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No consistently effective therapy is yet available for the treatment of chronic HBsAg, anti-HBe, HBV-DNA-positive hepatitis. A multicenter trial has shown that the response rates are not significantly different when patients with anti-HBe-positive hepatitis are treated with six-month course of thymosin-alpha1 or of interferon-alpha. However, since among these patients, interferon's real efficacy is still debated, with sustained biochemical response achieved in only a few of the treated patients, we conducted this controlled study to investigate the safety and efficacy of thymosin-alpha1 as compared with no treatment. Forty-four chronic hepatitis B virus (HBV) carriers, who were anti-HBe- and HBV-DNA-positive, were randomized, with stratification for the presence of cirrhosis at baseline liver biopsy, to receive either thymosin-alpha1 at a dose of 900 microg/m2 twice a week for six months or no treatment. At entry, both groups of patients were comparable for sex, age, liver histology, ALT, IgM anti-HBc, and HBV-DNA levels. Forty-two patients were followed-up for 20 months (median; range 12-32 months) after completion of therapy: one dropped out, and one developed hepatocellular carcinoma at six months. Thymosin-alpha1 treatment had no side effects. Six months after the end of the therapy, HBV-DNA was negative and ALT had normalized in 14% of treated cases and in 4.5% of control group, while IgM anti-HBc was negative (<0.200) in 14% of the treated patients and in 4.5% of the controls. Among the treated patients, the median ALT levels stayed significantly lower compared to the pretreatment values during the treatment period and six months of follow-up. During the first year, there were six flares of hepatitis in the control group and five among the treated patients (P = NS), yielding a per year average of 0.3 and 0.23 flares per patient, respectively. Among the treated patients, median IgM anti-HBc levels were low with respect to baseline values 4-10 months after treatment started. None became HBsAg negative. In conclusion, these results indicate that, in anti-HBe, HBV-DNA-positive chronic hepatitis B, thymosin-alpha1 therapy alone does not increase the response rate, but may contribute to reduce the immune-mediated liver cell necrosis as indirectly assessed by ALT and IgM anti-HBc levels. [ABSTRACT FROM AUTHOR]

From December 1985 to December 1990, 100 liver orthotopic transplantations (OLTX) were performed in 89 adults with cirrhosis and various other liver diseases; eight patients had two transplants and three of these had three transplants. Organ perfusion was done with Eurocollins in the first 30, then with UW solution. Immunosuppressants were a combination of cyclosporin A and steroids for the first 30 patients, and then a combination of antilymphocyte globulin, azathioprine, methylprednisolone and cyclosporin A. The OLTXs were examined as a whole and also divided into two groups, one for 1985-88 and one for 1989-90. The cumulative survival was 63% after 12 months, 40% after 36 and 42 months. It was poor for the patients who received transplants between 1985 and 1988, but for the second group, survival was improved to 78% after 12 and 18 months. For neoplastic patients, overall survival was 49% after 18 months and 23% after 36 and 42 months. In the second group it was markedly better (83% after 18 months). The recurrence rate for patients surviving more than three months was 17% for hepatocellular carcinoma and 50% for cholangiocarcinoma. Five patients (38%) out of 13 HBsAg-positives before the transplant and surviving more than three months had recurrent hepatitis-B virus. The remaining eight patients are HBsAg negative at present. The improved actuarial survival for the second group is accounted for by the better surgical and intensive care given now and the methodological differences.

Several metabolic (HbA1, HDL-C, triglycerides) and hemostatic (VIIIR: Ag, VIII:C, B-TG variables were investigated in 35 non-obese, insulin-dependent diabetics without clinically evident vascular complications. B-TG was high but did not correlate with other metabolic and hemostatic parameters, suggesting that elevated B-TG in diabetes might be an expression of in vitro platelet activation. VIIIR: Ag and the ratio of VIIIR: Ag to VIII: C were markedly increased. There was a significant correlation of the HbA1 and HDL-C levels with VIIIR: Ag, indicating that VIIIR:Ag is another reflection of metabolic control in diabetes. Additional pathogenic mechanisms, however, appear to be involved in causing the changes in VIIIR: Ag in diabetes.

A familial syndrome with hypo-alpha-lipoproteinemia is described. The affected propositus and his relatives have low levels of high density lipoprotein-cholesterol and apolipoprotein A, without any other lipid and lipoprotein abnormalities. Lipase activity and lecithin:cholesterol acyltransferase activity are also normal. A high prevalence of premature cardiac events was observed in this kindred, without any other established coronary risk factors present. The longevity analyses showed a shortening of life expectancy. The biochemical data and the pedigree are compatible with an autosomal dominant mode of inheritance.

In the literature there is no agreement on the prevalence of chronic liver disease (CLD) and the role of hepatitis B virus (HBV) infection in diabetics. We undertook an epidemiological case-control study of the prevalence of CLD and HBV infection in 394 diabetics and 265 healthy subjects from Seriate and Como. The results did not show any significant differences between: 1) the prevalence of CLD in the diabetic population and in controls (4.8% vs 4.5%); 2) the prevalence of HBV infection in diabetics (HBsAg+: 8.3%; HBVAb+: 55.8%) and in controls (HBsAg+: 8.6%; HBVAb+: 54.7%); 3) the prevalence of HBV infection in diabetics with CLD (HBsAg+: 21%; HBVAb+: 52.6%) and in controls with CLD (HBsAg+: 16.6%; HBVAb+: 50%); 4) the prevalence of HBV infection in diabetics with and without CLD (HBsAg+: 21% vs 7.7%; HBVAb+: 52.6% vs 56%); 5) the prevalence of HBV infection in diabetics treated by injection and orally (HBsAg+: 6.9% vs 8.6%; HBVAb+: 58.3% vs 55.2%). The relative risk of CLD for the factor HBsAg+ was 3.2 in the diabetic population vs 1.4 in controls. In view of the presence of antidelta antibodies (HDVAb) in 25% of HBsAg+ diabetics with CLD and the lack of HBV markers in 26.3% of diabetics with CLD, we assume that other viruses (Delta, nonA-nonB) may play roles. Probably the interaction of all possible etiopathogenetic factors (alcohol, viruses, glycometabolic derangement) is determinant for CLD in diabetics.

Several investigators have reported high levels of gamma-glutamyl-transpeptidase (GGT) in the diabetic population. Therefore, we undertook a study to see the prevalence of 'isolated' high GGT in a large population of diabetics without chronic liver disease (CLD), as compared to an age- and sex-matched control group of non-diabetic subjects without CLD, and the role of extrahepatic factors in 'isolated' high GGT, as possible etiopathogenetic causes. We selected 351 diabetics with normal hepatologic screening, without echographic abnormalities of the hepatic parenchyma or the biliary tract. Age, duration and therapy of diabetes, body mass index (BMI), alcohol consumption, glycosylated hemoglobin (HbA1), and the presence of hepatitis B virus (HBV) were studied to see if they are related to high GGT. The control group included 260 age- and sex-matched non-diabetic subjects. We did not find any significant difference between diabetics and the control group in the prevalence of high GGT (mean: 17.5% vs. 23%; women: 16% vs. 14.5%). Multiple regression analysis showed that alcohol consumption plays the major role in the high GGT of both men and women.