Comparison of two groups in primary dysmenorrhea: serum endocan, procalcitonin, malondialdehyde levels and antioxidants

Comparison of two groups in primary dysmenorrhea: serum endocan, procalcitonin, malondialdehyde levels and antioxidants | 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 Comparison of two groups in primary dysmenorrhea: serum endocan, procalcitonin, malondialdehyde levels and antioxidants Sibel EJDER TEKGUNDUZ, Serap EJDER APAY, Ayşe Nur AKSOY, Engin SEBIN This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9352726/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 7 You are reading this latest preprint version Abstract Purpose This study aimed to investigate the relationships between inflammatory, oxidative, and endothelial biomarkers—specifically serum endocan, procalcitonin, malondialdehyde and total antioxidant status —and primary dysmenorrhea. Methods This prospective cohort study was conducted a City Hospital. Women has moderate to severe primary dysmenorrhea and healthy controls without dysmenorrhea were enrolled. Participants underwent pelvic ultrasonography on the first day of menstruation. Venous blood samples were collected on the same day, and serum endocan, procalcitonin, malondialdehyde, and total antioxidant status levels were measured using ELISA. Results Women with primary dysmenorrhea had significantly higher serum procalcitonin and endocan levels compared with controls. No significant differences were observed in MDA or TAS levels between groups. Univariate logistic regression analysis revealed that serum procalcitonin, endocan, menstrual cycle length, follicle-stimulating hormone, and dehydroepiandrosterone sulfate were significantly associated with the presence of dysmenorrhea. TAS levels showed an inverse correlation with pain severity. Conclusion Primary dysmenorrhea is associated with increased inflammatory and endothelial activation, as reflected by elevated serum procalcitonin and endocan levels. These findings support the multifactorial nature of dysmenorrhea involving inflammatory, endothelial, and hormonal components. Further prospective studies are warranted to clarify the clinical utility of these biomarkers in the evaluation and management of primary dysmenorrhea. Antioxidant Status Dysmenorrhea Endocan Procalcitonin Malondialdehyde Introduction Dysmenorrhea is characterized by cramp-like pain in the lower abdomen that typically begins with the onset of menstruation and lasts between 8 and 72 hours [ 1 ]. This pain may be accompanied by systemic symptoms such as nausea, vomiting, headache, lower back pain, diarrhea, fatigue, and restlessness [ 2 , 3 ]. Dysmenorrhea significantly impairs quality of life, contributes to absenteeism from school or work, and is associated with an increased risk of anxiety and depressive symptoms [ 4 , 5 ]. Primary dysmenorrhea is defined as painful menstruation in the absence of identifiable pelvic pathology is primarily attributed to increased uterine contractility and inflammation mediated by elevated prostaglandin and leukotriene production following a decline in ovarian steroid hormones [ 6 , 7 ]. Symptoms typically emerge within one to two years after menarche, coincide with ovulatory cycles, and are most intense during the first 24–36 hours of menstruation [ 2 , 8 ]. In contrast, secondary dysmenorrhea arises from underlying pelvic pathology, including endometriosis, chronic pelvic inflammatory disease, uterine fibroids, cervical stenosis, or congenital and acquired reproductive tract anomalies [ 3 , 9 ]. According to World Health Organization data, dysmenorrhea affects up to 94% of adolescents aged 10–20 years and approximately 8.8% of women aged 19–41 years, highlighting its substantial global burden [ 10 ]. Although the precise pathophysiological mechanisms underlying dysmenorrhea remain incompletely understood, accumulating evidence supports a central role for inflammatory, vascular, and oxidative processes [ 11 – 13 ]. Luteal phase regression leads to progesterone withdrawal, triggering lysosomal enzyme release, cellular breakdown, and an inflammatory cascade characterized by prostaglandin synthesis and endometrial shedding [ 2 ]. These events initiate complex interactions between the endocrine, immune, and vascular systems [ 14 ]. Elevated prostaglandin levels, particularly PGF₂α and PGE₂, have been shown to induce uterine vasoconstriction, hypercontractility, ischemia, and heightened nociceptor sensitivity, thereby contributing to menstrual pain [ 15 , 16 ]. Concurrently, increased expression of inflammatory cytokines—including IL-1, IL-6, IL-8, and TNF-α—as well as matrix metalloproteinases has been documented during menstruation in women with dysmenorrhea [ 14 , 17 , 18 ]. Vascular and endothelial factors may further exacerbate dysmenorrhea. Vascular endothelial growth factor (VEGF) has been implicated in disease severity through its effects on leukocyte migration, endothelial permeability, and hypoxia-related pathways involving macrophage migration inhibitory factor (MMIF) and hypoxia-inducible factor-1α (HIF-1α) [ 19 ]. These findings suggest that endothelial dysfunction and microvascular impairment may play a role in endometrial ischemia and pain generation. Oxidative stress has also been proposed as a contributing mechanism in primary dysmenorrhea. Lipid peroxidation, a hallmark of oxidative injury, has been observed during inflammatory and ischemic conditions associated with menstruation [ 20 , 21 ]. Reactive oxygen species can damage lipids, proteins, and nucleic acids, amplifying tissue injury and inflammation [ 22 ]. Accordingly, biomarkers such as malondialdehyde (MDA) have been widely used to assess oxidative stress in clinical and experimental settings [ 23 , 24 ]. Endocan (endothelial cell-specific molecule-1) is a soluble dermatan sulfate proteoglycan secreted by activated endothelial cells and is increasingly recognized as a marker of endothelial dysfunction and inflammation [ 25 ]. Elevated circulating endocan levels have been reported in various inflammatory and vascular conditions, suggesting its potential relevance in disorders characterized by endothelial activation and ischemia [ 26 , 27 ]. Given the ischemic and inflammatory milieu of dysmenorrhea, endocan may serve as a novel biomarker reflecting endothelial involvement in disease pathophysiology. Procalcitonin, a precursor of calcitonin synthesized primarily by thyroid C cells, is an established acute-phase reactant. While traditionally associated with bacterial infections and sepsis, emerging evidence indicates that procalcitonin levels may also increase in non-infectious inflammatory states [ 28 – 30 ]. To date, among acute-phase reactants, only high-sensitivity C-reactive protein (hs-CRP) has been evaluated in primary dysmenorrhea, and data on procalcitonin in this context are lacking [ 31 ]. The balance between oxidative stress and antioxidant defense systems is critical in maintaining cellular homeostasis. Total antioxidant status reflects the combined activity of enzymatic and non-enzymatic antioxidants and provides an integrated measure of antioxidant capacity in biological fluids [ 24 ].Alterations in this balance may influence pain severity, inflammation, and endothelial function in dysmenorrhea. Given the limited data addressing the interplay between oxidative stress, antioxidant capacity, inflammatory activity, and endothelial dysfunction in primary dysmenorrhea, this study aimed to evaluate the association between serum endocan, procalcitonin, malondialdehyde levels, and total antioxidant status in women with primary dysmenorrhea. Material and Methods Study Design and Setting This study was designed as a prospective cohort study and conducted at the Gynecology and Pediatrics Clinics of Erzurum City Hospital. Study Population Inclusion Criteria Women aged 18–30 years who presented to Erzurum City Hospital with moderate to severe primary dysmenorrhea were eligible for inclusion. All participants were nulliparous, non-smokers, had normal findings on physical and ultrasonographic examinations, and had no history of chronic abdominal or pelvic inflammatory, circulatory, or surgical diseases. Dysmenorrhea was required to have started 2–3 years after menarche, to be cyclical in nature, to begin a few hours before the onset of menstruation, and to persist during the first three days of the menstrual cycle. Exclusion Criteria Participants were excluded if they had a body mass index (BMI) ≥30 kg/m², systemic diseases (including cardiovascular, pulmonary, endocrine, or metabolic disorders), a history of smoking or alcohol consumption, pelvic pathology (such as endometriosis, ovarian cysts, or previous pelvic surgery), or if they had used analgesic medications within 24 hours prior to blood sampling. Control Group The control group consisted of healthy women without dysmenorrhea and with no known gynecological or systemic diseases. Clinical Assessment and Sample Collection On the first day of menstruation, all participants underwent pelvic ultrasonography to exclude underlying pelvic pathology. Pain severity was assessed using a visual analog scale (VAS) ranging from 0 (no pain) to 10 (worst pain imaginable). Demographic and clinical data, including age, BMI, menstrual cycle length (days), and duration of menstrual bleeding (days), were recorded. Venous blood samples were collected from all participants on the same day. Samples were centrifuged at 3000 rpm for 10 minutes, and the separated serum was stored at −80°C until biochemical analysis. Laboratory Analysis Plasma procalcitonin and serum malondialdehyde (MDA) and endocan levels were measured using enzyme-linked immunosorbent assay (ELISA) kits on automated analyzers, in accordance with the manufacturers’ instructions. Results were recorded using the reference ranges and units specified by the assay kits. Sample Size and Power Analysis Based on power analysis, a minimum of 25 participants per group was required to achieve 85% statistical power. Statistical Analysis Statistical analyses were performed using SPSS software (latest version; IBM Corp., Armonk, NY, USA). Normality of continuous variables was assessed using the Kolmogorov–Smirnov test. Continuous variables were expressed as mean ± standard deviation or median (interquartile range), as appropriate, while categorical variables were presented as frequencies and percentages. Group comparisons were conducted using the independent samples t -test or Mann–Whitney U test for continuous variables and the chi-square test for categorical variables. Associations between clinical and biochemical variables and the presence of primary dysmenorrhea were evaluated using univariate logistic regression analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) were reported. A p value <0.05 was considered statistically significant. Funding : This study was supported by Atatürk University Scientific Research Project Directorate with project number 12205 and project code TKP-2023-12205. Ethics: Ethical approval was obtained from the Atatürk University Faculty of Health Sciences Ethics Committee (No: B.30.2.ATA.0.01.00/228 Date:30.03.2023). Informed consent was obtained from the participants in the study. The Helsinki Declaration rules were followed at every stage of the research. Results A total of 42 women with primary dysmenorrhea and 42 healthy controls were included in the study. Comparisons of sociodemographic and menstrual characteristics are presented in Table 1. There were no significant differences between the groups in terms of age, body mass index, or menstrual duration (all p > .05). However, women with dysmenorrhea had significantly shorter menstrual cycle lengths compared with controls (29.71 ± 3.98 vs. 32.98 ± 8.17 days, p=.02). As expected, VAS pain scores were markedly higher in the dysmenorrhea group than in the control group (7.82 ± 1.02 vs. 0.82 ± 0.93, p < .001). Table 1 . Comparison of Sociodemographic and Menstrual Characteristics Between Women With and Without Dysmenorrhea Characteristics With dysmenorrhea Without dysmenorrhea t (df) p Age (years), M ± SD 23.00 ± 3.26 22.09 ± 3.27 1.32 .18 Body mass index (kg/m²) 21.72 ± 3.66 22.40 ± 3.40 -0.91 .36 Cycle length (days) 29.71 ± 3.98 32.98 ± 8.17 -2.41 .02* Menstrual duration (days) 5.60 ± 1.60 5.93 ± 1.76 -0.93 .35 VAS pain score (0–10) 7.82 ± 1.02 0.82 ± 0.93 33.75 <.001*** Note. Values are presented as mean ± standard deviation (M ± SD). VAS = Visual Analogue Scale. p < .05; p < .01; p < .001. Biochemical and hormonal parameters are summarized in Table 2. Women with dysmenorrhea exhibited significantly higher serum levels of follicle-stimulating hormone (FSH), dehydroepiandrosterone sulfate (DHEA-S), procalcitonin, and endocan compared with controls (all p < .05). No statistically significant differences were observed between the groups for luteinizing hormone, estradiol, thyroid-stimulating hormone, prolactin, total testosterone, malondialdehyde (MDA), or total antioxidant status (TAS). Table 2 . Comparison of Biochemical Parameters Between Women With and Without Dysmenorrhea Parameter With dysmenorrhea Without dysmenorrhea t (df) p FSH (mIU/mL) 6.97 ± 1.67 6.18 ± 1.84 2.13 .03* LH (mIU/mL) 4.94 ± 2.20 5.79 ± 4.50 -1.13 .25 Estradiol (pg/mL) 38.94 ± 13.74 41.57 ± 18.67 -0.76 .44 TSH (µIU/mL) 1.94 ± 1.13 1.99 ± 0.90 -0.22 .82 Prolactin (ng/mL) 13.42 ± 5.68 13.50 ± 6.85 -0.06 .95 DHEA-S (µg/dL) 213.31 ± 101.78 169.60 ± 93.39 2.12 .03* Total testosterone (ng/dL) 25.81 ± 7.10 29.05 ± 9.62 -1.81 .07 Procalcitonin (ng/mL) 0.59 ± 0.41 0.08 ± 0.13 7.87 <.001*** MDA (µmol/L) 1.61 ± 1.37 2.14 ± 1.74 -1.60 .11 Endocan (pg/mL) 279.36 ± 362.53 126.43 ± 116.95 2.69 .008** TAS (µmol Trolox equiv/L) 32.41 ± 37.53 30.72 ± 27.01 0.24 .80 Note. Values are presented as mean ± standard deviation (M ± SD). FSH = follicle-stimulating hormone; LH = luteinizing hormone; TSH = thyroid-stimulating hormone; DHEA-S = dehydroepiandrosterone sulfate; MDA = malondialdehyde; TAS = total antioxidant status. p < .05; p < .01; p < .001. Correlation analyses stratified by study group are shown in Table 3. In the dysmenorrhea group, estradiol levels were positively correlated with body mass index, while prolactin levels were negatively correlated with VAS pain scores. Both DHEA-S and total testosterone demonstrated positive correlations with pain severity. TAS showed a strong positive correlation with body mass index and a strong inverse correlation with VAS scores. In the control group, FSH was negatively correlated with menstrual duration, MDA was positively correlated with body mass index, endocan was positively correlated with age, and procalcitonin showed a strong positive correlation with VAS scores. Table 3 . Pearson’s Correlation Coefficients Between Biochemical Parameters and Clinical Characteristics in Women With and Without Dysmenorrhea <table border="1" cellspacing="3" cellpadding="0" width="100%" Group Parameter Age BMI Cycle length Menstrual duration VAS With dysmenorrhea FSH .11 (.46) –.15 (.32) –.03 (.85) –.14 (.35) –.06 (.69) LH –.14 (.37) –.01 (.96) .04 (.77) .15 (.34) .03 (.84) Estradiol –.02 (.90) .30* (.048) –.06 (.69) –.11 (.49) .03 (.86) TSH –.04 (.77) .11 (.49) –.03 (.85) .09 (.58) –.08 (.61) Prolactin .19 (.22) .18 (.24) –.02 (.89) .28 (.07) –.30* (.048) DHEA-S –.10 (.50) –.20 (.19) –.26 (.08) .16 (.31) .38* (.011) Testosterone –.03 (.83) –.07 (.65) –.21 (.16) .25 (.10) .39** (.008) Procalcitonin –.18 (.24) .16 (.30) –.19 (.22) –.10 (.53) .19 (.22) MDA –.12 (.43) .01 (.93) –.06 (.67) .08 (.61) –.02 (.92) Endocan –.03 (.83) –.14 (.35) .14 (.36) –.24 (.11) .09 (.58) TAS .15 (.33) .56*** (.001) .23 (.13) .07 (.63) –.57*** (<.001) Without dysmenorrhea FSH .07 (.67) –.13 (.38) –.27 (.07) –.32* (.030) –.11 (.46) LH –.07 (.65) –.20 (.18) –.15 (.34) –.23 (.14) .02 (.91) Estradiol .01 (.95) –.05 (.77) .01 (.97) .02 (.88) –.15 (.34) TSH .05 (.76) .27 (.07) .04 (.78) –.05 (.76) .26 (.09) Prolactin .22 (.15) .02 (.88) –.06 (.70) –.10 (.53) –.18 (.23) DHEA-S .02 (.91) .14 (.37) .04 (.77) –.06 (.69) .18 (.24) Testosterone –.22 (.15) –.26 (.09) –.04 (.82) .05 (.75) –.09 (.56) Procalcitonin –.05 (.76) –.06 (.71) .03 (.84) –.20 (.20) .50*** (<.001) MDA .11 (.48) .31* (.039) –.12 (.42) .07 (.63) .06 (.71) Endocan .39** (.008) .28 (.07) –.12 (.45) –.22 (.15) –.15 (.34) TAS –.05 (.73) –.05 (.77) –.23 (.14) .04 (.79) –.21 (.17) Values are Pearson’s r (two-tailed p in parentheses). FSH = follicle-stimulating hormone; LH = luteinizing hormone; TSH = thyroid-stimulating hormone; DHEA-S = dehydroepiandrosterone sulfate; MDA = malondialdehyde; TAS = total antioxidant status; VAS = Visual Analogue Scale. p < .05; * p < .01; ** p < .001. Univariate binary logistic regression analyses identifying factors associated with dysmenorrhea are presented in Table 4. Endocan (OR = 0.996, p = .038), procalcitonin (OR = 0.002, p < .001), menstrual cycle length (OR = 1.099, p = .030), FSH (OR = 0.771, p = .040), and DHEA-S (OR = 0.995, p = .042) were significantly associated with the presence of dysmenorrhea. Higher procalcitonin levels were strongly associated with dysmenorrhea, whereas higher endocan, FSH, and DHEA-S levels showed inverse associations. Longer cycle length was positively associated with dysmenorrhea. The VAS pain score demonstrated quasi-complete separation in the logistic regression model, precluding reliable estimation of odds ratios. MDA, TAS, age, and menstrual duration were not significantly associated with dysmenorrhea (all p > .05). Table 4 . Regression analysis some Biochemical Parameters Women With and Without Dysmenorrhea Variable OR (Exp[B]) 95% CI p-value VAS score Not estimable — 0.994 Endocan 0.996 0.992 – 1.000 0.038 Procalcitonin 0.002 0.000 – 0.035 <0.001* Cycle length 1.099 1.009 – 1.197 0.030 FSH 0.771 0.602 – 0.988 0.040 DHEAS 0.995 0.991 – 1.000 0.042 MDA 1.260 0.938 – 1.692 0.124 TAS 0.998 0.986 – 1.011 0.804 Age 0.916 0.802 – 1.045 0.192 Menstrual duration 1.128 0.878 – 1.449 0.347 OR, odds ratio; CI, confidence interval; VAS, Visual Analog Scale; MDA, malondialdehyde; TAS, total antioxidant status; FSH, follicle-stimulating hormone; DHEAS, dehydroepiandrosterone sulfate. VAS demonstrated quasi-complete separation, resulting in non-estimable odds ratios. All analyses were performed using univariate binary logistic regression. * p < .001 Discussion The present study evaluated the associations between inflammatory, oxidative, and endothelial biomarkers and primary dysmenorrhea by integrating biochemical findings with clinical characteristics. Our results demonstrated significantly higher serum levels of procalcitonin and endocan in women with dysmenorrhea, along with increased follicle-stimulating hormone (FSH) and dehydroepiandrosterone sulfate (DHEA-S) concentrations. Furthermore, univariate binary logistic regression analyses identifiedprocalcitonin, endocan, menstrual cycle length, FSH, and DHEA-S as variables significantly associated with the presence of dysmenorrhea. Among the evaluated biomarkers, procalcitonin showed the strongest association with dysmenorrhea. Although procalcitonin is classically regarded as a biomarker of bacterial infection and systemic inflammation, accumulating evidence indicates that it may also reflect inflammatory activation in non-infectious conditions [32-34]. Its prognostic relevance in cardiovascular and neurological disorders, including acute myocardial infarction and intracerebral hemorrhage, further supports its role as a marker of systemic inflammatory burden rather than infection alone [35,36]. In this context, our findings suggest that elevated procalcitonin levels in dysmenorrhea may reflect inflammatory activation accompanying pain severity, consistent with broader clinical observations [37,38]. Importantly, given the cross-sectional design, procalcitonin should be interpreted as a biomarker associated with dysmenorrhea rather than a causal mediator of pain. Previous studies investigating dysmenorrhea have predominantly focused on oxidative stress and classical inflammatory mediators. Aksoy et al. [39]. (2017) reported increased levels of heme oxygenase-1, nitric oxide, and malondialdehyde (MDA) in women with dysmenorrhea, supporting a role for lipid peroxidation and oxidative injury. Similarly, elevated MDA and proinflammatory cytokines have been described during the menstrual phase in dysmenorrheic women [17,40]. In contrast, our study did not demonstrate significant differences in MDA or total antioxidant status (TAS) between groups. This discrepancy may be attributable to interindividual variability, dietary antioxidant intake, or the use of nonsteroidal anti-inflammatory drugs, which have been shown to attenuate oxidative stress markers in dysmenorrhea [41-43]. Nevertheless, the observed inverse correlation between TAS and pain severity in our cohort supports the hypothesis that antioxidant capacity may modulate symptom intensity. The significantly elevated serum endocan levels observed in women with dysmenorrhea further support the involvement of endothelial dysfunction in menstrual pain pathophysiology. Endocan is a proteoglycan secreted by activated endothelial cells and has been associated with vascular inflammation, endothelial activation, and adverse cardiovascular outcomes [44-46]. Our findings are consistent with previous reports suggesting that oxidative and endothelial stress responses play a central role in dysmenorrhea [39]. The association between endocan and dysmenorrhea highlights the potential contribution of microvascular dysfunction and endometrial ischemia to pain generation. Beyond biochemical parameters, menstrual cycle length emerged as a clinically relevant factor associated with dysmenorrhea. The positive association between longer cycle length and dysmenorrhea underscores the importance of menstrual characteristics in routine clinical assessment. In addition, the observed associations of FSH and DHEA-S with dysmenorrhea suggest that subtle endocrine variations may influence inflammatory responses or pain perception, consistent with prior observations linking hormonal milieu to menstrual pain severity. Interventional and experimental studies further support the clinical relevance of oxidative and inflammatory pathways in dysmenorrhea. Red-light photobiomodulation, herbal extracts, probiotic supplementation, and lifestyle interventions such as high-intensity interval training have all been shown to reduce inflammatory markers and improve pain outcomes [47-51]. These findings collectively suggest that targeting oxidative stress and inflammation may represent a promising therapeutic strategy. In conclusion, our findings highlight the multifactorial nature of primary dysmenorrhea, involving inflammatory, endothelial, oxidative, and hormonal components. Although causal relationships cannot be inferred, the observed associations suggest that biomarkers such as procalcitonin and endocan may complement clinical evaluation and improve the characterization of dysmenorrhea. Interventional and experimental studies further support the clinical relevance of oxidative and inflammatory pathways in dysmenorrhea. Red-light photobiomodulation, herbal extracts, probiotic supplementation, and lifestyle interventions such as high-intensity interval training have all been shown to reduce inflammatory markers and improve pain outcomes [47-51]. These findings collectively suggest that targeting oxidative stress and inflammation may represent a promising therapeutic strategy. Future prospective studies are warranted to clarify temporal relationships and to explore whether these biomarkers may contribute to risk stratification or individualized management strategies. Declarations Author Contribution SET: Protocol development, Data collection, Manuscript writing SEA: Protocol, Data analysis, Manuscript writing ANA: Protocol development, Data collection, Manuscript writing ES: Laboratory analysis Funding : This study was supported by Atatürk University Scientific Research Project Directorate with project number 12205 and project code TKP-2023-12205. Competing Interests: There is no conflict of interest among the authors. Ethics approval: Ethical approval was obtained from the Atatürk University Faculty of Health Sciences Ethics Committee (No: B.30.2.ATA.0.01.00/228 Date:30.03.2023). Consent to participate: Informed consent was obtained from the participants in the study. Data Availability Statement: The data that support the findings of this study are available from the corresponding author upon reasonable request References Latthe PM, Champaneria R, Khan KS. (2011) Dysmenorrhoea. BMJ Clinical Evidence 0813. Dawood MY. Primary dysmenorrhea: advances in pathogenesis and management. Obstet Gynecol. 2006;108(2):428–41. https://doi.org/10.1097/01.AOG.0000230214.26638.0c . Harel Z. Dysmenorrhea in adolescents and young adults: etiology and management. J Pediatr Adolesc Gynecol. 2006;19(6):363–71. https://doi.org/10.1016/j.jpag.2006.09.001 . Balık G, Ustüner I, Kağıtcı M, Sahin FK. Is there a relationship between mood disorders and dysmenorrhea? J Pediatr Adolesc Gynecol. 2014;27(6):371–4. https://doi.org/10.1016/j.jpag.2014.01.108 . Nur Azurah AG, Sanci L, Moore E, Grover S. The quality of life of adolescents with menstrual problems. J Pediatr Adolesc Gynecol. 2013;26(2):102–8. https://doi.org/10.1016/j.jpag.2012.11.004 . American College of Obstetricians and Gynecologists (ACOG). Committee opinion 760: Dysmenorrhea and endometriosis in the adolescent. Obstet Gynecol. 2018;132(6):e249–58. Oladosu FA, Tu FF, Hellman KM. Nonsteroidal antiinflammatory drug resistance in dysmenorrhea: epidemiology, causes, and treatment. Am J Obstet Gynecol. 2018;218(4):390–400. https://doi.org/10.1016/j.ajog.2017.08.108 . Burnett M, Lemyre M. 345-Primary Dysmenorrhea Consensus Guideline. J Obstet Gynecol Can. 2017;39(7):585–95. https://doi.org/10.1016/j.jogc.2016.12.023 . Iacovides S, Avidon I, Baker FC. What we know about primary dysmenorrhea today: a critical review. Hum Reprod Update. 2015;21(6):762–78. https://doi.org/10.1093/humupd/dmv039 . Latthe P, Latthe M, Say L, Gülmezoglu M, Khan KS. WHO systematic review of prevalence of chronic pelvic pain: a neglected reproductive health morbidity. BMC Public Health. 2006;6:177. https://doi.org/10.1186/1471-2458-6-177 . Rad M, Sabzevari MT, Rastaghi S, Dehnavi ZM. The relationship between anthropometric index and primary dysmenorehea in female high school students. J Educ Health Promotion. 2018;7:34. https://doi.org/10.4103/jehp.jehp_117_17 . Guimarães I, Póvoa AM. Primary Dysmenorrhea: Assessment and Treatment. Revista Brasileira de Ginecol e Obstet. 2020;42(8):501–7. https://doi.org/10.1055/s-0040-1712131 . Barcikowska Z, Rajkowska-Labon E, Grzybowska ME, Hansdorfer-Korzon R, Zorena K. Inflammatory markers in dysmenorrhea and therapeutic options. Int J Environ Res Public Health. 2020;17(4):1191. https://doi.org/10.3390/ijerph17041191 . Maybin JA, Critchley HO. Progesterone: a pivotal hormone at menstruation. Ann N Y Acad Sci. 2011;1221:88–97. https://doi.org/10.1111/j.1749-6632.2011.05953.x . Pickles VR, Hall WJ, Best FA, Smith GN. Prostaglandins in endometrium and menstrual fluid from normal and dysmenorrhoeic subjects. BJOG: Int J Obstet Gynecol. 1965;72:185–92. https://doi.org/10.1111/j.1471-0528.1965.tb01415.x . Dawood MY, Dysmenorrhea and prostaglandins. In Gynecologic endocrinology 405–421. Boston, MA: Springer US; 1987. Yeh ML, Chen HH, So EC, Liu CF. A study of serum malondialdehyde and interleukin-6 levels in young women with dysmenorrhea in Taiwan. Life Sci. 2004;75(6):669–73. https://doi.org/https://doi.org/10.1016/j.lfs.2003.11.034 . Konecna L, Yan MS, Miller LE, Schölmerich J, Falk W, Straub RH, Brain. Behav Immun 14(1), 49–61. https://doi.org/10.1006/brbi.1999.0570 . Zhang F, Liu XL, Wang W, Dong HL, Xia YF, Ruan LP, Liu LP. Expression of MMIF, HIF-1α and VEGF in serum and endometrial tissues of patients with endometriosis. Curr Med Sci. 2018;38(3):499–504. https://doi.org/10.1007/s11596-018-1906-1 . Guliaeva NV, Luzina NL, Levshina IP, Kryzhanovskiĭ GN. The inhibition stage of lipid peroxidation during stress. Biull Eksp Biol Med. 1988;106(12):660–3. De Sanctis V, Soliman A, Bernasconi S, Bianchin L, Bona G, Bozzola M, et al. Primary dysmenorrhea in adolescents: Prevalence, impact and recent knowledge. Pediatr Endocrinol Reviews. 2015;13:512–20. Baird DT, Cameron ST, Critchley HO, Drudy TA, Howe A, Jones RL, Lea RG, Kelly RW. Prostaglandins and menstruation. Eur J Obstet Gynecol Reproductive Biology. 1996;70(1):15–7. https://doi.org/10.1016/s0301-2115(96)02568-7 . Uttara B, Singh AV, Zamboni P, Mahajan RT. Oxidative stress and neurodegenerative diseases: a review of upstream and downstream antioxidant therapeutic options. Curr Neuropharmacol. 2009;7(1):65–74. https://doi.org/10.2174/157015909787602823 . Szmidt MK, Granda D, Sicinska E, Kaluza J. Primary Dysmenorrhea in Relation to Oxidative Stress and Antioxidant Status: A Systematic Review of Case-Control Studies. Antioxidants. 2020;9(10):994. https://doi.org/10.3390/antiox9100994 . Zhao T, Kecheng Y, Zhao X, Hu X, Zhu J, Wang Y, Ni J. The higher serum endocan levels may be a risk factor for the onset of cardiovascular disease: A meta-analysis. Medicine. 2018;97(49):e13407. https://doi.org/10.1097/MD.0000000000013407 . Poon PY, Ng JK, Fung WW, Chow KM, Kwan BC, Li PK, Szeto CC. Relationship between plasma endocan level and clinical outcome of chinese peritoneal dialysis patients. Kidney Blood Press Res. 2019;44(5):1259–70. https://doi.org/10.1159/000502961 . Oktar SF, Guney I, Eren SA, Oktar L, Kosar K, Buyukterzi Z, Alkan E, Biyik Z, Erdem SS. Serum endocan levels, carotid intima-media thickness and microalbuminuria in patients with newly diagnosed hypertension. Clin Exp Hypertens. 2019;41(8):787–94. https://doi.org/10.1080/10641963.2019.1652632 . Wacker C, Prkno A, Brunkhorst FM, Schlattmann P. Procalcitonin as a diagnostic marker for sepsis: a systematic review and meta-analysis. Lancet Infect Dis. 2013;13(5):426–35. https://doi.org/10.1016/S1473-3099(12)70323-7 . Aringer M. Inflammatory markers in systemic lupus erythematosus. J Autoimmun. 2020;110:102374. https://doi.org/10.1016/j.jaut.2019.102374 . Wang J, Niu R, Jiang L, Wang Y, Shao X, Wu M, Ma Y. The diagnostic values of C-reactive protein and procalcitonin in identifying systemic lupus erythematosus infection and disease activity. Medicine. 2019;98(33):e16798. https://doi.org/10.1097/MD.0000000000016798 . Bahrami A, Bahrami-Taghanaki H, Khorasanchi Z, Timar A, Jaberi N, Azaryan E, Tayefi M, Ferns GA, Sadeghnia HR, Ghayour-Mobarhan M. Menstrual problems in adolescence: relationship to serum vitamins A and E, and systemic inflammation. Arch Gynecol Obstet. 2020;301(1):189–97. https://doi.org/10.1007/s00404-019-05343-1 . Bektas F, Soyuncu S, Gunduz I, Basarici I, Akbas H, Eken C. The value of procalcitonin, a novel inflammatory marker,diagnosis of myocardial infarction and evaluation of acute coronary syndrome patients. J Emerg Med. 2011;41(5):524–30. https://doi.org/10.1016/j.jemermed.2010.05.073 . Smolle KH, Kaufmann P, Stadlbauer V, Tatzber F, Winklhofer-Roob BM, Aigner R, Khoschsorur G, Wonisch W. Intermittent haemodialysis-induced oxidative stress and the effect on inflammatory parameters in critically ill patients. Clin Experimental Med J. 2010;4(1):79–88. https://doi.org/https://doi.org/10.1556/CEMED.4.2010.1.8 . He D, Zhang Y, Zhang B, Jian W, Deng X, Yang Y, Xiao T, Yu H, Wen S, Huang K. Serum Procalcitonin Levels are Associated with Clinical Outcome in Intracerebral Hemorrhage. Cell Mol Neurobiol. 2018;38(3):727–33. https://doi.org/10.1007/s10571-017-0538-5 . Festic E, Siegel J, Stritt M, Freeman WD. The Utility of Serum Procalcitonin in Distinguishing Systemic Inflammatory Response Syndrome from Infection After Aneurysmal Subarachnoid Hemorrhage. Neurocrit Care. 2014;20(3):375–81. https://doi.org/10.1007/s12028-014-9960-4 . Firani NK, Prisilla J. Procalcitonin and Troponin-I as Predictor of Mortality in Acute Myocardial Infarction Patients. Indonesian J Clin Pathol Med Lab. 2022;28(2):170–4. https://doi.org/10.24293/ijcpml.v28i2.1817 . Schuetz P, Daniels LB, Kulkarni P, Anker SD, Mueller B. Procalcitonin: A new biomarker for the cardiologist. Int J Cardiol. 2016;223:390–7. https://doi.org/10.1016/j.ijcard.2016.08.204 . Oka K, Araki J, Yamamoto K, Hanayama Y, Tokumasu K, Hagiya H, Obika M, Ogawa H, Otsuka F. Interrelationships Between Serum Levels of Procalcitonin and Inflammatory Markers. J Endocr Soc. 2021;5(1):A264–5. https://doi.org/10.1210/jendso/bvab048.536 . Aksoy AN, Laloglu E, Ozkaya AL, Yilmaz EPT. Serum heme oxygenase-1 levels in patients with primary dysmenorrhea. Arch Gynecol Obstet. 2017;295(4):929–34. https://doi.org/10.1007/s00404-017-4312-1 . Dikensoy E, Balat O, Pençe S, Balat A, Çekmen M, Yurekli M. Malondialdehyde, nitric oxide and adrenomedullin levels in patients with primary dysmenorrhea. J Obstet Gynecol Res. 2008;34(6):1049–53. https://doi.org/https://doi.org/10.1111/j.1447-0756.2008.00802.x . Furniss LD. Nonsteroidal anti-inflammatory agents in the treatment of primary dysmenorrhea. Clin Pharm. 1982;1(4):327–33. Kaplan Ö, Nazıroğlu M, Güney M, Aykur M. Non-steroidal anti-inflammatory drug modulates oxidative stress and calcium ion levels in the neutrophils of patients with primary dysmenorrhea. J Reprod Immunol. 2013;100(2):87–92. https://doi.org/https://doi.org/10.1016/j.jri.2013.10.004 . Haidari F, Homayouni F, Helli B, Haghighizadeh MH, Farahmandpour F. Effect of chlorella supplementation on systematic symptoms and serum levels of prostaglandins, inflammatory and oxidative markers in women with primary dysmenorrhea. Eur J Obstetrics&Gynecology Reproductive Biology. 2018;229:185–9. https://doi.org/https://doi.org/10.1016/j.ejogrb.2018.08.578 . Sekercioglu N, Balci H, Pekpak M. Procalcitonin and Malondialdehyde as Markers of Inflammation in Hemodialysis Patients. J Clin Anal Med. 2017;8:346–50. https://doi.org/10.4328/JCAM.4899 . Hu J, Yang C, Yang G, Du H, Zhao H, Liu H. Effects of atorvastatin doses on serum level of procalcitonin and predictors for major adverse cardiovascular events in patients with acute myocardial infarction: a pilot study and post hoc analysis. Coron Artery Dis. 2022;33(1):e87–93. https://doi.org/10.1097/mca.0000000000001084 . Zakaria IA, Mohammed Zain NA, Teik CK, Abu MA, Zainuddin AA, Abdul Aziz NH, Safian N, Mohd Mokhtar N, Raja Ali RA, Beng Kwang N, Mohamed Ismail NA, Hamizan MR, Ab Razak WS, Nur Azurah AG. The role of probiotics in improving menstrual health in women with primary dysmenorrhoea: A randomized, double-blind, placebo-controlled trial. Women's Health. 2024;20:17455057241234524. https://doi.org/10.1177/17455057241234524 . Chen Y, Cao Y, Xie Y, Zhang X, Yang Q, Li X, Sun J, Qiu P, Cao W, Wang S. (2013) Traditional Chinese medicine for the treatment of primary dysmenorrhea: How do Yuanhu painkillers effectively treat dysmenorrhea? Phytomedicine 20(12), 1095–1104. https://doi.org/https://doi.org/10.1016/j.phymed.2013.05.003 Mukhoirotin M, Kurniawati K, Mawarti H. The Effect of Slow Stroke Back Massage on Primary Dysmenorrhea: Levels of Beta-Endorphin, Interleukin-6, Tumor Necrosis Factor-α, and Pain Intensity. Int J Women's Health Reprod Sci. 2020;8:376–82. https://doi.org/10.15296/ijwhr.2020.60 . Yang X, Tian Y, Liu J, Kou Y, Xie Y, Wang S, Zhao Y. (2023) Peony Pollen Protects against Primary Dysmenorrhea in Mice by Inhibiting Inflammatory Response and Regulating the COX2/PGE2 Pathway. International Journal of Molecular Sciences, 24(24), 17245. https://www.mdpi.com/1422-0067/24/24/17245 Fu Q, Yang J, Jiang H, Qin H, Li A, Huo L, Liu M. Pulsed red light photobiomodulation ameliorates oxytocin-induced primary dysmenorrhea in mice by inhibiting oxidative stress and lipid accumulation. J Photochem Photobiol B. 2025;264:113119. https://doi.org/https://doi.org/10.1016/j.jphotobiol.2025.113119 . Yang MY, Chen HY, Ho CH, Huang WC. (2025) Impact of Probiotic Supplementation and High-Intensity Interval Training on Primary Dysmenorrhea: A Double-Blind, Randomized Controlled Trial Investigating Inflammation and Hormonal Modulation. Nutrients 17(4), 622. https://www.mdpi.com/2072-6643/17/4/622 Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Reviewers agreed at journal 08 May, 2026 Reviewers agreed at journal 03 May, 2026 Reviewers invited by journal 03 May, 2026 Editor invited by journal 13 Apr, 2026 Editor assigned by journal 09 Apr, 2026 Submission checks completed at journal 09 Apr, 2026 First submitted to journal 08 Apr, 2026 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. 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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-9352726","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":637107257,"identity":"f3d78a21-4502-4f60-96af-612683b10da4","order_by":0,"name":"Sibel EJDER TEKGUNDUZ","email":"","orcid":"","institution":"University of Health Science","correspondingAuthor":false,"prefix":"","firstName":"Sibel","middleName":"EJDER","lastName":"TEKGUNDUZ","suffix":""},{"id":637107262,"identity":"5e6a2053-9eda-4799-9b60-a6eccf0baee1","order_by":1,"name":"Serap EJDER APAY","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAz0lEQVRIiWNgGAWjYHCCBAkGBpsECLOAeC1pCQxsIKYBkdYAtRyGaGEgRot8e8PDGx/3nM/jl+9O/PDAgEGeX+wAfi0GZw4kW854drtYso13swTQYYYzZycQ0CKRkCbNc+B24oZjvBtAWhIMbhPQIj//QZr0nwPnQFo2/yBKC8MNhjRphgMHQFq2EWeLwZmEZMueA8mJM9tyt1kkGEgQ9ot8+5nEGz8O2CX2M5/dfPNHhY08vzQhhzHwoKiQIKQcBNgPEKNqFIyCUTAKRjIAABSQRs1Lz3NJAAAAAElFTkSuQmCC","orcid":"","institution":"Atatürk University","correspondingAuthor":true,"prefix":"","firstName":"Serap","middleName":"EJDER","lastName":"APAY","suffix":""},{"id":637107265,"identity":"eb6f7b6d-ad34-4a0f-8e2f-2af7f366f64a","order_by":2,"name":"Ayşe Nur AKSOY","email":"","orcid":"","institution":"University of Health Science","correspondingAuthor":false,"prefix":"","firstName":"Ayşe","middleName":"Nur","lastName":"AKSOY","suffix":""},{"id":637107269,"identity":"5283b90a-2a9e-4bb5-a17f-2276073a075b","order_by":3,"name":"Engin SEBIN","email":"","orcid":"","institution":"University of Health Science","correspondingAuthor":false,"prefix":"","firstName":"Engin","middleName":"","lastName":"SEBIN","suffix":""}],"badges":[],"createdAt":"2026-04-08 06:53:37","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-9352726/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-9352726/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":108999676,"identity":"019a7a68-db62-4bdc-9164-8df075461244","added_by":"auto","created_at":"2026-05-11 14:43:33","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":400794,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9352726/v1/222e7054-2dd5-4788-9b6c-f028c4e69d5b.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Comparison of two groups in primary dysmenorrhea: serum endocan, procalcitonin, malondialdehyde levels and antioxidants","fulltext":[{"header":"Introduction","content":"\u003cp\u003eDysmenorrhea is characterized by cramp-like pain in the lower abdomen that typically begins with the onset of menstruation and lasts between 8 and 72 hours [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. This pain may be accompanied by systemic symptoms such as nausea, vomiting, headache, lower back pain, diarrhea, fatigue, and restlessness [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. Dysmenorrhea significantly impairs quality of life, contributes to absenteeism from school or work, and is associated with an increased risk of anxiety and depressive symptoms [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e].\u003c/p\u003e \u003cp\u003ePrimary dysmenorrhea is defined as painful menstruation in the absence of identifiable pelvic pathology is primarily attributed to increased uterine contractility and inflammation mediated by elevated prostaglandin and leukotriene production following a decline in ovarian steroid hormones [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. Symptoms typically emerge within one to two years after menarche, coincide with ovulatory cycles, and are most intense during the first 24\u0026ndash;36 hours of menstruation [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eIn contrast, secondary dysmenorrhea arises from underlying pelvic pathology, including endometriosis, chronic pelvic inflammatory disease, uterine fibroids, cervical stenosis, or congenital and acquired reproductive tract anomalies [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. According to World Health Organization data, dysmenorrhea affects up to 94% of adolescents aged 10\u0026ndash;20 years and approximately 8.8% of women aged 19\u0026ndash;41 years, highlighting its substantial global burden [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAlthough the precise pathophysiological mechanisms underlying dysmenorrhea remain incompletely understood, accumulating evidence supports a central role for inflammatory, vascular, and oxidative processes [\u003cspan additionalcitationids=\"CR12\" citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]. Luteal phase regression leads to progesterone withdrawal, triggering lysosomal enzyme release, cellular breakdown, and an inflammatory cascade characterized by prostaglandin synthesis and endometrial shedding [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. These events initiate complex interactions between the endocrine, immune, and vascular systems [\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eElevated prostaglandin levels, particularly PGF₂α and PGE₂, have been shown to induce uterine vasoconstriction, hypercontractility, ischemia, and heightened nociceptor sensitivity, thereby contributing to menstrual pain [\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e, \u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]. Concurrently, increased expression of inflammatory cytokines\u0026mdash;including IL-1, IL-6, IL-8, and TNF-α\u0026mdash;as well as matrix metalloproteinases has been documented during menstruation in women with dysmenorrhea [\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e, \u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e, \u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eVascular and endothelial factors may further exacerbate dysmenorrhea. Vascular endothelial growth factor (VEGF) has been implicated in disease severity through its effects on leukocyte migration, endothelial permeability, and hypoxia-related pathways involving macrophage migration inhibitory factor (MMIF) and hypoxia-inducible factor-1α (HIF-1α) [\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]. These findings suggest that endothelial dysfunction and microvascular impairment may play a role in endometrial ischemia and pain generation.\u003c/p\u003e \u003cp\u003eOxidative stress has also been proposed as a contributing mechanism in primary dysmenorrhea. Lipid peroxidation, a hallmark of oxidative injury, has been observed during inflammatory and ischemic conditions associated with menstruation [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e, \u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e]. Reactive oxygen species can damage lipids, proteins, and nucleic acids, amplifying tissue injury and inflammation [\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e]. Accordingly, biomarkers such as malondialdehyde (MDA) have been widely used to assess oxidative stress in clinical and experimental settings [\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e, \u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eEndocan (endothelial cell-specific molecule-1) is a soluble dermatan sulfate proteoglycan secreted by activated endothelial cells and is increasingly recognized as a marker of endothelial dysfunction and inflammation [\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e]. Elevated circulating endocan levels have been reported in various inflammatory and vascular conditions, suggesting its potential relevance in disorders characterized by endothelial activation and ischemia [\u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e, \u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e]. Given the ischemic and inflammatory milieu of dysmenorrhea, endocan may serve as a novel biomarker reflecting endothelial involvement in disease pathophysiology.\u003c/p\u003e \u003cp\u003eProcalcitonin, a precursor of calcitonin synthesized primarily by thyroid C cells, is an established acute-phase reactant. While traditionally associated with bacterial infections and sepsis, emerging evidence indicates that procalcitonin levels may also increase in non-infectious inflammatory states [\u003cspan additionalcitationids=\"CR29\" citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e]. To date, among acute-phase reactants, only high-sensitivity C-reactive protein (hs-CRP) has been evaluated in primary dysmenorrhea, and data on procalcitonin in this context are lacking [\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThe balance between oxidative stress and antioxidant defense systems is critical in maintaining cellular homeostasis. Total antioxidant status reflects the combined activity of enzymatic and non-enzymatic antioxidants and provides an integrated measure of antioxidant capacity in biological fluids [\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e].Alterations in this balance may influence pain severity, inflammation, and endothelial function in dysmenorrhea.\u003c/p\u003e \u003cp\u003eGiven the limited data addressing the interplay between oxidative stress, antioxidant capacity, inflammatory activity, and endothelial dysfunction in primary dysmenorrhea, this study aimed to evaluate the association between serum endocan, procalcitonin, malondialdehyde levels, and total antioxidant status in women with primary dysmenorrhea.\u003c/p\u003e"},{"header":"Material and Methods","content":"\u003cp\u003e\u003cstrong\u003eStudy Design and Setting\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study was designed as a prospective cohort study and conducted at the Gynecology and Pediatrics Clinics of Erzurum City Hospital.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eStudy Population\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eInclusion Criteria\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWomen aged 18–30 years who presented to Erzurum City Hospital with moderate to severe primary dysmenorrhea were eligible for inclusion. All participants were nulliparous, non-smokers, had normal findings on physical and ultrasonographic examinations, and had no history of chronic abdominal or pelvic inflammatory, circulatory, or surgical diseases. Dysmenorrhea was required to have started 2–3 years after menarche, to be cyclical in nature, to begin a few hours before the onset of menstruation, and to persist during the first three days of the menstrual cycle.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eExclusion Criteria\u003c/em\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eParticipants were excluded if they had a body mass index (BMI) ≥30 kg/m², systemic diseases (including cardiovascular, pulmonary, endocrine, or metabolic disorders), a history of smoking or alcohol consumption, pelvic pathology (such as endometriosis, ovarian cysts, or previous pelvic surgery), or if they had used analgesic medications within 24 hours prior to blood sampling.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eControl Group\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe control group consisted of healthy women without dysmenorrhea and with no known gynecological or systemic diseases.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical Assessment and Sample Collection\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOn the first day of menstruation, all participants underwent pelvic ultrasonography to exclude underlying pelvic pathology. Pain severity was assessed using a visual analog scale (VAS) ranging from 0 (no pain) to 10 (worst pain imaginable). Demographic and clinical data, including age, BMI, menstrual cycle length (days), and duration of menstrual bleeding (days), were recorded.\u003c/p\u003e\n\u003cp\u003eVenous blood samples were collected from all participants on the same day. Samples were centrifuged at 3000 rpm for 10 minutes, and the separated serum was stored at −80°C until biochemical analysis.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eLaboratory Analysis\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePlasma procalcitonin and serum malondialdehyde (MDA) and endocan levels were measured using enzyme-linked immunosorbent assay (ELISA) kits on automated analyzers, in accordance with the manufacturers’ instructions. Results were recorded using the reference ranges and units specified by the assay kits.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eSample Size and Power Analysis\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eBased on power analysis, a minimum of 25 participants per group was required to achieve 85% statistical power.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eStatistical Analysis\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eStatistical analyses were performed using SPSS software (latest version; IBM Corp., Armonk, NY, USA). Normality of continuous variables was assessed using the Kolmogorov–Smirnov test. Continuous variables were expressed as mean ± standard deviation or median (interquartile range), as appropriate, while categorical variables were presented as frequencies and percentages.\u003c/p\u003e\n\u003cp\u003eGroup comparisons were conducted using the independent samples \u003cem\u003et\u003c/em\u003e-test or Mann–Whitney \u003cem\u003eU\u003c/em\u003e test for continuous variables and the chi-square test for categorical variables. Associations between clinical and biochemical variables and the presence of primary dysmenorrhea were evaluated using univariate logistic regression analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) were reported. A \u003cem\u003ep\u003c/em\u003e value \u0026lt;0.05 was considered statistically significant.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e: This study was supported by Atatürk University Scientific Research Project Directorate with project number 12205 and project code TKP-2023-12205.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics:\u0026nbsp;\u003c/strong\u003eEthical approval was obtained from the Atatürk University Faculty of Health Sciences Ethics Committee (No: B.30.2.ATA.0.01.00/228 Date:30.03.2023). Informed consent was obtained from the participants in the study. The Helsinki Declaration rules were followed at every stage of the research.\u003c/p\u003e"},{"header":"Results","content":"\u003cp\u003eA total of 42 women with primary dysmenorrhea and 42 healthy controls were included in the study. Comparisons of sociodemographic and menstrual characteristics are presented in Table 1. There were no significant differences between the groups in terms of age, body mass index, or menstrual duration (all p \u0026gt; .05). However, women with dysmenorrhea had significantly shorter menstrual cycle lengths compared with controls (29.71 \u0026plusmn; 3.98 vs. 32.98 \u0026plusmn; 8.17 days, p=.02). As expected, VAS pain scores were markedly higher in the dysmenorrhea group than in the control group (7.82 \u0026plusmn; 1.02 vs. 0.82 \u0026plusmn; 0.93, p \u0026lt; .001).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 1\u003c/strong\u003e. Comparison of Sociodemographic and Menstrual Characteristics Between Women With and Without Dysmenorrhea\u003c/p\u003e\n\u003ctable border=\"0\" cellspacing=\"3\" cellpadding=\"0\"\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eCharacteristics\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eWith dysmenorrhea\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eWithout dysmenorrhea\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003et (df)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003ep\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eAge (years), M \u0026plusmn; SD\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e23.00 \u0026plusmn; 3.26\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e22.09 \u0026plusmn; 3.27\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.32\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.18\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eBody mass index (kg/m\u0026sup2;)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e21.72 \u0026plusmn; 3.66\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e22.40 \u0026plusmn; 3.40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e-0.91\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.36\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eCycle length (days)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e29.71 \u0026plusmn; 3.98\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e32.98 \u0026plusmn; 8.17\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e-2.41\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.02*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eMenstrual duration (days)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e5.60 \u0026plusmn; 1.60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e5.93 \u0026plusmn; 1.76\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e-0.93\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.35\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eVAS pain score (0\u0026ndash;10)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e7.82 \u0026plusmn; 1.02\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.82 \u0026plusmn; 0.93\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e33.75\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026lt;.001***\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cem\u003eNote.\u003c/em\u003e Values are presented as mean \u0026plusmn; standard deviation (M \u0026plusmn; SD). VAS = Visual Analogue Scale. \u003cem\u003ep\u003c/em\u003e \u0026lt; .05; \u003cstrong\u003ep\u003c/strong\u003e \u0026lt; .01; \u003cstrong\u003e\u003cem\u003ep\u003c/em\u003e\u003c/strong\u003e \u0026lt; .001.\u003c/p\u003e\n\u003cp\u003eBiochemical and hormonal parameters are summarized in Table 2. Women with dysmenorrhea exhibited significantly higher serum levels of follicle-stimulating hormone (FSH), dehydroepiandrosterone sulfate (DHEA-S), procalcitonin, and endocan compared with controls (all p \u0026lt; .05). No statistically significant differences were observed between the groups for luteinizing hormone, estradiol, thyroid-stimulating hormone, prolactin, total testosterone, malondialdehyde (MDA), or total antioxidant status (TAS).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 2\u003c/strong\u003e. Comparison of Biochemical Parameters Between Women With and Without Dysmenorrhea\u003c/p\u003e\n\u003ctable border=\"0\" cellspacing=\"3\" cellpadding=\"0\"\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eParameter\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eWith dysmenorrhea\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003eWithout dysmenorrhea\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003et (df)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u003cstrong\u003ep\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eFSH (mIU/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e6.97 \u0026plusmn; 1.67\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e6.18 \u0026plusmn; 1.84\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.13\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.03*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eLH (mIU/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e4.94 \u0026plusmn; 2.20\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e5.79 \u0026plusmn; 4.50\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e-1.13\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.25\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eEstradiol (pg/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e38.94 \u0026plusmn; 13.74\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e41.57 \u0026plusmn; 18.67\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e-0.76\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.44\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eTSH (\u0026micro;IU/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.94 \u0026plusmn; 1.13\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.99 \u0026plusmn; 0.90\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e-0.22\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.82\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eProlactin (ng/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e13.42 \u0026plusmn; 5.68\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e13.50 \u0026plusmn; 6.85\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e-0.06\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.95\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eDHEA-S (\u0026micro;g/dL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e213.31 \u0026plusmn; 101.78\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e169.60 \u0026plusmn; 93.39\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.12\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.03*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eTotal testosterone (ng/dL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e25.81 \u0026plusmn; 7.10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e29.05 \u0026plusmn; 9.62\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e-1.81\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.07\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eProcalcitonin (ng/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.59 \u0026plusmn; 0.41\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.08 \u0026plusmn; 0.13\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e7.87\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e\u0026lt;.001***\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eMDA (\u0026micro;mol/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e1.61 \u0026plusmn; 1.37\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.14 \u0026plusmn; 1.74\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e-1.60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.11\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eEndocan (pg/mL)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e279.36 \u0026plusmn; 362.53\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e126.43 \u0026plusmn; 116.95\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e2.69\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.008**\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd\u003e\n \u003cp\u003eTAS (\u0026micro;mol Trolox equiv/L)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e32.41 \u0026plusmn; 37.53\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e30.72 \u0026plusmn; 27.01\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e0.24\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd\u003e\n \u003cp\u003e.80\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003e\u003cem\u003eNote.\u003c/em\u003e Values are presented as mean \u0026plusmn; standard deviation (M \u0026plusmn; SD). FSH = follicle-stimulating hormone; LH = luteinizing hormone; TSH = thyroid-stimulating hormone; DHEA-S = dehydroepiandrosterone sulfate; MDA = malondialdehyde; TAS = total antioxidant status. \u003cem\u003ep\u003c/em\u003e \u0026lt; .05; \u003cstrong\u003ep\u003c/strong\u003e \u0026lt; .01; \u003cstrong\u003e\u003cem\u003ep\u003c/em\u003e\u003c/strong\u003e \u0026lt; .001.\u003c/p\u003e\n\u003cp\u003eCorrelation analyses stratified by study group are shown in Table 3. In the dysmenorrhea group, estradiol levels were positively correlated with body mass index, while prolactin levels were negatively correlated with VAS pain scores. Both DHEA-S and total testosterone demonstrated positive correlations with pain severity. TAS showed a strong positive correlation with body mass index and a strong inverse correlation with VAS scores. In the control group, FSH was negatively correlated with menstrual duration, MDA was positively correlated with body mass index, endocan was positively correlated with age, and procalcitonin showed a strong positive correlation with VAS scores.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 3\u003c/strong\u003e. Pearson\u0026rsquo;s Correlation Coefficients Between Biochemical Parameters and Clinical Characteristics in Women With and Without Dysmenorrhea\u003c/p\u003e\n\u003ctable border=\"1\" cellspacing=\"3\" cellpadding=\"0\" width=\"100%\" \u003cthead=\"\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 49px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eGroup\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eParameter\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAge\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eBMI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCycle length\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMenstrual duration\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eVAS\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"11\" style=\"width: 49px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eWith dysmenorrhea\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eFSH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.11 (.46)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026ndash;.15 (.32)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.03 (.85)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026ndash;.14 (.35)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u0026ndash;.06 (.69)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eLH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.14 (.37)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026ndash;.01 (.96)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.04 (.77)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e.15 (.34)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e.03 (.84)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eEstradiol\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.02 (.90)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e.30* (.048)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.06 (.69)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026ndash;.11 (.49)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e.03 (.86)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eTSH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.04 (.77)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e.11 (.49)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.03 (.85)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e.09 (.58)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u0026ndash;.08 (.61)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eProlactin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.19 (.22)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e.18 (.24)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.02 (.89)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e.28 (.07)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u0026ndash;.30* (.048)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eDHEA-S\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.10 (.50)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026ndash;.20 (.19)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.26 (.08)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e.16 (.31)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e.38* (.011)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eTestosterone\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.03 (.83)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026ndash;.07 (.65)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.21 (.16)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e.25 (.10)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e.39** (.008)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eProcalcitonin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.18 (.24)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e.16 (.30)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.19 (.22)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026ndash;.10 (.53)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e.19 (.22)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eMDA\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.12 (.43)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e.01 (.93)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.06 (.67)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e.08 (.61)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u0026ndash;.02 (.92)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eEndocan\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.03 (.83)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026ndash;.14 (.35)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.14 (.36)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026ndash;.24 (.11)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e.09 (.58)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eTAS\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.15 (.33)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e.56*** (.001)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.23 (.13)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e.07 (.63)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u0026ndash;.57*** (\u0026lt;.001)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd rowspan=\"11\" style=\"width: 49px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eWithout dysmenorrhea\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eFSH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.07 (.67)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026ndash;.13 (.38)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.27 (.07)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026ndash;.32* (.030)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u0026ndash;.11 (.46)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eLH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.07 (.65)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026ndash;.20 (.18)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.15 (.34)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026ndash;.23 (.14)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e.02 (.91)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eEstradiol\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.01 (.95)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026ndash;.05 (.77)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.01 (.97)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e.02 (.88)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u0026ndash;.15 (.34)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eTSH\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.05 (.76)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e.27 (.07)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.04 (.78)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026ndash;.05 (.76)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e.26 (.09)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eProlactin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.22 (.15)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e.02 (.88)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.06 (.70)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026ndash;.10 (.53)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u0026ndash;.18 (.23)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eDHEA-S\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.02 (.91)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e.14 (.37)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.04 (.77)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026ndash;.06 (.69)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e.18 (.24)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eTestosterone\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.22 (.15)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026ndash;.26 (.09)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.04 (.82)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e.05 (.75)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u0026ndash;.09 (.56)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eProcalcitonin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.05 (.76)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026ndash;.06 (.71)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.03 (.84)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026ndash;.20 (.20)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e.50*** (\u0026lt;.001)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eMDA\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.11 (.48)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e.31* (.039)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.12 (.42)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e.07 (.63)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e.06 (.71)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eEndocan\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e.39** (.008)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e.28 (.07)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.12 (.45)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026ndash;.22 (.15)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u0026ndash;.15 (.34)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd style=\"width: 89px;\"\u003e\n \u003cp\u003eTAS\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.05 (.73)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 78px;\"\u003e\n \u003cp\u003e\u0026ndash;.05 (.77)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 79px;\"\u003e\n \u003cp\u003e\u0026ndash;.23 (.14)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 91px;\"\u003e\n \u003cp\u003e.04 (.79)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd style=\"width: 97px;\"\u003e\n \u003cp\u003e\u0026ndash;.21 (.17)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eValues are Pearson\u0026rsquo;s \u003cem\u003er\u003c/em\u003e (two-tailed \u003cem\u003ep\u003c/em\u003e in parentheses). FSH = follicle-stimulating hormone; LH = luteinizing hormone; TSH = thyroid-stimulating hormone; DHEA-S = dehydroepiandrosterone sulfate; MDA = malondialdehyde; TAS = total antioxidant status; VAS = Visual Analogue Scale. \u003cem\u003ep\u003c/em\u003e \u0026lt; .05; *\u003cem\u003ep\u003c/em\u003e \u0026lt; .01; **\u003cem\u003ep\u003c/em\u003e \u0026lt; .001.\u003c/p\u003e\n\u003cp\u003eUnivariate binary logistic regression analyses identifying factors associated with dysmenorrhea are presented in Table 4. Endocan (OR = 0.996, p = .038), procalcitonin (OR = 0.002, p \u0026lt; .001), menstrual cycle length (OR = 1.099, p = .030), FSH (OR = 0.771, p = .040), and DHEA-S (OR = 0.995, p = .042) were significantly associated with the presence of dysmenorrhea. Higher procalcitonin levels were strongly associated with dysmenorrhea, whereas higher endocan, FSH, and DHEA-S levels showed inverse associations. Longer cycle length was positively associated with dysmenorrhea. The VAS pain score demonstrated quasi-complete separation in the logistic regression model, precluding reliable estimation of odds ratios. MDA, TAS, age, and menstrual duration were not significantly associated with dysmenorrhea (all p \u0026gt; .05).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eTable 4\u003c/strong\u003e. Regression analysis some Biochemical Parameters Women With and Without Dysmenorrhea\u003c/p\u003e\n\u003ctable border=\"0\" cellspacing=\"0\" cellpadding=\"0\"\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 200px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eVariable\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 107px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eOR (Exp[B])\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 130px;\"\u003e\n \u003cp\u003e\u003cstrong\u003e\u0026nbsp; \u0026nbsp; 95% CI\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e\u003cstrong\u003ep-value\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 200px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eVAS score\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 107px;\"\u003e\n \u003cp\u003eNot estimable\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 130px;\"\u003e\n \u003cp\u003e\u0026mdash;\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0.994\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 200px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eEndocan\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 107px;\"\u003e\n \u003cp\u003e0.996\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 130px;\"\u003e\n \u003cp\u003e0.992 \u0026ndash; 1.000\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0.038\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 200px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eProcalcitonin\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 107px;\"\u003e\n \u003cp\u003e0.002\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 130px;\"\u003e\n \u003cp\u003e0.000 \u0026ndash; 0.035\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e\u0026lt;0.001*\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 200px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eCycle length\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 107px;\"\u003e\n \u003cp\u003e1.099\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 130px;\"\u003e\n \u003cp\u003e1.009 \u0026ndash; 1.197\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0.030\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 200px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eFSH\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 107px;\"\u003e\n \u003cp\u003e0.771\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 130px;\"\u003e\n \u003cp\u003e0.602 \u0026ndash; 0.988\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0.040\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 200px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eDHEAS\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 107px;\"\u003e\n \u003cp\u003e0.995\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 130px;\"\u003e\n \u003cp\u003e0.991 \u0026ndash; 1.000\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0.042\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 200px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMDA\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 107px;\"\u003e\n \u003cp\u003e1.260\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 130px;\"\u003e\n \u003cp\u003e0.938 \u0026ndash; 1.692\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0.124\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 200px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eTAS\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 107px;\"\u003e\n \u003cp\u003e0.998\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 130px;\"\u003e\n \u003cp\u003e0.986 \u0026ndash; 1.011\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0.804\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 200px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eAge\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 107px;\"\u003e\n \u003cp\u003e0.916\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 130px;\"\u003e\n \u003cp\u003e0.802 \u0026ndash; 1.045\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0.192\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd valign=\"top\" style=\"width: 200px;\"\u003e\n \u003cp\u003e\u003cstrong\u003eMenstrual duration\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 107px;\"\u003e\n \u003cp\u003e1.128\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 130px;\"\u003e\n \u003cp\u003e0.878 \u0026ndash; 1.449\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd valign=\"top\" style=\"width: 91px;\"\u003e\n \u003cp\u003e0.347\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n\u003c/table\u003e\n\u003cp\u003eOR, odds ratio; CI, confidence interval; VAS, Visual Analog Scale; MDA, malondialdehyde; TAS, total antioxidant status; FSH, follicle-stimulating hormone; DHEAS, dehydroepiandrosterone sulfate. VAS demonstrated quasi-complete separation, resulting in non-estimable odds ratios. All analyses were performed using univariate binary logistic regression. *\u003cem\u003ep\u003c/em\u003e \u0026lt; .001\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThe present study evaluated the associations between inflammatory, oxidative, and endothelial biomarkers and primary dysmenorrhea by integrating biochemical findings with clinical characteristics. Our results demonstrated significantly higher serum levels of procalcitonin and endocan in women with dysmenorrhea, along with increased follicle-stimulating hormone (FSH) and dehydroepiandrosterone sulfate (DHEA-S) concentrations. Furthermore, univariate binary logistic regression analyses identifiedprocalcitonin, endocan, menstrual cycle length, FSH, and DHEA-S as variables significantly associated with the presence of dysmenorrhea.\u003c/p\u003e\n\u003cp\u003eAmong the evaluated biomarkers, procalcitonin showed the strongest association with dysmenorrhea. Although procalcitonin is classically regarded as a biomarker of bacterial infection and systemic inflammation, accumulating evidence indicates that it may also reflect inflammatory activation in non-infectious conditions [32-34]. Its prognostic relevance in cardiovascular and neurological disorders, including acute myocardial infarction and intracerebral hemorrhage, further supports its role as a marker of systemic inflammatory burden rather than infection alone [35,36]. In this context, our findings suggest that elevated procalcitonin levels in dysmenorrhea may reflect inflammatory activation accompanying pain severity, consistent with broader clinical observations [37,38]. Importantly, given the cross-sectional design, procalcitonin should be interpreted as a biomarker associated with dysmenorrhea rather than a causal mediator of pain.\u003c/p\u003e\n\u003cp\u003ePrevious studies investigating dysmenorrhea have predominantly focused on oxidative stress and classical inflammatory mediators. Aksoy et al. [39]. (2017) reported increased levels of heme oxygenase-1, nitric oxide, and malondialdehyde (MDA) in women with dysmenorrhea, supporting a role for lipid peroxidation and oxidative injury. Similarly, elevated MDA and proinflammatory cytokines have been described during the menstrual phase in dysmenorrheic women [17,40]. In contrast, our study did not demonstrate significant differences in MDA or total antioxidant status (TAS) between groups. This discrepancy may be attributable to interindividual variability, dietary antioxidant intake, or the use of nonsteroidal anti-inflammatory drugs, which have been shown to attenuate oxidative stress markers in dysmenorrhea [41-43]. Nevertheless, the observed inverse correlation between TAS and pain severity in our cohort supports the hypothesis that antioxidant capacity may modulate symptom intensity.\u003c/p\u003e\n\u003cp\u003eThe significantly elevated serum endocan levels observed in women with dysmenorrhea further support the involvement of endothelial dysfunction in menstrual pain pathophysiology. Endocan is a proteoglycan secreted by activated endothelial cells and has been associated with vascular inflammation, endothelial activation, and adverse cardiovascular outcomes [44-46]. Our findings are consistent with previous reports suggesting that oxidative and endothelial stress responses play a central role in dysmenorrhea [39]. The association between endocan and dysmenorrhea highlights the potential contribution of microvascular dysfunction and endometrial ischemia to pain generation.\u003c/p\u003e\n\u003cp\u003eBeyond biochemical parameters, menstrual cycle length emerged as a clinically relevant factor associated with dysmenorrhea. The positive association between longer cycle length and dysmenorrhea underscores the importance of menstrual characteristics in routine clinical assessment. In addition, the observed associations of FSH and DHEA-S with dysmenorrhea suggest that subtle endocrine variations may influence inflammatory responses or pain perception, consistent with prior observations linking hormonal milieu to menstrual pain severity.\u003c/p\u003e\n\u003cp\u003eInterventional and experimental studies further support the clinical relevance of oxidative and inflammatory pathways in dysmenorrhea. Red-light photobiomodulation, herbal extracts, probiotic supplementation, and lifestyle interventions such as high-intensity interval training have all been shown to reduce inflammatory markers and improve pain outcomes [47-51]. These findings collectively suggest that targeting oxidative stress and inflammation may represent a promising therapeutic strategy.\u003c/p\u003e\n\u003cp\u003eIn conclusion, our findings highlight the multifactorial nature of primary dysmenorrhea, involving inflammatory, endothelial, oxidative, and hormonal components. Although causal relationships cannot be inferred, the observed associations suggest that biomarkers such as procalcitonin and endocan may complement clinical evaluation and improve the characterization of dysmenorrhea. Interventional and experimental studies further support the clinical relevance of oxidative and inflammatory pathways in dysmenorrhea. Red-light photobiomodulation, herbal extracts, probiotic supplementation, and lifestyle interventions such as high-intensity interval training have all been shown to reduce inflammatory markers and improve pain outcomes [47-51]. These findings collectively suggest that targeting oxidative stress and inflammation may represent a promising therapeutic strategy. Future prospective studies are warranted to clarify temporal relationships and to explore whether these biomarkers may contribute to risk stratification or individualized management strategies.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eAuthor Contribution\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eSET: Protocol development, Data collection, Manuscript writing\u003c/p\u003e\n\u003cp\u003eSEA: Protocol, Data analysis, Manuscript writing\u003c/p\u003e\n\u003cp\u003eANA: Protocol development, Data collection, Manuscript writing\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eES: Laboratory analysis\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e: This study was supported by Atatürk University Scientific Research Project Directorate with project number 12205 and project code TKP-2023-12205.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting Interests:\u003c/strong\u003e There is no conflict of interest among the authors.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthics approval:\u003c/strong\u003e Ethical approval was obtained from the Atatürk University Faculty of Health Sciences Ethics Committee (No: B.30.2.ATA.0.01.00/228 Date:30.03.2023).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent to participate:\u003c/strong\u003e Informed consent was obtained from the participants in the study.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eData Availability Statement:\u003c/strong\u003e The data that support the findings of this study are available from the corresponding author upon reasonable request\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eLatthe PM, Champaneria R, Khan KS. (2011) Dysmenorrhoea. BMJ Clinical Evidence 0813.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDawood MY. Primary dysmenorrhea: advances in pathogenesis and management. Obstet Gynecol. 2006;108(2):428\u0026ndash;41. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1097/01.AOG.0000230214.26638.0c\u003c/span\u003e\u003cspan address=\"10.1097/01.AOG.0000230214.26638.0c\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHarel Z. Dysmenorrhea in adolescents and young adults: etiology and management. J Pediatr Adolesc Gynecol. 2006;19(6):363\u0026ndash;71. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/j.jpag.2006.09.001\u003c/span\u003e\u003cspan address=\"10.1016/j.jpag.2006.09.001\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBalık G, Ust\u0026uuml;ner I, Kağıtcı M, Sahin FK. Is there a relationship between mood disorders and dysmenorrhea? J Pediatr Adolesc Gynecol. 2014;27(6):371\u0026ndash;4. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/j.jpag.2014.01.108\u003c/span\u003e\u003cspan address=\"10.1016/j.jpag.2014.01.108\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNur Azurah AG, Sanci L, Moore E, Grover S. The quality of life of adolescents with menstrual problems. J Pediatr Adolesc Gynecol. 2013;26(2):102\u0026ndash;8. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/j.jpag.2012.11.004\u003c/span\u003e\u003cspan address=\"10.1016/j.jpag.2012.11.004\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAmerican College of Obstetricians and Gynecologists (ACOG). Committee opinion 760: Dysmenorrhea and endometriosis in the adolescent. Obstet Gynecol. 2018;132(6):e249\u0026ndash;58.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eOladosu FA, Tu FF, Hellman KM. Nonsteroidal antiinflammatory drug resistance in dysmenorrhea: epidemiology, causes, and treatment. Am J Obstet Gynecol. 2018;218(4):390\u0026ndash;400. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/j.ajog.2017.08.108\u003c/span\u003e\u003cspan address=\"10.1016/j.ajog.2017.08.108\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBurnett M, Lemyre M. 345-Primary Dysmenorrhea Consensus Guideline. J Obstet Gynecol Can. 2017;39(7):585\u0026ndash;95. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/j.jogc.2016.12.023\u003c/span\u003e\u003cspan address=\"10.1016/j.jogc.2016.12.023\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eIacovides S, Avidon I, Baker FC. What we know about primary dysmenorrhea today: a critical review. Hum Reprod Update. 2015;21(6):762\u0026ndash;78. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1093/humupd/dmv039\u003c/span\u003e\u003cspan address=\"10.1093/humupd/dmv039\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLatthe P, Latthe M, Say L, G\u0026uuml;lmezoglu M, Khan KS. WHO systematic review of prevalence of chronic pelvic pain: a neglected reproductive health morbidity. BMC Public Health. 2006;6:177. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1186/1471-2458-6-177\u003c/span\u003e\u003cspan address=\"10.1186/1471-2458-6-177\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRad M, Sabzevari MT, Rastaghi S, Dehnavi ZM. The relationship between anthropometric index and primary dysmenorehea in female high school students. J Educ Health Promotion. 2018;7:34. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.4103/jehp.jehp_117_17\u003c/span\u003e\u003cspan address=\"10.4103/jehp.jehp_117_17\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGuimar\u0026atilde;es I, P\u0026oacute;voa AM. Primary Dysmenorrhea: Assessment and Treatment. Revista Brasileira de Ginecol e Obstet. 2020;42(8):501\u0026ndash;7. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1055/s-0040-1712131\u003c/span\u003e\u003cspan address=\"10.1055/s-0040-1712131\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBarcikowska Z, Rajkowska-Labon E, Grzybowska ME, Hansdorfer-Korzon R, Zorena K. Inflammatory markers in dysmenorrhea and therapeutic options. Int J Environ Res Public Health. 2020;17(4):1191. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.3390/ijerph17041191\u003c/span\u003e\u003cspan address=\"10.3390/ijerph17041191\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMaybin JA, Critchley HO. Progesterone: a pivotal hormone at menstruation. Ann N Y Acad Sci. 2011;1221:88\u0026ndash;97. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1111/j.1749-6632.2011.05953.x\u003c/span\u003e\u003cspan address=\"10.1111/j.1749-6632.2011.05953.x\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePickles VR, Hall WJ, Best FA, Smith GN. Prostaglandins in endometrium and menstrual fluid from normal and dysmenorrhoeic subjects. BJOG: Int J Obstet Gynecol. 1965;72:185\u0026ndash;92. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1111/j.1471-0528.1965.tb01415.x\u003c/span\u003e\u003cspan address=\"10.1111/j.1471-0528.1965.tb01415.x\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDawood MY, Dysmenorrhea and prostaglandins. In Gynecologic endocrinology 405\u0026ndash;421. Boston, MA: Springer US; 1987.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eYeh ML, Chen HH, So EC, Liu CF. A study of serum malondialdehyde and interleukin-6 levels in young women with dysmenorrhea in Taiwan. Life Sci. 2004;75(6):669\u0026ndash;73. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/https://doi.org/10.1016/j.lfs.2003.11.034\u003c/span\u003e\u003cspan address=\"10.1016/j.lfs.2003.11.034\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKonecna L, Yan MS, Miller LE, Sch\u0026ouml;lmerich J, Falk W, Straub RH, Brain. Behav Immun 14(1), 49\u0026ndash;61. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1006/brbi.1999.0570\u003c/span\u003e\u003cspan address=\"10.1006/brbi.1999.0570\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZhang F, Liu XL, Wang W, Dong HL, Xia YF, Ruan LP, Liu LP. Expression of MMIF, HIF-1α and VEGF in serum and endometrial tissues of patients with endometriosis. Curr Med Sci. 2018;38(3):499\u0026ndash;504. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1007/s11596-018-1906-1\u003c/span\u003e\u003cspan address=\"10.1007/s11596-018-1906-1\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGuliaeva NV, Luzina NL, Levshina IP, Kryzhanovskiĭ GN. The inhibition stage of lipid peroxidation during stress. Biull Eksp Biol Med. 1988;106(12):660\u0026ndash;3.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDe Sanctis V, Soliman A, Bernasconi S, Bianchin L, Bona G, Bozzola M, et al. Primary dysmenorrhea in adolescents: Prevalence, impact and recent knowledge. Pediatr Endocrinol Reviews. 2015;13:512\u0026ndash;20.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBaird DT, Cameron ST, Critchley HO, Drudy TA, Howe A, Jones RL, Lea RG, Kelly RW. Prostaglandins and menstruation. Eur J Obstet Gynecol Reproductive Biology. 1996;70(1):15\u0026ndash;7. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/s0301-2115(96)02568-7\u003c/span\u003e\u003cspan address=\"10.1016/s0301-2115(96)02568-7\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eUttara B, Singh AV, Zamboni P, Mahajan RT. Oxidative stress and neurodegenerative diseases: a review of upstream and downstream antioxidant therapeutic options. Curr Neuropharmacol. 2009;7(1):65\u0026ndash;74. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.2174/157015909787602823\u003c/span\u003e\u003cspan address=\"10.2174/157015909787602823\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSzmidt MK, Granda D, Sicinska E, Kaluza J. Primary Dysmenorrhea in Relation to Oxidative Stress and Antioxidant Status: A Systematic Review of Case-Control Studies. Antioxidants. 2020;9(10):994. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.3390/antiox9100994\u003c/span\u003e\u003cspan address=\"10.3390/antiox9100994\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZhao T, Kecheng Y, Zhao X, Hu X, Zhu J, Wang Y, Ni J. The higher serum endocan levels may be a risk factor for the onset of cardiovascular disease: A meta-analysis. Medicine. 2018;97(49):e13407. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1097/MD.0000000000013407\u003c/span\u003e\u003cspan address=\"10.1097/MD.0000000000013407\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePoon PY, Ng JK, Fung WW, Chow KM, Kwan BC, Li PK, Szeto CC. Relationship between plasma endocan level and clinical outcome of chinese peritoneal dialysis patients. Kidney Blood Press Res. 2019;44(5):1259\u0026ndash;70. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1159/000502961\u003c/span\u003e\u003cspan address=\"10.1159/000502961\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eOktar SF, Guney I, Eren SA, Oktar L, Kosar K, Buyukterzi Z, Alkan E, Biyik Z, Erdem SS. Serum endocan levels, carotid intima-media thickness and microalbuminuria in patients with newly diagnosed hypertension. Clin Exp Hypertens. 2019;41(8):787\u0026ndash;94. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1080/10641963.2019.1652632\u003c/span\u003e\u003cspan address=\"10.1080/10641963.2019.1652632\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWacker C, Prkno A, Brunkhorst FM, Schlattmann P. Procalcitonin as a diagnostic marker for sepsis: a systematic review and meta-analysis. Lancet Infect Dis. 2013;13(5):426\u0026ndash;35. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/S1473-3099(12)70323-7\u003c/span\u003e\u003cspan address=\"10.1016/S1473-3099(12)70323-7\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAringer M. Inflammatory markers in systemic lupus erythematosus. J Autoimmun. 2020;110:102374. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/j.jaut.2019.102374\u003c/span\u003e\u003cspan address=\"10.1016/j.jaut.2019.102374\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWang J, Niu R, Jiang L, Wang Y, Shao X, Wu M, Ma Y. The diagnostic values of C-reactive protein and procalcitonin in identifying systemic lupus erythematosus infection and disease activity. Medicine. 2019;98(33):e16798. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1097/MD.0000000000016798\u003c/span\u003e\u003cspan address=\"10.1097/MD.0000000000016798\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBahrami A, Bahrami-Taghanaki H, Khorasanchi Z, Timar A, Jaberi N, Azaryan E, Tayefi M, Ferns GA, Sadeghnia HR, Ghayour-Mobarhan M. Menstrual problems in adolescence: relationship to serum vitamins A and E, and systemic inflammation. Arch Gynecol Obstet. 2020;301(1):189\u0026ndash;97. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1007/s00404-019-05343-1\u003c/span\u003e\u003cspan address=\"10.1007/s00404-019-05343-1\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBektas F, Soyuncu S, Gunduz I, Basarici I, Akbas H, Eken C. The value of procalcitonin, a novel inflammatory marker,diagnosis of myocardial infarction and evaluation of acute coronary syndrome patients. J Emerg Med. 2011;41(5):524\u0026ndash;30. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/j.jemermed.2010.05.073\u003c/span\u003e\u003cspan address=\"10.1016/j.jemermed.2010.05.073\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSmolle KH, Kaufmann P, Stadlbauer V, Tatzber F, Winklhofer-Roob BM, Aigner R, Khoschsorur G, Wonisch W. Intermittent haemodialysis-induced oxidative stress and the effect on inflammatory parameters in critically ill patients. Clin Experimental Med J. 2010;4(1):79\u0026ndash;88. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/https://doi.org/10.1556/CEMED.4.2010.1.8\u003c/span\u003e\u003cspan address=\"10.1556/CEMED.4.2010.1.8\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHe D, Zhang Y, Zhang B, Jian W, Deng X, Yang Y, Xiao T, Yu H, Wen S, Huang K. Serum Procalcitonin Levels are Associated with Clinical Outcome in Intracerebral Hemorrhage. Cell Mol Neurobiol. 2018;38(3):727\u0026ndash;33. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1007/s10571-017-0538-5\u003c/span\u003e\u003cspan address=\"10.1007/s10571-017-0538-5\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFestic E, Siegel J, Stritt M, Freeman WD. The Utility of Serum Procalcitonin in Distinguishing Systemic Inflammatory Response Syndrome from Infection After Aneurysmal Subarachnoid Hemorrhage. Neurocrit Care. 2014;20(3):375\u0026ndash;81. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1007/s12028-014-9960-4\u003c/span\u003e\u003cspan address=\"10.1007/s12028-014-9960-4\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFirani NK, Prisilla J. Procalcitonin and Troponin-I as Predictor of Mortality in Acute Myocardial Infarction Patients. Indonesian J Clin Pathol Med Lab. 2022;28(2):170\u0026ndash;4. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.24293/ijcpml.v28i2.1817\u003c/span\u003e\u003cspan address=\"10.24293/ijcpml.v28i2.1817\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSchuetz P, Daniels LB, Kulkarni P, Anker SD, Mueller B. Procalcitonin: A new biomarker for the cardiologist. Int J Cardiol. 2016;223:390\u0026ndash;7. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1016/j.ijcard.2016.08.204\u003c/span\u003e\u003cspan address=\"10.1016/j.ijcard.2016.08.204\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eOka K, Araki J, Yamamoto K, Hanayama Y, Tokumasu K, Hagiya H, Obika M, Ogawa H, Otsuka F. Interrelationships Between Serum Levels of Procalcitonin and Inflammatory Markers. J Endocr Soc. 2021;5(1):A264\u0026ndash;5. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1210/jendso/bvab048.536\u003c/span\u003e\u003cspan address=\"10.1210/jendso/bvab048.536\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAksoy AN, Laloglu E, Ozkaya AL, Yilmaz EPT. Serum heme oxygenase-1 levels in patients with primary dysmenorrhea. Arch Gynecol Obstet. 2017;295(4):929\u0026ndash;34. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1007/s00404-017-4312-1\u003c/span\u003e\u003cspan address=\"10.1007/s00404-017-4312-1\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDikensoy E, Balat O, Pen\u0026ccedil;e S, Balat A, \u0026Ccedil;ekmen M, Yurekli M. Malondialdehyde, nitric oxide and adrenomedullin levels in patients with primary dysmenorrhea. J Obstet Gynecol Res. 2008;34(6):1049\u0026ndash;53. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/https://doi.org/10.1111/j.1447-0756.2008.00802.x\u003c/span\u003e\u003cspan address=\"10.1111/j.1447-0756.2008.00802.x\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFurniss LD. Nonsteroidal anti-inflammatory agents in the treatment of primary dysmenorrhea. Clin Pharm. 1982;1(4):327\u0026ndash;33.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKaplan \u0026Ouml;, Nazıroğlu M, G\u0026uuml;ney M, Aykur M. Non-steroidal anti-inflammatory drug modulates oxidative stress and calcium ion levels in the neutrophils of patients with primary dysmenorrhea. J Reprod Immunol. 2013;100(2):87\u0026ndash;92. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/https://doi.org/10.1016/j.jri.2013.10.004\u003c/span\u003e\u003cspan address=\"10.1016/j.jri.2013.10.004\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHaidari F, Homayouni F, Helli B, Haghighizadeh MH, Farahmandpour F. Effect of chlorella supplementation on systematic symptoms and serum levels of prostaglandins, inflammatory and oxidative markers in women with primary dysmenorrhea. Eur J Obstetrics\u0026amp;Gynecology Reproductive Biology. 2018;229:185\u0026ndash;9. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/https://doi.org/10.1016/j.ejogrb.2018.08.578\u003c/span\u003e\u003cspan address=\"10.1016/j.ejogrb.2018.08.578\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSekercioglu N, Balci H, Pekpak M. Procalcitonin and Malondialdehyde as Markers of Inflammation in Hemodialysis Patients. J Clin Anal Med. 2017;8:346\u0026ndash;50. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.4328/JCAM.4899\u003c/span\u003e\u003cspan address=\"10.4328/JCAM.4899\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHu J, Yang C, Yang G, Du H, Zhao H, Liu H. Effects of atorvastatin doses on serum level of procalcitonin and predictors for major adverse cardiovascular events in patients with acute myocardial infarction: a pilot study and post hoc analysis. Coron Artery Dis. 2022;33(1):e87\u0026ndash;93. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1097/mca.0000000000001084\u003c/span\u003e\u003cspan address=\"10.1097/mca.0000000000001084\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eZakaria IA, Mohammed Zain NA, Teik CK, Abu MA, Zainuddin AA, Abdul Aziz NH, Safian N, Mohd Mokhtar N, Raja Ali RA, Beng Kwang N, Mohamed Ismail NA, Hamizan MR, Ab Razak WS, Nur Azurah AG. The role of probiotics in improving menstrual health in women with primary dysmenorrhoea: A randomized, double-blind, placebo-controlled trial. Women's Health. 2024;20:17455057241234524. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.1177/17455057241234524\u003c/span\u003e\u003cspan address=\"10.1177/17455057241234524\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eChen Y, Cao Y, Xie Y, Zhang X, Yang Q, Li X, Sun J, Qiu P, Cao W, Wang S. (2013) Traditional Chinese medicine for the treatment of primary dysmenorrhea: How do Yuanhu painkillers effectively treat dysmenorrhea? Phytomedicine 20(12), 1095\u0026ndash;1104. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/https://doi.org/10.1016/j.phymed.2013.05.003\u003c/span\u003e\u003cspan address=\"10.1016/j.phymed.2013.05.003\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMukhoirotin M, Kurniawati K, Mawarti H. The Effect of Slow Stroke Back Massage on Primary Dysmenorrhea: Levels of Beta-Endorphin, Interleukin-6, Tumor Necrosis Factor-α, and Pain Intensity. Int J Women's Health Reprod Sci. 2020;8:376\u0026ndash;82. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/10.15296/ijwhr.2020.60\u003c/span\u003e\u003cspan address=\"10.15296/ijwhr.2020.60\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eYang X, Tian Y, Liu J, Kou Y, Xie Y, Wang S, Zhao Y. (2023) Peony Pollen Protects against Primary Dysmenorrhea in Mice by Inhibiting Inflammatory Response and Regulating the COX2/PGE2 Pathway. International Journal of Molecular Sciences, 24(24), 17245. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.mdpi.com/1422-0067/24/24/17245\u003c/span\u003e\u003cspan address=\"https://www.mdpi.com/1422-0067/24/24/17245\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFu Q, Yang J, Jiang H, Qin H, Li A, Huo L, Liu M. Pulsed red light photobiomodulation ameliorates oxytocin-induced primary dysmenorrhea in mice by inhibiting oxidative stress and lipid accumulation. J Photochem Photobiol B. 2025;264:113119. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://doi.org/https://doi.org/10.1016/j.jphotobiol.2025.113119\u003c/span\u003e\u003cspan address=\"10.1016/j.jphotobiol.2025.113119\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eYang MY, Chen HY, Ho CH, Huang WC. (2025) Impact of Probiotic Supplementation and High-Intensity Interval Training on Primary Dysmenorrhea: A Double-Blind, Randomized Controlled Trial Investigating Inflammation and Hormonal Modulation. Nutrients 17(4), 622. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003ehttps://www.mdpi.com/2072-6643/17/4/622\u003c/span\u003e\u003cspan address=\"https://www.mdpi.com/2072-6643/17/4/622\" targettype=\"URL\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e\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":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-womens-health","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bmwh","sideBox":"Learn more about [BMC Women's Health](http://bmcwomenshealth.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bmwh/default.aspx","title":"BMC Women's Health","twitterHandle":"","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Antioxidant Status, Dysmenorrhea, Endocan, Procalcitonin, Malondialdehyde","lastPublishedDoi":"10.21203/rs.3.rs-9352726/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9352726/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003ePurpose\u003c/h2\u003e \u003cp\u003eThis study aimed to investigate the relationships between inflammatory, oxidative, and endothelial biomarkers\u0026mdash;specifically serum endocan, procalcitonin, malondialdehyde and total antioxidant status \u0026mdash;and primary dysmenorrhea.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e \u003cp\u003eThis prospective cohort study was conducted a City Hospital. Women has moderate to severe primary dysmenorrhea and healthy controls without dysmenorrhea were enrolled. Participants underwent pelvic ultrasonography on the first day of menstruation. Venous blood samples were collected on the same day, and serum endocan, procalcitonin, malondialdehyde, and total antioxidant status levels were measured using ELISA.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e \u003cp\u003eWomen with primary dysmenorrhea had significantly higher serum procalcitonin and endocan levels compared with controls. No significant differences were observed in MDA or TAS levels between groups. Univariate logistic regression analysis revealed that serum procalcitonin, endocan, menstrual cycle length, follicle-stimulating hormone, and dehydroepiandrosterone sulfate were significantly associated with the presence of dysmenorrhea. TAS levels showed an inverse correlation with pain severity.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003ePrimary dysmenorrhea is associated with increased inflammatory and endothelial activation, as reflected by elevated serum procalcitonin and endocan levels. These findings support the multifactorial nature of dysmenorrhea involving inflammatory, endothelial, and hormonal components. Further prospective studies are warranted to clarify the clinical utility of these biomarkers in the evaluation and management of primary dysmenorrhea.\u003c/p\u003e","manuscriptTitle":"Comparison of two groups in primary dysmenorrhea: serum endocan, procalcitonin, malondialdehyde levels and antioxidants","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-05-11 14:40:11","doi":"10.21203/rs.3.rs-9352726/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"reviewerAgreed","content":"310913366589418376877216589852533562552","date":"2026-05-08T20:42:43+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"294199101678579722710097116862553899621","date":"2026-05-03T22:29:41+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-05-03T20:19:56+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-04-13T15:57:41+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-04-09T23:06:33+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-04-09T23:06:26+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Women's Health","date":"2026-04-08T06:39:56+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-womens-health","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bmwh","sideBox":"Learn more about [BMC Women's Health](http://bmcwomenshealth.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bmwh/default.aspx","title":"BMC Women's Health","twitterHandle":"","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"54c7fde2-c7bb-40cf-ba68-4f79185c0536","owner":[],"postedDate":"May 11th, 2026","published":true,"recentEditorialEvents":[{"type":"reviewerAgreed","content":"310913366589418376877216589852533562552","date":"2026-05-08T20:42:43+00:00","index":23,"fulltext":""},{"type":"reviewerAgreed","content":"294199101678579722710097116862553899621","date":"2026-05-03T22:29:41+00:00","index":22,"fulltext":""},{"type":"reviewersInvited","content":"3","date":"2026-05-03T20:19:56+00:00","index":"","fulltext":""}],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-05-11T14:40:11+00:00","versionOfRecord":[],"versionCreatedAt":"2026-05-11 14:40:11","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-9352726","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-9352726","identity":"rs-9352726","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}