Journal of Research in Medical Sciences1735-19953165202602101173511735EN20260210<p><strong>Background:</strong> Previous studies indicated that metabolic and bariatric surgery (MBS) is a well?known procedure for considerable and sustainable weight loss. While the studies showed that MBS may unfavorably influence and stimulate hepatic dysfunction by raising the aspartate aminotransferase (AST) and alanine aminotransferase (ALT). It is not yet clear whether the ALT and AST alterations following MBS are transient or it is permanently dangerous for liver function. Thus, we aimed to compare the metabolic effect of three MBS methods on liver function status.</p><p><strong>Materials and Methods:</strong> In this retrospective cohort study, we focused on adults who underwent MBS without a history of liver disorders. The trends of liver function enzymes and albumin levels from the baseline to 3, 6, and 12 months postsurgery were explored for all patients with complete data using multiple binary logistic regressions.</p><p><strong>Results:</strong> The study involved 1378 participants who completed all of the measurements, with 366 (26.56%) undergoing sleeve gastrectomy (SG), 772 (56.02%) undergoing one?anastomosis gastric bypass (OAGB), and 240 (17.41%) ndergoing Roux?en?Y gastric bypass (RYGB). While there were no significant differences in the levels of AST, ALT, and albumin between the three surgical methods at baseline, the effect of bariatric procedures on the AST and ALT levels went through completely differed across time. Furthermore, each bariatric technique had a different trend of the levels of AST and ALT. The trend of the levels of AST and ALT of RYGB and OAGB reached a stable level after 12 months of surgery. On the other hand, the stability time of the AST and ALT levels for SG was observed at 6 months, and the reduction was significantly higher than other methods.</p><p><strong>Conclusion:</strong> Our findings suggest that the increasing trend of the AST and ALT levels and the stimulation of the liver function postoperatively were transient. The changes in the AST and ALT trend also reached a stable level after 12 months postoperative.<br /><br /></p>http://jrms.mui.ac.ir/index.php/jrms/article/view/11735http://jrms.mui.ac.ir/index.php/jrms/article/download/11735/6509

Journal of Research in Medical Sciences1735-19953165202602101174011740EN20260210<p><strong>Background:</strong> Acute coronary syndrome (ACS) is one of the leading causes of death, but there is no attention paid to the risk  stratification of patients with ACS. Aims: We evaluated the utility of the triglyceride?glucose (TyG) index in predicting the hospital and<br />intensive care unit (ICU) mortality of critically ill patients with ACS.</p><p><strong>Materials and Methods:</strong> The study patients were collected from the eICU Collaborative Research Database. TyG index was calculated as the ln (fasting glucose level [mg/dL] × triglyceride level [mg/ dL]/2). The endpoints were hospital and ICU mortality. The univariate and multivariate logistic regressions and subgroup analysis were used to determine the relationship between the TyG index and two endpoints. The scatter plots, bar graphs and smoothing curves further proved it.</p><p><strong> Results:</strong> 5237 critically ill patients with ACS were enrolled. The TyG index was obviously higher in nonsurvivors groups than survivors groups. TyG index was significantly associated with hospital mortality in univariate analysis (odds ratio [OR] 1.33, 95% confidence interval [CI] 1.15–1.53, P &lt; 0.001), adjusted model I (OR 1.59, 95% CI 1.36–1.85, P &lt; 0.001) and adjusted model II (OR 2.23, 95% CI 1.50–3.31, P &lt; 0.001). The ICU mortality showed the same trends (OR 1.50, 95% CI 1.26–1.78, OR 1.73, 95% CI 1.45–2.06, OR 2.53, 95% CI 1.59–4.03, P &lt; 0.001). The same trends were observed after stratified by tertiles and quartiles. There were continuous linear relations between the TyG index and hospital and ICU mortality.</p><p><strong>Conclusion:</strong> TyG index is an independent predictor of ICU and hospital mortality in critically ill patients with ACS.<br /><br /></p>http://jrms.mui.ac.ir/index.php/jrms/article/view/11740http://jrms.mui.ac.ir/index.php/jrms/article/download/11740/6513

Journal of Research in Medical Sciences1735-19953165202602101173611736EN20260210Diabetic kidney disease (DKD) affects 30%–40% of patients with diabetes mellitus (DM). Dyslipidemia is a key modifiable risk factor for the development and progression of DKD. Statins remain the mainstay of lipid management in DM, but concerns exist about their<br />renal effects and limited impact on high?density lipoprotein (HDL) and triglycerides.  Fibrates, which primarily target HDL elevation and triglyceride reduction, have shown promise in addressing the lipid profile most relevant to DKD; however, they initially raise<br />serum creatinine levels. This review aims to compare the effects of statins and fibrates on the development and progression of DKD, examining their mechanisms of action, clinical evidence, and limitations of current research. A comprehensive search of PubMed, Scopus, and Web of Science identified clinical studies published from 2000 onward, evaluating the renal effects of statins and/or fibrates in patients with DM, focusing on kidney function,  damage markers, and disease progression. According to our findings, statins offer modest, short?term kidney protection; however, their long?term renal effects, and their limited  impact on the specific dyslipidemia pattern associated with DKD, are a concern. Fibrates, which more effectively target triglycerides and HDL, show promise in preserving kidney function, though their use may be limited in advanced kidney disease. While some  evidence suggests fibrates may be superior, especially in patients with low HDL and high triglycerides, more long?term studies are needed to confirm their definitive advantage over statins. Future research should focus on long?term studies with comprehensive assessments of kidney function.<br /><br />http://jrms.mui.ac.ir/index.php/jrms/article/view/11736http://jrms.mui.ac.ir/index.php/jrms/article/download/11736/6510

Journal of Research in Medical Sciences1735-19953165202602101173711737EN20260210<p><strong>Background:</strong> Due to the anti?inflammatory and antioxidant effects of riboflavin, this vitamin can be effective in improving migraine. However, due to conflicting results in previous studies, the present study aimed to determine the effectiveness of riboflavin in improving migraine in a systematic review and dose–response meta?analysis.</p><p><strong>Methods:</strong> Scopus, ISI Web of Science, and PubMed databases, as well as Google Scholar, were searched up to March 15, 2025 to find trials, published in the English language, that investigated the effect of riboflavin on migraine. Quality assessment of trial studies was done using the Cochrane Collaboration tool. STATA software was used to analyze the data.</p><p><strong>Results:</strong> The present study included 12 trials with a total sample size 749. The dose–response meta?analysis revealed a significant linear relationship, showing that increasing riboflavin intake up to 400 mg/day was associated with greater reductions in migraine frequency and duration, without evidence of a threshold effect (P &lt; 0.001). Riboflavin had a significant effect on frequency (weighted mean difference [WMD]: ?1.39, 95%CI: ?2.52 to ?0.25; I2 = 91.7%, P &lt; 0.001) and duration of migraine (WMD: ?1.36, 95% CI: ?2.69 to ?0.03; I2 = 90.4%, P &lt; 0.001) in comparison to the control. In terms of  ethodological approach, eight trials had a good and four had a fair quality.</p><p><strong>Conclusion:</strong> Riboflavin exhibits promising effects in reducing the frequency and duration of migraine. The limitations of the present study include the absence of a control group and the small sample size in some included studies.<br /><br /></p>http://jrms.mui.ac.ir/index.php/jrms/article/view/11737http://jrms.mui.ac.ir/index.php/jrms/article/download/11737/6511

Journal of Research in Medical Sciences1735-19953165202602101173811738EN20260210Fractures pose a significant public health challenge due to their association with poor health outcomes and increased healthcare costs. While bone mineral density (BMD) remains a fundamental element of fracture risk assessment, it fails to fully capture bone<br />quality, including strength and microstructural integrity. Advanced glycation end products, particularly pentosidine, have emerged as critical determinants of bone fragility by altering collagen cross?linking and mechanical properties. This manuscript reviews current evidence on pentosidine as a biomarker for bone quality and fracture risk. Pentosidine, a stable advanced glycation end product, accumulates in bone collagen through  nonenzymatic cross?linking, impairing bone toughness and increasing fracture  susceptibility. Elevated pentosidine levels correlate with age, diabetes, and chronic kidney disease, conditions strongly linked to increased fracture risk. Clinical studies demonstrate that serum, plasma, and urinary pentosidine levels independently predict fracture risk, even in the absence of significant BMD changes. Advances in detection technologies, including liquid chromatography and enzyme?linked immunosorbent assay, have improved pentosidine quantification, though challenges remain in establishing bone?specific biomarkers. Future research should focus on refining detection strategies and validating pentosidine as a clinical tool for fracture risk assessment, particularly in high?risk populations.<br /><br /><br />http://jrms.mui.ac.ir/index.php/jrms/article/view/11738http://jrms.mui.ac.ir/index.php/jrms/article/download/11738/6512