PubMed Health⌕ Search

Biomedical subjects

M Lisker-Melman

Publications and source records attributed to M Lisker-Melman.

16 recordsLinked to original sources
PubMed1992

Development of thyroid disease during therapy of chronic viral hepatitis with interferon alfa.

Six of 237 (2.5%) patients with chronic viral hepatitis who were treated with recombinant interferon alfa developed thyroid disease while on treatment. Three patients developed hyperthyroidism, two of whom developed detectable levels of thyroid-stimulating immunoglobulin; three patients developed hypothyroidism in association with high titers of antithyroglobulin and/or antimicrosomal antibodies. The thyroid disease did not remit when interferon therapy was stopped, and all six patients required definitive therapy for the thyroid disease. These findings suggest that a small proportion of patients treated with interferon alfa develop autoimmune reactions and can develop autoimmune thyroid disease.

Adult↗
PubMed1990

Therapy of chronic hepatitis B with recombinant human alpha and gamma interferon.

Eight patients with chronic hepatitis B entered a pilot study of gamma interferon and alpha interferon in combination. Gamma interferon alone had minimal inhibitory effects on serum levels of hepatitis B virus as monitored by serum HBV DNA and DNA-polymerase activity. The drug also gave troublesome side effects. In contrast, alpha interferon had more potent inhibitory effects on serum HBV levels and fewer side effects. When combined, the two interferons showed no additive or synergistic effects in inhibiting serum levels of HBV DNA or DNA polymerase. These findings indicate that the addition of gamma interferon to alpha interferon provides no additional antiviral effects but contributes significantly to side effects.

Adult↗
PubMed1990

A randomized, double-blind, placebo-controlled trial of recombinant human alpha-interferon therapy for chronic non-A, non-B (type C) hepatitis.

The effects of alpha-interferon therapy were evaluated in a prospective, randomized, double-blind, controlled trial of recombinant human interferon alfa-2b versus placebo in patients with well-documented chronic non-A, non-B hepatitis (type C). Forty-one patients, of whom 37 (90%) had hepatitis C virus antibodies in their serum, were enrolled in the trial. Twenty-one patients received interferon (2 million units) and 20 received placebo as subcutaneous injections three times weekly for 6 months. Mean serum aminotransferase activities and liver histology improved significantly in interferon-treated patients but not in placebo recipients. Ten interferon-treated patients (48%) had a complete response to therapy as shown by a reduction of mean serum aminotransferase activities into the normal range during therapy; three more patients had a partial response with aminotransferase activities decreasing by more than 50% on average. In follow up, however, serum aminotransferase levels usually returned to pre-treatment levels; at 6 to 12 months after stopping interferon, only two (10%) patients still had normal aminotransferase activity. These results indicate that alpha-interferon therapy is beneficial in reducing the disease activity in chronic hepatitis C. Only a minority of patients, however, appear to have a long-term response. In this study, interferon was generally well tolerated, with only one patient discontinuing therapy because of adverse effects.

Adult↗
PubMed1990

Therapy of chronic delta hepatitis with interferon alfa-2b.

In this pilot study, 12 patients with chronic delta hepatitis were studied. The diagnosis was based on the presence of antibodies to the hepatitis delta antigen in the serum and hepatitis delta virus RNA and hepatitis delta antigen in the serum and liver. All patients were also positive for hepatitis B surface antigen. The infection was presumed to have been transmitted by intravenous drug abuse in six of the patients, blood transfusion in one and by sexual contact in four (two had antibodies to human immunodeficiency virus in their serum, but did not show signs of acquired immunodeficiency syndrome). In one further patient, the source of infection was unknown. Interferon alfa-2b (INTRON A, Schering-Plough Corporation) was initiated at 5 million units per day subcutaneously for at least 4 months, being reduced by half if side effects occurred. Serum alanine aminotransferase levels, hepatitis delta virus RNA and hepatitis delta antigen were measured at monthly intervals for up to 12 months in some patients. Interferon therapy resulted in decreased serum levels of these three markers. On cessation of therapy, most patients experienced a relapse over 6 months, but alanine amino transferase levels could be normalized once more by restarting interferon therapy. In conclusion, interferon decreased hepatic inflammation by the inhibition of hepatitis delta virus replication, although relapse occurred when interferon was stopped and long-term therapy is required to achieve permanent control of the disease. Care will be required when treating patients with advanced or decompensated liver disease.

Adult↗
PubMed1989

Recombinant interferon alfa therapy for chronic hepatitis C. A randomized, double-blind, placebo-controlled trial.

Infection with the hepatitis C virus may result in chronic liver disease for which no effective therapy is now available. We studied the effects of recombinant human interferon alfa in a prospective, randomized, double-blind, placebo-controlled trial in patients with well-documented chronic hepatitis C. Forty-one patients were enrolled in the trial, 37 of whom were later found to have antibody to hepatitis C virus. Twenty-one patients received interferon alfa (2 million units) subcutaneously three times weekly for six months, and 20 received placebo. The mean serum aminotransferase levels and the histologic features of the liver improved significantly in the patients treated with interferon but not in the patients given placebo. Ten patients treated with interferon (48 percent) had a complete response, defined as a decline in mean serum aminotransferase levels to the normal range during therapy; three others had a decrease in mean aminotransferase levels of more than 50 percent. After treatment ended, however, serum aminotransferases usually returned to pretreatment levels; 6 to 12 months after the discontinuation of interferon therapy, only two patients (10 percent) still had normal values. We conclude that interferon alfa therapy is beneficial in reducing disease activity in chronic hepatitis C; however, the beneficial responses are often transient.

Adult↗
PubMed1989

Glomerulonephritis caused by chronic hepatitis B virus infection: treatment with recombinant human alpha-interferon.

STUDY OBJECTIVES: To assess the efficacy of alpha-interferon therapy in patients with hepatitis B virus (HBV)-related glomerulonephritis. DESIGN: Prospective, nonrandomized study. PATIENTS: Five patients with persistence of hepatitis B surface antigen, hepatitis B e antigen (HBeAg) and HBV DNA in serum for at least 6 months and histologic changes of chronic hepatitis on liver biopsy as well as persistent proteinuria of greater than 2 g/d and histologic changes of glomerulonephritis on renal biopsy. INTERVENTIONS: Patients received a 4-month course of recombinant human alpha-interferon (alfa-2b) beginning at a dose of 5 million units administered subcutaneously each day. RESULTS: Serum levels of HBV DNA decreased in all patients and fell to undetectable levels during treatment in four of five patients. In the four responding patients, serum HBeAg disappeared, aminotransferases fell into the normal range, and a follow-up liver biopsy showed an improvement in the hepatocyte necrosis and inflammation. Urine protein excretion also decreased during treatment. In the four responding patients, urine protein excretion gradually fell to less than 1 g/d and serum albumin levels rose into the normal range. Resolution of the biochemical and serologic evidence of chronic hepatitis and glomerulonephritis was accompanied by disappearance of signs and symptoms of liver and kidney disease. CONCLUSIONS: A high proportion of patients with HBV-related glomerulonephritis will respond to a 4-month course of alpha-interferon with a clinical, biochemical, and serologic remission.

Adult↗
PubMed1989

Rapidly progressive non-A, non-B hepatitis in patients with human immunodeficiency virus infection.

No information is available on the role of non-A, non-B hepatitis in the various hepatic abnormalities described in patients with the acquired immune deficiency syndrome. Of 97 patients referred with suspected non-A, non-B hepatitis, 3 were found to have antibody to the human immunodeficiency virus. These latter 3 patients all developed symptomatic cirrhosis within 3 yr of onset of hepatitis. Such a rapid progression of liver disease was rare in patients with non-A, non-B hepatitis who did not have simultaneous human immunodeficiency infection. These findings suggest that human immunodeficiency virus infection may potentiate the liver injury of chronic non-A, non-B hepatitis.

HIV Seropositivity↗
PubMed1989

Primary biliary cirrhosis.

Primary biliary cirrhosis is a chronic liver disease of unknown etiology characterized by slowly progressive intrahepatic cholestasis due to an inflammatory destruction of small intrahepatic bile ducts. The clinical course of PBC is variable ranging from a few years in rapidly progressive cases to a normal life-expectancy in a proportion of asymptomatic cases. The typical patient is a middle-aged woman who may present with pruritus, increasing pigmentation of the skin, and eventually jaundice. The level of serum alkaline phosphatase is almost invariably elevated, serum mitochondrial antibodies are present in more than 90 per cent, and an elevated serum IgM is usually present. PBC is associated with many immunologic abnormalities and appears to be a classic autoimmune disease. Some of the immune defects may be epiphenomena; others such as a marked defect in suppressor T cell function seem to be related to the pathogenesis of the disease. All drug therapy that is aimed at slowing the disease process is experimental. A place for immunosuppressive drugs in the management of PBC would be anticipated. However, no drug has to date been definitively shown to have a beneficial effect on the disease. Currently, the main treatments used are aimed at preventing or correcting the complications of intractable cholestasis. Patients with PBC and evidence of hepatic decompensation and/or poor quality of life make good candidates for liver transplantation. The current aim of therapy is to find an effective regime of immunosuppression that will make hepatic transplantation redundant for this disease.

Antibodies↗
PubMed1989

Conditions associated with hepatocellular carcinoma.

The most important condition associated with hepatocellular carcinoma is chronic hepatitis B virus infection. This article summarizes the information linking hepatocellular carcinoma with conditions other than hepatitis B virus infection.

Aflatoxins↗
PubMed1989

Primary lymphoma of the liver in a patient with acquired immune deficiency syndrome and chronic hepatitis B.

We describe the case of a homosexual man with asymptomatic infection with human immunodeficiency virus and hepatitis B virus who developed primary hepatic lymphoma. The lymphoma presented with rapid enlargement of the liver, and ultrasound examination revealed multiple hypoechoic lesions within the liver. Histological examination of the liver showed massive replacement by lymphomatous tissue, as well as changes of chronic active hepatitis B. Immunohistochemical stains for hepatitis B surface and core antigens were strongly positive in almost all hepatocytes, but not in tumor tissue. Whereas the occurrence of lymphoma probably is related to HIV infection, possible interactions between hepatitis B virus and HIV infection are discussed. Thus, the presence of mass lesions within the liver in a patient with HIV infection should raise the possibility of hepatic lymphoma even if there is no evidence of generalized lymphadenopathy.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Phenytoin hepatotoxicity masked by corticosteroids.

The association of phenytoin and liver toxicity is well documented. This article describes a patient who underwent a transsphenoidal resection of a pituitary tumor who developed phenytoin-induced hepatotoxicity that was masked by the simultaneous administration of corticosteroids for treatment of cerebral edema. In a patient receiving both medications, the systemic manifestations of the hypersensitivity to phenytoin may go unrecognized, leading to delayed identification of a potentially lethal complication of this commonly prescribed anticonvulsant.

Brain Edema↗