INTRODUCTION: Gastrointestinal (GI) symptoms in coronavirus-19 disease (COVID-19) have been reported with great variability and without standardization. In hospitalized patients, we aimed to evaluate the prevalence of GI symptoms, factors associated with their occurrence, and variation at 1 month. METHODS: The GI-COVID-19 is a prospective, multicenter, controlled study. Patients with and without COVID-19 diagnosis were recruited at hospital admission and asked for GI symptoms at admission and after 1 month, using the validated Gastrointestinal Symptom Rating Scale questionnaire. RESULTS: The study included 2036 hospitalized patients. A total of 871 patients (575 COVID+ and 296 COVID−) were included for the primary analysis. GI symptoms occurred more frequently in patients with COVID-19 (59.7%; 343/575 patients) than in the control group (43.2%; 128/296 patients) (P < 0.001). Patients with COVID-19 complained of higher presence or intensity of nausea, diarrhea, loose stools, and urgency as compared with controls. At a 1-month follow-up, a reduction in the presence or intensity of GI symptoms was found in COVID-19 patients with GI symptoms at hospital admission. Nausea remained increased over controls. Factors significantly associated with nausea persistence in COVID-19 were female sex, high body mass index, the presence of dyspnea, and increased C-reactive protein levels. DISCUSSION: The prevalence of GI symptoms in hospitalized patients with COVID-19 is higher than previously reported. Systemic and respiratory symptoms are often associated with GI complaints. Nausea may persist after the resolution of COVID-19 infection.

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.

We aimed to examine the effect of remission status on thiol–disulfide homeostasis in celiac patients and thus to indirectly determine the effect of oxidative stress and inflammation caused by non-compliance with the diet.

Background and Aim: Several studies have suggested that treatment with direct-acting antivirals (DAAs) in patients with chronic hepatitis C virus (HCV) may be associated with an increased risk of developing hepatocellular carcinoma (HCC). We investigated the incidence and risk factors of HCC in HCV patients who achieved a sustained virologic response (SVR) following DAA therapies. Materials and Methods: The medical data of patients who were diagnosed with HCV and received DAA therapy in two tertiary centers in Turkey were retrospectively collected. Results: Among them, 75 patients (52.4%) were noncirrhotic and 68 patients (47.6%) were cirrhotic. The overall SVR rate was 97.2% (139/143). It was 100% in noncirrhotic and 94.1% in cirrhotic patients. HCC was developed in 5 (7.4%) patients, all of whom had baseline cirrhosis. The annual rate of HCC occurrence was 2.94%, and the 5-year cumulative incidence of HCC was 7.3%. The mean Child-Pugh score (CPS) and Model for End-Stage Liver Disease (MELD) score significantly decreased after DAA treatment (CPS 7.0 vs 5.9, p=0.001; MELD 10.8 vs 9.5, p=0.003). Conclusion: There was no significant increase in the rate of HCC in cirrhotic HCV patients treated with DAAs. This treatment led to a remarkably high SVR rate and lowered CPS and MELD scores in cirrhotic HCV patients.