ArticleInternational journal of general medicine2022
Clinical Features and CT Imaging Analysis of Hepatic Sinuscase-Syndrome and Budd-Chiari Syndrome.
Article in International journal of general medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 2 citations in OpenAlex.
- Clinicopathological Evolution of Pyrrolizidine Alkaloid-induced Liver Injury: Transition From SOS to PSVD?Journal of clinical and translational hepatology · 2026Article
- CT findings of primary hepatic angiosarcoma complicated with hepatic sinusoidal obstruction syndrome: a case description.Quantitative imaging in medicine and surgery · 2026Article
- Hepatic Venous Occlusion Type of Budd-Chiari Syndrome versus Pyrrolizidine Alkaloid-Induced Hepatic Sinusoidal Obstructive Syndrome: A Multi-Center Retrospective Study.Journal of personalized medicine · 2023Article
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7 authors at 2 institutions in 1 country.
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Abstract
Objective: This study aimed to analyze the clinical features and computed tomography (CT) manifestations of hepatic sinusoidal obstruction syndrome (HSOS) induced by Gynura segetum, a Chinese herbal medicine, so as to improve the clinical understanding and diagnosis of the disease. Methods: Relevant clinical and laboratory parameters and CT imaging data of 20 patients with HSOS confirmed by liver biopsy were retrospectively analyzed and compared with 16 patients with Budd-Chiari syndrome (BCS). Results: Levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and glutamyl transpeptidase increased significantly (p < 0.05) in HSOS patients compared to the BCS patients, while the albumin level and prothrombin time, which are indicators of liver synthesis function, decreased and prolonged significantly, respectively. All 20 patients with HSOS had manifestations of ascites and heterogeneous hypoattenuation on CT, including 18 cases (90%) with heterogeneous enhancement (characteristic map-like enhancement), 17 (85%) with hepatomegaly, 18 (90%) with gallbladder wall oedema, and 16 (80%) with stenosis of main hepatic veins and characteristic "clover-like" enhancement at the second porta hepatis. Conclusion: Both HSOS and BCS are post-sinusoidal portal hypertension, but have different etiologies and durations. Although they both cause liver congestion, the clinical manifestation of HSOS is acute liver injury. The CT manifestations are characterized by ascites, map-like enhancement and heterogeneous hypoattenuation of the liver parenchyma, and stenosis of the main hepatic veins. BCS is often found in the stage of decompensated liver cirrhosis, resulting in liver shrinkage, splenomegaly, and ascites.
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