It is known that esophageal varices (EV) appear or aggravate after balloon-occluded retrograde transvenous obliteration (B-RTO) for gastric varices (GV) in some patients. The aim of this study was to investigate a relationship between the appearance or aggravation of EV after B-RTO and the degree of development of left gastric vein (LGV) estimated by endoscopic ultrasonography (EUS) performed before B-RTO in 20 patients. EV appeared or aggravated in 11 patients (55%). Among them, 5 patients (25%) had to be treated. Diameter of LGV correlated with the progress of EV after B-RTO. On the other hand, EV did not aggravate in 4 patients with developed LGV, which had no intramural perforating vein and flowed into extramural collateral vessels. Assessment of LGV by EUS is useful to predict the aggravation of EV after B-RTO.

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Previous studies have shown that angiotensin II plays a role in the regulation of hepatic sinusoidal micro-circulation, and that angiotensin II receptor antagonist decreases portal venous pressure in liver cirrhosis. We examined changes in portal blood flow using pulsed-Doppler ultrasonography before and 2 weeks after the administration of daily oral candesartan 4 mg in 12 cirrhotic patients with portal hypertension. After 2 weeks administration, maximum blood velocity of portal vein significantly (p <0.05) increased from 16.7±5.6 to 22.9±6.7 cm/s, portal blood flow volume increased to approximately 115% of basal value and the congestion index significantly (p <0.05) decreased from 0.094±0.038 to 0.063±0.033 cm·s. Plasma ammonia and ICG R₁₅ levels also decreased significantly (p <0.05). These results suggest that the decrease in sinusoidal resistance due to candesartan led to an increase in portal venous blood flow. Therefore, it appears likely that continuous administration of candesartan will lead to reduced, collateral blood flow and improvement of hepatic dysfunction.

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To evaluate prophylactic injection sclerotherapy (EIS) for esophageal varices, a prospective randomized controlled trial was begun in 1993 by the Japanese Society for Portal Hypertension. 79 patients whom endoscopic findings suggested high risk of bleeding but who had no bleeding episode, were randomly allocated to the EIS group of 40 patients or non treated group of 39 patients. Patients were followed for 42 months to 89 months. Variceal hemorrhage occurred in 3 patients receiving EIS and 10 patients of the controls (p = 0.057). The survival curves (Kaplan-Meier) of both groups were similar (p= 0.61). We conclude that prophylactic sclerotherapy does not significantly reduce the risk of bleeding from esophageal varices and is not effective in improving survival.

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We analyzed the clinical characteristics of portal hypertensive gastropathy (PHG), focusing on the etiology of portal hypertension, the severity of esophagogastric varices, portal hemodynamics, and investigated the change of PHG after endoscopic therapy or non-shunt operation for varices. PHG was recognized in 208 cases (54.7%) among 380 patients with portal hypertension, and high incidence rates of PHG were found in the circumstances : extra-hepatic portal obstruction, Child's Class C, absence of portosystemic shunt, and hepatofugal or bidirectional blood flow in the left gastric vein. PHG were more frequently present in case with gastric varices alone, and the severe PHG were observed high in cases of high grade esophageal varices (F1<F3). Analysis of clinical outcomes after treatments for varices revealed a tendency for PHG to improve after non-shunt operation. These findings lead to the suggestion that the degree of gastric mucosal congestion is related to progression of PHG, and that increased portal hypertension is associated with the development of PHG. Selection of the appropriate treatment modality should be contingent upon evaluation of hemodynamics and take account of its effects on the gastric mucosa.

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Screening with colonoscopy revealed colonic varices in 30 out of 157 patients with portal hypertension (19%). Patients with extrahepatic portal obstruction (EHO) were most frequently accompanied with the varices (11/21 patients, 52%). Colonic varices ruptured in 8 patients (2 liver cirrhosis, 4 EHO, and 2 primary biliary cirrhosis). Arteriovenous malformation was visualized by angiography in the variceal regions of 4 of 7 patients and 3 of those were EHO. Colectomy, transanal variceal ligation or endoscopic sclerotherapy was performed successfully for these ruptured varices. Since various treatments for esophago-gastric varices were improved, the possibility of a long-term survival of these patients has been increased. Because incidence of colonic varices is expected to increase, a strict follow-up and appropriate selection of treatments for colonic varices are required.

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[in Japanese]

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