Background/Objectives: Catha edulis, also known as Khat, is a stimulant with hepatotoxic properties. Studies reporting laboratory patterns are scarce. The aim was to assess the patterns associated with hepatic dysfunction due to Khat usage. Methods: Patients with liver injury and self-reported Khat consumption presenting to the gastroenterology department at the King Fahad Central Hospital in Jazan between January 2017–May 2024 were retrospectively included in the study. Patients with any signs of cirrhosis or viral hepatitis were excluded to have a more homogenous inclusion. Normal distribution was not assumed; data were presented as the median (IQR or %). Results: Sixty-three patients (of which 62 (98.4%) were male) aged 35 (29–41) years were included in the study. An IgG > 20 g/L was present in 41 (61.5%) patients, and the majority (n = 48, 76.2%) had a hepatocellular injury pattern based on an R-factor > 5. Over half of the patients had at least one positive autoantibody(ANA 47.6%; SMA 55.6% and AMA 4.8%), while 57 (90.5%) patients received immunosuppressive therapy. Conclusions: Khat-induced liver injury seems to be predominantly AIH-like in nature, given the IgG elevation, hepatocellular injury pattern, and relatively high rate of autoantibody positivity.

Autoimmune liver diseases (AiLDs), including autoimmune hepatitis (AIH), primary biliary cholangitis (PBC), and primary sclerosing cholangitis (PSC), are immune-mediated conditions associated with significant hepatic and systemic manifestations. Among these, cytopenias—defined as reductions in blood cell counts affecting single or multiple lineages—represent a clinically important, though often under-recognized, complication. Cytopenias in AiLDs arise from diverse mechanisms, including immune-mediated destruction, hypersplenism due to portal hypertension, bone marrow suppression, and nutritional deficiencies. These abnormalities can exacerbate bleeding, infections, or fatigue, complicating the disease course and impacting therapeutic strategies. Immune-mediated cytopenias, such as autoimmune hemolytic anemia (AIHA), immune thrombocytopenic purpura (ITP), and autoimmune neutropenia (AIN), are more frequently associated with AIH, whereas cytopenias in PBC and PSC are largely attributed to hypersplenism. Diagnostic evaluation involves a systematic approach combining clinical history, laboratory testing (e.g., complete blood counts, Coombs tests, and nutritional assessments), imaging studies, and bone marrow evaluation in complex cases. Treatment strategies aim to address the underlying cause of cytopenias, including immunosuppressive therapy for autoimmune mechanisms, beta-blockers or splenectomy for hypersplenism, and supplementation for nutritional deficiencies. Challenges include distinguishing between immune- and hypersplenism-related cytopenias, managing drug-induced cytopenias, and optimizing care in transplant candidates. The recently recognized IgG4-related disease, often mimicking cholestatic AiLDs, adds another layer of complexity, given its association with autoimmune cytopenias and hypersplenism. This review aims to act as a guide for the clinician dealing with patients with AiLDs with respect to the occurrence of cytopenias, with a specific focus on pathophysiology and management of these cytopenias. Furthermore, there need to be enhanced multidisciplinary discussions about those patients between the hematologists and hepatologists, with a maintenance of a high index of suspicion for the rarer causes of cytopenias in AiLDs on the part of the treating physician, and there is a need for further studies to elucidate the mechanisms behind the occurrence of cytopenias in AiLDs.

Background: Hydrophilic polymer embolization (HPE) is a scarcely reported complication associated with endovascular procedures where the hydrophilic coating dislodges and disseminates to more distal vascular beds, leading to ischemic complications. The aim of this study is to assess the clinical outcomes associated with HPE in the literature and try to quantify it in a scoping manner. Methods: All reports with regard to HPE in the PubMed database where clinical data were available were included. Reports were excluded if no clinical data were available and only histopathological descriptions are available, if the language of the report was not in English, and if access could not be obtained to that specific report. Results: A total of 60 publications containing 111 patients were identified. The majority (N = 45, 75%) of the publications were “single-patient” case reports. An overwhelming minority of the reports reported underlying hypertension (N = 27, 45.0%) and ischemic heart disease (N = 28, 46.7%). The most common implicated procedures for HPE occurence were cardiac procedures (N = 28, 46.7%), intracranial procedures (N = 13, 21.7%) and aortic procedures (N = 10, 16.7%). Steroids were trialled in nine (15%) of the reports, mainly for HPE to the CNS (7/9), with no mortality in that specific group. However, HPE-related mortality, identified in 48/111 patients, was largely due to HPE with pulmonary and cardiac involvement (combined 36/48 of all deaths). Conclusions: HPE seems to be a rare occurrence, although low-quality evidence (mainly case reports) comprises most of the research on the subject. Fatal outcomes seem relatively common, and steroid therapy may be trialled in select cases. Further research, potentially through prospective registry studies may aid in providing more knowledge on HPE.

An 81-year-old woman with a history of rheumatoid arthritis and atrial fibrillation presented to the gastroenterology department with several months of postprandial abdominal pain, diarrhoea, and weight loss. Repeated ileocolonoscopies were normal. Magnetic resonance enterography and panenteric capsule endoscopy revealed a segment of ulcerated and narrowed small bowel ([Fig. 1], [Fig. 2], [Video 1]), raising initial suspicion of Crohn’s disease. The terminal ileum appeared normal. Treatment with intermittent steroids resulted in no improvement. A double-balloon enteroscopy was attempted but aborted due to a cardiac event. Over the following 5 years, the patient experienced intermittent symptoms and was treated empirically with steroids, without lasting improvement. Eventually, she presented with acute worsening of abdominal pain and malnutrition, prompting further investigation. Abdominal computed tomography imaging showed mural thickening and a “comb sign” in the distal jejunum/proximal ileum ([Fig. 3]). Shortly after admission, signs of peritonitis emerged. A repeat abdominal computed tomography scan revealed fat stranding, suspecting local perforation alongside an 18-mm small-bowel diverticulum ([Fig. 4]). Emergency laparotomy showed green pus originating from perforated jejunal diverticulitis. Subsequent macroscopic and microscopic pathological examination confirmed perforated jejunal diverticulitis ([Fig. 5]), with no features of malignancy or inflammatory bowel disease. The patient recovered uneventfully. Jejunal diverticulitis is rare and often underrecognized but may closely mimic small bowel Crohn’s disease on capsule endoscopy and cross-sectional imaging [1] [2] [3]. This case highlights the importance of maintaining a broad differential and considering IBD mimics in chronic small bowel disease, particularly in older adults with atypical features or poor response to immunosuppression [4]. The VIVA mnemonic – vascular (e.g., ischemia), infectious (e.g., TB and Yersinia), vasculitis (e.g., Behçet’s), autoimmune/other (e.g., NSAID enteropathy, neoplasia) – serves as a structured clinical reminder to consider IBD mimics early in the diagnostic process. The term “VIVA” also evokes the traditional oral examinations (“viva voce”) in medical training, reinforcing the intellectual rigor and diagnostic precision needed in such complex cases. Endoscopy_UCTN_Code_CCL_1AC_2AD Article published online: 08 December 2025 © 2025. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/). Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany

Background: Sodium-glucose cotransporter-2 inhibitors (SGLT2i) are increasingly used in patients with type 2 diabetes, chronic kidney disease, and heart failure. However, their safety and efficacy in patients with congenital or surgically altered urogenital anatomy remains underexplored. Methods: We conducted a narrative review of current evidence regarding the use of SGLT2i in patients with urinary tract malformations, urinary diversions, and functional voiding disorders. Key risks, clinical considerations, and management strategies were synthesized from the existing literature and case reports. Results: Patients with benign prostatic hyperplasia, vesicoureteral reflux, neurogenic bladder, nephrostomies, and ileal conduits may face increased risks of urinary tract infections, fungal colonization, and therapy-related complications due to persistent glycosuria and altered urinary flow. Nevertheless, these patients may still benefit from SGLT2i’s systemic renal and cardiovascular effects. Individualized risk assessment, close monitoring, and multidisciplinary management are essential. Conclusions: Patients with urological abnormalities represent a high-risk but potentially high-reward population for SGLT2i therapy. A cautious, tailored approach is necessary, and future dedicated research is urgently needed to better guide clinical practice.