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: Gaucher disease (GD) is a rare autosomal recessive lysosomal storage disorder caused by mutations in the GBA1 gene, leading to deficient β-glucocerebrosidase activity. This results in the accumulation of glucocerebroside in macrophages, primarily affecting the liver, spleen, bone marrow, and bones. Understanding the clinical outcomes and genetic mutation profiles in specific populations, such as Turkish patients, is essential for optimized disease management and personalized therapy and preventing morbidity and mortality. Method: This retrospective study analyzed data from 29 Turkish patients with previously diagnosed type 1 GD at a single center between September and December 2023. Genetic analyses were performed to identify GBA1 mutations using next-generation sequencing. Genetic mutations were the primary criterion for diagnosing GD. Clinical features, treatment responses, and outcomes were evaluated. Clinical parameters included hematological findings, organomegaly, and bone involvement. Data were analyzed to identify potential correlations between genetic mutations and clinical manifestations. Results: This study included 14 male and 15 female patients, with a mean diagnosis age of 22.1 years. A significant family history was observed in 93% of cases, and 52% had consanguineous parents. Epistaxis (72%) was the most common pre-diagnosis symptom. Most patients received enzyme replacement therapy with 60 units/kg. Treatment led to significant improvements, including increased hemoglobin (21.1%), higher platelet count (86.1%), and reduced organomegaly (liver (10.02%), spleen (25.22%)). Genetic analysis identified seven mutations, with c.1226A>G (p.N409S) being the most frequent. Conclusions: This study highlights the spectrum of clinical outcomes and genetic mutations in Turkish patients with GD, emphasizing the variability in disease severity based on genotype. GD should be considered for patients with unexplained nosebleeds, hepatosplenomegaly, bone pain, weakness, or siblings or other family members with similar symptoms. The genetic analysis revealed considerable heterogeneity among patients, which indicates the necessity of observing this in the development of personalized treatment strategies. Future studies with larger cohorts and long-term follow-up are needed to further elucidate genotype–phenotype correlations in this population.

Introduction: Oral lichen planus (OLP) is a chronic inflammatory condition and a precancerous lesion of OLP-based oral squamous cell carcinoma (OSCC), with possible esophageal involvement (esophageal lichen planus [ELP]), though the latter prevalence and clinical significance remain uncertain. This study aimed to determine ELP prevalence in OLP/OSCC patients, assess the diagnostic performance of white-light endoscopy (WLE), narrow-band imaging (NBI), and Lugol’s iodine staining-based chromoendoscopy, and evaluate histologic findings for potential prognostic implications. Methods: In this prospective single-center study (2011–2020), 81 adults with confirmed OLP and about 50% history of OSCC underwent esophagogastroduodenoscopy (EGD) using WLE, NBI, and chromoendoscopy. Biopsies were taken from visually suspicious areas and from normal-appearing mucosa throughout the esophagus, stomach, and duodenum. Results: ELP was identified in only 4 patients (4.9%), all of whom were asymptomatic or had minimal symptoms. In 3 cases, ELP was detected only via random biopsies despite normal endoscopic appearance. The sensitivity of WLE, NBI, and chromoendoscopy was low, with Lugol’s staining yielding false positives due to benign changes like glycogen acanthosis. No dysplasia or carcinoma was observed. Conclusion: Even in one of the largest prospective studies, ELP remained a rare finding, often clinically silent, and frequently undetectable on endoscopy. Step biopsies are essential for diagnosis. EGD screening in OLP may be considered as a one-time index endoscopy, supplemented by symptom-based evaluation in selected cases. ELP does not appear to increase short-term malignancy risk, and management should focus on symptom control and avoiding complications.

Background: Advanced cirrhosis induces profound CD4⁺ T-cell depletion through splenic sequestration and immune dysregulation. Pneumocystis jirovecii pneumonia risk thresholds remain undefined in non-HIV immunocompromised populations, necessitating investigation in cirrhotic patients. Objectives: To investigate the potential association between peripheral CD4⁺ T-cell counts and opportunistic infections (OI)—specifically Pneumocystis jirovecii (PJ)—in hospitalized patients with liver disease, and to characterize clinical outcomes across immunological risk strata. Methods: We retrospectively analyzed 455 adults hospitalized in a single institution with hepatic disorders. CD4⁺ T-cell counts were available in 227/455 patients. Among these, 22 patients met predefined immunological risk criteria (CD4⁺ < 500/µL and/or HIV positivity) and were classified into three immunological risk clusters (IRCs): IRC-A (HIV−, CD4⁺ < 200/µL; n = 9), IRC-B (HIV+, CD4⁺ < 200/µL; n = 7), and IRC-C (HIV−, CD4⁺ 200–499/µL; n = 6). PJ PCR testing was evaluated when available. Results: Among 455 patients, in-hospital mortality was 103/455 (22.6%). Of the 22 immunologically at risk patients, 15/22 had cirrhosis. PJ PCR was performed in 8/22 patients (IRC-A: 2; IRC-B: 4; IRC-C: 2), with 3/8 positive (37.5%): IRC-A (1/2), IRC-B (1/4), IRC-C (1/2). Ct values ranged from 27.0 to 31.7. Two PJ-PCR–positive cirrhotic patients (IRC-A: n = 1; IRC-C: n = 1) survived without specific anti-PJ therapy; one HIV-positive patient (IRC-B) received trimethoprim-sulfamethoxazole and survived. In-hospital mortality was 5/9 (55.6%) in IRC-A, 2/7 (28.6%) in IRC-B, and 3/6 (50.0%) in IRC-C; none of the deaths were attributable to PJ pneumonia. Conclusions: Severe CD4⁺ T-cell depletion (<200/µL) was common among cirrhotic patients and associated with PJ detection (3/8 tested), but not with PJ-related mortality (0/3). Mortality was primarily driven by hepatic decompensation and bacterial infections. CD4⁺ assessment may improve risk stratification in cirrhosis; however, prospective, multicenter studies are warranted to validate these findings and to evaluate CD4-guided strategies for the prevention of opportunistic infections.

Objectives: Clinical intent for laboratory testing (“indication”) is rarely recorded in structured form, limiting contextual interpretation, auditability, and utilization stewardship. We developed a comprehensive, and clinically applicable framework that standardizes laboratory test indications and links them to indication-dependent utilization and interpretation. Methods: A structured literature review on utilization, appropriateness, and request rationale informed an iterative, consensus-based process with a multidisciplinary expert panel to develop and operationalize an indication taxonomy and attribute schema. Structural coherence was assessed by comparing semantic distance hierarchies derived from indication labels alone with an enriched multi-layer (“layered prototype”) representation incorporating these attributes. Use cases were applied to assess feasibility of indication-to-interpretation mapping. Results: We defined 19 distinct indication types, grouped into five clusters across the clinical course: Initial Detection and Diagnostic Clarification, Disease Characterization and Prognosis, Therapy Guidance and Safety, Longitudinal Management and Reassessment, and Analytical and External Requirements. Each is specified with structured attributes and examples to support implementation. Semantic distance analyses supported a coherent hierarchy. Layered prototypes yielded more informative organization than labels alone, enabling context-dependent consolidation and guided deployment. Conclusions: By providing explicit indication-to-interpretation mapping/logic, the framework closes a key gap in the total testing process between order entry and post-analytical interpretation. It supports context-specific decision limits, reporting logic, and stewardship analytics, and is amenable to formalization as a machine-readable ontology for interoperable implementation.

This study presents a refined murine MetALD model designed to distinguish ethanol-modified features from FFC-driven metabolic steatohepatitis. Chronic ethanol did not uniformly worsen liver injury. Instead, it selectively modified disease trajectory through greater early collagen-positive fibrotic remodeling, altering lipid-droplet architecture, and context-dependent inflammatory chemokine signaling. By 24 wk, FFC and FFC/ethanol injury programs converged, supporting MetALD as a timing- and pathway-dependent modification of metabolic steatohepatitis.