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Improved Hepatic Reserve and Fibrosis in a Case of “Portal-Systemic Liver Failure” by Portosystemic Shunt Occlusion

Patient: Female, 67-year-old Final Diagnosis: Portal-systemic liver failure Symptoms: None (second opinion) Medication: None Clinical Procedure: Balloon-occluded retrograde transvenous obliteration (BRTO) Specialty: Radiology OBJECTIVE: Unusual or unexpected effect of treatment BACKGROUND: This is a...

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Detalles Bibliográficos
Autores principales: Ishikawa, Tsuyoshi, Sasaki, Ryo, Nishimura, Tatsuro, Iwamoto, Takuya, Takami, Taro, Yamasaki, Takahiro, Sakaida, Isao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7038637/
https://www.ncbi.nlm.nih.gov/pubmed/32063601
http://dx.doi.org/10.12659/AJCR.921236
Descripción
Sumario:Patient: Female, 67-year-old Final Diagnosis: Portal-systemic liver failure Symptoms: None (second opinion) Medication: None Clinical Procedure: Balloon-occluded retrograde transvenous obliteration (BRTO) Specialty: Radiology OBJECTIVE: Unusual or unexpected effect of treatment 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.