Gastric vascular ectasias in cirrhosis: association with hypoacidity not related to gastric atrophy.

To investigate whether hypergastrinemia and low serum levels of pepsinogen I are associated with gastric hypoacidity in cirrhosis with capillary ectasia of gastric mucosa and whether this alteration is secondary to the presence of atrophic gastritis, two groups of patients were studied: 1) 12 cirrhotic patients with diffuse gastric red spots at the endoscopic examination, and 2) 12 cirrhotic patients with endoscopically normal mucosa. Vascular ectasia of the gastric mucosa was histologically confirmed in all patients with gastric red spots. The study of base-line and stimulated acid gastric secretion showed that 9 of 12 (75%) cirrhotics with gastric vascular ectasia had achlorhydria and that 8 of these 9 patients had high base-line gastrin serum levels (greater than 130 pg/ml) and low base-line pepsinogen I serum levels (less than 20 ng/ml). Base-line gastrin and pepsinogen I serum levels were significantly greater and lower, respectively, in patients with gastric vascular ectasias than in cirrhotics without these lesions. None of the patients of either group had complete atrophy in the corpus of the stomach, and only 4 of the 9 cirrhotics with gastric vascular ectasia and achlorhydria had moderate atrophy. These results show that achlorhydria is frequently associated with hypergastrinemia and low pepsinogen I serum levels in patients with cirrhosis and gastric vascular ectasias and suggest that this disturbance is not secondary to a morphologic abnormality of the gastric mucosa.