Background and Aims: Ornidazole, a nitroimidazole antibiotic, is widely used for protozoal and anaerobic infections and is generally considered safe. However, ornidazole-induced liver injury (OILI) is an underrecognized yet potentially severe adverse reaction. This multicenter study aims to characterize the clinical features, histopathology, and outcomes of OILI to improve the awareness and management of this rare entity worldwide. Methods: We conducted a retrospective analysis of 101 patients with OILI from eight tertiary centers between 2006 and 2023. Cases were included based on liver enzyme elevations temporally linked to ornidazole and the exclusion of other causes. Causality was assessed using the Roussel Uclaf Causality Assessment Method (RUCAM) score. Clinical data, laboratory parameters, autoantibody profiles, histology, treatments, and outcomes were evaluated. Results: OILI was classified as highly probable in 42.6% of cases (n = 43), probable in 51.5% of cases (n = 52), and possible in 5.9% (n = 6) of cases. The predominant pattern was acute hepatocellular injury (83.2%) (n = 84). Autoimmune-like hepatitis occurred in 5% of cases (n = 5), with ANA positivity in 16.8% of cases (n = 17). Corticosteroids were used in 24.8% of cases (n = 25) and were associated with higher ANA positivity and a 20% (n = 5) relapse rate post-discontinuation. Recovery was achieved in 87.7% of cases (n = 88), while 7.9% of cases (n = 8) required liver transplantation and 4% (n = 4) died. Conclusions: Ornidazole can cause serious idiosyncratic liver injury, including autoimmune phenotypes, and should be considered in the differential diagnosis of acute hepatitis. Given the notable risk of liver failure and death, early recognition, drug discontinuation, and close monitoring are essential. In select cases, corticosteroids and plasmapheresis may be beneficial, though the evidence remains limited.

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: The global increase in metabolic dysfunction-associated steatotic liver disease underscores the need for accessible and reliable markers to assess hepatic steatosis. The triglyceride–glucose (TyG) index, derived from fasting plasma glucose and triglyceride levels, has emerged as a practical surrogate marker of insulin resistance and has been increasingly associated with metabolic liver involvement. This study aimed to evaluate the relationship between the TyG index and the severity of hepatic steatosis assessed by ultrasonography. Methods: This retrospective cross-sectional study included 480 adult patients without a prior diagnosis of diabetes mellitus or hypertension who underwent fasting laboratory testing and abdominal ultrasonography between January 2024 and May 2025. Fasting plasma glucose and triglyceride levels were obtained on the same day as ultrasonographic evaluation. Hepatic steatosis was assessed by a single experienced radiologist using standardized ultrasonographic criteria, and patients were categorized into three groups according to steatosis grade (grade 0, grade 1, and grade 2–3; n = 160 for each group). Demographic data and laboratory parameters, including glucose, triglycerides, HbA1c, platelet count, neutrophils, lymphocytes, monocytes, ALT, AST, and total cholesterol levels, were recorded. The TyG index was calculated using the formula: TyG = ln[(fasting triglycerides × fasting glucose)/2]. Results: A total of 480 patients (30.6% male) were included in the analysis. Mean fasting glucose, triglyceride, and TyG index values were 94.20 ± 11.15 mg/dL, 146.91 ± 83.94 mg/dL, and 8.70 ± 0.55, respectively. Metabolic and inflammatory parameters increased significantly with advancing steatosis grades (all p < 0.05). The TyG index demonstrated a clear stepwise increase from grade 0 (8.29 ± 0.42) to grade 1 (8.74 ± 0.42) and grade 2–3 steatosis (9.07 ± 0.49) (p < 0.001), with all pairwise comparisons remaining statistically significant. Receiver operating characteristic (ROC) analysis showed good discriminative performance of the TyG index for hepatic steatosis (AUC = 0.829), and an optimal cutoff value of 7.90 was identified using the Youden index, yielding high sensitivity for detection. In multivariable logistic regression analysis, the TyG index remained the strongest independent predictor of hepatic steatosis (adjusted OR 11.41, 95% CI 6.10–21.34; p < 0.001). Conclusions: The TyG index increased progressively with the severity of hepatic steatosis and showed strong associations with metabolic and inflammatory parameters. These findings support the TyG index as a simple and accessible marker reflecting metabolic dysfunction and hepatic steatosis, with potential value for early risk stratification in clinical practice.

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.

Karaciğer, vücudun en büyük iç organıdır ve metabolik fonksiyonların merkezi olarak birçok hayati işlevi üstlenir. Bu organ, protein sentezinden detoksifikasyona, enerji depolamasından sindirim enzimlerinin üretimine kadar birçok kritik süreçte rol oynar. Ancak karaciğerin bu çok yönlü işlevleri, onu çeşitli enfeksiyonlara karşı da savunmasız hale getirir. Karaciğere gelen kanın çoğu, portal ven yoluyla gastrointestinal sistemden gelir ve bu kan aynı zamanda potansiyel olarak patojenik mikroorganizmalar da taşıyabilir. Bu durum, karaciğerin birçok mikrobiyal organizma ile enfekte olmasına zemin hazırlar. Bakteriyel, parazitik ve fungal enfeksiyonlar karaciğerde ciddi patolojik değişikliklere neden olabilir. Bu enfeksiyonlar doğrudan karaciğerde başlayabilir veya sistemik ya da bulaşıcı hastalıkların bir parçası olarak ortaya çıkabilir. Karaciğer enfeksiyonlarının klinik seyri, enfeksiyonun etiyolojisine, konağın bağışıklık durumuna ve enfeksiyonun yayılma derecesine bağlı olarak büyük ölçüde değişir. Bu bölümün amacı, bakteriyel karaciğer hastalıklarının etiyolojisini, patogenezini, klinik semptomlarını, tanı yöntemlerini ve tedavi yaklaşımlarını ayrıntılı olarak ele almaktır.