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The correlation between portal hypertensive gastropathy and portal hypertension was strong enough to suggest which patients with these conditions could develop cirrhosis, but not hepatocellular carcinoma, according to research published in BMC Gastroenterology.
“Although portal hypertension is regarded as the main target for the prevention or treatment of complications of liver cirrhosis, portal hypertensive gastropathy is frequently overlooked and the clinical implications as a prognostic factor of liver cirrhosis or a predictive factor for the development of hepatocellular carcinoma have not been established,” Dong Joon Kim, MD, PhD, of the division of gastroenterology and hepatology at Hallym University College of Medicine in Korea, told Healio.com/Hepatology.
Kim and colleagues prospectively enrolled 587 patients with cirrhosis — the largest study of its kind — to determine the likelihood of developing HCC.
The mortality rate was 20.3% (n = 119), and HCC developed in 9.2% (n = 54) during the follow-up period (32.6 ± 27.8 months). The portal hypertensive gastropathy (PHG) grade was well correlated to hepatic vein pressure gradient (HVPG):
•no PHG: median 9.2 (interquartile ranges [IQR]: 7.2–16.7);
•mild PHG: 14.6 (IQR: 10.1–19.3); and
•severe PHG: 17.3 (IQR: 12.3–21.5; P < .001)
“The presence of advanced hepatic fibrosis is related to portal hypertension and the development of hepatocellular carcinoma. Thus, early detection and treatment of liver fibrosis and its complications are important,” Kim told Healio.com/Hepatology. “Although measurement of portal pressure gives us important information, routine checking for all the patients with liver cirrhosis is difficult.”
Child-Pugh class, MELD score and survival were also well-connected, researchers wrote, but not connected to patients developing HCC. The level of PHG (HR = 3.29; 95% CI, 1.12–9.63, severe vs. no PHG) and Child-Pugh class (HR = 3.53; 95% CI, 1.79–6.97, Child C vs. A) revealed a substantial connection to patients succumbing.
The researchers noted both treated and non-treated gastric and esophageal varices were present in the patients, meaning a connection between PHG’s creation and these varices could not be determined. In addition, researchers did not note differences between HVPG and PHG as it related to treating liver cirrhosis.
“We hope endoscopic determination of [PHG] will be used for the surrogate marker of portal hypertension and prognostic factor of liver cirrhosis,” Kim said.