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Biomedical subjects

H A Kessler

Publications and source records attributed to H A Kessler.

At least 73 records · Page 4Linked to original sources

Circulating human immunodeficiency virus (HIV) p24 antigen-positive lymphocytes: a flow cytometric measure of HIV infection.

Asymptomatic individuals seropositive for human immunodeficiency virus (HIV) progress in a heterogeneous fashion toward AIDS. To facilitate monitoring of disease progression and response to therapy, a rapid, new flow cytometric assay (FCA) lymphocyte p24-FCA, has been devised to quantify peripheral blood lymphocytes expressing cell-associated HIV-1 p24 antigen. Results from 55 asymptomatic, HIV-1-seropositive, serum p24 antigen-negative individuals ranged from undetectable (less than 0.1%) to 13.6% p24+ lymphocytes (mean, 2.0%). Mean values for three other groups studied were 0.1% for seronegative, viral culture-negative laboratory workers (n = 24); 4.2% for untreated patients with AIDS (n = 16); and 0.3% for AIDS patients receiving zidovudine (n = 11). Lymphocyte p24-FCA values were inversely related to the number of days to positive viral cultures and to levels of CD4+ lymphocytes. The ratio of p24+ lymphocytes to CD4+ lymphocytes may reflect the fraction of infected CD4+ lymphocytes. Lymphocyte p24-FCA determination may provide a method for monitoring response to antiretroviral therapy regardless of serum p24 antigen status.

CD4-Positive T-Lymphocytes↗

Analysis of lymphocytes, monocytes, and neutrophils from human immunodeficiency virus (HIV)-infected persons for HIV DNA.

The human immunodeficiency virus (HIV) infects and depletes or alters the function of cells involved in immune responsiveness. While both T helper lymphocytes and monocyte/macrophages can be infected via cell-surface CD4 in vitro, previous studies showed that few blood cells express HIV RNA in vivo. This study used DNA amplification to determine the levels of HIV DNA in purified lymphocytes, monocytes, and neutrophils from HIV-infected asymptomatic individuals and persons with AIDS. The average numbers of HIV DNA copies in lymphocytes from AIDS patients and asymptomatic individuals were similar (approximately 100-140 copies/150,000 cells). However, when expressed on the basis of numbers of CD4+ T cells, AIDS patients' cells contained approximately 2.5 times more HIV DNA. While HIV DNA was present in lymphocytes from all 27 subjects, little or no HIV DNA was observed in monocytes or neutrophils. Only 1 asymptomatic person contained levels of HIV DNA in monocytes (125 proviral copies/150,000 cells) that were comparable to levels expressed in lymphocytes (160/150,000). While expression of monocyte HIV DNA in this person was persistent over at least 8 months, it was not observed in neutrophils, suggesting that monocyte HIV DNA did not originate in myeloid precursors. This study shows that in AIDS or asymptomatic HIV infection, lymphocytes are the predominant infected cell found in blood.

Acquired Immunodeficiency Syndrome↗

In vitro activity of tosufloxacin (A-61827; T-3262) against selected genital pathogens.

The in vitro activity of tosufloxacin (A-61827; T-3262) against 15 clinical isolates of Chlamydia trachomatis and 31 recent clinical isolates of Neisseria gonorrhoeae, including 15 spectinomycin-resistant N. gonorrhoeae and 16 penicillinase-producing N. gonorrhoeae, was determined. Tosufloxacin was compared with doxycycline, ciprofloxacin, and temafloxacin against C. trachomatis. Susceptibility testing was performed by using McCoy cell monolayers. The in vitro activity of tosufloxacin against N. gonorrhoeae was compared with that of ciprofloxacin, temafloxacin, doxycycline, ceftriaxone, and spectinomycin by using an agar dilution method. Tosufloxacin was as active as temafloxacin against C. trachomatis (MIC for 90% of strains tested [MIC90], 0.25 microgram/ml; MBC for 90% of strains tested [MBC90], 0.25 microgram/ml) and was almost as active as doxycycline (MIC90, 0.06 microgram/ml; MBC90, 0.125 microgram/ml). Ciprofloxacin, temafloxacin, and tosufloxacin were extremely active against N. gonorrhoeae, including spectinomycin-resistant N. gonorrhoeae and penicillinase-producing N. gonorrhoeae, with MIC90s of 0.004, 0.015, and 0.008 microgram/ml, respectively. Ceftriaxone was slightly less active (MIC90, 0.03 microgram/ml), and doxycycline was the least active drug tested (MIC90, 4.0 micrograms/ml). Tosufloxacin and temafloxacin had excellent activity against the C. trachomatis and N. gonorrhoeae strains tested.

4-Quinolones↗

Major abdominal operations in acquired immunodeficiency syndrome.

Twenty-one major abdominal operations performed on 20 patients with Acquired Immunodeficiency Syndrome (AIDS) were reviewed. Fourteen operations were for therapeutic indications, eight were emergent. The array of pathology encountered included opportunistic infection with Mycobacterium avium intracellulare, Cytomegalovirus, Cryptosporidium, abdominal tuberculosis, lymphoma, Kaposi's sarcoma, AIDS-related immune thrombocytopenia, perforated appendicitis and colonic pseudo-obstruction. Hospital mortality was 20 per cent. Major morbidity occurred in 15 per cent of patients and was more common following emergency operations. Preoperative demographic, hematologic, or nutritional parameters examined or the presence of single-organ system dysfunction did not predict outcome. Fifty-three per cent of hospital survivors are alive with a nine-month median postoperative follow-up. It is concluded that major abdominal procedures in patients with AIDS should not be withheld due to fear of excessive morbidity or mortality. General surgeons are involved in the evaluation and treatment of increasing numbers of patients with HIV infection. Appropriate management requires recognition of a wide range of surgical pathology and attention to details of safe intraoperative conduct.

Abdominal Pain↗

Predictors of outcome in AIDS patients receiving zidovudine.

Fifty-eight AIDS patients who previously had Pneumocystis carinii pneumonia (PCP) were enrolled in an open trial of zidovudine therapy. We analyzed baseline clinical and laboratory parameters to identify predictors of outcome. Fifty-eight patients were followed for a mean of 26.5 weeks. There were 17 deaths; the probability of survival at 24 weeks was 0.81. Forty-one participants had unsuccessful outcomes, which included new opportunistic infections (24), progressive neurologic deterioration (2), and drug toxicity, excluding anemia, necessitating discontinuation of zidovudine (15). Only 24 subjects (41%) were receiving zidovudine at the end of the study period including 17 who had neither opportunistic infection nor toxicity. Low baseline hemoglobin level (p less than 0.001) and poor performance status as measured by the Karnofsky scale (p less than 0.01) independently predicted unsuccessful outcome and early death. Low hemoglobin (p = 0.001), low platelet count (p = 0.016), and increased time since PCP (p = 0.008) predicted development of drug toxicity. Neither CD4 lymphocyte count nor p24 antigenemia correlated with outcome.

Acquired Immunodeficiency Syndrome↗

Treatment of human immunodeficiency virus-related thrombocytopenia with zidovudine.

Human immunodeficiency virus (HIV)-related thrombocytopenia has been well described and requires therapy in about one half of the patients. Conventional modes of therapy with prednisone, danazol, immunoglobulin, and/or splenectomy have not been uniformly successful. We have administered zidovudine to three patients with HIV-related thrombocytopenia. All three patients responded with a sustained increase in their platelet counts, despite discontinuation of conventional therapy. Interruption of zidovudine therapy was associated with a decrease in platelet count. Concomitant with the elevation in platelet count with zidovudine therapy, there was a reduction in the circulating p24 antigen levels. Whether the elevations in the platelet count in these patients with HIV-related thrombocytopenia is due to the antiviral effect of zidovudine is unknown. It is clear that further studies examining the prospective use of zidovudine in the treatment of HIV-related thrombocytopenia are indicated.

Acquired Immunodeficiency Syndrome↗

Erythema nodosum associated with acute cytomegalovirus mononucleosis in an adult.

Acute cytomegalovirus mononucleosis has been associated with maculopapular rashes, petechiae, purpura, urticaria, ulcerative lesions, and vesicular eruptions. Although erythema nodosum has been reported in association with a number of infectious and noninfectious diseases, to our knowledge it has not been associated with cytomegalovirus infections. We report the first case of an adult patient with acute cytomegalovirus mononucleosis who presented with erythema nodosum.

Acute Disease↗

Update: Epstein-Barr virus-related disease.

The widespread application of molecular virologic technology has resulted in a rapid expansion in our knowledge of the physical, biologic, and clinical properties of EBV. As data continue to accumulate, we may better understand the pathogenesis of, and more clearly define diseases associated with, primary and reactivated infection due to this virus. The development of new antiviral agents and recombinant or subunit vaccines will permit more effective treatment, and possibly prevention, of disease and long-term sequelae associated with EBV infection.

Acute Disease↗

Regression of oral hairy leukoplakia during zidovudine therapy.

We describe two patients with human immunodeficiency virus infection and oral hairy leukoplakia whose tongue lesions resolved on oral zidovudine therapy. During therapy, each patient had a measurable reduction in human immunodeficiency virus antigen corresponding with clinical regression of oral lesions. The clinical course suggests that zidovudine may have contributed to the resolution of these lesions either indirectly through immunologic improvement or through an antiviral effect.

Acquired Immunodeficiency Syndrome↗

Diagnosis of human immunodeficiency virus infection in seronegative homosexuals presenting with an acute viral syndrome.

Early diagnosis of acute human immunodeficiency virus (HIV) infection is difficult because patients may be seronegative for HIV at the time of presentation. We have used a serum HIV antigen (HIV-Ag) enzyme immunoassay (EIA) to diagnose acute HIV infection in four high-risk patients. The clinical syndrome in these four patients was characterized by fever (four), rash (three), myalgias-arthralgias (three), and pharyngitis (two). All patients had spontaneous resolution of their symptoms within eight to 12 days. Serum HIV antibody, as measured by a commercially available screening EIA and by Western blot analysis, was negative in all patients at time of presentation and all seroconverted on subsequent testing. Human immunodeficiency virus was isolated from two of two patients during the acute illness. Initial serum samples from all four patients were positive for HIV-Ag. Serum samples of three of four patients became negative for HIV-Ag and positive for HIV antibody. These data suggest that serum HIV-Ag detection by EIA may be useful in the diagnosis of the acute syndrome caused by HIV infection.

Acquired Immunodeficiency Syndrome↗

Correlation of serum HIV antigen and antibody with clinical status in HIV-infected patients.

An enzyme immunoassay (EIA) has been developed which detects antigen(s) (Ag) of the human immunodeficiency virus (HIV) in the serum of patients with the acquired immunodeficiency syndrome (AIDS), AIDS-related complex (ARC), and patients at high risk for HIV infection. The test has a sensitivity of approximately 50 pg/ml of HIV protein. The specificity of the assay was determined with various virus infected cell lines, normal human sera/plasma, and serum from patients not known to be at risk for HIV infection. No false-positive HIV-Ag results were seen. Sera from 69% of patients with AIDS were positive for HIV-Ag as were 46% of patients with ARC and 19% of asymptomatic, HIV-antibody-positive individuals. There were significant associations between the stage of HIV infection--ie, AIDS vs ARC vs asymptomatic--and the detection of HIV-Ag in serum (p less than 0.0001) and the lack of detection of antibody to HIV core Ag (p less than 0.0001). HIV-Ag was also found in the serum of two asymptomatic antibody-negative individuals who were at high risk for AIDS and who later developed HIV antibody. The presence of HIV-Ag in sera was confirmed by an inhibition procedure. Thus, HIV-Ag can be detected in the serum of infected individuals prior to antibody production and correlates with the clinical stage of HIV infection.

Acquired Immunodeficiency Syndrome↗