Introduction: Hepatitis C Virus (HCV) is a blood borne virus that will progress to a chronic state in 55-85% of cases. Though direct acting antivirals (DAA) offers an effective cure, HCV remains underdiagnosed and the development of complications of cirrhosis including HCC may be the only clinical clue prompting diagnosis. Achieving sustained virological response (SVR) with direct acting antivirals (DAA) is a therapeutic imperative even in advanced HCC to prevent decompensation and to reduce tumor recurrence. However, drug interactions, suboptimal response in HCC, and risk of provoking decompensation in cirrhosis are important considerations in initiating treatment. We present the novel case of SVR with immune checkpoint inhibitor (ICI) therapy in a treatment naïve host. Case: Mr. M is a 53-year-old male with alcohol use disorder, and remote intravenous drug use, presented with severe abdominal pain, acute anemia (hemoglobin 7.6g/dL), hypotension (systolic BP 94mmHg). CT imaging revealed cirrhotic morphology and an 8cm liver lesion with tumor thrombosis and hemoperitoneum consistent tumor rupture. His Childs Pugh Score was B-9. AFP was 1972ng/mL. Liver biopsy confirmed mixed biphenotypic HCC/Cholangiocarcinoma. Etiological screen returned positive for HCV (antibody positive, RNA 20,500 IU/mL, genotype I). Treatment was deferred due to ‘advanced malignancy’. He started systemic therapy as tremelimumab and durvalumab, achieving significant tumor response. His HCV titer climbed to 895,000 IU/mL 5 months after starting treatment before declining and remaining persistently undetectable even after completion of immunotherapy. Subsequent disease progression was managed with TACE and SBRT. Systemic therapy was complicated by grade II ICI-hepatitis responsive to prednisone. Discussion: This case shows immune checkpoint inhibition can reverse immune tolerance of chronic HCV and can achieve SVR without DAAs. ICI is the backbone of systemic therapy for HCC and enhance anti-tumor immunity by promoting T-cell regulatory cell depletion and reversal of T-cell exhaustion. Only one other case of HCV clearance with ICI is published but this is the first in the absence of DAA therapy. This finding suggests that ICI may restore anti-viral immunity in chronic infections and has implications for treatment decisions for HCV.
Web-like mucus (WLM) is a recently recognized endoscopic finding associated with potassium-competitive acid blocker (P-CAB) therapy, particularly with vonoprazan (VPZ). However, its clinical significance, dose-dependency, and reversibility remain unclear. Here, we report a case of WLM that developed after VPZ treatment initiation and disappeared after dose reduction. A 78-year-old man with refractory gastroesophageal reflux disease switched from proton pump inhibitor therapy to VPZ 20 mg. Follow-up esophagogastroduodenoscopy revealed white transparent mucus resistant to water irrigation in the gastric fornix and upper body, consistent with WLM. Gastric mucus culture revealed the presence of oral commensal bacteria. Although VPZ therapy was continued, the dose was reduced to 10 mg because of improvement in reflux symptoms. Subsequent endoscopy performed 2 months after the dose reduction showed complete disappearance of the WLM. This case suggests that WLM may be a reversible gastric mucosal change associated with VPZ therapy and may exhibit dose-dependent behavior. Changes in gastric microbiota induced by profound acid suppression may contribute to its pathogenesis. Recognizing this finding is crucial since it may obscure the gastric mucosa and potentially interfere with careful endoscopic evaluation. Further studies are required to clarify the pathophysiological mechanisms and clinical implications of WLM in patients receiving P-CABs.
Biliary ascites is a rare form of ascites resulting from disruption of biliary tract integrity, and spontaneous, non-traumatic, non-iatrogenic perforation of the gallbladder or bile ducts is an exceptionally uncommon cause in adults. We report a 65-year-old man who presented with right upper quadrant pain, jaundice, fever, diarrhea, and progressive abdominal distension following an episode of untreated choledocholithiasis. Cross-sectional imaging, including ultrasound, MRCP, and contrast-enhanced CT, confirmed obstructive choledocholithiasis and moderate ascites but failed to demonstrate a bile leak. Diagnostic paracentesis revealed a low serum-ascites albumin gradient of 0.8 g/dL with a markedly elevated ascitic-to-serum bilirubin ratio of 6.7 and neutrophil-predominant ascitic fluid, consistent with biliary ascites complicated by secondary bacterial peritonitis. Hepatobiliary scintigraphy with SPECT/CT subsequently localized an active biliary leak. Exploratory laparotomy revealed approximately two liters of biliary ascites and a phlegmonous perforation of the gallbladder fundus; cholecystectomy with common bile duct exploration, stone extraction, and T-tube closure were performed, with an uneventful postoperative recovery. This case highlights spontaneous gallbladder perforation secondary to obstructive choledocholithiasis as a rare but treatable cause of biliary ascites and secondary bacterial peritonitis and reinforces the diagnostic value of ascitic fluid analysis and hepatobiliary scintigraphy when conventional imaging is inconclusive.
Introduction Intestinal tuberculosis (ITB) remains an important diagnostic challenge in gastroenterology because it frequently mimics Crohn’s disease clinically, radiologically, and endoscopically. Misdiagnosis may result in delayed treatment or inappropriate immunosuppression. Presentation with small bowel obstruction is uncommon and may prompt unnecessary surgical intervention. Case Presentation A 24-year-old woman with no significant medical history presented with colicky abdominal pain, bilious vomiting, abdominal distension, and constipation. Computed tomography demonstrated small bowel obstruction with a transition point at the distal jejunum/proximal ileum, associated with necrotic mesenteric lymphadenopathy, omental thickening, and free fluid. MRI enterography revealed terminal ileal inflammation, raising suspicion for Crohn’s disease. Fecal calprotectin was borderline elevated (120 µg/g). Further evaluation identified right upper lobe infiltrates on chest radiography and a positive interferon-gamma release assay. Bronchoscopy confirmed active tuberculosis by acid-fast bacilli smear and polymerase chain reaction. The patient was managed conservatively with nasogastric decompression and standard anti-tuberculosis therapy, leading to complete resolution of bowel obstruction without surgery. Conclusion This case highlights ITB as an essential differential diagnosis in patients with terminal ileitis or unexplained small bowel obstruction. Necrotic mesenteric lymphadenopathy and extraintestinal clues should prompt investigation for tuberculosis. Early multidisciplinary recognition may prevent unnecessary surgery and harmful immunosuppressive therapy.
Primary hepatic squamous cell carcinoma (SCC) is an exceptionally rare malignancy with vague clinical features and no characteristic biomarkers. We present a 64-year-old woman with right upper quadrant pain and significant weight loss, initially suspected to have a liver abscess. Imaging revealed hepatic masses, and biopsy confirmed SCC with no extrahepatic primary source. Immunohistochemistry supported a primary hepatic origin, and molecular profiling showed PD-L1 positivity. Despite palliative immunotherapy, the patient’s condition rapidly deteriorated. This case highlights the diagnostic challenges and limited therapeutic options in primary hepatic SCC, emphasizing the need for continued reporting and research.
