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Objective: The aim of this study was to evaluate the energy expenditure, substrate oxidation, and body composition in alcoholics during addiction and after several months of abstinence., Methods: A total of 32 alcoholics without liver cirrhosis and malabsorption were consecutively recruited. A total of 55 social drinkers, matched for gender and height, were studied as a control group. Anthropometry and bioimpedance analysis were performed to assess body composition, and indirect calorimetry was used to measure basal metabolic rate (BMR) and substrate oxidation. Total abstinence was then achieved in 15 subjects. At 1, 2, 3, and 6 months of abstinence, the metabolic variables and the energy intake were re-examined., Results: At enrollment (T0) alcoholics compared to controls showed a significant decrease in body mass index (22.2+/-2.71 vs 23.6+/-1.3 kg/m2; p < 0.05), fat mass (14.1+/-4.5 vs 16.7+/-3.3 kg; p < 0.01), an increased BMR normalized by fat-free mass (34.5+/-3.7 vs 32.1+/-2.01 kcal/kg/day; p < 0.01), a lower nonprotein respiratory quotient (npRQ: 0.76+/-0.03 vs 0.83+/-0.03; p < 0.001), with a consequently higher lipid oxidation (0.08+/-0.02 vs 0.04+/-0.02 g/min; p < 0.01), and a lower carbohydrate oxidation (0.05+/-0.02 vs 0.10+/-0.03 g/min; p < 0.01). Although at 1 and 2 months of abstinence the metabolic parameters had improved, only after 3 months of abstinence did alcoholics show values of body mass index (23.2+/-2.6 kg/ m2), fat mass (17.0+/-5.34 kg), BMR/fat-free mass (33.1+/-2.78 kcal/kg/day), npRQ (0.82+/-0.02), lipid oxidation (0.05+/-0.03 g/min) and carbohydrate oxidation (0.11+/-0.04 g/min) comparable to those of controls; these values remained constant at 6 months., Conclusion: Three months of abstinence from alcohol could represent the minimum time necessary to obtain a normalization of the metabolic variables considered and of the nutritional status for these patients, probably related to a regression of the functional alterations of the microsomal ethanol oxidizing system and of mitochondria secondary to chronic ethanol abuse.

Mesothelial lesions can present significant diagnostic problems. An accurate identification of the lesion is important in deciding what course of action to follow, as well as what the required treatment will be. We report the case of a man with untreatable ascites. Four years after the first symptom appeared, the patient suddenly began to lose weight. The CT scan showed a thickening of the peritoneal profile; a diffuse lesion of the mesothelium was then observed at laparotomy. Histological examination led to a diagnosis of malignant mesothelioma in a well-differentiated mesothelial lesion with diffuse involvement of the serosa of the small intestine and the lesser omentum.

Several studies on the usefulness of oral disodium cromoglycate (DSCG) in the treatment of systemic adverse reaction to foods have been performed, with less attention to gastroenterological symptoms. In the present study, we selected 101 patients with diarrheic-type irritable bowel syndrome which improved after an elimination diet and worsened after a challenge with specific food(s). All patients were then tested for 48 commercial alimentary antigens by skin prick test (SPT) and underwent 8 wk of oral DSCG (500 mg three times a day), and the results were evaluated by means of a semiquantitative subjective and objective score. We observed an improvement of the symptoms in 67% of the 74 SPT-positive patients, whereas only 41% of the 27 SPT-negative patients showed a positive response to DSCG (p less than 0.05). These data confirm the protective role of DSCG in food-dependent diarrheic-type irritable bowel syndrome with food allergy features.

Autologous mixed lymphocyte reaction (AMLR) and phenotypical composition of circulating lymphocytes obtained from nine subjects with untreated hepatocellular carcinoma (HCC); three HCC patients locally treated by means of intraarterial chemoembolization; six subjects with gut-derived carcinoma (GDC); nine chronic active liver disease patients (CALD), and 14 normal controls have been evaluated, using monoclonal antibodies (MAB) against CD5, CD8, CD4 glycoproteins and anti-LAK-1 molecule, a novel 120-KD surface antigen that is present on the membrane of large granular lymphocytes, by means of classical indirect immunofluorescence technique. Autologous mixed lymphocyte reaction was significantly reduced in all patients, along with CD4-positive cells that are the responder cells in this reaction. A relative increase in the percentage of LAK cells was also observed in neoplastic patients with a normalization after local treatment of the HCC. In the light of promising results obtained by Rosenberg et al. by adoptive transfer of LAK cells activated with Interleukin-2 (IL2) in various cancers, our results support a similar therapeutic trial in HCC patients.

Defects in T lymphocyte subpopulations and in the functional characteristics of such cells have been thought to play a role in the evolution of chronic hepatitis B, but the precise nature of the alterations and their significance remains unresolved. We studied lymphocyte subsets in 27 patients with chronic hepatitis B utilizing standard monoclonal antibodies including Leu 1,2a,3a,7 and D1/12 (against the common determinant of the Dr molecule), as well as a newly described monoclonal antibody, "5/9," which is thought to characterize a unique subpopulation of T4 cells with specific helper/inducer function. These results were compared with those obtained using the autologous mixed lymphocyte reaction assay for the same patients in order to further delineate the lymphocyte alterations in chronic hepatitis B. A significant reduction in the mean number of Leu 3a (T4) positive cells was observed as well as a reduction in the number of 5/9 positive cells. These changes were most evident in those positive for HBeAg in serum. Reduction in Leu 3a cells was associated with a reduced autologous mixed lymphocyte reaction assay response, and was most marked in the HBeAg-positive individuals. These findings suggest that HBeAg-positive patients in whom active viral replication is occurring have a defect in T lymphocyte number and function, which may be due in part to reduced 5/9 positive cells. These alterations may be related to the persistence of virus in chronic active hepatitis B patients.