How Common is Portal Hypertension in Patients With NAFLD?
Patients with nonalcoholic fatty liver disease (NAFLD) are at risk for portal hypertension and esophageal varices, according to the September issue of Clinical Gastroenterology and Hepatology.
The study also shows that factors such as advanced liver disease, type 2 diabetes, and obesity can be used to identify patients most likely to have portal hypertension, who should be examined by endoscopy for esophageal varices.
With the increasing prevalence of obesity, NAFLD has become a common liver disease. NAFLD is characterized by a range of liver disorders, ranging from simple steatosis to features of cellular injury including necrosis and inflammation, with or without fibrosis.
In some patients, NAFLD progresses to advanced fibrosis and cirrhosis, and even to end-stage liver disease and portal hypertension. In fact, portal hypertension might develop even before cirrhosis in patients with NAFLD. The most feared complication of portal hypertension is bleeding from esophageal varices, which can be fatal.
It is not clear whether patients with NAFLD should undergo endoscopy examinations for esophageal varices before they develop cirrhosis. And little is known about how to identify patients with NAFLD who are most likely to develop esophageal varices or other signs of portal hypertension.
Flavia Mendes et al. investigated the prevalence of portal hypertension and esophageal varices in a large series of patients with well-characterized and liver biopsy-confirmed NAFLD. They also looked at markers that could be used to identify patients most at risk for portal hypertension and esophageal varices.
They found that portal hypertension and esophageal varices were not uncommon among patients with NAFLD. Among the 354 patients with NAFLD, 100 had portal hypertension at the time they were diagnosed with NAFLD (28.2%). Of these, 88 also had septal fibrosis or cirrhosis—the remaining 12 patients had either no fibrosis (stage 0) or mild fibrosis (stages 1–2), based on biopsy analysis (see figure).
In fact, among 204 patients with no or mild fibrosis (stages 0–2), 12 had portal hypertension (6%). However, these patients had a significantly higher grade of steatosis, based on biopsy analysis, compared with the 192 patients without portal hypertension.
Splenomegaly was the most common sign of portal hypertension in patients with NAFLD; it was found in 25%, with ascites and portosystemic encephalopathy present in 12% and 7%, respectively. Splenomegaly might therefore be an early indicator of presence or risk of portal hypertension—spleen size should be measured routinely during abdominal imaging studies during diagnostic evaluation of patients with suspected NAFLD.
The patients that developed portal hypertension were also likely to have thrombocytopenia, hyperbilirubinemia, cirrhosis, and obesity. Esophageal varices were associated with thrombocytopenia, type 2 diabetes, and splenomegaly.
Mendes et al. conclude that portal hypertension and esophageal varices are common among patients with NAFLD. Signs of portal hypertension correlated with more advanced fibrosis, but also occurred in patients without fibrosis or with mild fibrosis.
Features of advanced liver disease and insulin resistance can be used to identify patients with NAFLD who are likely to have or to develop portal hypertension—these patients should undergo endoscopy to identify esophageal varices.
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Mendes FV, Suzuki A, Sanderson SO, et al. Prevalence and indicators of portal hypertension in patients with nonalcoholic fatty liver disease. Clin Gastroenterol Hepatol 2012;1028-1033.e2.