Background: Cirrhosis is a progressive liver disease often associated with sarcopenia. Vitamin D and IGF-1 alterations may contribute to muscle loss and disease progression. This study evaluated their relationship in cirrhotic patients. Methods: A total of 90 patients with liver cirrhosis were included in this retrospective observational study. Clinical and laboratory data were collected, and disease severity was assessed using Child–Pugh and MELD-Na scores. Sarcopenia was evaluated using CT-based skeletal muscle index at the L3 level with sex-specific cut-offs. Patients with malignancy, acute liver failure, recent surgery, or muscle-affecting conditions were excluded. Vitamin D and IGF-1 levels were classified using standard and age-adjusted reference ranges. Results: A total of 90 patients were included, of whom 42 were alive, and 48 died during follow-up. Gender distribution was similar between groups (p = 0.388). Skeletal muscle area was significantly lower in non-survivors (110 vs. 140 cm², p = 0.002), while body mass index did not differ (p = 0.570). Vitamin D levels were significantly lower (10.0 vs. 17.9 ng/mL, p < 0.001), and hemoglobin levels were reduced in the non-survivor group (10.76 ± 2.13 vs. 12.87 ± 2.57 g/dL, p = 0.001). In multivariate analysis, age (OR 1.046, p = 0.032), MELD-Na score (OR 1.200, p = 0.001), and vitamin D level (OR 0.920, p = 0.024) were independently associated with mortality. Conclusions: CT-based sarcopenia assessment is a useful adjunct in cirrhosis when interpreted with disease severity. Radiological muscle depletion is common and associated with worse outcomes, while vitamin D deficiency independently associated with mortality, highlighting its potential as a biomarker and therapeutic target.

Background/Objectives: Acute pancreatitis (AP) is a heterogeneous disease with outcomes ranging from mild to severe. Early risk stratification is essential, but commonly used scoring systems are often complex for routine use. This study aimed to evaluate the predictive value of systemic inflammatory indices derived from complete blood count parameters in assessing disease severity in AP. Methods: This retrospective study included 454 patients with AP. Demographic, clinical, and laboratory data were obtained from electronic medical records. Systemic inflammatory indices (NLR, PLR, MLR, dNLR, SII, SIRI, and AISI) were calculated from admission laboratory values, with logarithmic transformation applied to selected indices. Disease severity was classified according to the Revised Atlanta Classification, and patients were grouped as mild or moderate-to-severe. Statistical analyses included ROC curve analysis and logistic regression. Results: Among 454 patients, 371 (81.7%) had mild and 83 (18.3%) had moderate-to-severe AP. Patients with more severe disease were older and showed significant differences in several laboratory parameters. NLR, PLR, SII, dNLR, and Log-SII were significantly higher in the moderate-to-severe group. However, all indices demonstrated limited discriminative performance, with dNLR showing the highest AUC (0.612). In multivariate analysis, only age and C-reactive protein (CRP) remained independent predictors of disease severity. Conclusions: Systemic inflammatory indices are associated with disease severity in AP; however, their predictive performance is limited. Conventional parameters such as age and CRP remain more reliable for risk stratification.

Introduction: Intraductal papillary mucinous neoplasms (IPMNs) are precursor lesions of pancreatic cancer. This study investigated the association between MRI-derived pancreatic fat fraction and IPMN.. Material Methods: This retrospective case-control study included 60 patients with IPMN and 120 controls evaluated between 2018 and 2025. All participants underwent pancreatic MRI with proton density fat fraction (PDFF) imaging. Pancreatic fat fraction was measured in the pancreatic head, body, and tail on PDFF maps, and mean pancreatic fat fraction was calculated. Group comparisons, receiver operating characteristic analysis, and logistic regression analyses were performed to evaluate the association between pancreatic fat fraction and IPMN. Results: A total of 180 participants were included in the study, comprising 60 patients with IPMN and 120 controls without IPMN. Patients with IPMN were significantly older than controls (72.5 vs. 57.0 years, p=0.001). The IPMN group demonstrated higher glucose and LDH levels and lower HDL cholesterol, hemoglobin, hematocrit, and platelet counts compared with controls (all p<0.05). Pancreatic fat fraction measurements were significantly increased in patients with IPMN across all pancreatic regions. Head, body, tail, and mean pancreatic fat fractions were markedly higher in the IPMN group than in controls (all p=0.001). In multivariable logistic regression analyses, age and pancreatic fat fraction remained independently associated with IPMN presence. ROC analysis demonstrated excellent diagnostic performance, with mean pancreatic fat fraction showing the highest discriminative ability (AUC=0.968), followed by head (AUC=0.934), body (AUC=0.922), and tail fat fraction (AUC=0.876). Conclusion: Pancreatic fat fraction was significantly higher in patients with IPMN and remained independently associated with IPMN presence after multivariable adjustment. Mean pancreatic fat fraction demonstrated excellent diagnostic performance for distinguishing IPMN from non-IPMN individuals. Quantitative MRI-based assessment of pancreatic fat may represent a useful imaging biomarker for IPMN detection.

Background/Objectives: Numerous hematologic, inflammatory, biochemical, and nutritional indices have been proposed as prognostic markers in coronavirus disease 2019 (COVID-19), but direct comparison of a broad range of these indices within the same cohort remains limited. This study aimed to evaluate and compare the prognostic performance of multiple routinely available indices for in-hospital mortality. Methods: This retrospective observational cohort included 1952 adults hospitalized with COVID-19. Demographic, clinical, comorbidity, and laboratory data were obtained from medical records. Eighteen derived indices were evaluated, including NLR, PLR, SII, CAR, CLR, LAR, UAR, CPR, DAR, and PNI. Receiver operating characteristic analysis was performed to assess discrimination for in-hospital mortality, and optimal cut-offs were determined using the Youden index. Selected indices were further evaluated in separate multivariable logistic regression models adjusted for age, sex, diabetes mellitus, CAD/IHD, and eGFR. Results: In-hospital mortality occurred in 80 patients (4.1%). Non-survivors were older and had higher inflammatory and biochemical markers and lower lymphocyte counts and albumin levels. CAR and CLR showed the highest numerical AUCs for in-hospital mortality (0.870 for both), followed by PNI (0.857), CPR (0.852), DAR (0.829), UAR (0.823), LAR (0.815), and NLR (0.807). In separate multivariable models adjusted for age, sex, diabetes mellitus, CAD/IHD, and eGFR, ln(CLR), ln(CAR), ln(CPR), ln(LAR), ln(UAR), ln(NLR), ln(dNLR), and ln(DAR) remained independently associated with mortality (all p < 0.001). Among the adjusted models, the CLR model showed the highest explained variance (Nagelkerke R² = 0.511) with good calibration (Hosmer–Lemeshow p = 0.997); ln(CLR) remained independently associated with mortality (aOR 3.590, 95% CI 2.517–5.120; p < 0.001). Conclusions: Several routinely available composite indices were associated with in-hospital mortality in COVID-19. Among the evaluated indices, CAR and CLR showed the highest individual discrimination, while the CLR-based adjusted model showed the most favorable model-fit profile among the multivariable models evaluated. Multiple selected indices remained independently associated with mortality after adjustment for clinical covariates. These findings suggest that such markers may have potential value as adjunctive tools for mortality risk stratification.

Introduction: Intraductal papillary mucinous neoplasms (IPMNs) are precursor lesions of pancreatic cancer. This study investigated the association between MRI-derived pancreatic fat fraction and IPMN. Materials and Methods: This retrospective case–control study included 60 patients with IPMN and 120 controls evaluated between 2018 and 2025. All participants underwent pancreatic MRI with proton density fat fraction (PDFF) imaging. Pancreatic fat fraction was measured in the pancreatic head, body, and tail on PDFF maps, and mean pancreatic fat fraction was calculated. Group comparisons, receiver operating characteristic analysis, and logistic regression analyses were performed to evaluate the association between pancreatic fat fraction and IPMN. Results: A total of 180 participants were included in the study, comprising 60 patients with IPMN and 120 controls without IPMN. Patients with IPMN were significantly older than controls (72.5 vs. 57.0 years, p = 0.001). The IPMN group demonstrated higher glucose and LDH levels and lower HDL cholesterol, hemoglobin, hematocrit, and platelet counts compared with controls (all p < 0.05). Pancreatic fat fraction measurements were significantly increased in patients with IPMN across all pancreatic regions. Head, body, tail, and mean pancreatic fat fractions were markedly higher in the IPMN group than in controls (all p = 0.001). In multivariable logistic regression analyses, age and pancreatic fat fraction remained independently associated with IPMN presence. ROC analysis demonstrated excellent diagnostic performance, with mean pancreatic fat fraction showing the highest discriminative ability (AUC = 0.968), followed by head (AUC = 0.934), body (AUC = 0.922), and tail fat fraction (AUC = 0.876). Conclusions: Pancreatic fat fraction was significantly higher in patients with IPMN and remained independently associated with IPMN presence after multivariable adjustment. Mean pancreatic fat fraction demonstrated excellent diagnostic performance for distinguishing IPMN from non-IPMN individuals. Quantitative MRI-based assessment of pancreatic fat may represent a useful imaging biomarker for IPMN detection.

Chronic hepatitis B remains a major cause of cirrhosis and hepatocellular carcinoma worldwide. We investigated whether histologic hepatic steatosis affects hepatitis B virus deoxyribonucleic acid (HBV DNA) suppression in patients receiving antiviral therapy. This retrospective observational study included 307 adult patients with chronic hepatitis B who received tenofovir or entecavir therapy and underwent pretreatment liver biopsy. Demographic, laboratory, virological, radiological, and histopathological data were retrieved from the electronic medical record system. Laboratory parameters included complete blood count, liver function tests, alpha-fetoprotein, renal function tests, and lipid profile. Histopathological evaluation included fibrosis stage, histologic activity index, and hepatic steatosis percentage. Ultrasonographic findings included hepatic steatosis, liver echotexture, and contour. The primary outcome was HBV DNA suppression at 12 months. Long-term virological response was evaluated as time to first HBV DNA suppression during follow-up (maximum 60 months). A total of 307 patients receiving entecavir or tenofovir were included, of whom 258 (84.0%) achieved HBV DNA suppression at 12 months. Patients without suppression had higher baseline aspartate aminotransferase, histologic activity index, histologic steatosis, and baseline log ₁₀ HBV DNA levels (all P < .05). Histologic steatosis ≥5% was more frequent in patients without suppression (42.9% vs 23.6%, P = .005). In multivariable analysis, steatosis ≥5% (odds ratio 0.365, 95% confidence interval [CI] 0.179–0.746; P = .006) and higher baseline log ₁₀ HBV DNA (odds ratio 0.842, 95% CI 0.751–0.944; P = .003) were associated with a lower likelihood of 12-month suppression, with similar findings in the parsimonious sensitivity model. Kaplan–Meier analysis showed delayed suppression with steatosis (log-rank P = .016); however, this association was not significant in the conventional adjusted Cox model (hazard ratio 0.900, 95% CI 0.689–1.175; P = .438), and a significant time-dependent interaction indicated non-proportionality ( P < .001). Histologic steatosis and higher baseline log ₁₀ HBV DNA were associated with a lower likelihood of 12-month HBV DNA suppression. However, an independent longitudinal association with time to suppression was not demonstrated. Residual confounding by unmeasured metabolic factors cannot be excluded.