LES with BCAA supplementation significantly and rapidly improves liver functioning and CPS in LC patients who have undergone RFA for HCC. Control of blood sugar levels is necessary when calorie-containing BCAA is administrated to LC patients with impaired glucose tolerance.

Nitric oxide (NO) is known to play an important role in modulating both the hepatic and mesenteric circulation under physiological and pathological conditions. We investigated how L-arginine, a precursor of NO, modifies the hepatic and mesenteric circulation in patients with cirrhosis. The study design was a single-blind controlled study. We measured the systemic and portal hemodynamics before and following intravenous L-arginine and saline infusion using pulsed Doppler ultrasonography in 20 patients with cirrhosis, and then the effects were compared with those found in 20 healthy subjects. In these patients, the effects of L-arginine on hepatic circulation were investigated using hepatic catheterization. L-Arginine infusion induced systemic vasodilation in both the healthy controls and the cirrhotic patients in a similar hemodynamic manner. In these patients, the L-arginine-induced increase in the portal flow was significantly higher than that of cardiac output (CO); however, the relation was the inverse in healthy subjects. Moreover, the L-arginine-induced increase in the portal flow was greater in the cirrhotic patients than that seen in healthy subjects. As a result, L-arginine infusion was thus found to selectively augment the hepatopetal portal blood flow in the cirrhotic liver. In patients, L-arginine infusion induced marked hepatic vasodilation as demonstrated by the reduced hepatic sinusoidal resistance (HSR) and increased estimated hepatic blood flow (EHBF) associated with the ameliorated intrinsic clearance of indocyanine green. Despite the fall in HSR, the hepatic venous pressure gradient (HVPG) increased following L-arginine infusion. The mesenteric and hepatic vascular areas of cirrhosis exhibited an increased susceptibility to the dilator action of L-arginine. These findings suggest that the enhanced NO production in the splanchnic vascular area has an important role in the hepatic circulation in patients with cirrhosis. (HEPA-TOLOGY 1998;27:377-382.)Patients with cirrhosis exhibit circulatory abnormalities such as perturbation of the hepatic microcirculation, as well as systemic and mesenteric hyperemia. 1,2 It has recently been proposed that hepatic stellate cells play an important role in regulating hepatic sinusoidal tonus and the blood flow under physiological and pathological conditions. 3-7 The contractility of hepatic stellate cells depends on the dynamic control of the balance of two endothelium-derived vasoactive substances, endothelin 1 and nitric oxide (NO). [3][4][5][6][7] Endothelin produces sustained vasoconstriction in the liver, which appears to be related to the contraction of hepatic stellate cells. 3,4 In addition, NO is also a potent modulator of stellate cell contractility 5,6 and inhibits the vasoconstriction induced by endothelin in the perfused rat liver. 7 Therefore, both endothelin and NO play a critical role in modulating hepatic microcirculation.L-Arginine, a precursor of NO, induces systemic vasodilation and natriuresis when infused intravenously in humans. [8][9][10][...

We report a patient with chronic hepatitis C who developed eosinophilic enteritis while being treated with recombinant interferon alpha-2b. He had no history of either allergic disorders or recurring episodes of abdominal cramps, nausea, or diarrhea. He also had had a normal eosinophil count prior to the interferon treatment. After a 12-week course of interferon alpha-2b, he began to complain of severe abdominal pain, diarrhea, and abdominal fullness. His peripheral eosinophil count increased to 45% (absolute count, of 7,610/microl). Abdominal ultrasonography and computed tomography revealed diffuse thickness of the intestinal wall with gross ascites that contained numerous eosinophils. An upper gastrointestinal barium study with small bowel follow-through showed an edematous mucosal layer of the jejunum and ileum. There was a spectacular relief of the patient's subjective symptoms after the administration of prednisolone. Follow-up studies revealed resolution of the ascites and the mucosal layer edema and normalization of the peripheral eosinophil count. Prednisolone was tapered off, but the eosinophilic enteritis did not recur. As there had been no evident exposure to common causative factors for eosinophilic enteritis, we suggest that interferon alpha-2b could thus have played a role in the triggering of the eosinophilic enteritis.

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We found a significant decrease in the oxygen delivery in patients undergoing an endoscopic variceal ligation. Such deteriorated tissue oxygenation may be serious especially in patients with a low oxygen transport ability such as in patients with variceal hemorrhage with anemia. However, the clinical significance of these changes remains unclear and further studies are therefore warranted.