Clinical, laboratory, and hemodynamic parameters in portal hypertensive gastropathy: a study of 254 cirrhotics.

BACKGROUND: Portal hypertensive gastropathy (PHG) is the most common gastric mucosal injury in patients with liver cirrhosis. It is a cause of both acute and chronic upper gastrointestinal bleeding even in the absence of esophageal or gastric varices. The pathogenesis of PHG is unclear. It is not known whether PHG correlates more with portal hypertension or with liver dysfunction. It is also not clear whether altered vascular hemodynamics occurring in PHG is purely a local phenomenon of the stomach or is it a part of a generalized vascular abnormality of cirrhosis and portal hypertension. AIM: In the first part of our study, we aimed to assess any correlation of various clinical and laboratory parameters relating to portal hypertension and liver dysfunction with the presence or absence of PHG. In the second part of our study we examined whether systemic and pulmonary hemodynamics is significantly altered in patients with PHG. PATIENTS AND METHODS: In this retrospective study, the records of consecutive cirrhotic patients who had undergone complete portal, systemic, and pulmonary hemodynamic assessments were analyzed. We excluded patients who had had endoscopic variceal ligation, endoscopic sclerotherapy, cyanoacrylate glue injection or surgery for portal hypertension, patients on beta-blockers, and patients with gastric antral vascular ectasia. Clinical, laboratory, and hemodynamic parameters were compared between patients with and without PHG.
RESULTS: Two hundred and fifty-four patients were included in the study (mean age 44.3+/-12.6 y, 82% males). One hundred and three (41%) patients had a history of upper gastrointestinal bleeding. Alcohol, hepatitis B, and cryptogeny were the most common etiologies (27% each). One hundred and forty (55%) patients had PHG. Variables significantly associated with PHG on univariate analysis were history of gastrointestinal bleed, ascites, high bilirubin, deranged prothrombin time, higher variceal grade, high Child-Pugh score, and high hepatic venous pressure gradient. However, on multivariate analysis only Child-Pugh class C, large variceal size, and hepatic venous pressure gradient greater than 12 mm Hg were independently associated with the presence of PHG. Patients with PHG were significantly more vasodilated as indicated by the high mean cardiac index (5.3+/-2.3 vs. 4.6+/-1.9 L/min/m, P=0.012), mean cardiac output (8.9+/-4.0 vs. 7.6+/-3.2 L/min, P=0.004), low median systemic vascular resistance [869 (252-2651) vs. 974 (403-2590) dyn.s/cm, P=0.012], and low median pulmonary vascular resistance [51 (6-226) vs. 63 (6-512) dyn.s/cm, P=0.003].
CONCLUSIONS: PHG is more often associated with advanced portal hypertension and advanced liver failure. The presence of PHG also indicates the existence of an additional vasodilation to already existent hemodynamic anomalies seen in portal hypertension as evidenced by a higher cardiac index and output and lower systemic and pulmonary resistance compared with patients without PHG. Thus, PHG is not merely a local phenomenon in gastric mucosa but also a severe manifestation of generalized vascular alterations of cirrhosis and portal hypertension.