Pituitary luteinizing hormone reserve in elderly men with prostatic disease.
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Biomedical subjects
Publications and source records attributed to S Kleinman.
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CONTEXT: Persons at risk of human immunodeficiency virus 1 (HIV-1) infection, have been classified incorrectly as HIV infected because of Western blot results, but the frequency of false-positive Western blot results is unknown. OBJECTIVES: To determine the frequency of false-positive HIV-1 Western blot results in US blood donors and to make projections to other screened populations. Secondarily, to validate an algorithm for evaluating possible false-positive cases. DESIGN: A retrospective cohort study of HIV-1 enzyme immunoassay (EIA) and Western blot results from large blood donor screening programs in which donors with suspected false-positive Western blot results underwent HIV-1 RNA polymerase chain reaction (PCR) testing and follow-up HIV-1 serology. SETTING: Five US blood centers participating in the Retrovirus Epidemiology Donor Study. PARTICIPANTS: More than 5 million allogeneic and autologous blood donors who successfully donated blood at 1 of the 5 participating centers from 1991 through 1995. MAIN OUTCOME MEASURES: Rate of false positivity by Western blot and true HIV-1 infection status as determined by HIV-1 RNA PCR and by serologic follow-up of blood donors more than 5 weeks after donation. RESULTS: Of 421 donors who were positive for HIV-1 by Western blot, 39 (9.3%) met the criteria of possible false positivity because they lacked reactivity to p31. Of these, 20 (51.3%) were proven by PCR not to be infected with HIV-1. The false-positive prevalence was 4.8% of Western blot-positive donors and 0.0004% (1 in 251000) of all donors (95% confidence interval, 1 in 173000 to 1 in 379000 donors). CONCLUSIONS: A false diagnosis of HIV-1 infection can result from the combination of EIA and Western blot testing in blood donor and other HIV-1 screening programs. Individuals with a positive Western blot result lacking the p31 band should be counseled that, although they may be HIV infected, there is uncertainty about this conclusion. These individuals should be further evaluated by RNA PCR testing (if feasible) and HIV serologic analysis on a follow-up sample.
Exchange transfusion is a well-established procedure for the treatment of severe complications of sickle cell anemia. However, large-volume exchange is a difficult, time-consuming technique, and therefore rarely used. Exchange red blood cell pheresis, using automated equipment, can accomplish red blood cell exchange more rapidly and efficiently, and can be easily performed by a skilled team of nursing personnel. The recent introduction of a pediatric centrifuge bowl allows this technique to be applied to pediatric patients. This procedure was used in a 13-year-old male with sickle cell anemia, who presented with bilateral pulmonary infiltrates, respiratory distress, and hypoxemia, unresponsive to antibiotics and other means of conservative therapy. A one and one-half volume red blood cell exchange reduced the hemoglobin S concentration to 13 per cent. The patient experienced dramatic improvement within 24 hours, progressing to complete recovery within a few days.
A population of 73 donor samples was assembled on the basis of reactive results in routine screening with three different licensed human T-lymphotrophic virus type III (HTLV-III) antibody enzyme-linked immunosorbent assay (ELISA) procedures. The samples were retested by a number of licensed and developmental tests and by Western blot analysis. Our data indicate that nonspecific results are generated by ELISA tests and that many of these reactions appear to be directed against the cell substrate used to grow the virus. These findings suggest that combinations of currently licensed ELISA tests, based upon HTLV-III grown in H-9 cells, cannot be used to confirm the specificity of reactive samples.
We conducted anti-HIV testing on follow-up samples obtained at a mean interval of 20 weeks from 150 blood donors who had previously tested anti-HIV ELISA positive and Western blot atypical. Of 93 donors who demonstrated reactivity to HIV core protein p24, 4 progressed to positive Western blots. Most of the remaining donors showed a persistent p24 reactivity on Western blot and had no risk factors for HIV infection. Immunofluorescence testing of the initial sample from 93 donors could not definitively separate seroconverters from those with persistent p24 reactivity. Of 57 donors with p18 reactivity, none were positive on follow-up anti-HIV testing. Our findings suggest policies and strategies for notifying donors of atypical anti-HIV Western blot results.
We have estimated the risk of transmitting HIV infection from a unit of HIV seronegative blood collected in Los Angeles and Orange Counties, CA from March 1985 through February 1987. Our method consisted of lookback investigations and anti-HIV testing of living recipients of HIV seronegative units donated by persons who later tested HIV seropositive at the time of a subsequent donation. During these investigations we have documented 3 cases of HIV transmission from HIV seronegative blood; using several assumptions, and extrapolating from this data, we have calculated that the risk of HIV transmission from an HIV seronegative unit was 1 in 51,000 to 1 in 102,000 (with a best guess of 1 in 68,000). We believe that our model can be applied in other geographic regions in an ongoing fashion in order to update our estimates of HIV transmission from HIV seronegative blood.
A new, multiple-antigen enzyme immunoassay (EIA-2) for hepatitis C virus (HCV) antibodies was evaluated in parallel with the previously available c100-3 HCV EIA (EIA-1) in 14,068 volunteer blood donors as well as in 25 cases of transfusion-associated hepatitis C for which recipient and donor samples were available. When compared to EIA-1, the EIA-2 was more sensitive in detecting HCV-infected blood donors. The EIA-2 detected an additional 1 in 1000 EIA-1-negative, surrogate marker-negative donors who were infected with HCV as demonstrated by polymerase chain reaction (PCR). The specificity of the EIA-2 was comparable to that of the EIA-1, but the two tests appear to detect different populations of false-positive donors. Recombinant immunoblot assay-indeterminate donors were detected five times more frequently by the EIA-2; PCR demonstrated that 21 percent of these donors were infected with HCV. The greater sensitivity of EIA-2 was also found in 25 transfusion recipients with non-A, non-B hepatitis; however, in 16 percent of these cases of posttransfusion HCV infection, the EIA-2 failed to detect an HCV-seropositive donor. These data indicate that EIA-2 testing will significantly reduce, but probably not eliminate, the risk of transfusion-associated HCV infection; we estimate this residual per-unit risk to be 1 in 2000 to 1 in 6000 units transfused. On a national level, it is projected that the replacement of the anti-HCV EIA-1 with the EIA-2 will initially prevent up to 40 additional cases of transfusion-associated hepatitis C per day.
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