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Biomedical subjects

T C Merigan

Publications and source records attributed to T C Merigan.

At least 235 records · Page 13Linked to original sources
PubMed1981

Controlled clinical trial of intravenous acyclovir in heart-transplant patients with mucocutaneous herpes simplex infections.

Viral cultures of mucocutaneous herpes simplex lesions became negative in 5 heart-transplant patients given a 7-day course of intravenous acyclovir. Relief of pain and healing of lesions paralleled the virological response. Similar clinical and virological responses were not seen in the 5 placebo-treated patients in this double-blind placebo-controlled trial. No adverse reactions attributable to acyclovir were noted. Shedding of herpes simplex viruses recurred in 3 patients after acyclovir therapy.

Acyclovir↗
PubMed1981

Virology and immune mechanisms.

Epstein-Barr virus and hepatitis B virus are two agents which chronically infect man and have been associated with specific neoplasms. Such findings point the way to new methods of control and detection of human malignancies. Furthermore, immunosuppression is another major factor underlying the development of certain malignancies in human populations. It is clear that congenital immunodeficiency states as well as organ transplant recipients requiring iatrogenic immunosuppression and cancer patients requiring chemotherapy and/or x-irradiation are susceptible to particular malignancies at a higher rate than the normal population. Such findings also provide not only clues as to the mechanisms which control tumor development but argue for certain limitations to the extent of immunosuppressive therapy utilized for treatment of cancer.

Animals↗
PubMed1981

Treatment of NZB/NZW F1 hybrid mice with Mycobacterium bovis strain BCG or type II interferon preparations accelerates autoimmune disease.

NZB/NZW F1 hybrid mice develop a spontaneous autoimmune disease characterized by the appearance of antinuclear antibodies and premature death due to immune complex glomerulonephritis. To investigate the possible effects of cellular immune stimulation on this disorder, groups of female NZB/NZW mice, aged 2, 5, and 7 months, were treated either with the nonspecific immunostimulatory agent Mycobacterium bovis strain BCG or with saline. Mice treated with BCG at ages 5 and 7 months died sooner than age-matched controls, and death was associated with severe glomerulonephritis, suggesting that BCG may have accelerated autoimmunity in these mice. Since BCG is known to stimulate the production of type II (or gamma) interferon, a substance with potent immunoregulatory effects, a second study was carried out to assess the effects of type II interferon on NZB/NZW disease. A greater number of type II interferon-treated mice died by 9 months of age when compared to controls, and the increased death rate was associated with a more rapid development of antinuclear antibodies and histologically confirmed glomerulonephritis. These data, together with a recent report of increases in the level of serum type II interferon in patients with active systemic lupus erythematosus, suggest that type II interferon may play a role in the pathogenesis of autoimmune disease.

Animals↗
PubMed1981

Human leukocyte interferon treatment of two children with insulin dependent diabetes.

Two patients with newly diagnosed insulin dependent diabetes mellitus were treated with human leukocyte interferon based on the hypothesis that the diabetes was induced by an active viral infection in the pancreatic islets and could be arrested. High peak levels of serum interferon were achieved (100-200 U/ml) with minimal systemic side effects. There was no sustained therapeutic benefit as measured by increased production of endogenous insulin, or of C-peptide, or by a lower requirement for exogenous insulin. Further trials with interferon treatment should be undertaken only if evidence of active viral infection (culture, antigen detection) can be associated with insulin dependent diabetes onset and these markers followed during treatment.

Blood Glucose↗
PubMed1981

Antiviral treatment of chronic hepatitis B virus infection. I. Changes in viral markers with interferon combined with adenine arabinoside.

Twenty patients with chronic active hepatitis and 12 patients with chronic persistent hepatitis associated with hepatitis B virus (HBV) infection were treated with human leukocyte interferon or adenine arabinoside alone or in combination. With interferon alone, four of 16 patients showed a permanent disappearance of HBV-associated DNA polymerase (DNAP) activity from serum. Of six patients treated with adenine arabinoside alone, only one patient became permanently DNAP-negative. With a regimen of multiple cycles of combined interferon and adenine arabinoside, seven of 16 male patients became permanently DNAP-negative. Of 69 patients who met the criteria for admission to the program, spontaneous decreases in DNAP activity without treatment were observed in only 9% during a mean observation period of 10 months. In general, patients with chronic active hepatitis, those who are female, and those with a history of recent steroid therapy responded to the antiviral agents significantly better than did the other patients.

Adult↗
PubMed1981

Short-course human leukocyte interferon in treatment of herpes zoster in patients with cancer.

Because of encouraging results when human leukocyte interferon was given for 5 to 7 days to treat early localized herpes zoster in patients with cancer, a small placebo-controlled, randomized, double-blind trial was set up involving only 48 h of therapy. In this trial, there was no effect on acute pain or disease progression in the primary dermatome. However, a modest but significant effect was noted in that distal cutaneous spread was diminished in the treated patients compared with the controls and the treated patients had diminished severity and duration of postherpetic neuralgia. No evidence of impairment in varicella-zoster-specific lymphocyte transformation was observed in interferon-treated patients.

Clinical Trials as Topic↗
PubMed1981

Follow-up observations on the effect of human leukocyte interferon in non-Hodgkin's lymphoma.

Follow-up data for 11 patients with non-Hodgkin's lymphoma treated with partially purified human leukocyte interferon is presented. The interferon preparation used was 0.1% pure and treatment consisted of 5 x 10(6) U given intramuscularly twice daily for 60 injections. One complete, three partial, and three minimal responses were observed in five of seven evaluable patients with nodular non-Hodgkin's lymphoma. Duration of response appears to be from 6 to 12 mo. One patient achieved a second partial response on retreatment with interferon in spite of having received chemotherapy in the interval between interferon treatments. No responses were seen in three patients with rapidly progressive diffuse histiocytic lymphoma. Dose-limiting toxicity is leukopenia, which necessitated modification or cessation of treatment in three patients. Nonhematologic toxicities consisted of fever, malaise, arthralgia, and loss of appetite. In conclusion, interferon has activity against non-Hodgkin's lymphoma, and prior treatment with chemotherapy does not preclude a response to interferon.

Adult↗
PubMed1981

Interferon acts directly on human B lymphocytes to modulate immunoglobulin synthesis.

At different times of exposure, interferon (IFN) enhanced and suppressed pokeweed mitogen- (PWM) induced IgG synthesis by human peripheral blood lymphocytes (PBL). Pretreatment of PBL and IFN frequently increased antibody production by more than 100% when compared with that by untreated PBL. Results of experiments in which PBL were separated into T and B subpopulations indicated that IFN preparations acted directly on B cells. Thus, mixtures of IFN-treated B cells and untreated T cells from 5 of 7 persons tested produced 81% to 500% more IgG than untreated, matched control cells. However, IFN-treated monocytes mixed with untreated B and T cells or IFN-treated T cells mixed with untreated B cells failed to enhance IgG production significantly in similar assays. In contrast to the pretreatment protocol, when IFN was present in the incubation mixture throughout the PWM assay, IgG production decreased. Sephadex chromatography of the IFN and tests of the resulting fractions indicated that the IgG production-enhancing activity was located in the fraction carrying the antiviral activity.

Adolescent↗
PubMed1981

Effects of immunosuppressive therapy on viral markers in chronic active hepatitis B.

Hepatitis B virus associated DNA polymerase activity, hepatitis b surface antigen (HBsAg), and serum aspartate aminotransferase were followed in 21 patients with chronic active hepatitis while immunosuppressive therapy (prednisone +/- azathioprine) was being withdrawn. In every case, DNA polymerase activity fell within 6-10 wk of decreasing treatment and became undetectable in 8 patients. This was usually accompanied by a fall in HbsAg titer and a transient rise in serum aspartate aminotransferase activity. Four additional patients with previously untreated HbsAg positive chronic active hepatitis were placed on prednisone for 12 wk. There was a rise in DNA polymerase activity and HBsAg titer with a fall in serum aspartate aminotransferase values during treatment. Upon discontinuing therapy, DNa polymerase activity fell dramatically in all 3 patients who completed their course of prednisone and became undetectable in 1. These findings suggest that immunosuppressive therapy has a potentiating effect on hepatitis B viral replication in patients with chronic active hepatitis.

Adult↗
PubMed1980

Role of G0-G1 arrest in the inhibition of tumor cell growth by interferon.

We report here that human leukocyte interferon preparations are capable of influencing the transition of human melanoma cells from the "A" state to the "B" phase. Human melanoma cells that enter a quiescent stage at high cell density are more sensitive to the cytostatic action of interferon than those that continue to proliferate under similar conditions. Cell cycle perturbations caused by interferon in these cells include a decreased transition rate out of G0-G1 ("A" state) into S ("B" phase) and a prolongation of S. These findings support the idea that some metabolic event is required for progress through the G0-G1 phase of the cell cycle and is susceptible to interferon action.

Blood↗
PubMed1980

Effect of interferon therapy on circulating lymphocytes in humans.

The effect of interferon treatment on both lymphocyte subpopulation numbers and function was studied in two groups of patients who were being treated systemically with 0.5 to 1.0 x 10(7) units of human leukocyte-derived interferon (HulFN-alpha) daily. Patients with nodular lymphocytic, poorly differentiated non-Hodgkin's lymphoma (NLPD) were given interferon for 30 days and those with chronic hepatitis B infection were treated in cycles for 4 to 7 days. In both patient groups, B lymphocytes numbers were reduced during treatment, but T lymphocyte numbers were unaffected. T lymphocyte responses, measured by blast transformation to herpesvirus antigens were generally low before treatment in NLPD patients. The responses were restored after termination of therapy. In two NLPD patients given two courses of treatment separated by a 3 month interval, the restored T lymphocyte responses were inhibited during the second course of treatment. In patients with chronic hepatitis B virus infection, lymphocyte blast transformation to the viral antigens were also depressed during treatment compared to pretreatment responses. Changes in lymphocyte responses to phytohemagglutinin and pokeweed mitogen were not observed in either patient group.

Antigens, Viral↗
PubMed1980

Type I and type II interferons: differential antiviral actions in transformed cells.

In transformed mouse embryo cells, type II interferon had much less antiviral activity than type I interferon. In non-transformed cells, the two interferons had similar high activity, Reversal of the phenotype of Moloney sarcoma virus (MSV) transformed cells by sodium butyrate restored their sensitivity to the antiviral action of type II interferon. Additional evidence for a role of the cytoskeletal network in the action of type II interferon is that its antiviral effect is reduced by cytochalasin B, colchicine or vinblastine. MSV-transformed cells, selected for their resistance to the antiviral action of type I interferon, were sensitive to type II interferon. These differences in the effects of type I and II interferon on transformed cells are at present unexplained, but suggest that they have at least partially separate mechanisms of action.

Animals↗