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Postprandial hyperemia is associated with a significant increase in portal pressure in cirrhosis, which may contribute to progressive dilation and rupture of gastroesophageal varices. In cirrhosis, an insufficient hepatic production of nitric oxide (NO) may impair the expected hepatic vasodilatory response to increased blood flow, further exaggerating the postprandial increase in portal pressure. This study was aimed at investigating whether low doses of an oral NO donor might counteract the postprandial peak in portal pressure. Twenty-three portal hypertensive cirrhotics, 8 of them under propranolol therapy, were randomized to receive orally 5-isosorbide mononitrate (ISMN; 10 mg; n ‫؍‬ 11) or placebo (n ‫؍‬ 12) and a standard liquid meal 15 minutes later. S everal studies have shown that, in normal subjects, food intake induces marked changes in splanchnic hemodynamics. [1][2][3][4][5] The main finding is a postprandial increase in splanchnic blood flow, caused by splanchnic arteriolar vasodilatation occurring in the submucosal and mucosal layers of the small intestine. This postprandial splanchnic vasodilatation and hyperemia occur owing to the interaction of intrinsic mechanisms (such as changes in arteriolar transmural pressure and/or increase in vasodilator tissue metabolites) and extrinsic mechanisms (action of autonomic nervous system) and to the effect of gastrointestinal hormones. [1][2][3][4]6,7 On the other hand, in cirrhotic patients, the postprandial hyperemia determines a significant increase of portal and collateral blood flow, which results in an increased hepatic venous pressure gradient (HVPG). 3,[7][8][9][10][11][12][13][14][15] This is observed rapidly, the maximum changes in splanchnic hemodynamics being observed at 30 minutes after the meal, returning to basal levels at 120 minutes. 3,8,9,[11][12][13][14] These data suggest that, in cirrhotic patients, the repeated increase in portal venous pressure because of food intake may contribute to the progressive portal-systemic collateral dilation and to the development and dilation of the varices that eventually lead to variceal bleeding.Propranolol administration has been reported to reduce the postprandial peak in portal pressure, 10 but sub-

Age, ingestion of a strong acid, leucocytosis, deep gastric ulcers, and gastric necrosis are predictive of death after caustic ingestion. A risk score system including these predictors may be useful in prognostic evaluation.

Portopulmonary hypertension (PPHTN) is a rare complication in patients with portal hypertension. A role of endothelin 1 (ET-1) and other cytokines was demonstrated in primary pulmonary hypertension but not in PPHTN. We evaluated the possible role of ET-1, interleukin 6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor alpha (TNF-α) in the pathogenesis of PPHTN. Plasmatic concentrations of ET-1, IL-6, IL-1β, and TNF-α were measured in patients with pulmonary systolic arterial pressure (PAPs) >30 mm Hg and in patients with cirrhosis. In all, Six out of 11 patients with PAPs >30 mm Hg had PPHTN on right heart catheterization. The remaining 10 patients had an hyperdynamic circulation (HC). In PPHTN patients, ET-1 and IL-6 were significantly higher compared with HC and patients with cirrhosis. Endothelin 1 and IL-6 could be implicated in the pathogenesis of PPHTN. On the basis of these results, ET-1 receptor antagonists or anti-IL-6 could have a rationale in the treatment of PPHTN.

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