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In an attempt to improve the prognostic capacity of Child-Pugh score in nonbleeding cirrhotics. 110 consecutive in-patients without gastrointestinal hemorrhage at admission were studied and followed up for 24 months or until death. Fifty-five of the 110 patients (50%) died during this period. Mean survival time was 18.8 ± 1.4 months (mean ± SKM). In addition to Child-Pugh score, eight variables, including anthropometric nutritional parameters, routine renal function tests, and alcoholism markers, were recorded at admission. the ability of these variables to improve the prognostic capacity of the Child-Pugh score was assessed with the proportional hazard Cox's regression procedure, using a stepwise method for covariate selection, after including the Child-Pugh score at the first step. Thus, in addition to Child-Pugh score (0 = 0.302). three variables were included in the final model: serum urea (0 = 0.M3), MCV (0 = 0.027), and mid-arm muscle circumference (0 = -0.025). According to the contribution of each of these factors to the model, a prognostic index was obtained to estimate survival in the individual patient. An assessment of the predictive power of the model was made by means of a split-sample technique. The prognostic index described in ths study may contribute to improve the selection of nonbleeding patients with advanced cirrhosis to receive specific therapies such as transplantation. However, its true clinical relevance will he established only by prospectively comparing its prognostic value with that of the Child-Pugh score in a new sample of patients. [ABSTRACT FROM AUTHOR]

Twenty-five patients with abdominopelvic malignant tumors receiving irradiation were studied. The following items were assessed before, during, and at the end of the radiation period: 1) clinical symptoms, scored on the basis of their severity; 2) orocecal transit time (lactulose-H2 breath test); and 3) absorption of lactose and bile salts. Ninety-two percent of the patients showed clinical symptoms suggestive of acute radiation enteropathy, mainly diarrhea. A significant acceleration of the orocecal transit was observed during the study: 70 ± 6.9 min vs 63.3 ± 6.3 min vs 44.3 ± 5.1 min (F = 5.49, p = 0.008), being faster in patients with severe diarrhea (F = 3.25, p = 0.05). Forty-four percent and 57% of the patients developed lactose and bile salt malabsorption, respectively. A decrease in the transit time was observed, independent of the absorption or malabsorption of such substances. However, the orocecal transit was faster in those lactose malabsorbers with severe diarrhea, than in those with mild diarrhea (F = 4.2, p = 0.03). The results suggest that acceleration of orocecal transit may be a major factor in the pathophysiology of radiation-induced diarrhea, whereas lactose malabsorption may contribute to the severity of the diarrhea. [ABSTRACT FROM AUTHOR]

Fatty acid (FA) profile of plasma total lipids, phospholipids (PL), cholesteryl esters (CE), and triglycerides (TG) were measured in 101 patients with advanced liver cirrhosis and in 44 age- and sex-matched healthy controls, Plasma levels of lipidic phosphorus, esterified cholesterol, and TG also were measured, and the unsaturation index (UI) was calculated for each fraction. Total plasma concentrations of saturated FA, linoleate, and polyunsaturated FA (PUFA) were lower in cirrhotics than in controls. This profile was also found in plasma levels of PL- and CE-associated FA. No detectable amounts of C20:3n9 were found in cirrhotic patients. Percent FA distribution of lipid fractions showed a lower percentage of linoleate and PUFA and a higher relative amount of saturated and monoenoic FA in cirrhotics than in controls. As a consequence, the UI of PL and CE was diminished in liver cirrhosis. Linoleate and PUFA deficiency was more marked in CE than in PL, as shown by the number of patients with values below the 5th percentile of the control group, suggesting an attempt to maintain the unsaturation of PL as the most important component of cell membranes. Hepatic failure, poor essential FA intake, and malnutrition are some of the possible etiologic factors for PUFA deficiency in cirrhosis. Their relative contribution to plasma FA abnormalities, as well as the clinical and pathophysiological consequences of PUFA deficit in cirrhotic patients, requires further investigation. [ABSTRACT FROM AUTHOR]