Chronic Blood-Borne Viral Hepatitis and Treatment Outcomes in a Major Hospital in Al-Baha City: A Retrospective Cross-Sectional Study.

Chronic Blood-Borne Viral Hepatitis and Treatment Outcomes in a Major Hospital in Al-Baha City: A Retrospective Cross-Sectional Study. | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Chronic Blood-Borne Viral Hepatitis and Treatment Outcomes in a Major Hospital in Al-Baha City: A Retrospective Cross-Sectional Study. Talal A. Sallam, Rabei M. El-Badry, Turki Hamid Alkully, Hasan H. Alfahemi, and 3 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7767890/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 12 Jan, 2026 Read the published version in BMC Infectious Diseases → Version 1 posted 16 You are reading this latest preprint version Abstract Background In Al-Baha viral hepatitis in clinical settings has not been adequately investigated. This study examined chronic HBV and HCV infections and treatment outcomes among patients at King Fahd Hospital in Al-Baha. Methodology: Patients records were retrieved anonymously for clinical, demographic, virological and biochemical data from January 2019 and December 2022. Results A total of 148 patients infected with HBV and/or HCV attended during the 4-year study period. The mean age was 49.6 ± 13.2 (20–88 years); 84 (56.8%) males and 64 (43.2%) females. A total of 119 (80.4%) were infected with HBV, 27 (18.2%) with HCV while only 2 (1.4%) had dual HBV/HCV infection. Higher HBV viral loads correlated with higher ALT levels (r = 0.317, p = 0.001). Higher HCV viral loads did not associate with higher ALT levels (r = 0.246, p = 0.23). Of all cases 144 were clinically characterized and encompassed 117 chronic HBV, 25 chronic HCV, 1 acute HCV and 1 dual HBV/ HCV infection. Forty-seven (32.6%) were HBeAg-negative chronic infections, 69 (47.2%) were HBeAg- undesignated chronic infections. Cirrhosis was present in 6% of HBV cases and 18.5% of HCV cases. Through the course of HBV treatment, patients treated with tenofovir alafenamide (n = 15) achieved viral load suppression in 93.3%, with ALT either maintained or normalized in most cases. Treatment with entecavir (n = 8) also resulted in undetectable or markedly reduced viral load with generally unchanging ALT levels. All 16 HCV patients achieved viral clearance after 12 weeks treatment course; sofosbuvir–daclatasvir (n = 14) was highly effective though 2 showed elevated post-treatment ALT. Single patients on glecaprevir/pibrentasvir and elbasvir/grazoprevir also achieved viral clearance. Conclusions Chronic HBV and HCV infections remain clinical challenges. Viral load of HBV but not that of HCV correlated with ALT. Tenofovir alafenamide, entecavir, and sofosbuvir/daclatasvir showed strong efficacy, though limited follow-up and small sample sizes restrict conclusions. Overall, treatment responses merit further investigation. HBV HCV Chronic hepatitis Blood-borne viral hepatitis Al-Baha Saudi Arabia Background The threat of hepatitis B virus (HBV) and hepatitis C virus (HCV) remains enormous owing to the life-threatening complications that result from their infections. The WHO updated global estimate reveals that 254 million are living with HBV and 50 million with HCV, which together pose the second leading infectious cause of death with an annual death of 1.3 million of which 83% were due to HBV, and 17% due to HCV ( 1 ). Currently there is a protective vaccine against HBV while vaccine to HCV infection is unavailable ( 2 ). Even though direct-acting antiviral therapy (DAAs) to HCV infections can cure more than 95% of the infected individuals, access to diagnosis and subsequent treatment remains a challenge ( 3 ). In Saudi Arabia the mass immunization program initiated in 1990 has led to a dramatic decline in prevalence HBsAg( 4 – 6 ). As a result, in 2017, an overall prevalence of HBsAg of 1.7%, and of 0.1% among 5-year-olds and < 0.1% among infants have been reported( 7 ). However, an incidence of 490 cases of decompensated cirrhosis, 1500 cases of hepatocellular carcinoma (HCC) and 1,740 liver-related deaths due to HBV have been reported ( 7 ). Additionally, since 2006, the crude incidence rate of acute hepatitis B cases per 100,000 population has fluctuated, reaching 18.0 in 2021( 8 ). This undoubtedly suggests that HBV infection remains a significant health problem. Control of HCV in Saudi Arabia began in the early 1990s with the introduction of blood donor screening. In 2016, the estimated prevalence was approximately 0.7% overall and 0.5%, corresponding to roughly 100,000 individuals with active infection, the majority of whom remained untreated and therefore at risk of progression to cirrhosis and hepatocellular carcinoma (HCC) ( 9 ). A modeling study projected a continued increase in HCV-related cases of cirrhosis (both compensated and decompensated), HCC, and liver-related mortality in the coming years ( 10 ). Thus, despite progress in controlling HBV and HCV, as reflected by the decline in prevalence, a parallel reduction in morbidity and mortality associated with these infections has not yet been observed.( 6 , 7 ). To tackle the challenge of chronic HBV and HCV infection an accurate estimate of the magnitude of this health problem is needed. To achieve this the status of chronic viral hepatitis, need to be fully elucidated in all regions of the Saudi Arabia. Therefore, his study aims to investigate the examined chronic HBV and HCV infections and treatment outcomes at King Fahd Hospital in Al-Baha, thereby contributing to a more comprehensive national estimate of disease burden. Methods This retrospective cross-sectional study investigated chronic blood-borne viral hepatitis and treatment outcomes among patients who attended a major hospital In Al-Baha city. The study included all consecutive patients with HBV or HCV infection who attended King Fahd Hospital, Al-Baha, between January 2019 and December 2022 for assessment, follow-up, and treatment. King Fahd Hospital is designated as a tertiary care center by the Ministry of Health (MOH), with a capacity of over 400 beds, and serves as the main referral hospital for the seven governorates of the Al-Baha region. The Al-Baha region is located in the southwest of the Kingdom of Saudi Arabia, between the holy city of Makkah and the Aseer region. It has a population of 461,360 and covers an area of 10,362 square kilometers ( 11 ). The region consists of mountainous governorates, characterized by cold winters and mild summers, as well as lowland coastal governorates in Tehama, which experience mild winters and hot summers. Patient records were retrieved in anonymized form and reviewed for demographic, clinical, and laboratory data, including HBsAg, HBeAg, Anti-HBe, anti-HCV, HBV and HCV, viral load, and liver function tests. The study protocol was approved by the Ethics Research Committee (ERC) of the Faculty of Medicine, Al-Baha University, in accordance with the Declaration of Helsinki (approval number: REC/MIC/BU-FM/2022/63R). Access to patient records was granted with written authorization from King Fahd Hospital Whole blood samples were collected in a plain tube for serological testing and in an EDTA tube when plasma was required for nucleic acid testing. Serum or plasma were separated and tested immediately. All testing was performed according to the instructions of the manufacturer. HBsAg primary and confirmatory testing was performed using a commercial ELISA (DS-ELA-0.01 HBsAg, Diagnostic system, Germany), HBeAg and anti-HBe testing were accomplished using a commercial Monolisa HBe Ag-Ab PLUS ELISA (Bio-Rad, France),while primary anti-HCV testing was carried out using a commercial fourth generation (EIAgen HCV Ab (v.4), ADALTIS, Italy Y) and confirmatory testing was achieved using a third-generation immune assay INNO-LIA HCV Score (Fujirebia, Belgium) Levels of total and direct bilirubin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT) were measured using a quantitative enzymatic colorimetric assay (Beckman Coulter ALT Assay Kit, Beckman Coulter-Ireland Y). The HBV viral load was determined using a commercial real-time PCR-based assay (Abbott Real Time Viral Load Assay, Abbott, Germany Y). The assay is an in vitro real-time PCR for the quantification of hepatitis B virus DNA in human plasma or serum from HBV-infected individuals with 100% specificity and a limit of detection of 10 IU/mL for the 0.5mL sample preparation procedure. The HCV viral load was determined using a commercial real-time PCR-based assay (Abbott Real Time Viral Load Assay, Abbott, Germany Y). The assay is an in vitro reverse transcription polymerase chain reaction (RT-PCR) for the quantitation HCV-RNA in human plasma or serum from HCV-infected individuals. The assay has 100% specificity and a 30 IU/mL limit of detection for the 0.2mL sample preparation procedure. Both assays were performed according to the manufacturer's instructions. Data was coded, entered, and analyzed using IBM SPSS Statistics for Windows, Version 25.0 (IBM Corp., Armonk, NY, USA, 2017). Continuous variables were summarized as means with standard deviations using independent-samples t -tests, with p < 0.05 considered statistically significant. Categorical variables were expressed as absolute and relative frequencies. Associations between independent and dependent variables were evaluated using the chi -square test, with statistical significance defined as p < 0.05. Correlation analyses were conducted following logarithmic transformation of values to normalize distributions and reduce skewness. Results A total of 148 patients with HBV and/or HCV infection attended the hospital during the four-year study period, corresponding to a mean annual incidence of 37.5 cases. The patients mean age was 49.6 ± 13.2 years (range: 20–88), distributed across three age groups: 20–40, 41–60, and >60 years and included 84 males (56.8%) and 64 females (43.2%) (Table 1). Table 1: Demographic characteristics of patients with HBV and HCV infections Demographic characteristic n (%) Age groups 20-40 37 (25.0) 41-60 85 (57.4) > 60 26 (17.6) Sex Male 84 (56.8) Female 64 (43.2) Total 148 (100) Of all patients (n=148), 119 (80.4%) had HBV infection, 27 (18.2%) had HCV infection while 2 (1.4%) patients had dual HBV/HCV infections. The rate of infection differed, although insignificantly, between males and females with male: female ratios of 1.5:1 for HBV and 1.1: 1 for HCV (Table 2). Rates of infection with HBV and HCV among different age groups varied insignificantly with the highest HBV infection rate (84.7%) being among subjects aged 41-60 years while the highest HCV infection rate (27.8%) was among those aged 20-40 years (Table 2). Table 2: HBV and HCV infections among various age groups of males and females (n=148). HBV n (%) HCV n (%) p Age groups 20-40 26/36 (72.2) 10/36 (27.8) 0.20 41-60 72/85 (84.7) 13/85(15.3) > 60 19/26 (73.1) 7/ 26 (26.9) Sex Males 70/84 (83.3) 14/84 (16.7) 0.20 Females 47/63 (74.6) 16/63 (25.4) Total 117/147 (79.6) 30/147* (20.4) HBV infection was based on positivity HBsAg and HBV-DNA. *One patient was infected with both HBV and HCV. HBV infection was significantly more common than HCV among males across age groups (p = 0.02), with the highest prevalence in those aged 41–60 years (91.7%). Among females, however, no significant difference between HBV and HCV infection rates was observed (p = 0.32) (Table 3). Table 3. Infections with HBV versus infections of HCV among males and females of various age groups. Sex Age groups HBV HCV p Male 20-40 12/19 (63.2) 7/19 (36.8) 0.02 41-60 44/48 (91.7) 4/48 (8.3) >60 14/17 (82.4) 3/17 (17.6) Female 20-40 14/17 (82.4) 3/ 17 (17.6) 0.32 41-60 28/37 (75.7) 9/37 (24.3) >60 5/9 (55.6) 4/9 (44.4) With progress of age, HBV infection rates increased, albeit insignificantly (p>0.05) among males but decreased among females while HCV infection rates significantly decreased (p=0.02) among males and insignificantly ((>0.05) increased among females (Table 4). Table 4 . Rates of infections with HBV and HCV among males and females of various age groups. Virus Sex Age groups Infection rate p n (%) HBV Male 20-40 12/19 (63.2) 0.37 41-60 44/48 (91.7) >60 14/17 (82.4) Female 20-40 14/17 (82.4) 0.55 41-60 28/37 (75.7) >60 5/9 (55.6) HCV Male 20-40 7/19 (36.8) 0.02 41-60 4/48 (8.3) >60 3/17 (17.6) Female 20-40 3/ 17 (17.6) 0.26 41-60 9/37 (24.3) >60 4/9 (44.4) Of all patients, 111 (75.5%) had complete data of ALT, AST and HBV viral load. Among these, 28 (25.2%) exhibited elevated ALT levels with higher mean log 10 viral load, albeit insignificantly (p= 0.16), than those with normal ALT levels while patients with elevated AST levels had a significantly higher mean log 10 viral load ( p =0.001), than those with [99, (89.2%)] normal AST (Table 5). Additionally, 26 (92.3%) patients had complete ALT, AST and HCV viral load data. Of these 15 (57.7%) had elevated ALT with significantly ( p =0.03) higher log 10 viral load than those with normal ALT levels (n=11, 42.3%) while 16 (61.5%) exhibited abnormal AST levels had significantly ( p =0.003) higher log 10 viral load (Table 5). Table 5. Correlation between viral load and ALT/AST enzyme levels among HBV and HCV p atients Virus Liver enzyme No (%) Viral load range t p 95% CI Type Levels (IU/L) (IU/ml) Mean ± SD (Log 10 ) HBV (n=111) ALT ≤40 83 (74.7) 9.0 – 1,000,000,000 2.72 ± 1.25 1.4 0.16 -0.25, 1.44 >40 28 (25.2) 19- 561,141,163 3.32 ± 2.10 AST ≤40 99 (89.2) 10.0- 561,141,163 2.70 ± 1.28 3.7 40 12 (10.8) 20 - 561,141,163 4.32 ± 2.43 HCV (n=26) ALT ≤40 11 (42.3) 13,976-3,070,024 5.4±0.65 2.3 0.03 0.06- 1.12 >40 15 (57.7) 43,403-9,791,933 6.05±0.64 AST ≤40 10 (38.5) 13,976- 3,070,024 5.2±0.66 3.3 0.003 0.29- 1.28 >40 16 (61.5) 168,921-9,791,933 6.01±0.55 Correlation between viral load and the levels of ALT and AST were assessed using bivariate correlation analysis with logarithmic transformation of these values to normalize data distribution and to reduce skewness for more reliable statistical analysis. This has revealed higher HBV viral loads associated with higher ALT levels (r = 0.317, p = 0.001) and higher AST levels (r = 0.369, p < 0.001) (Table 6). Furthermore, higher HCV viral loads were not associated with higher ALT levels (r = 0.246, p = 0.23) but significantly associated with higher AST levels ( r = 0.473, p =0.02) (Table 6) Table 6: Correlation between Log 10 ALT and Log 10 viral load among patients with HBV and HCV infections. Log 10 viral load AST levels ALT levels HBV r 0.369 0.317 p 0.000 0.001 N 111 111 HCV r 0.473 0.246 p 0.02 0.23 N 26 26 Of all viral hepatitis patients (n=148), 144 were designated chronic infections, the majority of which were due to HBV rather than HCV. The predominant among these were HBeAg undesignated chronic HBV infection [69, (47.2%)] due to unknown HBeAg status, followed by 47 (32.6%) patients with HBeAg-negative chronic HBV infections (Table 7). Among these, 33 (70.2%) patients were HBeAg-negative/anti-HBe-positive with viral loads between <2,000 and <20,000 IU/ml, suggesting inactive HBV infection (Table 7). In addition, one patient had immune-tolerant chronic HBV infection, 7 (6.0%) patients had compensated cirrhosis; of these; 6 (85.7%) were male and 1 (14.3%) was a female (Table 7). Twenty-six of 27 patients were clinically characterized. of these 25 were designated chronic infection while 1 had acute infection. Of 25 had chronic infection 3 (11.1%), who were all females, had compensated cirrhosis and 2 (7.4%), 1 male and 1 female, presented with decompensated cirrhosis while 20 (80.0%) were noncirrhotic. Of the patients treated with tenofovir alafenamide (n = 15), 7 (46.7%) achieved undetectable HBV viral load, 7 (46.7%) had a >2 log10 reduction in post-treatment viral load, and 1 (6.7%) showed <1 log10 difference between pre- and post-treatment viral load. Normal ALT levels were observed both pre- and post-treatment in 8 patients (47.1%), while 5 patients (29.4%) had elevated ALT before treatment that normalized after treatment. Among the 8 HBV patients treated with entecavir, 4 (50.0%) achieved undetectable viral load with normalized ALT, 2 (25.0%) achieved undetectable viral load with ALT that was normal or only slightly elevated both pre- and post-treatment, and 2 (25.0%) had a 5 log10 reduction in viral load with ALT remaining normal pre- and post-treatment Of 16 chronic HCV patients treated, 14 received sofosbuvir–daclatasvir, 1 received glecaprevir/pibrentasvir, and 1 received elbasvir/grazoprevir. All patients treated with sofosbuvir–daclatasvir achieved undetectable viral load at the end of treatment; among them, 11 achieved normalizations of ALT, 1 had persistently normal ALT pre- and post-treatment, and 2 had higher ALT levels post-treatment than before treatment. The patient treated with glecaprevir/pibrentasvir achieved undetectable viral load with ALT remaining normal both pre- and post-treatment. The patient treated with elbasvir/grazoprevir also achieved undetectable viral load and had a normal pretreatment ALT level; however, post-treatment ALT data were not available. Sustained virological response data 12 weeks (SVR12) post treatment for HCV infected patients were not available. Table 7. Clinical characteristics of patients (n= 143) with HBV and HCV infections. Clinical characteristic No (%) HBeAg negative chronic HBV infection 47 (32.9%) Undesignated chronic HBV infections 69 (48.3%) Immune tolerant HBV infections 1 (0.7) Acute HCV 1 (0.7) Chronic HCV 25 (17.4) Discussion In Saudi Arabia HBV vaccine was included in EPI in 1989 ( 12 ) paralleled with a conjunct vaccination program for children at school entry, healthcare workers and hemodialysis patients initiated in 1990 ( 6 ). This led to a sharp reduction in HBsAg prevalence, with rates of 1.7% overall, 0.1% among 5-year-olds, and less than 0.1% among infants being reported.( 7 ). Additionally, the control program of HCV which was initiated almost 4 decades ago, have contributed to maintaining seroprevalence of as low as 0.4% to 1.7%( 13 ). Our findings have shown that 148 cases 119 HBV and 28 HCV infections and 1 case of dual HBV/HCV infection, have attended the major hospital in Al-Baha region seeking health care during the 4-year study period, accounting for an average of 37 (29.5 HBV vs 7.75 HCV) annual cases. This suggests that HBV and HCV infections remain a major challenge in Al-Baha region. Previously an average annual seropositivity incidence per 100,000 of 104.6 for HBV, and 78.4 for HCV ( 14 ) have been reported in other regions of Saudi Arabia. Additionally, an estimate of 70,000 to 80,000 cases of active HCV infections have been reported in 2016 with the majority that have not been treated ( 9 )and subsequently will go on to develop cirrhosis and HCC. Furthermore in 2017 an estimate of 574,000 HBV infections, an incidence of 490 cases of decompensated cirrhosis, 1500 cases of (HCC) and 1,740 liver-related deaths have been reported in Saudi Arabia( 7 ). Additionally, a modelling study has estimated an increase of HCV cases, HCC decompensated and compensated cirrhosis cases and liver-related deaths in the ensuing years( 9 ). A recent study reported that a total of 79,282 HBV cases with an overall 4,955 annual cases with a crude incidence rate (CIR) of HBV infections over the years from 2006 to 2021 have shown rates that fluctuated between 15.1/100,000 and 24.2/100,000, suggesting that HBV remains a challenge( 8 ). In Al-Baha region 960 HBV infected cases have been reported between the years 2006 and 2021 with mean annual cases of 60 and with an overall mean CIR of 14/100,000 ( 8 ). Taken together, these reports are in line with the findings of the current study that the HBV infection remains challenge despite the control efforts. However, this increase could reflect a recent development in epidemiological surveillance and the reporting system( 15 ) rather than factual increase in the number of cases. In the current study most, infections were due to HBV (79.1%) as compared to 20.3% HCV infections. This reflects the common type of blood-borne viral hepatitis in Saudi Arabia where incidence per 100, 000 has been previously reported to be 104.6 for HBV and 78.4 for HCV( 14 ). Likewise, global HBV infections are more common than those caused by HCV( 1 ). However, the relatively lower incidence of HCV infections is attributable to the elusive nature of its infection that tends to be mild with nonspecific symptoms ( 16 ) or in many cases asymptomatic ( 16 , 17 )and consequently many cases do not seek health care and as a result go undiagnosed. The current estimate is that 70,000 to 80,000 Saudi individuals with active HCV infection remain undiagnosed( 9 ). This can be a major challenge facing identification of infected cases and accordingly referring them for treatment to fulfil the WHO goal of Glob al Health Sector on Viral Hepatitis (GHSS), for HCV elimination by 2030( 18 ). In the current study, the HBV infection rate among the youngest age group (20–40 years) remains high (73%) despite the fact that this age group encompassed 20.7% patients who aged 20 to 35 years and these were born during the era of HBV vaccination and consequently were likely to have received the vaccine. However, these patients represent small minority of the total number of patients (6.1%) who may have remained susceptible due to perhaps missed vaccination opportunity as a result of low vaccination coverage or were vaccine non-responders. On the other hand, the highest HBV infection rate was among those aged 41–60 years while those aged > 60 have lower infection rate. However, the infection rates among these two groups despite variation still high and reflect the pre-vaccination era where most of the Saudi public of this age were unlikely to have been immune. Therefore, the small minority of patients in this study who were ≤ 35 years of age clearly suggest an impact of vaccination. The current study has shown that males: female HBV infection rate of 1.5:1 which is in line with 1.34:1 that has been previously reported ( 19 )although 2.5:1( 20 )3.8:1( 21 )have also been reported. Low HBV infection rates among females can be ascribed to the characteristic female immunological variation that gives rise to disparities in disease outcome( 19 ).The present study has shown rather an inverted male: female HCV ratio of 1:1.1 which is not in accordance with previous reports which suggesting male: female ratios of 1.6:1 to 1.3:1( 18 , 22 ). This could be recounted to the small HCV sample size as HCV infections are less common and consequently less frequently diagnosed. Infections with HBV among males aged 20 to 40 years were significantly ( p = 0.02) more common than HCV (65% vs 35%) indicating HBV as a more prevalent than HCV. Infection rates with HBV among males increased from 65% in those who aged 20–40 years to 89.8% in males who were 41–60 years old although slightly decreased to 82.4% in those aged > 60 years. This decrease may have been related to the small sample size of this latter age group. The high infection rate among old -aged males is likely to reflect the nature of the horizontal transmission of HBV among Saudi publics of this age in general given the fact that they were not vaccinated as they were borne before the era of vaccine. Additionally, during their early life over four decades ago less awareness of HBV infections existed, and males might have been exposed to occupational risk hazards involving percutaneous exposure. In contrast, in areas with high perinatal, mother-to-child transmission, HBV prevalence can be high even in younger age groups( 23 ). With progress of age the current study revealed a notably high HBV infection rates with decreasing trend, albeit insignificantly ( p = 0.55), among the youngest age group (20–40 years) of females. This trend is inverted in the case of HCV of which infection rates rather insignificantly ( p = 0.26) increased with progress of age, as compared to males where HCV infection rates peaked in the young 20–40 age group but dropped significantly (p = 0.02) in older age. This finding is inconsistent with previous reports which suggested that unlike males, females increasingly clear HCV infections ( 22 ) meaning that female infection rates decline with progress of age which is not the case in the current study. The female small size in the current study was likely to be decreed by the prevailing social norms which may have limited female presentation to health services and thus less women seek health care. Therefore, female infection rates warrant further investigation using a larger sample size. Patients with abnormal ALT levels tended to have higher HBV viral loads although this difference did not reach statistical significance ( p = 0.16). Additionally bivariate analysis has shown a significantly moderate positive correlation between ALT and viral load ( r = 0.317, p = 0.001). Given the limited sample size, the detected correlation may underrate the true association. It is likely that a stronger and statistically significant correlation would have been detected with a larger cohort. Correlation between ALT levels and HBV viral load has been previously reported among HBeAg positive and HBeAg negative chronic hepatitis B patients ( 24 – 28 ). This provides additional evidence that in chronic HBV infection, elevated viral load is closely associated with increased ALT levels, emphasizing the role of viral replication as a main contributor to liver inflammation and injury. The positive correlation between AST levels and viral load ( r = 0.369 p ≤ 0.001) in this study aligns with earlier findings in HBeAg-negative chronic hepatitis B patients( 24 ). Although AST has been previously linked to liver pathology, disease stage( 24 ), and severity of liver injury( 25 ), this is likely true here as well. However, further virological and clinical data are essential to substantiate this inference. HCV infected patients in the present study with higher ALT have shown significantly ( p = 0.03) higher mean log 10 viral load compared to those with normal ALT despite the lack of correlation with levels and log 10 viral load ( r = 0.246, p = 0.23) likely due to the lack of linear variation between ALT and viral loads. Although ALT is a marker of liver injury, it does not always correlate with viral load in HCV patients( 24 , 25 , 29 – 31 ). Some patients may have high viral loads but normal ALT levels due to a less efficient immune response, while others with stronger immune systems may show elevated ALT despite having lower viral loads. Additionally, viral load in this study reflects the viral level in blood rother than reflecting the viral status in the liver. On the other hand, patients in this study with abnormal AST levels had significantly ( p = 0.003) higher log 10 viral load associated with higher AST levels (r = 0.473, p = 0.02). Although a previous report has demonstrated absence of significant correlation of HCV viral load with ALT (r = 0.06) and AST(r = 0.004) ( 32 ) another report has demonstrated absence of correlation between HCV viral load and serum ALT level (r = 0.15) but a significant correlation with AST (r = 0.42)( 33 ). Studies vary in their evidence of ALT and AST association with viral load from weak to significant according to the viral genotype, stage of the diseases and individual immune status( 27 , 28 , 34 ),. Arriving to clear inferences on the significances ALT and AST our patients merit further investigation. Only 2 patients had dual HBV and HCV infections reflecting the rarity of dual infections due likely to the differences in mode of transmission of the two viruses in Saudi Arabia. In addition to common percutaneous route HBV and HCV infection, HBV can also be transmitted sexually and by close contact while HCV is merely blood and blood products associated. The predominance of HBV chronic viral hepatitis is likely to be related to the fact that HBV infections are more frequently diagnosed in Saudi Arabia than HCV. The low prevalence of HBeAg-positive HBV infections in our cohort, coupled with the more frequent occurrence of HBeAg-negative/anti-HBe–positive cases with viral loads between < 2,000 and < 20,000 IU/mL, is consistent with the profile commonly observed in the Saudi HBV-infected population( 35 , 36 ). This pattern is likely attributable to the predominance of HBV genotype D, which is associated with a lower rate of HBeAg positivity( 37 ). However, the 69 patients with unknown HBeAg status may undermine this inference. Therefore, for the common chronic HBV infection profiles in our region merits further investigation. In the present study the proportions of cirrhotic patients due to chronic HBV (6.0%) were far less than that caused by chronic HCV (18.5%) although one expects HBV to be more prevalent viral cause of cirrhosis given the more frequently diagnosed hepatitis B than hepatitis C in Saudi Arabia. Global pooled data, as well as findings from countries with high HBV endemicity, indicate that HBV infection is more common than HCV among cirrhotic patients( 38 ). In regions where HBV vaccination programs have successfully reduced HBV transmission, HCV infection rates have overtaken those of HBV( 38 ). This trend may be explained by the generally slower progression of chronic HBV compared to HCV. Supporting this, a large proportion of our HBV-infected cohort appeared to be inactive carriers, as most were HBeAg-negative/anti-HBe–positive with viral loads between < 2,000 and < 20,000 IU/mL. Nonetheless, the limited sample size in our study restricts definitive conclusions, underscoring the need for further research with a larger cohort. The two only patients with decompensated cirrhosis had HCV infection and none of the HBV infected patients had decompensated cirrhosis which more commonly develops among HCV patients. The annual of hepatic decompensation rates were around 5.6% per year for HCV-related cirrhosis and about 3.2% per year HBV-related cirrhosis( 39 ). This necessitates treatment of chronic HCV-infected patients to reduce the risk of progression to liver decompensation. Direct acting antiviral therapy was associated with 62% lower incidence of HCV- associated decompensated cirrhosis ( 40 ). Despite the small number (n = 7) of patients with HBV cirrhosis, 6 (85.7%) were males. This is in accordance with previous reports of male sex as a risk for cirrhosis( 20 , 21 ). Of the cohort with chronic HBV, treated with tenofovir/alafenamide (n = 15), the undetectable viral load in almost half of the patients and its significant decline in another half of them along with normal ALT levels either maintained from baseline or normalized during therapy, suggest tenofovir/alafenamide therapy was associated with high rates of virologic suppression and ALT normalization. However, interpretation remains restricted by the absence of data on treatment duration and lack of follow-up to confirm sustained virological response. Tenofovir/alafenamide treatment of HBeAg-negative/HBeAg‐positive patients with chronic HBV infection have been reported for its high virological and biochemical response rates, with improvements in liver fibrosis. It also shows a favorable long‐term benefit–risk profile, with good renal safety and no evidence of resistance( 41 , 42 ). Future studies in our region are needed to confirm these outcomes ideally using larger sample sizes and more robust data on treatment duration and follow-up. Similarly, the undetectable viral load observed in 75% of patients treated with entecavir, along with a significant reduction in the remaining 25%, and the normalization or maintenance of normal ALT levels during therapy, support the regimen strong virologic suppression and ALT normalization effects. However, definitive conclusions about the response to entecavir in our cohort were limited by the absence of treatment duration and follow-up data. Previous studies have shown that prolonged entecavir therapy yielded excellent virologic responses( 43 , 44 ) in treatment-naive HBeAg-positive and -negative patients, with a very low incidence of resistance over a 7-year follow-up period ( 44 ). Given that both entecavir and tenofovir/alafenamide have high barriers to resistance, they are considered first-line options for long-term antiviral therapy [39]. Therefore, it is reasonable to expect favorable long-term treatment outcomes in our patient population. The undetectable viral load and the normal levels of ALT in 12 (85.7%) HCV infected patients after 12 weeks of treatment with sofosbuvir/ daclatasvir indicates high treatment efficacy although the lacking data on sustained virological response would have provided a clear conclusion. Previously reported treatment outcomes demonstrated sustained virologic response rates with sofosbuvir and daclatasvir of 90 to 98% of noncirrhotic and 84 to 92% for cirrhotic patients ( 45 – 48 ) in addition to > 90% of treatment naive ( 45 , 47 ) and as high as 87% of treatment experienced( 45 ). Since data on treatment with 2 glecaprevir/ pibrentasvir and elbasvir/grazoprevir were available from only one patient each, and both achieved undetectable viral loads with ALT levels remaining normal before and after therapy in one patient, the findings are not considered significant due to the very limited sample size. However, pangenotypic efficacy trials of glecaprevir/pibrentasvir have reported SVR12 of 98% after 8 weeks treatment and 99% after12 weeks treatment in non-cirrhotic patients ( 49 ). Eight -week treatment with glecaprevir/pibrentasvir have shown SVR12 83–94% for genotype 3 and 96–100% for the other genotypes [52]. The SVR12 rates were 97.9% and > 95% across cirrhosis status, genotypes, illicit drug use, alcohol consumption, and treatment experience ( 50 ). Grazoprevir–elbasvir achieved an overall 95 to 96% SVR12 rates in treatment-naive cirrhotic and noncirrhotic patients with genotype 1, 4, or 6 infections ( 26 , 51 ). This curative regimen along with the comparatively low HCV viraemia prevalence reported across the Kingdom makes elimination of HCV as a public health threat, by an achievable goal—through case finding, linkage to care, and early treatment—in line with the global targets set by the WHO. Conclusions Despite control programs, chronic HBV and HCV remain clinical challenges. Among Saudi HBV patients, HBeAg-negative/anti-HBe–positive cases were common. Chronic HBV infections peaked in ages 41–60 and HCV in ages 20–40. Levels of ALT correlated with HBV viral load, underlining viral replication as a key driver of liver injury, while no such correlation was observed for HCV. Tenofovir alafenamide and entecavir showed strong virologic suppression and ALT normalization, though data on treatment duration and follow-up were lacking. Sofosbuvir/daclatasvir also showed high efficacy, but absence of sustained response data limits conclusions. Small sample size of patients treated with tenofovir/alafenamide (n = 15), suggest tenofovir/alafenamide therapy was associated with high rates of virologic suppression and ALT normalization. However, interpretation remains restricted by the absence of data on treatment duration and lack of follow-up to confirm sustained virological response. Abbreviations - HBV : Hepatitis B virus - HCV : Hepatitis C virus - ALT: Alanine Aminotransferase - AST: Aspartate Aminotransferase - ALP: alkaline phosphatase - GGT: gamma-glutamyl transferase - HCC: Hepatocellular carcinoma - RES: Research Ethics Committee - EDTA: Ethylenediaminetetraacetic acid - ELISA: Enzyme linked immunosorbent assay - RT-PCR: reverse transcription polymerase chain reaction - SVR12: Sustained Virological Response at 12 weeks post completing antiviral therapy Declarations Ethical consideration and informed consent. The study protocol was approved by the Ethics Research Committee (ERC) of the Faculty of Medicine, Al-Baha University (Ethical approval number: REC/MIC//BU-FM/2022/63R). Data was obtained on written consent to the King Fahd Hospital, and no consent was required from participants as the study is retrospective. Consent for publication This manuscript does not contain any individual person’s data in any form either individual details, images or videos. Availability of data and materials Data sharing is not applicable to this article as no datasets were generated or analysed during the current study. Competing interests The authors declare that they have no competing interests. Funding The authors did not receive support from any organization for the submitted work. Authors contributions Concept and design: TAS, RME, Analysis and interpretation of data: TAS, RME. Drafting of the manuscript: TAS, HHA. Assistance in interpretation of results, formulation of methodology and critical review of the manuscript for important intellectual content: RME, THA, HHA, MAH, KIA, MAA Supervision: TAS, THA, RME. Actively engaged in the data collection process, ensuring comprehensive and accurate gathering of relevant patient information. All authors approved the final manuscript. Limitations of the study One important limitation of this study was the absence of comprehensive clinical, virological, histopathological, and treatment-related data, which could have provided deeper insight into the true burden of blood-borne viral hepatitis. The retrospective design also introduced potential selection bias. To establish clearer inferences regarding viral hepatitis in the region, a prospective cross-sectional study is warranted. Furthermore, the relatively small sample size, along with the limited number of patients with available data on clinical complications, restricts the strength of conclusions and highlights the need for larger cohorts that better represent different age groups. Finally, the small sample size and lack of sufficient treatment duration and follow-up data further limit definitive assessment of antiviral treatment responses. Acknowledgements The authors would like to express their sincere gratitude to the staff at the special chemistry section at the laboratory and blood bank department of King Fahd hospital in Al-Baha, Saudi Arabia for their unwavering support through the period of this study. References WHO sounds alarm on viral hepatitis infections. claiming 3500 lives each day [Internet]. [cited 2025 Aug 20]. Available from: https://www.who.int/news/item/09-04-2024-who-sounds-alarm-on-viral-hepatitis-infections-claiming-3500-lives-each-day Papatheodoridis G, Hatzakis A. Public health issues of hepatitis C virus infection. Best Pract Res Clin Gastroenterol. 2012;26(4):371–80. Hepatitis C. [Internet]. [cited 2025 Aug 20]. Available from: https://www.who.int/news-room/fact-sheets/detail/hepatitis-c Al-Faleh FZ, Al-Jeffri M, Ramia S, Al-Rashed R, Arif M, Rezeig M, et al. Seroepidemiology of hepatitis B virus infection in Saudi children 8 years after a mass hepatitis B vaccination programme. J Infect. 1999;38(3):167–70. Mohammed Abdullah S. Prevalence of hepatitis B and C in donated blood from the jazan region of saudi arabia. Malays J Med Sci MJMS. 2013;20(2):41–6. Abdo AA, Sanai FM, Al-Faleh FZ. Epidemiology of Viral Hepatitis in Saudi Arabia: Are We Off the Hook? Saudi J Gastroenterol Off J Saudi Gastroenterol Assoc. 2012;18(6):349–57. Sanai FM, Alghamdi M, Dugan E, Alalwan A, Al-Hamoudi W, Abaalkhail F, et al. A tool to measure the economic impact of Hepatitis B elimination: A case study in Saudi Arabia. J Infect Public Health. 2020;13(11):1715–23. Alghamdi IG, Alghamdi RM, Alghamdi MS, Alghamdi AM, Alghamdi MI, Alghamdi ZI, et al. Epidemiology of Hepatitis B in Saudi Arabia from 2006 to 2021. Hepatic Med Evid Res. 2023;15:233–47. Altraif I. Can hepatitis C virus be eliminated by 2030? Saudi Arabia as an example. Saudi Med J. 2018;39(8):842–5. Aljumah AA, Abaalkhail F, Al-Ashgar H, Assiri A, Babatin M, Al Faleh F, et al. Epidemiology, disease burden, and treatment strategies of chronic hepatitis C virus infections in Saudi Arabia in the new treatment paradigm shift. Saudi J Gastroenterol Off J Saudi Gastroenterol Assoc. 2016;22(4):269–81. Abdul Salam A, Elsegaey I, Khraif R, Al-Mutairi A. Population distribution and household conditions in Saudi Arabia: reflections from the 2010 Census. SpringerPlus. 2014;3:530. Al-Faleh FZ, Ayoola EA, Al-Jeffry M, Arif M, Al-Rashed RS, Ramia S. Integration of hepatitis B vaccine into the expanded program on immunization: The Saudi Arabian experience. Ann Saudi Med. 1993;13(3):231–6. Madani TA. Hepatitis C virus infections reported in Saudi Arabia over 11 years of surveillance. Ann Saudi Med. 2007;27(3):191–4. Memish ZA, Knawy BA, El-Saed A. Incidence trends of viral hepatitis A, B, and C seropositivity over eight years of surveillance in Saudi Arabia. Int J Infect Dis IJID Off Publ Int Soc Infect Dis. 2010;14(2):e115–120. Aljumah AA, Babatin M, Hashim A, Abaalkhail F, Bassil N, Safwat M, et al. Hepatitis B care pathway in Saudi Arabia: Current situation, gaps and actions. Saudi J Gastroenterol Off J Saudi Gastroenterol Assoc. 2019;25(2):73–80. Schillie S, CDC Recommendations for Hepatitis C Screening Among Adults — United States., 2020. MMWR Recomm Rep [Internet]. 2020 [cited 2025 Aug 20];69. Available from: https://www.cdc.gov/mmwr/volumes/69/rr/rr6902a1.htm McCaughan GW, McGuinness PH, Bishop GA, Painter DM, Lien AS, Tulloch R, et al. Clinical assessment and incidence of hepatitis C RNA in 50 consecutive RIBA-positive volunteer blood donors. Med J Aust. 1992;157(4):231–3. CGHE [Internet]. [cited 2025 Aug 20]. Global Health Sector Strategy on Viral Hepatitis: 2016–2021 Towards Ending Viral Hepatitis. Available from: https://www.globalhep.org/tools-resources/action-plans/global-health-sector-strategy-viral-hepatitis-2016-2021-towards-ending Brown R, Goulder P, Matthews PC. Sexual Dimorphism in Chronic Hepatitis B Virus (HBV) Infection: Evidence to Inform Elimination Efforts. Wellcome Open Res. 2022;7:32. Liu M, Li L, Zhao J, Ungvari GS, Ng CH, Duan Z, et al. Gender differences in demographic and clinical characteristics in patients with HBV-related liver diseases in China. PeerJ. 2022;10:e13828. Baig S. Gender disparity in infections of Hepatitis B virus. J Coll Physicians Surg–Pak JCPSP. 2009 Sept;19(9):598–600. Hepatitis C-. Annual Epidemiological Report for 2022 [Internet]. 2024 [cited 2025 Aug 20]. Available from: https://www.ecdc.europa.eu/en/publications-data/hepatitis-c-annual-epidemiological-report-2022 Kolou M, Katawa G, Salou M, Gozo-Akakpo KS, Dossim S, Kwarteng A, et al. High Prevalence of Hepatitis B Virus Infection in the Age Range of 20–39 Years Old Individuals in Lome. Open Virol J. 2017;11:1–7. Esmaeelzadeh A, Saadatnia H, Memar B, Mokhtari Amirmajdi E, Ganji A, Goshayeshi L, et al. Evaluation of serum HBV viral load, transaminases and histological features in chronic HBeAg-negative hepatitis B patients. Gastroenterol Hepatol Bed Bench. 2017;10(1):39–43. Hasanjani Roushan MR, Hajiahmadi M, Shafaie S. Histopathological features of liver and its relation to serum transaminase levels in 91 cases of anti-HBe-positive chronic hepatitis B. Int J Clin Pract. 2005 July;59(7):791–4. Zeuzem S, Ghalib R, Reddy KR, Pockros PJ, Ari ZB, Zhao Y, et al. Grazoprevir–Elbasvir Combination Therapy for Treatment-Naive Cirrhotic and Noncirrhotic Patients With Chronic Hepatitis C Virus Genotype 1, 4, or 6 Infection. Ann Intern Med. 2015 July;7(1):1–13. McCormick SE, Goodman ZD, Maydonovitch CL, Sjogren MH. Evaluation of liver histology, ALT elevation, and HCV RNA titer in patients with chronic hepatitis C. Am J Gastroenterol. 1996;91(8):1516–22. Lau JY, Davis GL, Kniffen J, Qian KP, Urdea MS, Chan CS et al. Significance of serum hepatitis C virus RNA levels in chronic hepatitis C. Lancet Lond Engl. 1993 June 12;341(8859):1501–4. Rabbi FJ, Rezwan MK, Shirin T. HBeAg/anti-HBe, alanine aminotransferase and HBV DNA levels in HBsAg positive chronic carriers. Bangladesh Med Res Counc Bull. 2008;34(2):39–43. Kim KH, Na IH, Cha JM, Cho YK, Park SY, Kim HP, et al. [Serum ALT and HBV DNA levels in patients with HBeAg-negative chronic hepatitis B]. Taehan Kan Hakhoe Chi Korean J Hepatol. 2003;9(4):284–92. Ljunggren KK, Nordenfelt E, Kidd A. Correlation of HBeAg/anti-HBe, ALT levels, and HBV DNA PCR results in HBsAg-positive patients. J Med Virol. 1993;39(4):297–302. Anand BS, Velez M. Assessment of correlation between serum titers of hepatitis c virus and severity of liver disease. World J Gastroenterol WJG. 2004;10(16):2409–11. Amjad S, Akram A, Iqbal M, Hussain M, Khan M. Analysis of ALT and AST levels in HCV infected patients. Zeuzem S, Franke A, Lee JH, Herrmann G, Ruster B, Roth WK. Phylogenetic analysis of hepatitis C virus isolates and their correlation to viremia, liver function tests, and histology. Hepatol Baltim Md. 1996;24(5):1003–9. Babair Y, Elsafi S, Ghamdi MA, Gezery ME. Frequency and Pattern of Chronic Hepatitis B Infection in the Eastern Region of Saudi Arabia: A Cross-sectional Study. Biosci Biotechnol Res Asia [Internet]. 2016 May 7 [cited 2025 Aug 20];9(2). Available from: https://www.biotech-asia.org/vol9no2/frequency-and-pattern-of-chronic-hepatitis-b-infection-in-the-eastern-region-of-saudi-arabia-a-cross-sectional-study/ Sallam TA, El-Bingawi HM, Alzahrani KI, Alzahrani BH, Alzahrani AA. Prevalence of hepatitis B and hepatitis C viral infections and impact of control program among blood donors in Al-Baha region, Saudi Arabia. Saudi J Health Sci. 2020;9(1):56. Asaad AM, Al-Ayed MSZ, Aleraky M, Qureshi MA. Hepatitis B virus genotyping in chronic hepatitis B patients in southwestern Saudi Arabia. Braz J Infect Dis. 2015 Sept 1;19(5):525–8. Alberts CJ, Clifford GM, Georges D, Negro F, Lesi OA, Hutin YJF, et al. Worldwide prevalence of hepatitis B virus and hepatitis C virus among patients with cirrhosis at country, region, and global levels: a systematic review. Lancet Gastroenterol Hepatol. 2022;7(8):724–35. Toshikuni N, Arisawa T, Tsutsumi M. Hepatitis C-related liver cirrhosis - strategies for the prevention of hepatic decompensation, hepatocarcinogenesis, and mortality. World J Gastroenterol WJG. 2014;20(11):2876–87. Park H, Wang W, Henry L, Nelson DR. Impact of All-Oral Direct‐Acting Antivirals on Clinical and Economic Outcomes in Patients With Chronic Hepatitis C in the United States. Hepatology. 2019;69(3):1032. Buti M, Lim Y, Chan HLY, Agarwal K, Marcellin P, Brunetto MR, et al. Eight-year efficacy and safety of tenofovir alafenamide for treatment of chronic hepatitis B virus infection: Final results from two randomised phase 3 trials. Aliment Pharmacol Ther. 2024;60(11–12):1573–86. Chan HLY, Buti M, Lim YS, Agarwal K, Marcellin P, Brunetto M, et al. Long-Term Treatment With Tenofovir Alafenamide for Chronic Hepatitis B Results in High Rates of Viral Suppression and Favorable Renal and Bone Safety. Am J Gastroenterol. 2024;119(3):486–96. Ridruejo E, Marciano S, Galdame O, Reggiardo MV, Muñoz AE, Adrover R, et al. Efficacy and safety of long term entecavir in chronic hepatitis B treatment naïve patients in clinical practice. Ann Hepatol. 2014;13(3):327–36. Lee HW, Kwon JC, Oh IS, Chang HY, Cha YJ, Choi IS, et al. Prolonged Entecavir Therapy Is Not Effective for HBeAg Seroconversion in Treatment-Naive Chronic Hepatitis B Patients with a Partial Virological Response. Antimicrob Agents Chemother. 2015 Sept;59(9):5348–56. Sulkowski MS, Gardiner DF, Rodriguez-Torres M, Reddy KR, Hassanein T, Jacobson I, et al. Daclatasvir plus Sofosbuvir for Previously Treated or Untreated Chronic HCV Infection. N Engl J Med. 2014;370(3):211–21. Shiha G, Soliman R, ElBasiony M, Hassan AA, Mikhail NNH. Sofosbuvir plus Daclatasvir with or without ribavirin for treatment of chronic HCV genotype 4 patients: real-life experience. Hepatol Int. 2018 July;12(4):339–47. Ahmed OA, Elsebaey MA, Fouad MHA, Elashry H, Elshafie AI, Elhadidy AA, et al. Outcomes and predictors of treatment response with sofosbuvir plus daclatasvir with or without ribavirin in Egyptian patients with genotype 4 hepatitis C virus infection. Infect Drug Resist. 2018;11:441–5. Farrag AN, Kamel AM. Efficacy of 8-week daclatasvir-sofosbuvir regimen in chronic hepatitis C: a systematic review and meta-analysis. Virol J. 2024;21:275. Puoti M, Foster GR, Wang S, Mutimer D, Gane E, Moreno C, et al. High SVR12 with 8-week and 12-week glecaprevir/pibrentasvir therapy: An integrated analysis of HCV genotype 1–6 patients without cirrhosis. J Hepatol. 2018;69(2):293–300. Real-World Effectiveness and Safety of Glecaprevir/Pibrentasvir for the Treatment of Chronic Hepatitis C. A Prospective Cohort Study in Portugal [Internet]. [cited 2025 Sept 9]. Available from: https://www.natap.org/2024/HCV/021324_01.htm?utm_source=chatgpt.com Asselah T, Reesink H, Gerstoft J, de Ledinghen V, Pockros PJ, Robertson M, et al. Efficacy of elbasvir and grazoprevir in participants with hepatitis C virus genotype 4 infection: A pooled analysis. Liver Int Off J Int Assoc Study Liver. 2018 Sept;38(9):1583–91. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Published Journal Publication published 12 Jan, 2026 Read the published version in BMC Infectious Diseases → Version 1 posted Editorial decision: Revision requested 07 Nov, 2025 Reviews received at journal 06 Nov, 2025 Reviewers agreed at journal 06 Nov, 2025 Reviewers agreed at journal 06 Nov, 2025 Reviewers agreed at journal 06 Nov, 2025 Reviewers agreed at journal 05 Nov, 2025 Reviews received at journal 05 Nov, 2025 Reviewers agreed at journal 05 Nov, 2025 Reviewers agreed at journal 05 Nov, 2025 Reviewers agreed at journal 04 Nov, 2025 Reviewers agreed at journal 04 Nov, 2025 Reviewers invited by journal 27 Oct, 2025 Editor invited by journal 07 Oct, 2025 Editor assigned by journal 05 Oct, 2025 Submission checks completed at journal 05 Oct, 2025 First submitted to journal 02 Oct, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7767890","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":540218691,"identity":"b7819cb8-3404-4d92-b278-9214c5da42b3","order_by":0,"name":"Talal A. Sallam","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAwUlEQVRIiWNgGAWjYHACxgMMDDYJIJYEUep5gBioJY10LYdJ0GLPf/jBgZ855/MMDjAfvM3DUCdP2BaJNIODvdtuFxscYEu25mE4bNhAWAuDwQHebbcTNxzgMZPmYTjASFgL//EPB/9uOwfUwv8NqKXOnrAWhhyDw7zbDoBsYQNqYU4krOVGTsFh2W3JxZKH2Ywt5xgcTiaohb3/+MaHb7fZ5fEdb354401FnS1BLQjADCIMiFc/CkbBKBgFowAPAADUbz02XAFN2gAAAABJRU5ErkJggg==","orcid":"","institution":"Department of Medical Microbiology, Faculty of Medicine, Al-Baha University","correspondingAuthor":true,"prefix":"","firstName":"Talal","middleName":"A.","lastName":"Sallam","suffix":""},{"id":540218693,"identity":"a104c929-9bf0-4501-907b-4d2c4d1c84b4","order_by":1,"name":"Rabei M. El-Badry","email":"","orcid":"","institution":"Department of Pathology, Faculty of Medicine, Al-Baha University, Al-Baha","correspondingAuthor":false,"prefix":"","firstName":"Rabei","middleName":"M.","lastName":"El-Badry","suffix":""},{"id":540218694,"identity":"62e4bee2-9a5c-426a-a8c0-e393d01203e7","order_by":2,"name":"Turki Hamid Alkully","email":"","orcid":"","institution":"Department of Internal Medicine, Faculty of Medicine, Al-Baha University","correspondingAuthor":false,"prefix":"","firstName":"Turki","middleName":"Hamid","lastName":"Alkully","suffix":""},{"id":540218698,"identity":"733e1f15-67ea-488a-9a22-5b2c98f4cc37","order_by":3,"name":"Hasan H. Alfahemi","email":"","orcid":"","institution":"Al-Baha University","correspondingAuthor":false,"prefix":"","firstName":"Hasan","middleName":"H.","lastName":"Alfahemi","suffix":""},{"id":540218699,"identity":"08e10aad-484c-4602-b171-8181fed6f176","order_by":4,"name":"Muhammad A. Halwani","email":"","orcid":"","institution":"Department of Medical Microbiology, Faculty of Medicine, Al-Baha University","correspondingAuthor":false,"prefix":"","firstName":"Muhammad","middleName":"A.","lastName":"Halwani","suffix":""},{"id":540218700,"identity":"5d225185-6438-461c-bb85-ad4b0d87b6ed","order_by":5,"name":"Khaled I. Alzahrani","email":"","orcid":"","institution":"Training and intern, Faculty of Medicine, Al-Baha University","correspondingAuthor":false,"prefix":"","firstName":"Khaled","middleName":"I.","lastName":"Alzahrani","suffix":""},{"id":540218701,"identity":"6b49f6f1-a8de-4f3a-b8e4-c0f3be00e5a3","order_by":6,"name":"Manal A. Alghamdi","email":"","orcid":"","institution":"Laboratory Department, King Fahd Hospital","correspondingAuthor":false,"prefix":"","firstName":"Manal","middleName":"A.","lastName":"Alghamdi","suffix":""}],"badges":[],"createdAt":"2025-10-02 16:08:17","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-7767890/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-7767890/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1186/s12879-025-12432-x","type":"published","date":"2026-01-12T16:29:54+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":95260317,"identity":"6f6241f8-e1cc-4f32-99dc-0aae49ba86d1","added_by":"auto","created_at":"2025-11-06 04:17:18","extension":"docx","order_by":0,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":148383,"visible":true,"origin":"","legend":"","description":"","filename":"ChronicbloodborneViralHepatitisandTreatmentOutcomesforBMC02102025.docx","url":"https://assets-eu.researchsquare.com/files/rs-7767890/v1/ee3a06c05a57540055ea46af.docx"},{"id":95260322,"identity":"74707f95-3d76-475b-91cc-8d5a7f4b5a7f","added_by":"auto","created_at":"2025-11-06 04:17:19","extension":"json","order_by":1,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":9077,"visible":true,"origin":"","legend":"","description":"","filename":"120c9b4771f2483f8a352d3f17df9729.json","url":"https://assets-eu.researchsquare.com/files/rs-7767890/v1/fe778ec2b42c85625780669f.json"},{"id":95312848,"identity":"aa8fae59-7248-40e5-8e6a-7f4ce859f1f5","added_by":"auto","created_at":"2025-11-06 15:50:25","extension":"xml","order_by":2,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":136862,"visible":true,"origin":"","legend":"","description":"","filename":"120c9b4771f2483f8a352d3f17df97291enriched.xml","url":"https://assets-eu.researchsquare.com/files/rs-7767890/v1/45cbcacfb615a64014e3c1e1.xml"},{"id":95260321,"identity":"cd5ffac4-554c-41c2-8b3c-19fb5e51b975","added_by":"auto","created_at":"2025-11-06 04:17:19","extension":"xml","order_by":3,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":137056,"visible":true,"origin":"","legend":"","description":"","filename":"120c9b4771f2483f8a352d3f17df97291structuring.xml","url":"https://assets-eu.researchsquare.com/files/rs-7767890/v1/59b1881c1e3f5cca415f9f42.xml"},{"id":95260318,"identity":"3c733ec1-92cf-4b0f-9f26-a29f3bdf275b","added_by":"auto","created_at":"2025-11-06 04:17:19","extension":"html","order_by":4,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":146702,"visible":true,"origin":"","legend":"","description":"","filename":"earlyproof.html","url":"https://assets-eu.researchsquare.com/files/rs-7767890/v1/c3251e88364cbb4308b1e866.html"},{"id":100614770,"identity":"debd2894-4bcb-42fa-9760-845721e4627a","added_by":"auto","created_at":"2026-01-19 17:24:33","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1039105,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7767890/v1/3a104d8d-bf18-45cb-b860-24bc16674df5.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Chronic Blood-Borne Viral Hepatitis and Treatment Outcomes in a Major Hospital in Al-Baha City: A Retrospective Cross-Sectional Study.","fulltext":[{"header":"Background","content":"\u003cp\u003eThe threat of hepatitis B virus (HBV) and hepatitis C virus (HCV) remains enormous owing to the life-threatening complications that result from their infections. The WHO updated global estimate reveals that 254\u0026nbsp;million are living with HBV and 50\u0026nbsp;million with HCV, which together pose the second leading infectious cause of death with an annual death of 1.3\u0026nbsp;million of which 83% were due to HBV, and 17% due to HCV (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). Currently there is a protective vaccine against HBV while vaccine to HCV infection is unavailable (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). Even though direct-acting antiviral therapy (DAAs) to HCV infections can cure more than 95% of the infected individuals, access to diagnosis and subsequent treatment remains a challenge (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eIn Saudi Arabia the mass immunization program initiated in 1990 has led to a dramatic decline in prevalence HBsAg(\u003cspan additionalcitationids=\"CR5\" citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e). As a result, in 2017, an overall prevalence of HBsAg of 1.7%, and of 0.1% among 5-year-olds and \u0026lt;\u0026thinsp;0.1% among infants have been reported(\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). However, an incidence of 490 cases of decompensated cirrhosis, 1500 cases of hepatocellular carcinoma (HCC) and 1,740 liver-related deaths due to HBV have been reported (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). Additionally, since 2006, the crude incidence rate of acute hepatitis B cases per 100,000 population has fluctuated, reaching 18.0 in 2021(\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e). This undoubtedly suggests that HBV infection remains a significant health problem.\u003c/p\u003e\u003cp\u003eControl of HCV in Saudi Arabia began in the early 1990s with the introduction of blood donor screening. In 2016, the estimated prevalence was approximately 0.7% overall and 0.5%, corresponding to roughly 100,000 individuals with active infection, the majority of whom remained untreated and therefore at risk of progression to cirrhosis and hepatocellular carcinoma (HCC) (\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). A modeling study projected a continued increase in HCV-related cases of cirrhosis (both compensated and decompensated), HCC, and liver-related mortality in the coming years (\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). Thus, despite progress in controlling HBV and HCV, as reflected by the decline in prevalence, a parallel reduction in morbidity and mortality associated with these infections has not yet been observed.(\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eTo tackle the challenge of chronic HBV and HCV infection an accurate estimate of the magnitude of this health problem is needed. To achieve this the status of chronic viral hepatitis, need to be fully elucidated in all regions of the Saudi Arabia. Therefore, his study aims to investigate the examined chronic HBV and HCV infections and treatment outcomes at King Fahd Hospital in Al-Baha, thereby contributing to a more comprehensive national estimate of disease burden.\u003c/p\u003e"},{"header":"Methods","content":"\u003cp\u003eThis retrospective cross-sectional study investigated chronic blood-borne viral hepatitis and treatment outcomes among patients who attended a major hospital In Al-Baha city. The study included all consecutive patients with HBV or HCV infection who attended King Fahd Hospital, Al-Baha, between January 2019 and December 2022 for assessment, follow-up, and treatment. King Fahd Hospital is designated as a tertiary care center by the Ministry of Health (MOH), with a capacity of over 400 beds, and serves as the main referral hospital for the seven governorates of the Al-Baha region. The Al-Baha region is located in the southwest of the Kingdom of Saudi Arabia, between the holy city of Makkah and the Aseer region. It has a population of 461,360 and covers an area of 10,362 square kilometers (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e). The region consists of mountainous governorates, characterized by cold winters and mild summers, as well as lowland coastal governorates in Tehama, which experience mild winters and hot summers.\u003c/p\u003e\u003cp\u003ePatient records were retrieved in anonymized form and reviewed for demographic, clinical, and laboratory data, including HBsAg, HBeAg, Anti-HBe, anti-HCV, HBV and HCV, viral load, and liver function tests. The study protocol was approved by the Ethics Research Committee (ERC) of the Faculty of Medicine, Al-Baha University, in accordance with the Declaration of Helsinki (approval number: REC/MIC/BU-FM/2022/63R). Access to patient records was granted with written authorization from King Fahd Hospital\u003c/p\u003e\u003cp\u003eWhole blood samples were collected in a plain tube for serological testing and in an EDTA tube when plasma was required for nucleic acid testing. Serum or plasma were separated and tested immediately. All testing was performed according to the instructions of the manufacturer.\u003c/p\u003e\u003cp\u003eHBsAg primary and confirmatory testing was performed using a commercial ELISA (DS-ELA-0.01 HBsAg, Diagnostic system, Germany), HBeAg and anti-HBe testing were accomplished using a commercial Monolisa HBe Ag-Ab PLUS ELISA (Bio-Rad, France),while primary anti-HCV testing was carried out using a commercial fourth generation (EIAgen HCV Ab (v.4), ADALTIS, Italy Y) and confirmatory testing was achieved using a third-generation immune assay \u003cem\u003eINNO-LIA HCV Score (Fujirebia, Belgium)\u003c/em\u003e\u003c/p\u003e\u003cp\u003eLevels of total and direct bilirubin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT) were measured using a quantitative enzymatic colorimetric assay (Beckman Coulter ALT Assay Kit, Beckman Coulter-Ireland Y).\u003c/p\u003e\u003cp\u003eThe HBV viral load was determined using a commercial real-time PCR-based assay (Abbott Real Time Viral Load Assay, Abbott, Germany Y). The assay is an in vitro real-time PCR for the quantification of hepatitis B virus DNA in human plasma or serum from HBV-infected individuals with 100% specificity and a limit of detection of 10 IU/mL for the 0.5mL sample preparation procedure.\u003c/p\u003e\u003cp\u003eThe HCV viral load was determined using a commercial real-time PCR-based assay (Abbott Real Time Viral Load Assay, Abbott, Germany Y). The assay is an in vitro reverse transcription polymerase chain reaction (RT-PCR) for the quantitation HCV-RNA in human plasma or serum from HCV-infected individuals. The assay has 100% specificity and a 30 IU/mL limit of detection for the 0.2mL sample preparation procedure. Both assays were performed according to the manufacturer's instructions.\u003c/p\u003e\u003cp\u003eData was coded, entered, and analyzed using IBM SPSS Statistics for Windows, Version 25.0 (IBM Corp., Armonk, NY, USA, 2017). Continuous variables were summarized as means with standard deviations using independent-samples \u003cem\u003et\u003c/em\u003e-tests, with p\u0026thinsp;\u0026lt;\u0026thinsp;0.05 considered statistically significant. Categorical variables were expressed as absolute and relative frequencies. Associations between independent and dependent variables were evaluated using the \u003cem\u003echi\u003c/em\u003e-square test, with statistical significance defined as \u003cem\u003ep\u003c/em\u003e\u0026thinsp;\u0026lt;\u0026thinsp;0.05. Correlation analyses were conducted following logarithmic transformation of values to normalize distributions and reduce skewness.\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003eA total of 148 patients with HBV and/or HCV infection attended the hospital during the four-year study period, corresponding to a mean annual incidence of 37.5 cases. The patients mean age was 49.6 \u0026plusmn; 13.2 years (range: 20\u0026ndash;88), distributed across three age groups: 20\u0026ndash;40, 41\u0026ndash;60, and \u0026gt;60 years and included 84 males (56.8%) and 64 females (43.2%) (Table 1).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 1: Demographic characteristics of patients with HBV and HCV infections\u003c/strong\u003e\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" align=\"\" width=\"457\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 174px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eDemographic characteristic\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 100px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 183px;\"\u003e\n \u003cp\u003en \u0026nbsp; (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 174px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAge groups\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 100px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e20-40\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 183px;\"\u003e\n \u003cp\u003e37 (25.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 100px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e41-60\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 183px;\"\u003e\n \u003cp\u003e85 (57.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 100px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026gt; 60\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 183px;\"\u003e\n \u003cp\u003e26 (17.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 174px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eSex\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 100px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMale\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 183px;\"\u003e\n \u003cp\u003e84 (56.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 100px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eFemale\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 183px;\"\u003e\n \u003cp\u003e64 (43.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 100px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eTotal\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 183px;\"\u003e\n \u003cp\u003e148 (100)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eOf all patients (n=148), 119 (80.4%) had HBV infection, 27 (18.2%) had HCV infection while 2 (1.4%) patients had dual HBV/HCV infections. The rate of infection differed, although insignificantly, between males and females with male: female ratios of 1.5:1 for HBV and 1.1: 1 for HCV (Table 2). \u0026nbsp;Rates of infection with HBV and HCV among different age groups varied insignificantly with the highest HBV infection rate (84.7%) being among subjects aged 41-60 years while the highest HCV infection rate (27.8%) was among those aged 20-40 years (Table 2).\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 2: HBV and HCV infections among various age groups of males and females (n=148).\u003c/strong\u003e\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" align=\"\" width=\"543\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e\u0026nbsp;\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 74px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e\u0026nbsp;\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 154px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eHBV \u0026nbsp; \u0026nbsp; \u0026nbsp;n (%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 150px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eHCV \u0026nbsp;n (%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 72px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003ep\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAge groups\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 74px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e20-40\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 154px;\"\u003e\n \u003cp\u003e26/36 (72.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 150px;\"\u003e\n \u003cp\u003e10/36 (27.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 72px;\"\u003e\n \u003cp\u003e0.20\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 74px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e41-60\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 154px;\"\u003e\n \u003cp\u003e72/85 (84.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 150px;\"\u003e\n \u003cp\u003e13/85(15.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 74px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026gt; 60\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 154px;\"\u003e\n \u003cp\u003e19/26 (73.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 150px;\"\u003e\n \u003cp\u003e7/ 26 (26.9)\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eSex\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 74px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMales\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 154px;\"\u003e\n \u003cp\u003e70/84 (83.3)\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 150px;\"\u003e\n \u003cp\u003e14/84 (16.7)\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 72px;\"\u003e\n \u003cp\u003e0.20\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 74px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eFemales\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 154px;\"\u003e\n \u003cp\u003e47/63 (74.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 150px;\"\u003e\n \u003cp\u003e16/63 (25.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 94px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eTotal\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 74px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 154px;\"\u003e\n \u003cp\u003e117/147 (79.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 150px;\"\u003e\n \u003cp\u003e30/147* (20.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 72px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cem\u003eHBV infection was based on positivity HBsAg and HBV-DNA. *One patient was infected with both HBV and HCV.\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eHBV infection was significantly more common than HCV among males across age groups (p = 0.02), with the highest prevalence in those aged 41\u0026ndash;60 years (91.7%). Among females, however, no significant difference between HBV and HCV infection rates was observed (p = 0.32) (Table 3).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 3. Infections with HBV versus infections of HCV among males and females of various age groups.\u003c/strong\u003e\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" align=\"\" width=\"510\"\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 89px;\"\u003e\n \u003cp\u003eSex\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 89px;\"\u003e\n \u003cp\u003eAge groups\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" style=\"width: 122px;\"\u003e\n \u003cp\u003eHBV\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" style=\"width: 132px;\"\u003e\n \u003cp\u003eHCV\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 89px;\"\u003e\n \u003cp\u003eMale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 89px;\"\u003e\n \u003cp\u003e20-40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 122px;\"\u003e\n \u003cp\u003e12/19 (63.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 132px;\"\u003e\n \u003cp\u003e7/19 (36.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e0.02\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 89px;\"\u003e\n \u003cp\u003e41-60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 122px;\"\u003e\n \u003cp\u003e44/48 (91.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 132px;\"\u003e\n \u003cp\u003e4/48 (8.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 89px;\"\u003e\n \u003cp\u003e\u0026gt;60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 122px;\"\u003e\n \u003cp\u003e14/17 (82.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 132px;\"\u003e\n \u003cp\u003e3/17 (17.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 89px;\"\u003e\n \u003cp\u003eFemale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 89px;\"\u003e\n \u003cp\u003e20-40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 122px;\"\u003e\n \u003cp\u003e14/17 (82.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 132px;\"\u003e\n \u003cp\u003e3/ 17 (17.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e0.32\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 89px;\"\u003e\n \u003cp\u003e41-60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 122px;\"\u003e\n \u003cp\u003e28/37 (75.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 132px;\"\u003e\n \u003cp\u003e9/37 (24.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 89px;\"\u003e\n \u003cp\u003e\u0026gt;60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 122px;\"\u003e\n \u003cp\u003e5/9 (55.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 132px;\"\u003e\n \u003cp\u003e4/9 (44.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n\u003c/table\u003e\n\u003cp\u003eWith progress of age, HBV infection rates increased, albeit insignificantly (p\u0026gt;0.05) among males but decreased among females while HCV infection rates significantly decreased (p=0.02) among males and insignificantly ((\u0026gt;0.05) increased among females (Table 4).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003e\u003cspan dir=\"RTL\"\u003e4\u003c/span\u003e\u003c/strong\u003e\u003cstrong\u003e.\u003c/strong\u003e Rates of infections with HBV and HCV among males and females of various age groups.\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" align=\"\" width=\"444\"\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 48px;\"\u003e\n \u003cp\u003eVirus\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003eSex\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003eAge groups\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" style=\"width: 126px;\"\u003e\n \u003cp\u003eInfection rate\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"bottom\" style=\"width: 126px;\"\u003e\n \u003cp\u003en \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; (%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"6\" valign=\"top\" style=\"width: 48px;\"\u003e\n \u003cp\u003eHBV\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003eMale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e20-40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e12/19 (63.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e0.37\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e41-60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e44/48 (91.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e\u0026gt;60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e14/17 (82.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003eFemale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e20-40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e14/17 (82.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e0.55\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e41-60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e28/37 (75.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e\u0026gt;60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e5/9 (55.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"6\" valign=\"top\" style=\"width: 48px;\"\u003e\n \u003cp\u003eHCV\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003eMale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e20-40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e7/19 (36.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e0.02\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e41-60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e4/48 (8.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e\u0026gt;60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e3/17 (17.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003eFemale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e20-40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e3/ 17 (17.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 54px;\"\u003e\n \u003cp\u003e0.26\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e41-60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e9/37 (24.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 108px;\"\u003e\n \u003cp\u003e\u0026gt;60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 126px;\"\u003e\n \u003cp\u003e4/9 (44.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n\u003c/table\u003e\n\u003cp\u003eOf all patients, 111 (75.5%) had complete data of ALT, AST and HBV viral load. Among these, 28 (25.2%) exhibited elevated ALT levels with higher mean log\u003csub\u003e10\u003c/sub\u003e viral load, albeit insignificantly (p= 0.16), than those with normal ALT levels while patients with elevated AST levels had a significantly higher mean log\u003csub\u003e10\u003c/sub\u003e viral load (\u003cem\u003ep\u003c/em\u003e=0.001), than those with [99, (89.2%)] normal AST (Table 5). Additionally, 26 (92.3%) patients had complete ALT, AST and HCV viral load data. Of these 15 (57.7%) had elevated ALT with significantly (\u003cem\u003ep\u003c/em\u003e=0.03) higher log\u003csub\u003e10\u003c/sub\u003e viral load than those with normal ALT levels (n=11, 42.3%) while 16 (61.5%) exhibited abnormal AST levels had significantly (\u003cem\u003ep\u003c/em\u003e=0.003) higher log\u003csub\u003e10\u003c/sub\u003e viral load (Table 5).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 5. Correlation between viral load and ALT/AST enzyme levels among HBV and HCV\u003c/strong\u003e\u003cstrong\u003e\u0026nbsp;p\u003c/strong\u003e\u003cstrong\u003eatients\u003c/strong\u003e\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" align=\"\" width=\"767\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 67px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eVirus\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" valign=\"top\" style=\"width: 131px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eLiver enzyme\u003c/strong\u003e\u003c/p\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNo \u0026nbsp; (%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd colspan=\"2\" valign=\"top\" style=\"width: 282px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eViral load range\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 48px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003et\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u003cem\u003ep\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e95% CI\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 67px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 65px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eType\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eLevels (IU/L)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e(IU/ml)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMean \u0026plusmn; SD (Log\u003csub\u003e10\u003c/sub\u003e)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"4\" valign=\"top\" style=\"width: 67px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eHBV (n=111)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 65px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; ALT \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026le;40 \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e83 (74.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e9.0 \u0026ndash; 1,000,000,000\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e2.72 \u003cstrong\u003e\u0026plusmn;\u0026nbsp;\u003c/strong\u003e1.25\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 48px;\"\u003e\n \u003cp\u003e1.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e0.16\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e-0.25, 1.44\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026gt;40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e28 (25.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e19- 561,141,163\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e3.32\u003cstrong\u003e\u0026plusmn;\u0026nbsp;\u003c/strong\u003e2.10\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 65px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAST\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026le;40 \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e99 (89.2)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e10.0- 561,141,163\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e2.70\u003cstrong\u003e\u0026plusmn;\u003c/strong\u003e1.28\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 48px;\"\u003e\n \u003cp\u003e3.7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e\u0026lt;0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e0.07\u0026ndash;3.18)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026gt;40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e12 (10.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e20 - 561,141,163\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e4.32\u003cstrong\u003e\u0026plusmn;\u003c/strong\u003e2.43\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"4\" valign=\"top\" style=\"width: 67px;\"\u003e\n \u003cp\u003eHCV\u003c/p\u003e\n \u003cp\u003e\u003cstrong\u003e(n=26)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 65px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eALT\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026le;40 \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e11 (42.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e13,976-3,070,024\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e5.4\u0026plusmn;0.65\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 48px;\"\u003e\n \u003cp\u003e2.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e0.03\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e0.06- \u0026nbsp; \u0026nbsp;1.12\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026gt;40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e15 (57.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e43,403-9,791,933\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e6.05\u0026plusmn;0.64\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 65px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAST\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026le;40 \u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e10 (38.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e13,976- 3,070,024\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e5.2\u0026plusmn;0.66\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 48px;\"\u003e\n \u003cp\u003e3.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 60px;\"\u003e\n \u003cp\u003e0.003\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd rowspan=\"2\" valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e0.29- \u0026nbsp; \u0026nbsp;1.28\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 66px;\"\u003e\n \u003cp\u003e\u0026gt;40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 78px;\"\u003e\n \u003cp\u003e16 (61.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e168,921-9,791,933\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e6.01\u0026plusmn;0.55\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eCorrelation between viral load and the levels of ALT and AST were assessed using bivariate correlation analysis with logarithmic transformation of these values to normalize data distribution and to reduce skewness for more reliable statistical analysis. This has revealed higher HBV viral loads associated with higher ALT levels (r = 0.317, \u003cem\u003ep\u003c/em\u003e = 0.001) and higher AST levels (r = 0.369, \u003cem\u003ep\u003c/em\u003e \u0026lt; 0.001) (Table 6). Furthermore, higher HCV viral loads were not associated with higher ALT levels (r = 0.246, p = 0.23) but significantly associated with higher AST levels (\u003cem\u003er\u003c/em\u003e = 0.473, p =0.02) (Table 6)\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 6: Correlation between Log\u003csub\u003e10\u003c/sub\u003e ALT and Log\u003csub\u003e10\u003c/sub\u003e viral load among patients with HBV and HCV infections.\u003c/strong\u003e\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"504\"\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003eLog\u003csub\u003e10\u0026nbsp;\u003c/sub\u003eviral load\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" style=\"width: 102px;\"\u003e\n \u003cp\u003eAST levels\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" style=\"width: 138px;\"\u003e\n \u003cp\u003eALT levels\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003eHBV\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e\u003cem\u003er\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 102px;\"\u003e\n \u003cp\u003e0.369\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 138px;\"\u003e\n \u003cp\u003e0.317\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 102px;\"\u003e\n \u003cp\u003e0.000\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 138px;\"\u003e\n \u003cp\u003e0.001\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eN\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 102px;\"\u003e\n \u003cp\u003e111\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 138px;\"\u003e\n \u003cp\u003e111\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"3\" valign=\"top\" style=\"width: 120px;\"\u003e\n \u003cp\u003eHCV\u0026nbsp;\u003c/p\u003e\n \u003cp\u003e\u0026nbsp;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e\u003cem\u003er\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e0.473\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e0.246\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003e\u003cem\u003ep\u003c/em\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e0.02\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e0.23\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 144px;\"\u003e\n \u003cp\u003eN\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 102px;\"\u003e\n \u003cp\u003e26\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 138px;\"\u003e\n \u003cp\u003e26\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n\u003c/table\u003e\n\u003cp\u003eOf all viral hepatitis patients (n=148), 144 were designated chronic infections, the majority of which were due to HBV rather than HCV. The predominant among these were HBeAg undesignated chronic HBV infection [69, (47.2%)] due to unknown HBeAg status, followed by 47 (32.6%) patients with HBeAg-negative chronic HBV infections (Table 7). Among these, 33 (70.2%) patients were HBeAg-negative/anti-HBe-positive with viral loads between \u0026lt;2,000 and \u0026lt;20,000 IU/ml, suggesting inactive HBV infection (Table 7). In addition, one patient had immune-tolerant chronic HBV infection, 7 (6.0%) patients had compensated cirrhosis; of these; 6 (85.7%) were male and 1 (14.3%) was a female (Table 7).\u003c/p\u003e\n\u003cp\u003eTwenty-six of 27 patients were clinically characterized. of these 25 were designated chronic infection while 1 had acute infection. Of 25 had chronic infection 3 (11.1%), who were all females, had compensated cirrhosis and 2 (7.4%), 1 male and 1 female, presented with decompensated cirrhosis while 20 (80.0%) were noncirrhotic.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eOf the patients treated with tenofovir alafenamide (n = 15), 7 (46.7%) achieved undetectable HBV viral load, 7 (46.7%) had a \u0026gt;2 log10 reduction in post-treatment viral load, and 1 (6.7%) showed \u0026lt;1 log10 difference between pre- and post-treatment viral load. Normal ALT levels were observed both pre- and post-treatment in 8 patients (47.1%), while 5 patients (29.4%) had elevated ALT before treatment that normalized after treatment.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eAmong the 8 HBV patients treated with entecavir, 4 (50.0%) achieved undetectable viral load with normalized ALT, 2 (25.0%) achieved undetectable viral load with ALT that was normal or only slightly elevated both pre- and post-treatment, and 2 (25.0%) had a 5 log10 reduction in viral load with ALT remaining normal pre- and post-treatment\u003c/p\u003e\n\u003cp\u003eOf 16 chronic HCV patients treated, 14 received sofosbuvir\u0026ndash;daclatasvir, 1 received glecaprevir/pibrentasvir, and 1 received elbasvir/grazoprevir. All patients treated with sofosbuvir\u0026ndash;daclatasvir achieved undetectable viral load at the end of treatment; among them, 11 achieved normalizations of ALT, 1 had persistently normal ALT pre- and post-treatment, and 2 had higher ALT levels post-treatment than before treatment. The patient treated with glecaprevir/pibrentasvir achieved undetectable viral load with ALT remaining normal both pre- and post-treatment. The patient treated with elbasvir/grazoprevir also achieved undetectable viral load and had a normal pretreatment ALT level; however, post-treatment ALT data were not available. Sustained virological response data 12 weeks (SVR12) post treatment for HCV infected patients were not available.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 7. Clinical characteristics of patients (n=\u003c/strong\u003e\u003cstrong\u003e143)\u003c/strong\u003e \u003cstrong\u003ewith HBV and HCV infections.\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"0\" cellpadding=\"0\" width=\"456\"\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 300px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eClinical characteristic\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"bottom\" style=\"width: 156px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eNo (%)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 300px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eHBeAg negative chronic HBV infection\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 156px;\"\u003e\n \u003cp\u003e47 (32.9%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 300px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eUndesignated\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003echronic HBV infections\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 156px;\"\u003e\n \u003cp\u003e69 (48.3%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 300px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eImmune tolerant HBV infections\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 156px;\"\u003e\n \u003cp\u003e1 (0.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 300px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAcute HCV\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 156px;\"\u003e\n \u003cp\u003e1 (0.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 300px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eChronic HCV\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 156px;\"\u003e\n \u003cp\u003e25 (17.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n\u003c/table\u003e"},{"header":"Discussion","content":"\u003cp\u003eIn Saudi Arabia HBV vaccine was included in EPI in 1989 (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e) paralleled with a conjunct vaccination program for children at school entry, healthcare workers and hemodialysis patients initiated in 1990 (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e). This led to a sharp reduction in HBsAg prevalence, with rates of 1.7% overall, 0.1% among 5-year-olds, and less than 0.1% among infants being reported.(\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). Additionally, the control program of HCV which was initiated almost 4 decades ago, have contributed to maintaining seroprevalence of as low as 0.4% to 1.7%(\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). Our findings have shown that 148 cases 119 HBV and 28 HCV infections and 1 case of dual HBV/HCV infection, have attended the major hospital in Al-Baha region seeking health care during the 4-year study period, accounting for an average of 37 (29.5 HBV vs 7.75 HCV) annual cases. This suggests that HBV and HCV infections remain a major challenge in Al-Baha region. Previously an average annual seropositivity incidence per 100,000 of 104.6 for HBV, and 78.4 for HCV (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e) have been reported in other regions of Saudi Arabia. Additionally, an estimate of 70,000 to 80,000 cases of active HCV infections have been reported in 2016 with the majority that have not been treated (\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e)and subsequently will go on to develop cirrhosis and HCC. Furthermore in 2017 an estimate of 574,000 HBV infections, an incidence of 490 cases of decompensated cirrhosis, 1500 cases of (HCC) and 1,740 liver-related deaths have been reported in Saudi Arabia(\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). Additionally, a modelling study has estimated an increase of HCV cases, HCC decompensated and compensated cirrhosis cases and liver-related deaths in the ensuing years(\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). A recent study reported that a total of 79,282 HBV cases with an overall 4,955 annual cases with a crude incidence rate (CIR) of HBV infections over the years from 2006 to 2021 have shown rates that fluctuated between 15.1/100,000 and 24.2/100,000, suggesting that HBV remains a challenge(\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e). In Al-Baha region 960 HBV infected cases have been reported between the years 2006 and 2021 with mean annual cases of 60 and with an overall mean CIR of 14/100,000 (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e). Taken together, these reports are in line with the findings of the current study that the HBV infection remains challenge despite the control efforts. However, this increase could reflect a recent development in epidemiological surveillance and the reporting system(\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e) rather than factual increase in the number of cases.\u003c/p\u003e\u003cp\u003eIn the current study most, infections were due to HBV (79.1%) as compared to 20.3% HCV infections. This reflects the common type of blood-borne viral hepatitis in Saudi Arabia where incidence per 100, 000 has been previously reported to be 104.6 for HBV and 78.4 for HCV(\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). Likewise, global HBV infections are more common than those caused by HCV(\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). However, the relatively lower incidence of HCV infections is attributable to the elusive nature of its infection that tends to be mild with nonspecific symptoms (\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e) or in many cases asymptomatic (\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e, \u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e)and consequently many cases do not seek health care and as a result go undiagnosed. The current estimate is that 70,000 to 80,000 Saudi individuals with active HCV infection remain undiagnosed(\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). This can be a major challenge facing identification of infected cases and accordingly referring them for treatment to fulfil the WHO goal of Glob al Health Sector on Viral Hepatitis (GHSS), for HCV elimination by 2030(\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eIn the current study, the HBV infection rate among the youngest age group (20\u0026ndash;40 years) remains high (73%) despite the fact that this age group encompassed 20.7% patients who aged 20 to 35 years and these were born during the era of HBV vaccination and consequently were likely to have received the vaccine. However, these patients represent small minority of the total number of patients (6.1%) who may have remained susceptible due to perhaps missed vaccination opportunity as a result of low vaccination coverage or were vaccine non-responders. On the other hand, the highest HBV infection rate was among those aged 41\u0026ndash;60 years while those aged\u0026thinsp;\u0026gt;\u0026thinsp;60 have lower infection rate. However, the infection rates among these two groups despite variation still high and reflect the pre-vaccination era where most of the Saudi public of this age were unlikely to have been immune. Therefore, the small minority of patients in this study who were \u0026le;\u0026thinsp;35 years of age clearly suggest an impact of vaccination.\u003c/p\u003e\u003cp\u003eThe current study has shown that males: female HBV infection rate of 1.5:1 which is in line with 1.34:1 that has been previously reported (\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e)although 2.5:1(\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e)3.8:1(\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e)have also been reported. Low HBV infection rates among females can be ascribed to the characteristic female immunological variation that gives rise to disparities in disease outcome(\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e).The present study has shown rather an inverted male: female HCV ratio of 1:1.1 which is not in accordance with previous reports which suggesting male: female ratios of 1.6:1 to 1.3:1(\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e, \u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e). This could be recounted to the small HCV sample size as HCV infections are less common and consequently less frequently diagnosed.\u003c/p\u003e\u003cp\u003eInfections with HBV among males aged 20 to 40 years were significantly (\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.02) more common than HCV (65% vs 35%) indicating HBV as a more prevalent than HCV. Infection rates with HBV among males increased from 65% in those who aged 20\u0026ndash;40 years to 89.8% in males who were 41\u0026ndash;60 years old although slightly decreased to 82.4% in those aged\u0026thinsp;\u0026gt;\u0026thinsp;60 years. This decrease may have been related to the small sample size of this latter age group. The high infection rate among old -aged males is likely to reflect the nature of the horizontal transmission of HBV among Saudi publics of this age in general given the fact that they were not vaccinated as they were borne before the era of vaccine. Additionally, during their early life over four decades ago less awareness of HBV infections existed, and males might have been exposed to occupational risk hazards involving percutaneous exposure. In contrast, in areas with high perinatal, mother-to-child transmission, HBV prevalence can be high even in younger age groups(\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eWith progress of age the current study revealed a notably high HBV infection rates with decreasing trend, albeit insignificantly (\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.55), among the youngest age group (20\u0026ndash;40 years) of females. This trend is inverted in the case of HCV of which infection rates rather insignificantly (\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.26) increased with progress of age, as compared to males where HCV infection rates peaked in the young 20\u0026ndash;40 age group but dropped significantly (p\u0026thinsp;=\u0026thinsp;0.02) in older age. This finding is inconsistent with previous reports which suggested that unlike males, females increasingly clear HCV infections (\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e) meaning that female infection rates decline with progress of age which is not the case in the current study. The female small size in the current study was likely to be decreed by the prevailing social norms which may have limited female presentation to health services and thus less women seek health care. Therefore, female infection rates warrant further investigation using a larger sample size.\u003c/p\u003e\u003cp\u003ePatients with abnormal ALT levels tended to have higher HBV viral loads although this difference did not reach statistical significance (\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.16). Additionally bivariate analysis has shown a significantly moderate positive correlation between ALT and viral load (\u003cem\u003er\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.317, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.001). Given the limited sample size, the detected correlation may underrate the true association. It is likely that a stronger and statistically significant correlation would have been detected with a larger cohort. Correlation between ALT levels and HBV viral load has been previously reported among HBeAg positive and HBeAg negative chronic hepatitis B patients (\u003cspan additionalcitationids=\"CR25 CR26 CR27\" citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e). This provides additional evidence that in chronic HBV infection, elevated viral load is closely associated with increased ALT levels, emphasizing the role of viral replication as a main contributor to liver inflammation and injury. The positive correlation between AST levels and viral load (\u003cem\u003er\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.369 \u003cem\u003ep\u003c/em\u003e\u0026thinsp;\u0026le;\u0026thinsp;0.001) in this study aligns with earlier findings in HBeAg-negative chronic hepatitis B patients(\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e). Although AST has been previously linked to liver pathology, disease stage(\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e), and severity of liver injury(\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e), this is likely true here as well. However, further virological and clinical data are essential to substantiate this inference.\u003c/p\u003e\u003cp\u003eHCV infected patients in the present study with higher ALT have shown significantly (\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.03) higher mean log\u003csub\u003e10\u003c/sub\u003e viral load compared to those with normal ALT despite the lack of correlation with levels and log\u003csub\u003e10\u003c/sub\u003e viral load (\u003cem\u003er\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.246, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.23) likely due to the lack of linear variation between ALT and viral loads. Although ALT is a marker of liver injury, it does not always correlate with viral load in HCV patients(\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e, \u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e, \u003cspan additionalcitationids=\"CR30\" citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e). Some patients may have high viral loads but normal ALT levels due to a less efficient immune response, while others with stronger immune systems may show elevated ALT despite having lower viral loads. Additionally, viral load in this study reflects the viral level in blood rother than reflecting the viral status in the liver. On the other hand, patients in this study with abnormal AST levels had significantly (\u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.003) higher log\u003csub\u003e10\u003c/sub\u003e viral load associated with higher AST levels (r\u0026thinsp;=\u0026thinsp;0.473, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.02). Although a previous report has demonstrated absence of significant correlation of HCV viral load with ALT (r\u0026thinsp;=\u0026thinsp;0.06) and AST(r\u0026thinsp;=\u0026thinsp;0.004) (\u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e) another report has demonstrated absence of correlation between HCV viral load and serum ALT level (r\u0026thinsp;=\u0026thinsp;0.15) but a significant correlation with AST (r\u0026thinsp;=\u0026thinsp;0.42)(\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e). Studies vary in their evidence of ALT and AST association with viral load from weak to significant according to the viral genotype, stage of the diseases and individual immune status(\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e, \u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e, \u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e),. Arriving to clear inferences on the significances ALT and AST our patients merit further investigation.\u003c/p\u003e\u003cp\u003eOnly 2 patients had dual HBV and HCV infections reflecting the rarity of dual infections due likely to the differences in mode of transmission of the two viruses in Saudi Arabia. In addition to common percutaneous route HBV and HCV infection, HBV can also be transmitted sexually and by close contact while HCV is merely blood and blood products associated.\u003c/p\u003e\u003cp\u003eThe predominance of HBV chronic viral hepatitis is likely to be related to the fact that HBV infections are more frequently diagnosed in Saudi Arabia than HCV. The low prevalence of HBeAg-positive HBV infections in our cohort, coupled with the more frequent occurrence of HBeAg-negative/anti-HBe\u0026ndash;positive cases with viral loads between \u0026lt;\u0026thinsp;2,000 and \u0026lt;\u0026thinsp;20,000 IU/mL, is consistent with the profile commonly observed in the Saudi HBV-infected population(\u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e, \u003cspan citationid=\"CR36\" class=\"CitationRef\"\u003e36\u003c/span\u003e). This pattern is likely attributable to the predominance of HBV genotype D, which is associated with a lower rate of HBeAg positivity(\u003cspan citationid=\"CR37\" class=\"CitationRef\"\u003e37\u003c/span\u003e). However, the 69 patients with unknown HBeAg status may undermine this inference. Therefore, for the common chronic HBV infection profiles in our region merits further investigation.\u003c/p\u003e\u003cp\u003eIn the present study the proportions of cirrhotic patients due to chronic HBV (6.0%) were far less than that caused by chronic HCV (18.5%) although one expects HBV to be more prevalent viral cause of cirrhosis given the more frequently diagnosed hepatitis B than hepatitis C in Saudi Arabia. Global pooled data, as well as findings from countries with high HBV endemicity, indicate that HBV infection is more common than HCV among cirrhotic patients(\u003cspan citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e). In regions where HBV vaccination programs have successfully reduced HBV transmission, HCV infection rates have overtaken those of HBV(\u003cspan citationid=\"CR38\" class=\"CitationRef\"\u003e38\u003c/span\u003e). This trend may be explained by the generally slower progression of chronic HBV compared to HCV. Supporting this, a large proportion of our HBV-infected cohort appeared to be inactive carriers, as most were HBeAg-negative/anti-HBe\u0026ndash;positive with viral loads between \u0026lt;\u0026thinsp;2,000 and \u0026lt;\u0026thinsp;20,000 IU/mL. Nonetheless, the limited sample size in our study restricts definitive conclusions, underscoring the need for further research with a larger cohort. The two only patients with decompensated cirrhosis had HCV infection and none of the HBV infected patients had decompensated cirrhosis which more commonly develops among HCV patients. The annual of hepatic decompensation rates were around 5.6% per year for HCV-related cirrhosis and about 3.2% per year HBV-related cirrhosis(\u003cspan citationid=\"CR39\" class=\"CitationRef\"\u003e39\u003c/span\u003e). This necessitates treatment of chronic HCV-infected patients to reduce the risk of progression to liver decompensation. Direct acting antiviral therapy was associated with 62% lower incidence of HCV- associated decompensated cirrhosis (\u003cspan citationid=\"CR40\" class=\"CitationRef\"\u003e40\u003c/span\u003e). Despite the small number (n\u0026thinsp;=\u0026thinsp;7) of patients with HBV cirrhosis, 6 (85.7%) were males. This is in accordance with previous reports of male sex as a risk for cirrhosis(\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e, \u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eOf the cohort with chronic HBV, treated with tenofovir/alafenamide (n\u0026thinsp;=\u0026thinsp;15), the undetectable viral load in almost half of the patients and its significant decline in another half of them along with normal ALT levels either maintained from baseline or normalized during therapy, suggest tenofovir/alafenamide therapy was associated with high rates of virologic suppression and ALT normalization. However, interpretation remains restricted by the absence of data on treatment duration and lack of follow-up to confirm sustained virological response. Tenofovir/alafenamide treatment of HBeAg-negative/HBeAg‐positive patients with chronic HBV infection have been reported for its high virological and biochemical response rates, with improvements in liver fibrosis. It also shows a favorable long‐term benefit\u0026ndash;risk profile, with good renal safety and no evidence of resistance(\u003cspan citationid=\"CR41\" class=\"CitationRef\"\u003e41\u003c/span\u003e, \u003cspan citationid=\"CR42\" class=\"CitationRef\"\u003e42\u003c/span\u003e). Future studies in our region are needed to confirm these outcomes ideally using larger sample sizes and more robust data on treatment duration and follow-up.\u003c/p\u003e\u003cp\u003eSimilarly, the undetectable viral load observed in 75% of patients treated with entecavir, along with a significant reduction in the remaining 25%, and the normalization or maintenance of normal ALT levels during therapy, support the regimen strong virologic suppression and ALT normalization effects. However, definitive conclusions about the response to entecavir in our cohort were limited by the absence of treatment duration and follow-up data. Previous studies have shown that prolonged entecavir therapy yielded excellent virologic responses(\u003cspan citationid=\"CR43\" class=\"CitationRef\"\u003e43\u003c/span\u003e, \u003cspan citationid=\"CR44\" class=\"CitationRef\"\u003e44\u003c/span\u003e) in treatment-naive HBeAg-positive and -negative patients, with a very low incidence of resistance over a 7-year follow-up period (\u003cspan citationid=\"CR44\" class=\"CitationRef\"\u003e44\u003c/span\u003e). Given that both entecavir and tenofovir/alafenamide have high barriers to resistance, they are considered first-line options for long-term antiviral therapy [39]. Therefore, it is reasonable to expect favorable long-term treatment outcomes in our patient population.\u003c/p\u003e\u003cp\u003eThe undetectable viral load and the normal levels of ALT in 12 (85.7%) HCV infected patients after 12 weeks of treatment with sofosbuvir/ daclatasvir indicates high treatment efficacy although the lacking data on sustained virological response would have provided a clear conclusion. Previously reported treatment outcomes demonstrated sustained virologic response rates with sofosbuvir and daclatasvir of 90 to 98% of noncirrhotic and 84 to 92% for cirrhotic patients (\u003cspan additionalcitationids=\"CR46 CR47\" citationid=\"CR45\" class=\"CitationRef\"\u003e45\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR48\" class=\"CitationRef\"\u003e48\u003c/span\u003e) in addition to \u0026gt;\u0026thinsp;90% of treatment naive (\u003cspan citationid=\"CR45\" class=\"CitationRef\"\u003e45\u003c/span\u003e, \u003cspan citationid=\"CR47\" class=\"CitationRef\"\u003e47\u003c/span\u003e) and as high as 87% of treatment experienced(\u003cspan citationid=\"CR45\" class=\"CitationRef\"\u003e45\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eSince data on treatment with 2 glecaprevir/ pibrentasvir and elbasvir/grazoprevir were available from only one patient each, and both achieved undetectable viral loads with ALT levels remaining normal before and after therapy in one patient, the findings are not considered significant due to the very limited sample size. However, pangenotypic efficacy trials of glecaprevir/pibrentasvir\u003c/p\u003e\u003cp\u003ehave reported SVR12 of 98% after 8 weeks treatment and 99% after12 weeks treatment in non-cirrhotic patients (\u003cspan citationid=\"CR49\" class=\"CitationRef\"\u003e49\u003c/span\u003e). Eight -week treatment with glecaprevir/pibrentasvir have shown SVR12 83\u0026ndash;94% for genotype 3 and 96\u0026ndash;100% for the other genotypes [52]. The SVR12 rates were 97.9% and \u0026gt;\u0026thinsp;95% across cirrhosis status, genotypes, illicit drug use, alcohol consumption, and treatment experience (\u003cspan citationid=\"CR50\" class=\"CitationRef\"\u003e50\u003c/span\u003e). Grazoprevir\u0026ndash;elbasvir achieved an overall 95 to 96% SVR12 rates in treatment-naive cirrhotic and noncirrhotic patients with genotype 1, 4, or 6 infections (\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e, \u003cspan citationid=\"CR51\" class=\"CitationRef\"\u003e51\u003c/span\u003e). This curative regimen along with the comparatively low HCV viraemia prevalence reported across the Kingdom makes elimination of HCV as a public health threat, by an achievable goal\u0026mdash;through case finding, linkage to care, and early treatment\u0026mdash;in line with the global targets set by the WHO.\u003c/p\u003e"},{"header":"Conclusions","content":"\u003cp\u003eDespite control programs, chronic HBV and HCV remain clinical challenges. Among Saudi HBV patients, HBeAg-negative/anti-HBe\u0026ndash;positive cases were common. Chronic HBV infections peaked in ages 41\u0026ndash;60 and HCV in ages 20\u0026ndash;40. Levels of ALT correlated with HBV viral load, underlining viral replication as a key driver of liver injury, while no such correlation was observed for HCV. Tenofovir alafenamide and entecavir showed strong virologic suppression and ALT normalization, though data on treatment duration and follow-up were lacking. Sofosbuvir/daclatasvir also showed high efficacy, but absence of sustained response data limits conclusions. Small sample size of patients treated with tenofovir/alafenamide (n\u0026thinsp;=\u0026thinsp;15), suggest tenofovir/alafenamide therapy was associated with high rates of virologic suppression and ALT normalization. However, interpretation remains restricted by the absence of data on treatment duration and lack of follow-up to confirm sustained virological response.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003e-\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;HBV : Hepatitis B virus\u003c/p\u003e\n\u003cp\u003e-\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;HCV : Hepatitis C virus\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e-\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;ALT: Alanine Aminotransferase\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e-\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;AST: Aspartate Aminotransferase\u003c/p\u003e\n\u003cp\u003e-\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;ALP: alkaline phosphatase\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e-\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;GGT: gamma-glutamyl transferase\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e-\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;HCC: Hepatocellular carcinoma\u003c/p\u003e\n\u003cp\u003e-\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;RES: Research Ethics Committee\u003c/p\u003e\n\u003cp\u003e-\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;EDTA: Ethylenediaminetetraacetic acid\u003c/p\u003e\n\u003cp\u003e-\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;ELISA: Enzyme linked immunosorbent assay\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e-\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;RT-PCR: reverse transcription polymerase chain reaction\u003c/p\u003e\n\u003cp\u003e- \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; SVR12: Sustained Virological Response at 12 weeks post completing antiviral therapy \u0026nbsp;\u0026nbsp;\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthical consideration and informed consent.\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe study protocol was approved by the Ethics Research Committee (ERC) of the Faculty of Medicine, Al-Baha University (Ethical approval number:\u0026nbsp;REC/MIC//BU-FM/2022/63R). Data was obtained on written consent to the King Fahd Hospital, and no consent was required from participants as the study is retrospective.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis manuscript does not contain any individual person’s data in any form either individual details, images or videos.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eData sharing is not applicable to this article as no datasets were generated or analysed during the current study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors did not receive support from any organization for the submitted work.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eConcept and design: TAS, RME,\u0026nbsp;Analysis and interpretation of data: TAS, RME. Drafting of the manuscript: TAS, HHA.\u0026nbsp;Assistance in interpretation of results, formulation of methodology and critical review of the manuscript for important intellectual content: RME, THA, HHA, MAH, KIA, MAA Supervision: TAS, THA,\u0026nbsp;RME. Actively engaged in the data collection process, ensuring comprehensive and accurate gathering of relevant patient information. All authors approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eLimitations of the study\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOne important limitation of this study was the absence of comprehensive clinical, virological, histopathological, and treatment-related data, which could have provided deeper insight into the true burden of blood-borne viral hepatitis. The retrospective design also introduced potential selection bias. To establish clearer inferences regarding viral hepatitis in the region, a prospective cross-sectional study is warranted. Furthermore, the relatively small sample size, along with the limited number of patients with available data on clinical complications, restricts the strength of conclusions and highlights the need for larger cohorts that better represent different age groups. Finally, the small sample size and lack of sufficient treatment duration and follow-up data further limit definitive assessment of antiviral treatment responses.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors would like to express their sincere gratitude to the staff at the special chemistry section at the laboratory and blood bank department of King Fahd hospital in Al-Baha, Saudi Arabia for their unwavering support through the period of this study. \u0026nbsp;\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eWHO sounds alarm on viral hepatitis infections. claiming 3500 lives each day [Internet]. [cited 2025 Aug 20]. Available from: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.who.int/news/item/09-04-2024-who-sounds-alarm-on-viral-hepatitis-infections-claiming-3500-lives-each-day\u003c/span\u003e\u003cspan address=\"https://www.who.int/news/item/09-04-2024-who-sounds-alarm-on-viral-hepatitis-infections-claiming-3500-lives-each-day\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003ePapatheodoridis G, Hatzakis A. Public health issues of hepatitis C virus infection. Best Pract Res Clin Gastroenterol. 2012;26(4):371\u0026ndash;80.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eHepatitis C. [Internet]. [cited 2025 Aug 20]. Available from: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.who.int/news-room/fact-sheets/detail/hepatitis-c\u003c/span\u003e\u003cspan address=\"https://www.who.int/news-room/fact-sheets/detail/hepatitis-c\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAl-Faleh FZ, Al-Jeffri M, Ramia S, Al-Rashed R, Arif M, Rezeig M, et al. Seroepidemiology of hepatitis B virus infection in Saudi children 8 years after a mass hepatitis B vaccination programme. J Infect. 1999;38(3):167\u0026ndash;70.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMohammed Abdullah S. Prevalence of hepatitis B and C in donated blood from the jazan region of saudi arabia. Malays J Med Sci MJMS. 2013;20(2):41\u0026ndash;6.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAbdo AA, Sanai FM, Al-Faleh FZ. Epidemiology of Viral Hepatitis in Saudi Arabia: Are We Off the Hook? Saudi J Gastroenterol Off J Saudi Gastroenterol Assoc. 2012;18(6):349\u0026ndash;57.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eSanai FM, Alghamdi M, Dugan E, Alalwan A, Al-Hamoudi W, Abaalkhail F, et al. A tool to measure the economic impact of Hepatitis B elimination: A case study in Saudi Arabia. J Infect Public Health. 2020;13(11):1715\u0026ndash;23.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAlghamdi IG, Alghamdi RM, Alghamdi MS, Alghamdi AM, Alghamdi MI, Alghamdi ZI, et al. Epidemiology of Hepatitis B in Saudi Arabia from 2006 to 2021. Hepatic Med Evid Res. 2023;15:233\u0026ndash;47.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAltraif I. Can hepatitis C virus be eliminated by 2030? Saudi Arabia as an example. Saudi Med J. 2018;39(8):842\u0026ndash;5.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAljumah AA, Abaalkhail F, Al-Ashgar H, Assiri A, Babatin M, Al Faleh F, et al. Epidemiology, disease burden, and treatment strategies of chronic hepatitis C virus infections in Saudi Arabia in the new treatment paradigm shift. Saudi J Gastroenterol Off J Saudi Gastroenterol Assoc. 2016;22(4):269\u0026ndash;81.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAbdul Salam A, Elsegaey I, Khraif R, Al-Mutairi A. Population distribution and household conditions in Saudi Arabia: reflections from the 2010 Census. SpringerPlus. 2014;3:530.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAl-Faleh FZ, Ayoola EA, Al-Jeffry M, Arif M, Al-Rashed RS, Ramia S. Integration of hepatitis B vaccine into the expanded program on immunization: The Saudi Arabian experience. Ann Saudi Med. 1993;13(3):231\u0026ndash;6.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMadani TA. Hepatitis C virus infections reported in Saudi Arabia over 11 years of surveillance. Ann Saudi Med. 2007;27(3):191\u0026ndash;4.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMemish ZA, Knawy BA, El-Saed A. Incidence trends of viral hepatitis A, B, and C seropositivity over eight years of surveillance in Saudi Arabia. Int J Infect Dis IJID Off Publ Int Soc Infect Dis. 2010;14(2):e115\u0026ndash;120.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAljumah AA, Babatin M, Hashim A, Abaalkhail F, Bassil N, Safwat M, et al. Hepatitis B care pathway in Saudi Arabia: Current situation, gaps and actions. Saudi J Gastroenterol Off J Saudi Gastroenterol Assoc. 2019;25(2):73\u0026ndash;80.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eSchillie S, CDC Recommendations for Hepatitis C Screening Among Adults \u0026mdash; United States., 2020. MMWR Recomm Rep [Internet]. 2020 [cited 2025 Aug 20];69. Available from: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.cdc.gov/mmwr/volumes/69/rr/rr6902a1.htm\u003c/span\u003e\u003cspan address=\"https://www.cdc.gov/mmwr/volumes/69/rr/rr6902a1.htm\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMcCaughan GW, McGuinness PH, Bishop GA, Painter DM, Lien AS, Tulloch R, et al. Clinical assessment and incidence of hepatitis C RNA in 50 consecutive RIBA-positive volunteer blood donors. Med J Aust. 1992;157(4):231\u0026ndash;3.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eCGHE [Internet]. [cited 2025 Aug 20]. Global Health Sector Strategy on Viral Hepatitis: 2016\u0026ndash;2021 Towards Ending Viral Hepatitis. Available from: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.globalhep.org/tools-resources/action-plans/global-health-sector-strategy-viral-hepatitis-2016-2021-towards-ending\u003c/span\u003e\u003cspan address=\"https://www.globalhep.org/tools-resources/action-plans/global-health-sector-strategy-viral-hepatitis-2016-2021-towards-ending\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBrown R, Goulder P, Matthews PC. Sexual Dimorphism in Chronic Hepatitis B Virus (HBV) Infection: Evidence to Inform Elimination Efforts. Wellcome Open Res. 2022;7:32.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eLiu M, Li L, Zhao J, Ungvari GS, Ng CH, Duan Z, et al. Gender differences in demographic and clinical characteristics in patients with HBV-related liver diseases in China. PeerJ. 2022;10:e13828.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBaig S. Gender disparity in infections of Hepatitis B virus. J Coll Physicians Surg\u0026ndash;Pak JCPSP. 2009 Sept;19(9):598\u0026ndash;600.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eHepatitis C-. Annual Epidemiological Report for 2022 [Internet]. 2024 [cited 2025 Aug 20]. Available from: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.ecdc.europa.eu/en/publications-data/hepatitis-c-annual-epidemiological-report-2022\u003c/span\u003e\u003cspan address=\"https://www.ecdc.europa.eu/en/publications-data/hepatitis-c-annual-epidemiological-report-2022\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eKolou M, Katawa G, Salou M, Gozo-Akakpo KS, Dossim S, Kwarteng A, et al. High Prevalence of Hepatitis B Virus Infection in the Age Range of 20\u0026ndash;39 Years Old Individuals in Lome. Open Virol J. 2017;11:1\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eEsmaeelzadeh A, Saadatnia H, Memar B, Mokhtari Amirmajdi E, Ganji A, Goshayeshi L, et al. Evaluation of serum HBV viral load, transaminases and histological features in chronic HBeAg-negative hepatitis B patients. Gastroenterol Hepatol Bed Bench. 2017;10(1):39\u0026ndash;43.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eHasanjani Roushan MR, Hajiahmadi M, Shafaie S. Histopathological features of liver and its relation to serum transaminase levels in 91 cases of anti-HBe-positive chronic hepatitis B. Int J Clin Pract. 2005 July;59(7):791\u0026ndash;4.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eZeuzem S, Ghalib R, Reddy KR, Pockros PJ, Ari ZB, Zhao Y, et al. Grazoprevir\u0026ndash;Elbasvir Combination Therapy for Treatment-Naive Cirrhotic and Noncirrhotic Patients With Chronic Hepatitis C Virus Genotype 1, 4, or 6 Infection. Ann Intern Med. 2015 July;7(1):1\u0026ndash;13.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eMcCormick SE, Goodman ZD, Maydonovitch CL, Sjogren MH. Evaluation of liver histology, ALT elevation, and HCV RNA titer in patients with chronic hepatitis C. Am J Gastroenterol. 1996;91(8):1516\u0026ndash;22.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eLau JY, Davis GL, Kniffen J, Qian KP, Urdea MS, Chan CS et al. Significance of serum hepatitis C virus RNA levels in chronic hepatitis C. Lancet Lond Engl. 1993 June 12;341(8859):1501\u0026ndash;4.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eRabbi FJ, Rezwan MK, Shirin T. HBeAg/anti-HBe, alanine aminotransferase and HBV DNA levels in HBsAg positive chronic carriers. Bangladesh Med Res Counc Bull. 2008;34(2):39\u0026ndash;43.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eKim KH, Na IH, Cha JM, Cho YK, Park SY, Kim HP, et al. [Serum ALT and HBV DNA levels in patients with HBeAg-negative chronic hepatitis B]. Taehan Kan Hakhoe Chi Korean J Hepatol. 2003;9(4):284\u0026ndash;92.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eLjunggren KK, Nordenfelt E, Kidd A. Correlation of HBeAg/anti-HBe, ALT levels, and HBV DNA PCR results in HBsAg-positive patients. J Med Virol. 1993;39(4):297\u0026ndash;302.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAnand BS, Velez M. Assessment of correlation between serum titers of hepatitis c virus and severity of liver disease. World J Gastroenterol WJG. 2004;10(16):2409\u0026ndash;11.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAmjad S, Akram A, Iqbal M, Hussain M, Khan M. Analysis of ALT and AST levels in HCV infected patients.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eZeuzem S, Franke A, Lee JH, Herrmann G, Ruster B, Roth WK. Phylogenetic analysis of hepatitis C virus isolates and their correlation to viremia, liver function tests, and histology. Hepatol Baltim Md. 1996;24(5):1003\u0026ndash;9.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eBabair Y, Elsafi S, Ghamdi MA, Gezery ME. Frequency and Pattern of Chronic Hepatitis B Infection in the Eastern Region of Saudi Arabia: A Cross-sectional Study. Biosci Biotechnol Res Asia [Internet]. 2016 May 7 [cited 2025 Aug 20];9(2). Available from: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.biotech-asia.org/vol9no2/frequency-and-pattern-of-chronic-hepatitis-b-infection-in-the-eastern-region-of-saudi-arabia-a-cross-sectional-study/\u003c/span\u003e\u003cspan address=\"https://www.biotech-asia.org/vol9no2/frequency-and-pattern-of-chronic-hepatitis-b-infection-in-the-eastern-region-of-saudi-arabia-a-cross-sectional-study/\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eSallam TA, El-Bingawi HM, Alzahrani KI, Alzahrani BH, Alzahrani AA. Prevalence of hepatitis B and hepatitis C viral infections and impact of control program among blood donors in Al-Baha region, Saudi Arabia. Saudi J Health Sci. 2020;9(1):56.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAsaad AM, Al-Ayed MSZ, Aleraky M, Qureshi MA. Hepatitis B virus genotyping in chronic hepatitis B patients in southwestern Saudi Arabia. Braz J Infect Dis. 2015 Sept 1;19(5):525\u0026ndash;8.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAlberts CJ, Clifford GM, Georges D, Negro F, Lesi OA, Hutin YJF, et al. Worldwide prevalence of hepatitis B virus and hepatitis C virus among patients with cirrhosis at country, region, and global levels: a systematic review. Lancet Gastroenterol Hepatol. 2022;7(8):724\u0026ndash;35.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eToshikuni N, Arisawa T, Tsutsumi M. Hepatitis C-related liver cirrhosis - strategies for the prevention of hepatic decompensation, hepatocarcinogenesis, and mortality. World J Gastroenterol WJG. 2014;20(11):2876\u0026ndash;87.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003ePark H, Wang W, Henry L, Nelson DR. Impact of All-Oral Direct‐Acting Antivirals on Clinical and Economic Outcomes in Patients With Chronic Hepatitis C in the United States. Hepatology. 2019;69(3):1032.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eButi M, Lim Y, Chan HLY, Agarwal K, Marcellin P, Brunetto MR, et al. Eight-year efficacy and safety of tenofovir alafenamide for treatment of chronic hepatitis B virus infection: Final results from two randomised phase 3 trials. Aliment Pharmacol Ther. 2024;60(11\u0026ndash;12):1573\u0026ndash;86.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eChan HLY, Buti M, Lim YS, Agarwal K, Marcellin P, Brunetto M, et al. Long-Term Treatment With Tenofovir Alafenamide for Chronic Hepatitis B Results in High Rates of Viral Suppression and Favorable Renal and Bone Safety. Am J Gastroenterol. 2024;119(3):486\u0026ndash;96.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eRidruejo E, Marciano S, Galdame O, Reggiardo MV, Mu\u0026ntilde;oz AE, Adrover R, et al. Efficacy and safety of long term entecavir in chronic hepatitis B treatment na\u0026iuml;ve patients in clinical practice. Ann Hepatol. 2014;13(3):327\u0026ndash;36.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eLee HW, Kwon JC, Oh IS, Chang HY, Cha YJ, Choi IS, et al. Prolonged Entecavir Therapy Is Not Effective for HBeAg Seroconversion in Treatment-Naive Chronic Hepatitis B Patients with a Partial Virological Response. Antimicrob Agents Chemother. 2015 Sept;59(9):5348\u0026ndash;56.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eSulkowski MS, Gardiner DF, Rodriguez-Torres M, Reddy KR, Hassanein T, Jacobson I, et al. Daclatasvir plus Sofosbuvir for Previously Treated or Untreated Chronic HCV Infection. N Engl J Med. 2014;370(3):211\u0026ndash;21.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eShiha G, Soliman R, ElBasiony M, Hassan AA, Mikhail NNH. Sofosbuvir plus Daclatasvir with or without ribavirin for treatment of chronic HCV genotype 4 patients: real-life experience. Hepatol Int. 2018 July;12(4):339\u0026ndash;47.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAhmed OA, Elsebaey MA, Fouad MHA, Elashry H, Elshafie AI, Elhadidy AA, et al. Outcomes and predictors of treatment response with sofosbuvir plus daclatasvir with or without ribavirin in Egyptian patients with genotype 4 hepatitis C virus infection. Infect Drug Resist. 2018;11:441\u0026ndash;5.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eFarrag AN, Kamel AM. Efficacy of 8-week daclatasvir-sofosbuvir regimen in chronic hepatitis C: a systematic review and meta-analysis. Virol J. 2024;21:275.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003ePuoti M, Foster GR, Wang S, Mutimer D, Gane E, Moreno C, et al. High SVR12 with 8-week and 12-week glecaprevir/pibrentasvir therapy: An integrated analysis of HCV genotype 1\u0026ndash;6 patients without cirrhosis. J Hepatol. 2018;69(2):293\u0026ndash;300.\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eReal-World Effectiveness and Safety of Glecaprevir/Pibrentasvir for the Treatment of Chronic Hepatitis C. A Prospective Cohort Study in Portugal [Internet]. [cited 2025 Sept 9]. Available from: \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.natap.org/2024/HCV/021324_01.htm?utm_source=chatgpt.com\u003c/span\u003e\u003cspan address=\"https://www.natap.org/2024/HCV/021324_01.htm?utm_source=chatgpt.com\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e\u003cli\u003e\u003cspan\u003eAsselah T, Reesink H, Gerstoft J, de Ledinghen V, Pockros PJ, Robertson M, et al. Efficacy of elbasvir and grazoprevir in participants with hepatitis C virus genotype 4 infection: A pooled analysis. Liver Int Off J Int Assoc Study Liver. 2018 Sept;38(9):1583\u0026ndash;91.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-infectious-diseases","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"infd","sideBox":"Learn more about [BMC Infectious Diseases](http://bmcinfectdis.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/infd","title":"BMC Infectious Diseases","twitterHandle":"#bmcinfectdis","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"HBV, HCV, Chronic hepatitis, Blood-borne viral hepatitis, Al-Baha, Saudi Arabia","lastPublishedDoi":"10.21203/rs.3.rs-7767890/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7767890/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e\u003cp\u003eIn Al-Baha viral hepatitis in clinical settings has not been adequately investigated. This study examined chronic HBV and HCV infections and treatment outcomes among patients at King Fahd Hospital in Al-Baha.\u003c/p\u003e\u003ch2\u003eMethodology:\u003c/h2\u003e\u003cp\u003ePatients records were retrieved anonymously for clinical, demographic, virological and biochemical data from January 2019 and December 2022.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e\u003cp\u003eA total of 148 patients infected with HBV and/or HCV attended during the 4-year study period. The mean age was 49.6\u0026thinsp;\u0026plusmn;\u0026thinsp;13.2 (20\u0026ndash;88 years); 84 (56.8%) males and 64 (43.2%) females. A total of 119 (80.4%) were infected with HBV, 27 (18.2%) with HCV while only 2 (1.4%) had dual HBV/HCV infection. Higher HBV viral loads correlated with higher ALT levels (r\u0026thinsp;=\u0026thinsp;0.317, p\u0026thinsp;=\u0026thinsp;0.001). Higher HCV viral loads did not associate with higher ALT levels (r\u0026thinsp;=\u0026thinsp;0.246, p\u0026thinsp;=\u0026thinsp;0.23). Of all cases 144 were clinically characterized and encompassed 117 chronic HBV, 25 chronic HCV, 1 acute HCV and 1 dual HBV/ HCV infection. Forty-seven (32.6%) were HBeAg-negative chronic infections, 69 (47.2%) were HBeAg- undesignated chronic infections. Cirrhosis was present in 6% of HBV cases and 18.5% of HCV cases. Through the course of HBV treatment, patients treated with tenofovir alafenamide (n\u0026thinsp;=\u0026thinsp;15) achieved viral load suppression in 93.3%, with ALT either maintained or normalized in most cases. Treatment with entecavir (n\u0026thinsp;=\u0026thinsp;8) also resulted in undetectable or markedly reduced viral load with generally unchanging ALT levels. All 16 HCV patients achieved viral clearance after 12 weeks treatment course; sofosbuvir\u0026ndash;daclatasvir (n\u0026thinsp;=\u0026thinsp;14) was highly effective though 2 showed elevated post-treatment ALT. Single patients on glecaprevir/pibrentasvir and elbasvir/grazoprevir also achieved viral clearance.\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e\u003cp\u003eChronic HBV and HCV infections remain clinical challenges. Viral load of HBV but not that of HCV correlated with ALT. Tenofovir alafenamide, entecavir, and sofosbuvir/daclatasvir showed strong efficacy, though limited follow-up and small sample sizes restrict conclusions. Overall, treatment responses merit further investigation.\u003c/p\u003e","manuscriptTitle":"Chronic Blood-Borne Viral Hepatitis and Treatment Outcomes in a Major Hospital in Al-Baha City: A Retrospective Cross-Sectional Study.","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-11-06 04:17:14","doi":"10.21203/rs.3.rs-7767890/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2025-11-07T08:33:29+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-11-06T14:05:22+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"19281770595783619476375207739332414488","date":"2025-11-06T13:53:19+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"73932014221811738295520429953169731632","date":"2025-11-06T13:51:32+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"44130101037777640788256309248566194278","date":"2025-11-06T09:46:54+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"104027705307145610099668208971404694008","date":"2025-11-05T19:27:05+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-11-05T17:56:10+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"98129700712027425442970976624309548412","date":"2025-11-05T15:46:46+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"5240207907723577782943303260578802328","date":"2025-11-05T07:18:03+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"21006172996339097515048933471900963243","date":"2025-11-04T18:10:43+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"273436118892937511958640704378824089528","date":"2025-11-04T14:38:42+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-10-27T11:01:05+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2025-10-07T19:04:07+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-10-05T23:55:07+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-10-05T23:54:47+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Infectious Diseases","date":"2025-10-02T16:03:18+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-infectious-diseases","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"infd","sideBox":"Learn more about [BMC Infectious Diseases](http://bmcinfectdis.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/infd","title":"BMC Infectious Diseases","twitterHandle":"#bmcinfectdis","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"c7e2a606-bb38-4f55-8507-a5c8a27a451f","owner":[],"postedDate":"November 6th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2026-01-19T16:47:56+00:00","versionOfRecord":{"articleIdentity":"rs-7767890","link":"https://doi.org/10.1186/s12879-025-12432-x","journal":{"identity":"bmc-infectious-diseases","isVorOnly":false,"title":"BMC Infectious Diseases"},"publishedOn":"2026-01-12 16:29:54","publishedOnDateReadable":"January 12th, 2026"},"versionCreatedAt":"2025-11-06 04:17:14","video":"","vorDoi":"10.1186/s12879-025-12432-x","vorDoiUrl":"https://doi.org/10.1186/s12879-025-12432-x","workflowStages":[]},"version":"v1","identity":"rs-7767890","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7767890","identity":"rs-7767890","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}