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Gut Disease May Play a Role in Non-cirrhotic Intrahepatic Portal Hypertension
Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
He is a member of both the National Writers Union, the International Federation of Journalists, and covers San Francisco Health News for Examiner.com.View all articles by Jefferson Adams
New study indicates gut disease may play a role in non-cirrhotic intrahepatic portal hypertension.
Celiac.com 11/25/2010 - Portal hypertension is high blood pressure within the portal vein and its tributaries. Non-cirrhotic intrahepatic portal hypertension (NCIPH) is portal hypertension that occurs within the liver, that is not triggered by cirrhosis. NCIPH is generally regarded to have a benign prognosis.
A research team examined whether gut-derived prothrombotic factors may contribute to the pathogenesis and prognosis of non-cirrhotic intrahepatic portal hypertension (NCIPH). Their results led them to conclude that gut-derived prothrombotic factors may in fact contribute to the pathogenesis and prognosis of NCIPH.
The team included C. E. Eapen, Peter Nightingale, Stefan G. Hubscher, Peter J. Lane, Timothy Plant, Dimitris Velissaris, and Elwyn Elias.
For their study, the team followed a cohort at a tertiary referral center. They analyzed prognostic indicators in 34 NCIPH patients. The team also looked for associated gut disorders.
Survival rates for transplant-free NCIPH patients from ﬁrst presentation with NCIPH at 1, 5, and 10 years was 94% (SE: 4.2%), 84% (6.6%), and 69% (9.8%), respectively.
Importantly, 18 patients (53%) showed decompensated liver disease.
Three patients (9%) showed ulcerative colitis while ﬁve of 31 patients (16%) tested had celiac disease. Kaplan–Meier analysis showed that the presence of celiac disease was a predictor of shorter transplant-free survival for these patients (p = 0.018).
Multivariable Cox regression analysis showed that people who were older when ﬁrst presenting with NCIPH, those with hepatic encephalopathy, and those with portal vein thrombosis had lower rates of transplant-free survival
More than one-third (36%) of NCIPH patients showed elevated levels of initial serum IgA anticardiolipin antibody (CLPA), compared with just 6% with Budd–Chiari syndrome (p = 0.032, Fisher’s exact test) and no patients with celiac disease
without concomitant liver disease (p = 0.007).
Under the team's prognostic factors, 53% of NCIPH patients ultimately progress to liver failure, and their data suggest that intestinal disease plays a role in the pathogenesis of intrahepatic portal vein occlusion leading to NCIPH.
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