Underlying mechanism of portal hypertensive gastropathy in cirrhosis: a hemodynamic and morphological approach.
OBJECTIVE
Portal hypertensive gastropathy (PHG) is an important cause of bleeding in patients with cirrhosis associated with portal hypertension. Histologically, the condition is characterized by dilation of the mucosal and submucosal vessels of the stomach; however, its mechanisms remain unclear. The aim of the present cross-sectional study was to evaluate the role of portal and systemic hemodynamic features, humoral factors and hepatocellular function in the development and severity of PHG in patients with cirrhosis.


METHODS
Forty-six patients with cirrhosis of different etiologies underwent endoscopy. Portal hypertension was evaluated by hepatic venous pressure gradient (HVPG). The gastric mucosa was analyzed using two diagnostic methods: endoscopy according to the McCormack criteria and histological by histomorphometric analysis.


RESULTS
The prevalence of PHG according to the endoscopic and histomorphometric methods was 93.4% and 76.1%, respectively. There were no statistically significant differences in HVPG measurements between the patients with mild (16.0 +/- 5.9 mmHg) and severe PHG (16.9 +/- 6.5 mmHg; P = 0.80) or between patients who did not have (15.2 +/- 8.0 mmHg) and those who had PHG (16.3 +/- 5.7 mmHg). No correlation was found between the presence or severity of PHG and systemic vascular resistance index (P = 0.53 and 0.34, respectively), Child-Pugh classification (P = 0.73 and 0.78, respectively) or glucagon levels (P = 0.59 and 0.62, respectively).


CONCLUSIONS
The present data show no correlation between the presence or the severity of PHG and portal pressure, Child-Pugh classification or systemic hemodynamics, suggesting that other factors may be involved in the physiopathology of PHG, such as local gastric mucosal factors or other underlying factors.
Curvêlo
Lílian Amorim
LA
Department of Medicine, Division of Gastroenterology and Hepatology, Federal University of São Paulo, São Paulo, Brazil. liliancurvelo@uol.com.br
Brabosa
Walnei
W
Rhor
Rachel
R
Lanzoni
Valéria
V
Parise
Edison Roberto
ER
Ferrari
Angelo Paulo
AP
Kondo
Mario
M
D000328:Adult; D015415:Biomarkers / Q000097:blood; D003430:Cross-Sectional Studies; D004932:Esophageal and Gastric Varices / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D004945:Esophagoscopy; D005260:Female; D005753:Gastric Mucosa / Q000098:blood supply / Q000378:metabolism / Q000473:pathology*; D005773:Gastroscopy; D005934:Glucagon / Q000097:blood; D006439:Hemodynamics; D006801:Humans; D006975:Hypertension, Portal / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D008103:Liver Cirrhosis / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D008111:Liver Function Tests; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D012307:Risk Factors; D012720:Severity of Illness Index; D013152:Splanchnic Circulation; D013272:Stomach Diseases / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D014655:Vascular Resistance; D014664:Vasodilation; D014690:Venous Pressure
D015415:Biomarkers; D005934:Glucagon