Development and Progression of Portal Hypertensive Gastropathy in Patients With Chronic Hepatitis C

Abstract

OBJECTIVES To determine the incidence and risk factors associated with new onset and worsening portal hypertensive gastropathy (PHG) in patients with chronic hepatitis C (CHC). METHODS 831 CHC patients with bridging fibrosis or cirrhosis at entry were prospectively monitored for clinical and histological liver disease progression while receiving either low dose peginterferonα2a or no antiviral therapy in the HALT-C Trial. Upper endoscopy with grading of PHG was performed at baseline and year 4 of the study. The presence and severity of PHG were determined using the NIEC criteria and worsening PHG was defined as a score increase of > 1 point. RESULTS During a median follow-up of 3.85 years, 50% of the 514 subjects without PHG developed new onset PHG while 26% of the 317 patients with baseline PHG had worsening PHG. Independent predictors of new onset PHG included higher alkaline phosphatase and being diabetic, while predictors of worsening PHG were Caucasian race, lower albumin, and higher serum AST/ ALT ratio and HOMA levels. New onset and worsening PHG were significantly associated with clinical as well as histological progression. New onset and worsening PHG were also associated with new onset and worsening of gastroesophageal varices. CONCLUSIONS New onset and worsening PHG develops at a rate of 12.9% per year and 6.7% per year, respectively, in non-responder CHC patients with advanced fibrosis. If confirmed in other studies, endoscopic surveillance for PHG may need to be tailored to individual patient risk factors.

Portal hypertensive gastropathy: A systematic review of the pathophysiology, clinical presentation, natural history and therapy

“…This mechanism is supported by finding that gastric mucosal blood flow increases after variceal ligation [91] . Another theory is that delayed gastric emptying after sclerotherapy from extravasation of sclerosant, may cause development of PHG [69] . No direct Itha et al [11] 163 children with extrahepatic portal vein obstruction presenting with variceal bleeding underwent endoscopic injection sclerotherapy Not reported 12% overall PHG (actual number not stated), 1 patient with severe PHG 41% overall PHG (actual number not stated), 12 patients with severe PHG P < 0.001 for overall PHG; P < 0.001 for severe PHG Poddar et al [83] 186 children with extrahepatic portal vein obstruction presenting with variceal bleeding undergoing endoscopic sclerotherapy, and mean follow up of 38 ± 30 mo [10] 967 patients with variceal bleeding underwent endoscopic sclerotherapy; out of whom 88 patients fulfilled the inclusion criteria (including presence of endoscopic lesions consistent with PHG or GAVE, before or within 4 wk after obliteration) were prospectively followed (out of whom 2 had only GAVE) [30] 230 patients with liver cirrhosis; of which 44 underwent variceal eradication with sclerotherapy Prospective study 24/44 (54%) 33/44 (75%) P < 0.05…”

“…For example, in a study of 373 cirrhotic patients, 299 (80.2%) had PHG [34] . In the HALT-C trial, 374 (37%) of 1011 patients with biopsy-proven cirrhosis or bridging fibrosis from hepatitis C had PHG [69] . This wide variability likely reflects variability in classification criteria, interpretation of endoscopic lesions, study populations, and natural history of PHG [10,70,71] .…”

Appropriate Use of Beta Blockers in Cirrhosis

“…include ascites, gastroesophageal varices, portosystemic encephalopathy, renal dysfunction, and hepatopulmonary syndrome [8,9]. The increase in portal pressure is due to increased resistance to blood flow resulting from disruption of normal liver architecture due to underlying fibrosis and scarring.…”

Gastric Antral Vascular Ectasia and Portal Hypertensive Gastropathy

“…According to the HALT-C trial, approximately 37% of patients (364 of 1011) with biopsy conirmed cirrhosis or bridging ibrosis from hepatitis C had PHG [8]. While PHG can present at any age, its severity can vary from mild to severe.…”