ArticleThe American journal of case reports2020
Improved Hepatic Reserve and Fibrosis in a Case of "Portal-Systemic Liver Failure" by Portosystemic Shunt Occlusion.
Article in The American journal of case reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 5 citations in OpenAlex.
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7 authors at 1 institution in 1 country.
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Abstract
BACKGROUND This is a case report validating our previous studies showing clinical benefit of balloon-occluded retrograde transvenous obliteration (BRTO) in improving hepatic function and outcomes in patients with a low liver stiffness (LS) and with procedural indication of encephalopathy. Here, we present the case of a woman in her late 60s suffering from hepatitis C virus-related decompensated liver cirrhosis with refractory encephalopathy. CASE REPORT The patient presented with a Child-Pugh score of 11, Model for End-Stage Liver Disease-Sodium (MELD-Na) score of 16, and LS of 21.5 kPa. BRTO was expected to improve both the intractable encephalopathy and hepatic function and prolong her vital prognosis. Portosystemic shunt (PSS) occlusion induced drastic changes in the portal-splenic vein hemodynamics, resulting in dramatically improved Child-Pugh and MELD-Na scores. This status was maintained for 1 year postoperatively. However, her LS increased 1 month postoperatively and declined steadily thereafter. The postoperative levels of hepatic fibrosis markers, including Mac-2 binding protein glycosylation isomer, decreased markedly. No ascites, pleural effusion, esophagogastric varices, or relapse of encephalopathy were observed during a 1-year postoperative follow-up period. CONCLUSIONS Liver failure caused mainly by the advanced development of PSSs (as in our case), rather than hepatic parenchymal cell dysfunction, is considered reversible and controllable via PSS occlusion. We herein propose a novel concept, "portal-systemic liver failure," to describe liver failure with a non-stiff liver and giant PSSs, as in the present case. In patients with "portal-systemic liver failure," BRTO could potentially improve the prognosis in association with improved hepatic reserve and fibrosis.
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