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Welcome to the Grand Rounds Further Reading List, Gastroenterology edition, brought to you by the Clinical Library, on Level 4, next to the Auditorium.
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When the liver is not the cause
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Gioia, S., et al. (2020). "Causes and Management of Non-cirrhotic Portal Hypertension​." Curr Gastroenterol Rep 22(12): 56 1534-312x
Curr Gastroenterol Rep. 2020 Sep 17;22(12):56. doi: 10.1007/s11894-020-00792-0.
file:///C:/Users/25133492/Downloads/s11894-020-00792-0%20(1).pdf PDF AVAILABLE AT LINK
PURPOSE OF THE REVIEW: Non-cirrhotic portal hypertension (NCPH) includes a heterogeneous group of conditions. The aim of this paper is to make an overview on the denominations, diagnostical features and management of porto-sinusoidal vascular disease (PSVD) and chronic portal vein thrombosis (PVT) being the main causes of NCPH in the Western world. RECENT FINDINGS: The management of NCPH consists in the treatment of associated diseases and of portal hypertension (PH). PH due to PSVD or PVT is managed similarly to PH due to cirrhosis. TIPS placement and liver transplantation are considerable options in patients with refractory variceal bleeding/ascites and with progressive liver failure. Anticoagulation is a cornerstone both in the treatment of thrombosis in PSVD and in the prevention of thrombosis recurrence in patients with portal cavernoma. Physicians should be aware of the existence of PSVD and chronic PVT and actively search them in particular settings. To now, the management of portal hypertension-related complications in NCPH is the same of those of cirrhosis. Large cooperative studies on the natural history of NCPH are necessary to better define its management.
Giri, S., et al. (2023). "Prevalence of hepatic encephalopathy in patients with non-cirrhotic portal hypertension: A systematic review and meta-analysis." Indian Journal of Gastroenterology 42(5): 642-650 https://doi.org/10.1007/s12664-023-01412-1 https://link.springer.com/article/10.1007/s12664-023-01412-1 PDF AVAILABLE AT LINK
Hepatic encephalopathy, (HE) although commonly associated with cirrhosis, has also been reported in non-cirrhotic portal hypertension (NCPH). The importance of identifying and treating HE in NCPH lies in the fact that many patients may be wrongly diagnosed as having psychiatric or neurologic disorders. Hence, we aimed to systematically review the prevalence of HE in NCPH.
Kmeid, M., et al. (2021). "Idiopathic Non-Cirrhotic Portal Hypertension and Porto-Sinusoidal Vascular Disease: Review of Current Data." Gastroenterology Res 14(2): 49-65 1918-2813
Gastroenterology Res. 2021 Apr;14(2):49-65. doi: 10.14740/gr1376. Epub 2021 Apr 21. https://pmc.ncbi.nlm.nih.gov/articles/PMC8110235/ PDF AVAILABLE AT LINK
Idiopathic non-cirrhotic portal hypertension (INCPH) is a clinicopathologic disease entity characterized by the presence of clinical signs and symptoms of portal hypertension (PH) in the absence of liver cirrhosis or known risk factors accountable for PH. Multiple hematologic, immune-related, infectious, hereditary and metabolic risk factors have been associated with this disorder. Still, the exact etiopathogenesis is largely unknown. The recently proposed porto-sinusoidal vascular disease (PSVD) scheme broadens the spectrum of the disease by also including patients without clinical PH who are found to have similar histopathologic findings on core liver biopsies. Three histomorphologic lesions have been identified as specific for PSVD to include obliterative portal venopathy, nodular regenerative hyperplasia and incomplete septal cirrhosis/fibrosis. However, these findings are often subtle, under-recognized and subjective with low interobserver agreement among pathologists. Additionally, the natural history of the subclinical forms of the disease remains unexplored. The clinical course is more favorable compared to cirrhosis patients, especially in the absence of clinical PH or liver dysfunction. There are no universally accepted guidelines in regard to diagnosis and treatment of INCPH/PSVD. Hence, this review emphasizes the need to raise awareness of this entity by highlighting its complex pathophysiology and clinicopathologic associations. Lastly, formulation of standardized diagnostic criteria with clinical validation is necessary to avoid misclassifying vascular diseases of the liver and to develop and implement targeted therapeutic strategies.
Sarma, M. S. and J. Seetharaman (2021). "Pediatric non-cirrhotic portal hypertension: Endoscopic outcome and perspectives from developing nations." World J Hepatol 13(10): 1269-1288 1948-5182 World J Hepatol. 2021 Oct 27;13(10):1269-1288. doi: 10.4254/wjh.v13.i10.1269
https://pmc.ncbi.nlm.nih.gov/articles/PMC8568571/ PDF AVAILABLE AT LINK
Non-cirrhotic portal hypertension (NCPH) forms an important subset of portal hypertension in children. Variceal bleed and splenomegaly are their predominant presentation. Laboratory features show cytopenias (hypersplenism) and preserved hepatic synthetic functions. Repeated sessions of endoscopic variceal ligation or endoscopic sclerotherapy eradicate esophageal varices in almost all cases. After variceal eradication, there is an increased risk of other complications like secondary gastric varices, cholangiopathy, colopathy, growth failure, especially in extra-hepatic portal vein obstruction (EHPVO). Massive splenomegaly-related pain and early satiety cause poor quality of life (QoL). Meso-Rex bypass is the definitive therapy when the procedure is anatomically feasible in EHPVO. Other portosystemic shunt surgeries with splenectomy are indicated when patients present late and spleen-related issues predominate. Shunt surgeries prevent rebleed, improve growth and QoL. Non-cirrhotic portal fibrosis (NCPF) is a less common cause of portal hypertension in children in developing nations. Presentation in the second decade, massive splenomegaly and patent portal vein are discriminating features of NCPF. Shunt surgery is required in severe cases when endotherapy is insufficient for the varices. Congenital hepatic fibrosis (CHF) presents with firm palpable liver and splenomegaly. Ductal plate malformation forms the histological hallmark of CHF. CHF is commonly associated with Caroli's disease, renal cysts, and syndromes associated with neurological defects. Isolated CHF has a favourable prognosis requiring endotherapy. Liver transplantation is required when there is decompensation or recurrent cholangitis, especially in Caroli's syndrome. Combined liver-kidney transplantation is indicated when both liver and renal issues are present.
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