Blackwater fever after halofantrine.
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Biomedical subjects
Publications and source records attributed to A Cargnel.
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A polymerase chain reaction (PCR) that amplifies the internal transcribed spacers of rRNA genes of Pneumocystis carinii (Pc-ITS-PCR) was compared with dihydrofolate reductase (DHFR) gene PCR to determine its usefulness in the diagnosis of Pneumocystis carinii pneumonia. All specimens from non-P. carinii pneumonia AIDS patients were both Pc-ITS-PCR- and DHFR PCR-negative. Twenty-six (96%) of 27 bronchoalveolar lavage specimens from P. carinii pneumonia patients were Pc-ITS-PCR-positive, and all 27 of these patients had at least 1 serum sample positive by Pc-ITS-PCR. In contrast, DHFR PCR detected P. carinii in only 4 (17%) of 24 P. carinii-positive lavage specimens and 2 (10%) of the 20 sera from P. carinii pneumonia patients. These results suggest that serum Pc-ITS-PCR may be useful for the diagnosis of P. carinii pneumonia.
OBJECTIVE: To examine the involvement of cognitive function in HIV-seropositive drug users (DU) in a pre-AIDS state. DESIGN: Fifty-six HIV-positive DU were prospectively evaluated. They belonged to groups II, III and IV (subgroups A, C2 and E) of the 1987 Centers for Disease Control and Prevention classification, with anamnesis negative for neurological pathology. HIV-negative DU (n = 19) and non-DU (n = 27) were used as controls. Infection with HIV and use of toxic drugs were considered variables of influence on cognitive function. METHOD: Subjects underwent neuropsychological evaluation by tests designed to explore cortical and subcortical function. RESULTS: HIV-positive DU showed worse performance scores at the psychometric tests than HIV-negative non-DU, but there was no difference when compared with HIV-negative DU. Ex-DU showed better performance than active DU. No difference with regard to degree of disease evolution was observed among HIV-positive individuals (i.e., groups II and III versus group IV). CONCLUSIONS: There was no evidence of cognitive deficits in HIV-positive individuals in non-AIDS phases to indicate early involvement by HIV at the cerebral level. Progression of the disease, prior to the AIDS phase, did not determine a worsening of intellectual performance. Instead, cognitive function was affected by the chronic and current use of toxic substances. In HIV-positive DU, a decline in cognitive function was found to be attributable to the chronic use of toxic substances rather than HIV infection.
Twenty-five HIV-seropositive drug abusers (DA+HIV+) (groups II-III and IV [A, C2 and E] of the CDC classification) were evaluated by use of the WAIS scale to determine any possible involvement of cognitive functions in the not yet overt phases of AIDS. The results were compared with those obtained in two control populations composed of 19 seronegative drug abusers (DA+HIV-) and 24 healthy subjects (DA-HIV-) to evaluate, in addition to the disease, the possible effect of the use of alcohol and toxic substances on cognitive performance. In spite of the small number of subjects, the study indicated that drug abuse is the main factor, among those analyzed, in determining a decline in cognitive functions.
The seroprevalence of HTLV-I/II was evaluated in 1247 Italian individuals at high risk for HIV infection. The population studied consisted of 985 intravenous drug users (IVDUs), 474 of whom on methadone maintenance and 511 in a therapeutic community, 110 HIV-infected patients in various stages of HIV-related disease and 152 hemophiliacs. Sera were screened for antibody to HTLV-I/II by enzyme immunoassay (EIA) and confirmed by Western blot and radioimmunoprecipitation assay. Confirmed positive samples were further differentiated by EIA using HTLV-I and HTLV-II specific peptides. The overall prevalence of anti-HTLV-I/II was 4.0% in IVDUs, with the highest prevalence (8.2%) among HIV-infected symptomatic patients. None of the hemophiliacs was anti-HTLV-I/II positive, even though 63.1% tested positive for HIV antibodies. The trend of seroprevalence in drug users and the evaluation of possible risk factors demonstrated that HTLV-I/II infection has been present in Italy before the onset of HIV epidemic. The overall seroprevalence showed no significant changes during the 10 year period covered by this survey but correlated with HIV seropositivity, age and duration of drug use. Peptide testing showed that HTLV infection was mainly due to HTLV-II.
OBJECTIVES: To assess whether the use of autologous blood transfusion may affect the incidence of post-transfusion hepatitis in transfused patients who undergo cardiac surgery. METHODS: One thousand one hundred and twelve polytransfused patients having undergone cardiac surgery were studied from October 1982 through September 1990. Patients were transfused with homologous blood from selected volunteer donors; autologous blood collection or blood saving were introduced in September 1986. Routine laboratory tests were carried out upon hospitalization and monthly for a six-month period. Patients with hepatitis were followed for at least 24 months and liver biopsy was performed in those with chronic hepatitis. RESULTS: Ninety-four (9.8%) of the 959 polytransfused patients developed non-A, non-B post-transfusion hepatitis; anti-hepatitis C virus antibodies were present in 52 out of the 72 patients tested. The mean incubation period for post-transfusion hepatitis was 70 days; hospitalization was required in 47.9% of the patients. The mean number of transfused units was 12.9 in patients who developed post-transfusion hepatitis and 6.96 in the those who did not. Hepatitis was chronic in 42% of the 94 patients; in the others alanine aminotransferase levels normalized in a mean period of 10.3 months. None of the 237 patients who received autologous blood had hepatitis. CONCLUSION: In our study the role of surgical teams in preventing post-transfusion hepatitis was shown to be essential. The high percentage of chronicity and symptom-free hepatitis observed is a further reason to reduce homologous blood transfusions and instore careful follow-up of polytransfused patients.
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Mycobacterial infections can be found in 10% of AIDS patients. Seventy cases with HIV+ infection were examined: they exhibited clear alterations of the chest and contemporaneous isolation and identification of mycobacteria. Primary tuberculosis is the most frequent manifestation in these patients. Alveolar parenchymal mono/bilateral infiltrates are the radiographic patterns of this pulmonary condition; they usually present without excavation (45.7%). Hilar and/or mediastinal lymph nodes are usually associated, and no pleural effusions. The main problem is the differential diagnosis with pneumocystis carinii pneumonia, especially the form involving lung apices. A correlation has been observed between the blood level of T-lymphocytes and their subsets (CD4 level) and the radiographic patterns of tuberculosis in AIDS patients. In fact, pleural effusion is frequent in patients with CD4 less than 200, while miliary nodules and cavitations are more frequent in the cases with CD4 greater than 200.
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The kinetics of antibody response to the group determinant a and subdeterminants d and y of hepatitis B virus were studied after infection and following immunisation with two recombinant DNA yeast-derived hepatitis B vaccines. The initial antibody response was to the subdeterminant epitopes, whereas anti-a antibody, which provides protection against different subtypes of the virus, was not detected for some weeks or months. The delay in the development of anti-a antibody after active immunisation raises important issues of early protection against infection.
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Two reactive sequences of the pre-S regions of hepatitis B surface antigen were synthesized chemically and used in micro-ELISAs for the assay of pre-S1 and pre-S2 antigens in serum from patients with acute and chronic hepatitis B. Pre-S1 antigen correlated well with the presence of HBV-DNA and was no longer detectable on cessation of viral replication, after natural recovery and after successful treatment with alpha-interferon. Pre-S2 proteins were also lost after treatment with alpha-interferon. The results show that the assay of pre-S1 and pre-S2 proteins in serum provides additional useful markers for assessing patients with acute and chronic hepatitis B infection and for monitoring the response to treatment with interferon.
In an Italian cooperative study on AIDS and cancer a diagnosis of Hodgkin's disease was established in 36 HIV-positive patients. The series was characterized by a high proportion of drug abusers, a high proportion of mixed cellularity and lymphocytic depletion subtypes and short survival. It is still unclear if HIV infection promotes the development of Hodgkin's disease or only modifies the course of the disease. According to the authors, however, patients who are HIV seropositive and have biopsy-proven Hodgkin's disease should be considered as fulfilling the criteria for AIDS.
A patient with peripheral cranial nerve paresis and bilateral myokymia is described during the course of acute co-infection with hepatitis B and delta viruses. Specific circulating hepatitis B immune complexes were found by electron microscopy concomitantly with the neurological symptoms.
Forty-six liver biopsies from HBsAg Delta/anti-Delta serum positive patients with chronic hepatitis were compared with liver specimens from HBsAg positive Delta/antiDelta negative patients. The results indicate more severe histologic damage and inflammation among subjects who are serum-positive to the Delta system. Specific virus antigen was found in liver cell nuclei of almost all the Delta IR patients (93.5%). The rate of diffusion was directly proportional to the severity of histological lesions, which is in linea with the direct cytopathic effect of the Delta virus as ascertained in various other studies.
Clinical and histologic valuation of delta chronic hepatitis is performed by a comparison between 46 HDV markers seropositive patients and an analogous group of HBsAg seropositive and delta system negative patients. It is possible to point out a greater seriousness of clinical and biohumoral situation during a HDV induced disease which is joined up with a more marked histologic damage and a greater inflammatory activity. The presence of specific viral antigen in hepatocyte nucleus suggests a delta-virus direct cytopathic effect.