The Impact of Hyperinsulinemia on Short-term Prognosis in Patients with Hyperlipidemia-induced Acute Pancreatitis

The Impact of Hyperinsulinemia on Short-term Prognosis in Patients with Hyperlipidemia-induced Acute Pancreatitis | 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 The Impact of Hyperinsulinemia on Short-term Prognosis in Patients with Hyperlipidemia-induced Acute Pancreatitis Mengjun Wang, Ruilin Luo, Shasha Sun, Lei Zheng, Wen Jiang, Yu Ge, and 3 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-3829400/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Purpose The short-term prognosis of hyperinsulinemia in patients with hyperlipidemia resulting in acute pancreatitis is remains uncertain. Material and Methods This study presents a retrospective analysis of patients who underwent treatment for hyperlipidemic acute pancreatitis at Wuhu Hospital of Traditional Chinese Medicine from January 2020 to April 2023. The patients were categorized into two groups based on their fasting insulin levels: the hyperinsulinemia group (HINS) and the non-hyperinsulinemia group (NHINS). The study aimed to observe and record the outcomes related to metabolic disease, short-term recurrence rate, and quality of life (QOL) score. Results In this study, a total of 92 patients with hyperlipidemic pancreatitis were enrolled prior to lipid-lowering therapy, including 59 patients in the HINS group and 33 patients in the NHINS group. Significant differences were observed between the two groups in terms of white blood cell count (WBC), hypersensitive C-reactive protein (CRP) levels, and fasting blood glucose at 2, 3–4, and 5–7 days after initiation of lipid-lowering intervention (P < 0.05). Following admission, anti-inflammatory treatment, lipid-lowering therapy, blood glucose control measures, and other symptomatic interventions were administered. Both groups exhibited a reduction in serum triglyceride levels; however, there was a significant difference in the magnitude of decrease compared to baseline on the fifth to seventh day (P < 0.05). There were statistically significant differences between the two groups in readmission for recurrent pancreatitis within 30 days after ICU transfer and discharge (P < 0.05). There was no statistically significant difference observed between the length of hospital stay or quality of life scores fifteen days after discharge. Conclusion The presence of hyperinsulinemia exerts a detrimental impact on the recovery process of patients with hyperlipidemia-induced acute pancreatitis, while the favorable baseline physical condition observed in the NHINS group contributes to a more advantageous recuperation from hyperlipidemic pancreatitis. Acute pancreatitis Hyperlipidemic Hyperinsulinemia short-term prognosis Figures Figure 1 Background The incidence of hyperlipidemic pancreatitis (HP) accounts for 2% to 4% of all cases of pancreatitis 1 , indicating a widespread increase of widespread increase 2 . The main symptoms include abdominal tenderness, indigestion, nausea and vomiting, which can lead of danger and fatality 3 . Acute pancreatitis is diagnosed when at least two out of the following three features are present: characteristic abdominal pain, elevated levels (three or more times the upper limit of normal) of pancreatic enzymes (amylase and/or lipase), or imaging findings showing specific abnormalities 4 . Upon diagnosis, the most appropriate treatment plan within 72 hours primarily involves fluid rehydration and enteral nutrition support 5 . Approximately 70% to 80% of patients with pancreatitis achieve control through timely diagnosis and systematic treatment, resulting in a relatively mild prognosis 6 .However, hyperlipidemic pancreatitis is more likely to have a severe disease course with a greater likelihood of persistent organ failure; if necessary, insulin should be administered as part of the treatment 7 . At normal plasma insulin levels, target tissues are unable to exhibit the normal synergistic hypoglycemic effects, inhibition of endogenous glucose production, suppression of lipolysis, and facilitation of glucose uptake by cells. This inability is defined as insulin resistance. Insulin resistance can be compensated by increasing the amount of insulin produced by the body itself, thus leading to an increase in fasting plasma insulin levels, which can eventually deteriorate into hyperinsulinemia 89 .Hyperinsulinemia, a state of elevated circulating insulin concentration 10 , is positively associated with obesity and is a clinical reflection of a small number of patients with insulin resistance 11 .Studies have shown that hyperinsulinemia is currently more likely to cause type 2 diabetes than insulin resistance 12 .The insufficiency of insulin function then causes compensatory hyperinsulinemia, and the islet beta cells need to secrete insulin continuously for this, which accelerates the failure of pancreatic beta cells and even leads to their apoptosis 13 , so that the pancreatic function is impaired. Long-term chronic inflammation induces hyperinsulinemia, which in turn promotes inflammation 14 . Although hyperinsulinemia is closely associated with fat metabolism and pancreatic function, there is currently a lack of relevant studies investigating the impact of hyperinsulinemia on the short-term prognosis of patients with hyperlipidemia-induced acute pancreatitis. This study aims to explore the influence of hyperinsulinemia on changes in pertinent laboratory indicators and disease severity following standard treatment in patients with acute pancreatitis caused by hyperlipidemia, thereby providing a novel theoretical foundation for the management of this condition. Clinical data and experimental methodologies 1.1 Introduction The present study retrospectively analyzed a total of ninety-two patients with acute pancreatitis and hyperlipidemia who were admitted to the surgery department of Wuhu Hospital of Traditional Chinese Medicine affiliated to Anhui University of Chinese Medicine from January 2020 to April 2023. Patients were categorized into two groups based on their hyperinsulinemic status: the Hyperinsulinemia (HINS) group, which included forty-four patients, and the Non-hyperinsulinemia (NHINS) group, which included forty-eight patients. After statistical analysis, no significant differences in baseline characteristics were observed between the two groups (p > 0.05), indicating comparability. 1.2 Criteria for inclusion and exclusion The study enrolled a total of 92 patients who received treatment for hyperlipidemia-induced acute pancreatitis at the Department of Surgery, Wuhu Hospital of Traditional Chinese Medicine affiliated with Anhui University of Chinese Medicine, from January 2020 to April 2023. Acute pancreatitis (AP) was diagnosed based on abdominal pain, elevated levels of blood amylase/lipase, and/or typical radiological findings. Hyperlipidemia acute pancreatitis (HLAP) was defined as a triglyceride (TG) level exceeding 5.6mmol/L after excluding other potential causes. Patients younger than 18 years old, pregnant individuals, or those with pancreatic cancer or chronic pancreatitis were excluded from the study population. General clinical markers including fasting blood glucose (GLU), total cholesterol (TC), triglyceride (TG), white blood cells (WBC), and high-sensitivity C-reactive protein (CRP) were measured at predetermined time points: one day before lipid-lowering intervention and two days, three to four days, and five to seven days after lipid-lowering intervention. The diagnostic criteria for acute uncomplicated pancreatitis and mild acute pancreatitis meet the diagnostic criteria for acute pancreatitis, satisfying one of the following conditions: absence of organ failure, absence of local or systemic complications, Ranson score < 3 points. The diagnostic criteria for acute pancreatitis were referenced from the 2013 Chinese Guidelines for Diagnosis and Treatment of Pancreatitis. The diagnostic criteria for mild acute pancreatitis align with the diagnostic criteria for acute pancreatitis and fulfill any of the following conditions: absence of organ failure, absence of local or systemic complications, Ranson score < 3 points, Acute Physiology And Chronic Health Evaluation (APACHE) score < 8, Bedside Index For Severity In Acute Pancreatitis (BISAP) < 3 points, Modified CT Severity Index (MCTSI) score < four points. QOL score upon admission and within 15 days of discharge was recorded. Qol score was taken by Moorehead-Ardelt QOL Questionnaire II, ranging from -3 to +3, the higher the score, the better. Revised Atlanta Grading standards classify acute pancreatitis severity as mild acute pancreatitis (MAP), moderately severe acute pancreatitis (MSAP), or severe acute pancreatitis (SAP) based on the presence of pancreatic necrosis, peripancreatic fluid collections, organ failure, and mortality. Organ failure is defined by respiratory insufficiency (PaO2/FiO2 ≤300 mmHg), renal failure (serum creatinine ≥170 μmol/L after rehydration), and/or shock (SBP ≤90 mmHg). Length of hospital stay and ICU days are also used to assess outcomes. The severity of acute pancreatitis was concurrently assessed using scoring systems such as the Ranson score, BISAP score, APACHE-II score, and Marshall score. Ranson scores are typically employed within 24 hours of symptom onset. BISAP scores indicate the progression of persistent organ failure in patients with acute pancreatitis. An APACHE-II score equal to or exceeding 9 is indicative of severe pancreatitis. The modified Marshall score effectively evaluates pancreatic severity by mitigating the statistical influence of renal function 151617181920 . 1.3 Improved gathering of patient information and clinical data, with an emphasis on ethical considerations. The patient's clinical history, such as age, sex, body mass index (BMI), drinking history, diabetes mellitus (DM) and fatty liver were recorded retrospectively. Patients with a history of heavy alcohol use, defined as alcohol intake ≥40 g/d for ≥5 years, were excluded from this study based on alcohol etiology 21 .The levels of serum calcium (Ca), C-reactive protein (CRP), white blood cells (WBC), and triglycerides (TG) were also measured. The initial management of hyperlipidemic pancreatitis involves symptomatic measures such as fasting, fluid resuscitation, analgesia, and nutritional support. Following the initial treatment, specific interventions aimed at reducing serum triglyceride levels, including insulin infusion, heparin administration, and anti-hyperlipidemic medications, were documented. This retrospective observational study protocol was approved by the Institute's Ethics Committee while ensuring complete patient anonymity in accordance with the Declaration of Helsinki. Methods of statistical analysis The data were processed using Graphpad Prism9.5.1 statistical software. Measurement data were presented the mean ± SD, and the t-test was employed for normally distributed data while the rank sum test was used for non-normally distributed data. Count data were expressed as percentages, and comparison was conducted using the χ2 test. A statistically significant difference was defined as P<0.05 at a significance level of α=0.05. Results 1. Baseline Characteristics The study retrospectively included a total of 100 patients, excluding one patient under the age of 18 and seven patients with incomplete follow-up. None of these excluded patients were considered in this research. Patients diagnosed with hyperinsulinemia (n=44) were categorized as HINS, while those without hyperinsulinemia (n=48) were classified as NHINS based on oral glucose tolerance test (OGTT), past medical history, and clinical manifestations. Figure 1 illustrates the detailed methodology employed in this study. The laboratory data and basic information measured by the two patient groups are presented in Table 1. Retrospective analysis was conducted on the patients' age, gender, body mass index (BMI), history of fatty liver disease, quality of life score at admission, blood lipid index, blood glucose index, and inflammatory response index. Statistical comparison revealed no significant difference between the two groups at baseline except for fasting blood glucose levels. 2. Prognostic indicators 2.1 Lipid Level The levels of TG exhibited a rapid decrease. Specifically, the HINS group and NHINS group displayed TG levels of 8.1 (3.5) and 7.5 (2.3), respectively, during days 5-7, with no statistically significant difference observed between the two groups. However, notable differences in TG levels were observed at baseline and during days 5-7 between the two groups (Table 2). 2.2 Blood glucose level The baseline fasting blood glucose (FBG) levels in the HINS group and NHINS group were 9.6(1.7) mmol/L and 9.1(1.5) mmol/L, respectively, which significantly differed from the FBG levels on day 2. In addition, the decline of FBG data in the NIHINS group was more pronounced (Table 3). 2.3 The short-term prognosis and rate of recurrence. The duration of hospitalization was recorded for both groups, and statistically, there was no significant difference observed. The readmissions within 30 days after discharge were documented for patients with recurrent pancreatitis in both groups. In the HINS group, 4 patients (9.1%) experienced readmission, while none were reported in the NHINS group (0%) (P < 0.05), indicating a significant disparity between the two groups. A total of 7 patients in the HINS group and 1 patient in the NHINS group required transfer to ICU due to severe condition, revealing a notable distinction between the two groups (Table 4). 2.4 The quality of life The quality of life scores 15 days after discharge were recorded for both groups. At baseline, the mean (SD) quality of life scores for patients in the HINS and NHINS groups were 0.23 (0.79) and 0.19 (0.98), respectively. After 15 days of discharge, the mean (SD) quality of life score was 1.05 (0.59) in the HINS group and 1.09 (0.68) in the NHINS group, with no statistically significant difference observed between the two groups. Furthermore, there was a statistically significant increase in quality of life scores for all patients at day 15 post-discharge when comparing their total scores before and after treatment (Table 5). 2.5 The comparison of scoring systems The Ranson score, BISAP score, APACHE-II score, and Marshall score were documented for both the HINS and NHINS groups upon discharge. Upon calculation, significant differences in the scores among the four groups were observed (P < 0.005) (Table 6). Topic under discussion The primary etiologies of acute pancreatitis include pancreatic hyperstimulation and obstruction of the bile pancreatic duct, resulting in elevated pressure within the pancreatic duct and reflux of active trypsin.Acute pancreatitis occurs when the protective mechanisms that prevent trypsinogen activation or reduce trypsin activity are compromised by overload 22 . The main factor contributing to AP is an imbalance in lipid metabolism-related pathways. Hyperlipidemia has surpassed alcohol as the second leading cause of AP, and the proportion of hyperlipidemia-induced pancreatitis in AP cases is also increasing. This suggests that genes regulating the lipid metabolism pathway may influence susceptibility to secondary infectious pancreatic necrosis in individuals with AP 23 . Pancreatitis is influenced by multiple factors. Over the past decade, numerous studies have demonstrated that acute pancreatitis can result in metabolic complications (such as exocrine pancreatic dysfunction and new-onset diabetes), regardless of the severity of the initial condition 24 . The management of acute pancreatitis is multifaceted, encompassing a spectrum of severity and clinical course. However, timely and aggressive fluid resuscitation along with early initiation of enteral nutrition have demonstrated efficacy in reducing mortality rates and the incidence of infections 25 . The development of hyperlipidemic pancreatitis, a type of acute pancreatitis, is triggered by the enzymatic action of pancreatic lipase on excessive fat, resulting in the generation of fatty acids. The subsequent accumulation of lipid toxicity induces robust inflammatory responses 26 . The mortality rate and incidence of organ necrosis in acute pancreatitis have been found to be positively correlated with the severity of hyperlipidemia 27 . Therefore, in the diagnosis and treatment of acute pancreatitis, clinicians consider triglyceride as a crucial adjunctive parameter: regular monitoring of triglyceride levels and serum glucose is necessary during insulin administration; cessation of intravenous insulin can be considered when the serum triglyceride concentration falls below 500mg/dL. The secretion of insulin by pancreatic beta cells plays a pivotal role in regulating glucose, amino acid, and free fatty acid metabolism in the human body 282930 . Maintaining optimal homeostasis of insulin concentration is achieved through a negative feedback regulatory mechanism. Any impairment to this mechanism can lead to symptoms associated with insufficient or excessive insulin secretion. Patients with hyperinsulinemia exhibit impaired response to normal insulin levels, and it is hypothesized that obesity induces insulin resistance. This reciprocal relationship between insulin resistance and obesity further exacerbates the condition 31 . The connection between insulin and obesity cannot be ignored 3233 . The management of hyperinsulinemia encompasses pharmacological and non-pharmacological interventions 34 . The drug treatment options for diabetes include sulfonylureas, glucagon-like peptide 1 (GLP-1) agonists, and dipeptidyl peptide-4 (DPP-4) inhibitors 35 ;the non-pharmacological interventions encompass the regulation of dietary energy intake, augmentation of physical activity, and enhancement of energy expenditure 36 . The non-drug treatment concept, although innovative and effective, necessitates a certain level of self-discipline and regularity 3738 , rendering it unsuitable for the acute stage of pancreatitis. Nevertheless, this study has certain limitations including a small sample size leading to biased sample selection, failure to follow up on long-term effects of pancreatitis treatment, and inability to refine the study based on different concentrations of serum triglycerides. Therefore, future research should focus on these aspects for further exploration. Conclusion In summary, during the course of hyperlipidemia pancreatitis, symptomatic treatment was administered to both groups of patients after hospitalization, resulting in significant improvement in clinical symptoms and laboratory indicators. However, due to their own pancreatic function impairment, patients in the HINS group experienced a slower recovery rate and disease aggravation, which had a negative impact. After conventional treatment, patients in the NHINS group exhibited milder abdominal signs and blood test reports compared to those in the HINS group. The HINS group did not significantly affect the hospital days and quality of life after discharge. Declarations Disclosure The authors declare that they have no conflict of interest. Funding This work was supported by the Scientific research project of colleges and universities in Anhui Province (grant number 2022AH052638), Anhui university natural science research project (grant number 2023AH053197) Conflict of Interest NONE Ethics Statement Our study was approved by the Ethics Review Committee of Wuhu Hospital of Anhui University of Traditional Chinese Medicine. Informed Consent. N/A Registry and the Registration No. of the study/trial. N/A Animal Studies. N/A Consent for publication Not applicable. Availability of data and materials Not applicable. 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19:07:19","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":365511,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-3829400/v1/82d8e3d6-54bb-4961-95a0-e76c51a43ba2.pdf"},{"id":49237791,"identity":"4d64b374-92a4-4c5b-8fb1-d5cb402a7354","added_by":"auto","created_at":"2024-01-05 18:02:50","extension":"pdf","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":71373,"visible":true,"origin":"","legend":"","description":"","filename":"tabel.pdf","url":"https://assets-eu.researchsquare.com/files/rs-3829400/v1/30b4ca94005ab1b39835d201.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"The Impact of Hyperinsulinemia on Short-term Prognosis in Patients with Hyperlipidemia-induced Acute Pancreatitis","fulltext":[{"header":"Background","content":"\u003cp\u003eThe incidence of hyperlipidemic pancreatitis (HP) accounts for 2% to 4% of all cases of pancreatitis\u003csup\u003e1\u003c/sup\u003e, indicating a widespread increase of widespread increase\u003csup\u003e2\u003c/sup\u003e.\u0026nbsp;The main symptoms include abdominal tenderness, indigestion, nausea and vomiting, which can lead of danger and fatality\u003csup\u003e3\u003c/sup\u003e. Acute pancreatitis is diagnosed when at least two out of the following three features are present: characteristic abdominal pain, elevated levels (three or more times the upper limit of normal) of pancreatic enzymes (amylase and/or lipase), or imaging findings showing specific abnormalities\u003csup\u003e4\u003c/sup\u003e. Upon diagnosis, the most appropriate treatment plan within 72 hours primarily involves fluid rehydration and enteral nutrition support\u003csup\u003e5\u003c/sup\u003e. Approximately 70% to 80% of patients with pancreatitis achieve control through timely diagnosis and systematic treatment, resulting in a relatively mild prognosis \u003csup\u003e6\u003c/sup\u003e.However, hyperlipidemic pancreatitis is more likely to have a severe disease course with a greater likelihood of persistent organ failure; if necessary, insulin should be administered as part of the treatment\u003csup\u003e7\u003c/sup\u003e.\u003c/p\u003e\n\u003cp\u003eAt normal plasma insulin levels, target tissues are unable to exhibit the normal synergistic hypoglycemic effects, inhibition of endogenous glucose production, suppression of lipolysis, and facilitation of glucose uptake by cells. This inability is defined as insulin resistance. Insulin resistance can be compensated by increasing the amount of insulin produced by the body itself, thus leading to an increase in fasting plasma insulin levels, which can eventually deteriorate into hyperinsulinemia\u003csup\u003e89\u003c/sup\u003e.Hyperinsulinemia, a state of elevated circulating insulin concentration\u003csup\u003e10\u003c/sup\u003e, is positively associated with obesity and is a clinical reflection of a small number of patients with insulin resistance\u003csup\u003e11\u003c/sup\u003e.Studies have shown that hyperinsulinemia is currently more likely to cause type 2 diabetes than insulin resistance\u003csup\u003e12\u003c/sup\u003e.The insufficiency of insulin function then causes compensatory hyperinsulinemia, and the islet beta cells need to secrete insulin continuously for this, which accelerates the failure of pancreatic beta cells and even leads to their apoptosis\u003csup\u003e13\u003c/sup\u003e, so that the pancreatic function is impaired. Long-term chronic inflammation induces hyperinsulinemia, which in turn promotes inflammation\u003csup\u003e14\u003c/sup\u003e.\u003c/p\u003e\n\u003cp\u003eAlthough hyperinsulinemia is closely associated with fat metabolism and pancreatic function, there is currently a lack of relevant studies investigating the impact of hyperinsulinemia on the short-term prognosis of patients with hyperlipidemia-induced acute pancreatitis. This study aims to explore the influence of hyperinsulinemia on changes in pertinent laboratory indicators and disease severity following standard treatment in patients with acute pancreatitis caused by hyperlipidemia, thereby providing a novel theoretical foundation for the management of this condition.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical data and experimental methodologies\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e1.1 Introduction\u003c/p\u003e\n\u003cp\u003eThe present study retrospectively analyzed a total of ninety-two patients with acute pancreatitis and hyperlipidemia who were admitted to the surgery department of Wuhu Hospital of Traditional Chinese Medicine affiliated to Anhui University of Chinese Medicine from January 2020 to April 2023. Patients were categorized into two groups based on their hyperinsulinemic status: the Hyperinsulinemia (HINS) group, which included forty-four patients, and the Non-hyperinsulinemia (NHINS) group, which included forty-eight patients. After statistical analysis, no significant differences in baseline characteristics were observed between the two groups (p \u0026gt; 0.05), indicating comparability.\u003c/p\u003e\n\u003cp\u003e1.2 Criteria for inclusion and exclusion\u003c/p\u003e\n\u003cp\u003eThe study enrolled a total of 92 patients who received treatment for hyperlipidemia-induced acute pancreatitis at the Department of Surgery, Wuhu Hospital of Traditional Chinese Medicine affiliated with Anhui University of Chinese Medicine, from January 2020 to April 2023. Acute pancreatitis (AP) was diagnosed based on abdominal pain, elevated levels of blood amylase/lipase, and/or typical radiological findings. Hyperlipidemia acute pancreatitis (HLAP) was defined as a triglyceride (TG) level exceeding 5.6mmol/L after excluding other potential causes. Patients younger than 18 years old, pregnant individuals, or those with pancreatic cancer or chronic pancreatitis were excluded from the study population. General clinical markers including fasting blood glucose (GLU), total cholesterol (TC), triglyceride (TG), white blood cells (WBC), and high-sensitivity C-reactive protein (CRP) were measured at predetermined time points: one day before lipid-lowering intervention and two days, three to four days, and five to seven days after lipid-lowering intervention.\u003c/p\u003e\n\u003cp\u003eThe diagnostic criteria for acute uncomplicated pancreatitis and mild acute pancreatitis meet the diagnostic criteria for acute pancreatitis, satisfying one of the following conditions: absence of organ failure, absence of local or systemic complications, Ranson score \u0026lt; 3 points. The diagnostic criteria for acute pancreatitis were referenced from the 2013 Chinese Guidelines for Diagnosis and Treatment of Pancreatitis. The diagnostic criteria for mild acute pancreatitis align with the diagnostic criteria for acute pancreatitis and fulfill any of the following conditions: absence of organ failure, absence of local or systemic complications, Ranson score \u0026lt; 3 points, Acute Physiology And Chronic Health Evaluation (APACHE) score \u0026lt; 8, Bedside Index For Severity In Acute Pancreatitis (BISAP) \u0026lt; 3 points, Modified CT Severity Index (MCTSI) score \u0026lt; four points.\u003c/p\u003e\n\u003cp\u003eQOL score upon admission and within 15 days of discharge was recorded. Qol score was taken by Moorehead-Ardelt QOL Questionnaire II, ranging from -3 to +3, the higher the score, the better.\u003c/p\u003e\n\u003cp\u003eRevised Atlanta Grading standards classify acute pancreatitis severity as mild acute pancreatitis (MAP), moderately severe acute pancreatitis (MSAP), or severe acute pancreatitis (SAP) based on the presence of pancreatic necrosis, peripancreatic fluid collections, organ failure, and mortality. Organ failure is defined by respiratory insufficiency (PaO2/FiO2 \u0026le;300 mmHg), renal failure (serum creatinine \u0026ge;170 \u0026mu;mol/L after rehydration), and/or shock (SBP \u0026le;90 mmHg). Length of hospital stay and ICU days are also used to assess outcomes.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThe severity of acute pancreatitis was concurrently assessed using scoring systems such as the Ranson score, BISAP score, APACHE-II score, and Marshall score. Ranson scores are typically employed within 24 hours of symptom onset. BISAP scores indicate the progression of persistent organ failure in patients with acute pancreatitis. An APACHE-II score equal to or exceeding 9 is indicative of severe pancreatitis. The modified Marshall score effectively evaluates pancreatic severity by mitigating the statistical influence of renal function\u003csup\u003e151617181920\u003c/sup\u003e.\u003c/p\u003e\n\u003cp\u003e1.3 Improved gathering of patient information and clinical data, with an emphasis on ethical considerations.\u003c/p\u003e\n\u003cp\u003eThe patient\u0026apos;s clinical history, such as age, sex, body mass index (BMI), drinking history, diabetes mellitus (DM) and fatty liver were recorded retrospectively. Patients with a history of heavy alcohol use, defined as alcohol intake \u0026ge;40 g/d for \u0026ge;5 years, were excluded from this study based on alcohol etiology\u003csup\u003e21\u003c/sup\u003e.The levels of serum calcium (Ca), C-reactive protein (CRP), white blood cells (WBC), and triglycerides (TG) were also measured.\u003c/p\u003e\n\u003cp\u003eThe initial management of hyperlipidemic pancreatitis involves symptomatic measures such as fasting, fluid resuscitation, analgesia, and nutritional support. Following the initial treatment, specific interventions aimed at reducing serum triglyceride levels, including insulin infusion, heparin administration, and anti-hyperlipidemic medications, were documented.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThis retrospective observational study protocol was approved by the Institute\u0026apos;s Ethics Committee while ensuring complete patient anonymity in accordance with the Declaration of Helsinki.\u003c/p\u003e"},{"header":"Methods of statistical analysis","content":"\u003cp\u003eThe data were processed using Graphpad Prism9.5.1 statistical software. Measurement data were presented the mean \u0026plusmn; SD, and the t-test was employed for normally distributed data while the rank sum test was used for non-normally distributed data. Count data were expressed as percentages, and comparison was conducted using the \u0026chi;2 test. A statistically significant difference was defined as P\u0026lt;0.05 at a significance level of \u0026alpha;=0.05.\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003e1. Baseline Characteristics\u003c/p\u003e\n\u003cp\u003eThe study retrospectively included a total of 100 patients, excluding one patient under the age of 18 and seven patients with incomplete follow-up. None of these excluded patients were considered in this research. Patients diagnosed with hyperinsulinemia (n=44) were categorized as HINS, while those without hyperinsulinemia (n=48) were classified as NHINS based on oral glucose tolerance test (OGTT), past medical history, and clinical manifestations. Figure 1 illustrates the detailed methodology employed in this study.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThe laboratory data and basic information measured by the two patient groups are presented in Table 1. Retrospective analysis was conducted on the patients\u0026apos; age, gender, body mass index (BMI), history of fatty liver disease, quality of life score at admission, blood lipid index, blood glucose index, and inflammatory response index. Statistical comparison revealed no significant difference between the two groups at baseline except for fasting blood glucose levels.\u003c/p\u003e\n\u003cp\u003e2. Prognostic indicators\u003c/p\u003e\n\u003cp\u003e2.1 Lipid Level\u003c/p\u003e\n\u003cp\u003eThe levels of TG exhibited a rapid decrease. Specifically, the HINS group and NHINS group displayed TG levels of 8.1 (3.5) and 7.5 (2.3), respectively, during days 5-7, with no statistically significant difference observed between the two groups. However, notable differences in TG levels were observed at baseline and during days 5-7 between the two groups (Table 2).\u003c/p\u003e\n\u003cp\u003e2.2 Blood glucose level\u003c/p\u003e\n\u003cp\u003eThe baseline fasting blood glucose (FBG) levels in the HINS group and NHINS group were 9.6(1.7) mmol/L and 9.1(1.5) mmol/L, respectively, which significantly differed from the FBG levels on day 2. In addition, the decline of FBG data in the NIHINS group was more pronounced (Table 3).\u003c/p\u003e\n\u003cp\u003e2.3 The short-term prognosis and rate of recurrence.\u003c/p\u003e\n\u003cp\u003eThe duration of hospitalization was recorded for both groups, and statistically, there was no significant difference observed. The readmissions within 30 days after discharge were documented for patients with recurrent pancreatitis in both groups. In the HINS group, 4 patients (9.1%) experienced readmission, while none were reported in the NHINS group (0%) (P \u0026lt; 0.05), indicating a significant disparity between the two groups. A total of 7 patients in the HINS group and 1 patient in the NHINS group required transfer to ICU due to severe condition, revealing a notable distinction between the two groups (Table 4).\u003c/p\u003e\n\u003cp\u003e2.4 The quality of life\u003c/p\u003e\n\u003cp\u003eThe quality of life scores 15 days after discharge were recorded for both groups. At baseline, the mean (SD) quality of life scores for patients in the HINS and NHINS groups were 0.23 (0.79) and 0.19 (0.98), respectively. After 15 days of discharge, the mean (SD) quality of life score was 1.05 (0.59) in the HINS group and 1.09 (0.68) in the NHINS group, with no statistically significant difference observed between the two groups. Furthermore, there was a statistically significant increase in quality of life scores for all patients at day 15 post-discharge when comparing their total scores before and after treatment (Table 5).\u003c/p\u003e\n\u003cp\u003e2.5 The comparison of scoring systems\u003c/p\u003e\n\u003cp\u003eThe Ranson score, BISAP score, APACHE-II score, and Marshall score were documented for both the HINS and NHINS groups upon discharge. Upon calculation, significant differences in the scores among the four groups were observed (P \u0026lt; 0.005) (Table 6).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTopic under discussion\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe primary etiologies of acute pancreatitis include pancreatic hyperstimulation and obstruction of the bile pancreatic duct, resulting in elevated pressure within the pancreatic duct and reflux of active trypsin.Acute pancreatitis occurs when the protective mechanisms that prevent trypsinogen activation or reduce trypsin activity are compromised by overload\u003csup\u003e22\u003c/sup\u003e. The main factor contributing to AP is an imbalance in lipid metabolism-related pathways. Hyperlipidemia has surpassed alcohol as the second leading cause of AP, and the proportion of hyperlipidemia-induced pancreatitis in AP cases is also increasing. This suggests that genes regulating the lipid metabolism pathway may influence susceptibility to secondary infectious pancreatic necrosis in individuals with AP\u003csup\u003e23\u003c/sup\u003e. Pancreatitis is influenced by multiple factors. Over the past decade, numerous studies have demonstrated that acute pancreatitis can result in metabolic complications (such as exocrine pancreatic dysfunction and new-onset diabetes), regardless of the severity of the initial condition\u003csup\u003e24\u003c/sup\u003e.\u003c/p\u003e\n\u003cp\u003eThe management of acute pancreatitis is multifaceted, encompassing a spectrum of severity and clinical course. However, timely and aggressive fluid resuscitation along with early initiation of enteral nutrition have demonstrated efficacy in reducing mortality rates and the incidence of infections\u003csup\u003e25\u003c/sup\u003e. The development of hyperlipidemic pancreatitis, a type of acute pancreatitis, is triggered by the enzymatic action of pancreatic lipase on excessive fat, resulting in the generation of fatty acids. The subsequent accumulation of lipid toxicity induces robust inflammatory responses\u003csup\u003e26\u003c/sup\u003e. The mortality rate and incidence of organ necrosis in acute pancreatitis have been found to be positively correlated with the severity of hyperlipidemia\u003csup\u003e27\u003c/sup\u003e. Therefore, in the diagnosis and treatment of acute pancreatitis, clinicians consider triglyceride as a crucial adjunctive parameter: regular monitoring of triglyceride levels and serum glucose is necessary during insulin administration; cessation of intravenous insulin can be considered when the serum triglyceride concentration falls below 500mg/dL. The secretion of insulin by pancreatic beta cells plays a pivotal role in regulating glucose, amino acid, and free fatty acid metabolism in the human body\u003csup\u003e282930\u003c/sup\u003e. Maintaining optimal homeostasis of insulin concentration is achieved through a negative feedback regulatory mechanism. Any impairment to this mechanism can lead to symptoms associated with insufficient or excessive insulin secretion.\u003c/p\u003e\n\u003cp\u003ePatients with hyperinsulinemia exhibit impaired response to normal insulin levels, and it is hypothesized that obesity induces insulin resistance. This reciprocal relationship between insulin resistance and obesity further exacerbates the condition\u003csup\u003e31\u003c/sup\u003e. The connection between insulin and obesity cannot be ignored\u003csup\u003e3233\u003c/sup\u003e. The management of hyperinsulinemia encompasses pharmacological and non-pharmacological interventions\u003csup\u003e34\u003c/sup\u003e. The drug treatment options for diabetes include sulfonylureas, glucagon-like peptide 1 (GLP-1) agonists, and dipeptidyl peptide-4 (DPP-4) inhibitors\u003csup\u003e35\u003c/sup\u003e;the non-pharmacological interventions encompass the regulation of dietary energy intake, augmentation of physical activity, and enhancement of energy expenditure\u003csup\u003e36\u003c/sup\u003e. The non-drug treatment concept, although innovative and effective, necessitates a certain level of self-discipline and regularity\u003csup\u003e3738\u003c/sup\u003e, rendering it unsuitable for the acute stage of pancreatitis.\u003c/p\u003e\n\u003cp\u003e\u0026nbsp; Nevertheless, this study has certain limitations including a small sample size leading to biased sample selection, failure to follow up on long-term effects of pancreatitis treatment, and inability to refine the study based on different concentrations of serum triglycerides. Therefore, future research should focus on these aspects for further exploration.\u0026nbsp;\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eIn summary, during the course of hyperlipidemia pancreatitis, symptomatic treatment was administered to both groups of patients after hospitalization, resulting in significant improvement in clinical symptoms and laboratory indicators. However, due to their own pancreatic function impairment, patients in the HINS group experienced a slower recovery rate and disease aggravation, which had a negative impact. After conventional treatment, patients in the NHINS group exhibited milder abdominal signs and blood test reports compared to those in the HINS group. The HINS group did not significantly affect the hospital days and quality of life after discharge.\u0026nbsp;\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eDisclosure\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no conflict of interest.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis work was supported by the Scientific research project of colleges and universities in Anhui Province (grant number 2022AH052638), Anhui university natural science research project (grant number 2023AH053197)\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConflict of Interest\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNONE\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics Statement\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOur study was approved by the Ethics Review Committee of Wuhu Hospital of Anhui University of Traditional Chinese Medicine.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eInformed Consent.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eN/A\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eRegistry and the Registration No. of the study/trial.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eN/A\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAnimal Studies.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eN/A\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe author reports no financial interest or other conflict of interest statement in this work.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n \u003cli\u003eZheng CB, Zheng ZH, Zheng YP. 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Management of Severe Acute Pancreatitis: An Update. \u003cem\u003eDigestion\u003c/em\u003e. 2021;102(4):503-507.\u003c/li\u003e\n \u003cli\u003eKarabuga B, Gemcioglu E, Konca Karabuga E, et al. Comparison of the predictive values of CRP, CRP/albumin, RDW, neutrophil/lymphocyte, and platelet/lymphocyte levels in determining the severity of acute pancreatitis in patients with acute pancreatitis according to the BISAP score. \u003cem\u003eBratisl Lek Listy\u003c/em\u003e. 2022;123(2):129-135.\u003c/li\u003e\n \u003cli\u003eWoo SM, Noh MH, Kim BG, et al. Comparison of serum procalcitonin with Ranson, APACHE-II, Glasgow and Balthazar CT severity index scores in predicting severity of acute pancreatitis. \u003cem\u003eKorean J Gastroenterol\u003c/em\u003e. 2011;58(1):31-37.\u003c/li\u003e\n \u003cli\u003eHarshit Kumar A, Singh Griwan M. A comparison of APACHE II, BISAP, Ranson\u0026apos;s score and modified CTSI in predicting the severity of acute pancreatitis based on the 2012 revised Atlanta Classification. \u003cem\u003eGastroenterol Rep (Oxf)\u003c/em\u003e. 2018;6(2):127-131.\u003c/li\u003e\n \u003cli\u003eDong X,\u0026nbsp;Pan S,\u0026nbsp;Zhang D,\u0026nbsp;et al. Hyperlipemia pancreatitis onset time affects the association between elevated serum triglyceride levels and disease severity. \u003cem\u003eLipids Health Dis\u003c/em\u003e. 2022;21(1):49. Published 2022 May 30.\u003c/li\u003e\n \u003cli\u003eWang GJ,\u0026nbsp;Gao CF,\u0026nbsp;Wei D,\u0026nbsp;Wang C,\u0026nbsp;Ding SQ. Acute pancreatitis：\u0026nbsp;etiology and common pathogenesis. \u003cem\u003eWorld J Gastroenterol\u003c/em\u003e. 2009;15（12）：1427-1430.\u003c/li\u003e\n \u003cli\u003eWolbrink DRJ,Kolwijck E,Ten Oever J,et al.Management of of infected pancreatic necrosis in the intensive care unit :a narrative review[J].Clin Microbiol Infect,2020,26(1);18-25. \u0026nbsp;\u003c/li\u003e\n \u003cli\u003ePetrov MS. Metabolic Trifecta After Pancreatitis: Exocrine Pancreatic Dysfunction, Altered Gut Microbiota, and New-Onset Diabetes. Clin Transl Gastroenterol. 2019;10(10):e00086.\u003c/li\u003e\n \u003cli\u003eMederos MA,\u0026nbsp;Reber HA,\u0026nbsp;Girgis MD. Acute Pancreatitis：\u0026nbsp;A Review [published correction appears in JAMA. 2021 Jun 15;325（23）：2405]. \u003cem\u003eJAMA\u003c/em\u003e. 2021;325（4）：382-390.\u003c/li\u003e\n \u003cli\u003eSaluja A,\u0026nbsp;Dudeja V,\u0026nbsp;Dawra R,\u0026nbsp;Sah RP. Early Intra-Acinar Events in Pathogenesis of Pancreatitis. \u003cem\u003eGastroenterology\u003c/em\u003e. 2019;156（7）：1979-1993.\u003c/li\u003e\n \u003cli\u003eZhang R,\u0026nbsp;Deng L,\u0026nbsp;Jin T,\u0026nbsp;et al. Hypertriglyceridaemia-associated acute pancreatitis：\u0026nbsp;diagnosis and impact on severity. \u003cem\u003eHPB\u0026nbsp;\u003c/em\u003e\u003cem\u003e（\u003c/em\u003e\u003cem\u003eOxford\u003c/em\u003e\u003cem\u003e）\u003c/em\u003e. 2019;21（9）：1240-1249.\u003c/li\u003e\n \u003cli\u003eNorton L,\u0026nbsp;Shannon C,\u0026nbsp;Gastaldelli A,\u0026nbsp;DeFronzo RA. Insulin：The master regulator of glucose metabolism. \u003cem\u003eMetabolism\u003c/em\u003e. 2022;129：155142.\u003c/li\u003e\n \u003cli\u003eLiu R,\u0026nbsp;Zhang L,\u0026nbsp;You H. Insulin Resistance and Impaired Branched-Chain Amino Acid Metabolism in Alzheimer\u0026apos;s Disease. \u003cem\u003eJ Alzheimers Dis\u003c/em\u003e. 2023;93（3）：847-862.\u003c/li\u003e\n \u003cli\u003eStefanovski D,\u0026nbsp;Punjabi NM,\u0026nbsp;Boston RC,\u0026nbsp;Watanabe RM. Insulin Action,\u0026nbsp;Glucose Homeostasis and Free Fatty Acid Metabolism：\u0026nbsp;Insights From a Novel Model [published correction appears in Front Endocrinol\u0026nbsp;（Lausanne）. 2021 Oct 27;12：789390]. \u003cem\u003eFront Endocrinol\u0026nbsp;\u003c/em\u003e\u003cem\u003e（\u003c/em\u003e\u003cem\u003eLausanne\u003c/em\u003e\u003cem\u003e）\u003c/em\u003e. 2021;12：625701. Published 2021 Mar 16.\u003c/li\u003e\n \u003cli\u003eLee SH,\u0026nbsp;Park SY,\u0026nbsp;Choi CS. Insulin Resistance：\u0026nbsp;From Mechanisms to Therapeutic Strategies. \u003cem\u003eDiabetes Metab J\u003c/em\u003e. 2022;46（1）：15-37.\u003c/li\u003e\n \u003cli\u003eKoh HE,\u0026nbsp;Cao C,\u0026nbsp;Mittendorfer B. Insulin Clearance in Obesity and Type 2 Diabetes. \u003cem\u003eInt J Mol Sci\u003c/em\u003e. 2022;23（2）：596. Published 2022 Jan 6.\u003c/li\u003e\n \u003cli\u003eKolb H,\u0026nbsp;Kempf K,\u0026nbsp;R\u0026ouml;hling M,\u0026nbsp;Martin S. Insulin：\u0026nbsp;too much of a good thing is bad. \u003cem\u003eBMC Med\u003c/em\u003e. 2020;18（1）：224. Published 2020 Aug 21.\u003c/li\u003e\n \u003cli\u003eFerguson D,\u0026nbsp;Finck BN. Emerging therapeutic approaches for the treatment of NAFLD and type 2 diabetes mellitus. \u003cem\u003eNat Rev Endocrinol\u003c/em\u003e. 2021;17（8）：484-495.\u003c/li\u003e\n \u003cli\u003ePadhi S,\u0026nbsp;Nayak AK,\u0026nbsp;Behera A. Type II diabetes mellitus：\u0026nbsp;a review on recent drug based therapeutics. \u003cem\u003eBiomed Pharmacother\u003c/em\u003e. 2020;131：110708.\u003c/li\u003e\n \u003cli\u003eMirabelli M,\u0026nbsp;Chiefari E,\u0026nbsp;Arcidiacono B,\u0026nbsp;et al. Mediterranean Diet Nutrients to Turn the Tide against Insulin Resistance and Related Diseases. \u003cem\u003eNutrients\u003c/em\u003e. 2020;12（4）：1066.\u003c/li\u003e\n \u003cli\u003eBanaszak,\u0026nbsp;Michalina et al. \u0026ldquo;Non-Pharmacological Treatments for Insulin Resistance：\u0026nbsp;Effective Intervention of Plant-Based Diets-A Critical Review.\u0026rdquo; \u003cem\u003eNutrients\u003c/em\u003e vol. 14,7 1400. 27 Mar. 2022.\u003c/li\u003e\n \u003cli\u003eNapole\u0026atilde;o,\u0026nbsp;Ana et al. \u0026ldquo;Effects of Calorie Restriction on Health Span and Insulin Resistance：Classic Calorie Restriction Diet vs. Ketosis-Inducing Diet.\u0026rdquo; \u003cem\u003eNutrients\u003c/em\u003e vol. 13,4 1302. 15 Apr. 2021.\u003c/li\u003e\n\u003c/ol\u003e"},{"header":"Tables","content":"\u003cp\u003eTable 1 to 6 are available in the Supplementary Files section.\u003c/p\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Acute pancreatitis, Hyperlipidemic, Hyperinsulinemia, short-term prognosis","lastPublishedDoi":"10.21203/rs.3.rs-3829400/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-3829400/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003ePurpose\u003c/h2\u003e \u003cp\u003eThe short-term prognosis of hyperinsulinemia in patients with hyperlipidemia resulting in acute pancreatitis is remains uncertain.\u003c/p\u003e\u003ch2\u003eMaterial and Methods\u003c/h2\u003e \u003cp\u003eThis study presents a retrospective analysis of patients who underwent treatment for hyperlipidemic acute pancreatitis at Wuhu Hospital of Traditional Chinese Medicine from January 2020 to April 2023. The patients were categorized into two groups based on their fasting insulin levels: the hyperinsulinemia group (HINS) and the non-hyperinsulinemia group (NHINS). The study aimed to observe and record the outcomes related to metabolic disease, short-term recurrence rate, and quality of life (QOL) score.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003eIn this study, a total of 92 patients with hyperlipidemic pancreatitis were enrolled prior to lipid-lowering therapy, including 59 patients in the HINS group and 33 patients in the NHINS group. Significant differences were observed between the two groups in terms of white blood cell count (WBC), hypersensitive C-reactive protein (CRP) levels, and fasting blood glucose at 2, 3\u0026ndash;4, and 5\u0026ndash;7 days after initiation of lipid-lowering intervention (P\u0026thinsp;\u0026lt;\u0026thinsp;0.05). Following admission, anti-inflammatory treatment, lipid-lowering therapy, blood glucose control measures, and other symptomatic interventions were administered. Both groups exhibited a reduction in serum triglyceride levels; however, there was a significant difference in the magnitude of decrease compared to baseline on the fifth to seventh day (P\u0026thinsp;\u0026lt;\u0026thinsp;0.05). There were statistically significant differences between the two groups in readmission for recurrent pancreatitis within 30 days after ICU transfer and discharge (P\u0026thinsp;\u0026lt;\u0026thinsp;0.05). There was no statistically significant difference observed between the length of hospital stay or quality of life scores fifteen days after discharge.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eThe presence of hyperinsulinemia exerts a detrimental impact on the recovery process of patients with hyperlipidemia-induced acute pancreatitis, while the favorable baseline physical condition observed in the NHINS group contributes to a more advantageous recuperation from hyperlipidemic pancreatitis.\u003c/p\u003e","manuscriptTitle":"The Impact of Hyperinsulinemia on Short-term Prognosis in Patients with Hyperlipidemia-induced Acute Pancreatitis","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-01-05 18:02:45","doi":"10.21203/rs.3.rs-3829400/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"057c7b0f-fbdf-460f-812d-881dafffdc17","owner":[],"postedDate":"January 5th, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2024-01-24T18:59:12+00:00","versionOfRecord":[],"versionCreatedAt":"2024-01-05 18:02:45","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-3829400","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-3829400","identity":"rs-3829400","version":["v1"]},"buildId":"qtupq5eGEP_6zYnWcrvyt","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}