Transient worsening of tuberculous symptomatology and lesions following antituberculous therapy (paradoxical response) has previously been described as a rare occurrence. To determine the incidence of paradoxical responses in patients with AIDS and TB who are treated with antituberculous therapy and subsequently with combination antiretroviral therapy (ARV), we conducted a prospective study of 33 HIV-seropositive TB patients treated with anti-TB therapy and antiretroviral therapy (Group 1) compared with 55 HIV-seronegative TB patients treated with anti-TB therapy (Group 2) and 28 HIV-seropositive TB patients treated with anti-TB therapy but not on antiretrovirals (historical control; Group 3). In Group 1 patients, paradoxical responses were temporally more related to the initiation of ARV than to the initiation of anti-TB therapy (mean +/- SD: 15 +/- 11 d versus 109 +/- 72 d [p < 0.001]) and occurred much more frequently (12 of 33; 36%) compared with Group 2 (1 of 55; 2%) (p < 0.001) or with Group 3 (2 of 28; 7%) (p = 0.013). The majority of patients who experienced paradoxical responses and received tuberculin purified protein derivative (PPD) in Group 1 had their tuberculin skin tests convert from negative to strongly positive after ARV. These observations suggest that a paradoxical response associated with enhanced tuberculin skin reactivity may occur after the initiation of ARV in HIV-infected TB patients. Furthermore, the skin test conversion after the initiation of ARV may have important public health implications.
The increased risk of developing lung diseases in cigarette smokers has been well recognized. The association between smoking and the risk of developing pulmonary infections in HIV-1-infected patients, however, which has not been established, was evaluated in the present study. Twenty-seven cases with lower respiratory infections (15 Pneumocystis carinii pneumonia (PCP), 12 TB cases) were compared with 27 age, gender, socio-economic and HIV status-matched patients, without history of respiratory diseases. Medical history and physical examinations were obtained every 6 months. Blood was drawn for CD4 and viral load measurements. A substantial number of HIV + smokers who developed PCP (one-third) had been on highly active retroviral therapy (HAART) for more than 6 months and prophylaxis had been discontinued. Multivariate analyses indicated that in HIV-infected people, after controlling for HIV status and antiretrovirals, cigarette smoking doubled the risk for developing PCP (p = 0.01). Multivariate analyses demonstrated that long-term smoking also increased the risk (2 x) of developing tuberculosis (p = 0.04). Moreover, daily tobacco use seemed to attenuate by 40% the immune and virological response to antiretroviral therapies. These findings indicate that tobacco use significantly increases the risk of pulmonary diseases in HIV infected subjects and has a potential deleterious impact on antiretroviral treatment.
In an attempt to define guidelines for the assessment of acute asthma, we evaluated 205 patients who presented to the emergency room for treatment of asthma. Of the 205, 120 were successfully treated and discharged from the emergency room, 45 were hospitalized, and 40 were treated and discharged from the emergency room but had relapses within 10 days. A predictive index using a combination of presenting factors was developed: pulse rate greater than or equal to 120 per minute, respiratory rate greater than or equal to 30 per minute, pulsus paradoxus greater than or equal to 18 mm Hg, peak expiratory flow rate less than or equal to 120 liters per minute, moderate to severe dyspnea, accessory-muscle use, and wheezing. The index ranged from 0 to 7, increasing with the severity of symptoms. The index scores of the relapse group (4.9 +/- 1.0) and the admitted group (5.1 +/- 1.0) were both significantly different (p less than 0.001) from that of the successfully treated group (1.6 +/- 1.2). An index of 4 or higher was 95 per cent accurate in predicting the risk of relapse and 96 per cent accurate in predicting the need for hospitalization.
Tobacco use, which is widespread among HIV-infected subjects, increases the risk of pulmonary diseases, particularly PCP and CAP, two respiratory infections with high prevalence and morbidity risks even in the era of HAART.
To study the association between mycobacterial disease and the acquired immunodeficiency syndrome, we reviewed the records of all cases of tuberculosis and all cases of the syndrome reported in Dade County, Florida, from January 1980 through June 1983. Tuberculosis was diagnosed in 27 of 45 Haitians with the syndrome, but in only 1 of 37 non-Haitians with the syndrome (p less than 0.001). Among the 27 Haitians with the syndrome and tuberculosis, 19 had extrapulmonary tuberculosis, whereas among 286 Haitian patients with tuberculosis without the syndrome, only 56 had extrapulmonary tuberculosis (p less than 0.001). Tuberculosis preceded the syndrome by 1 to 17 months (mean, 6) in 22 patients. In 10 patients with the syndrome and positive sputum cultures who were treated with conventional antituberculosis drugs, the cultures became negative within 1 to 4 months and tuberculosis did not recur. The frequency of disseminated atypical mycobacteriosis or positive sputum cultures for atypical mycobacteria was not significantly different between Haitian (11.3%) and non-Haitian (8.3%) patients with the syndrome.
Twenty Haitian patients, hospitalized from 1 April 1980 to 20 June 1982, had Pneumocystis carinii pneumonia, central nervous system toxoplasmosis, esophageal candidiasis, cryptococcosis, disseminated cytomegalovirus, progressive herpes simplex virus, chronic enteric coccidiosis, or invasive Kaposi's sarcoma. Ten patients died. Opportunistic infections were frequently multiple and were recurrent in three patients. In seven patients disseminated tuberculosis preceded the other infections by 2 to 15 months. There was no evidence of an underlying immunosuppressive disease, and no history of homosexuality or intravenous drug abuse. At least three patients probably acquired the syndrome in Haiti. Lymphadenopathy was common. Seventeen patients tested had anergy, and 18 had lymphopenia. Monoclonal antibody analysis of peripheral-blood T-cell subsets done on 11 patients showed a marked decrease in T-helper cells and an inversion of the normal ratio of T-helper cells to T-suppressor cells. This syndrome among heterosexual Haitians is strikingly similar to the syndrome of immunodeficiency described recently among American homosexuals.
Until recently it was thought that age greater than 35 yr was the main risk factor for the development of drug-induced hepatitis (DIH) in patients receiving antituberculosis therapy. We conducted a study to determine whether infection with either the hepatitis C virus or the human immunodeficiency virus (HIV) were significant risk factors for the development of DIH in patients receiving antituberculosis therapy. Our study consisted of two parts. In the first part, 134 consecutive patients admitted for the treatment of tuberculosis (TB) were followed for the development of DIH. All of these patients were also screened for the presence of hepatitis C and HIV. In the second part of the study, those patients who were hepatitis C positive and who developed DIH on repeated reintroduction of the anti-TB drugs were offered a liver biopsy. If active inflammation, which may be suggestive of hepatitis C infection, was present on the biopsy specimen, treatment with alpha-interferon was begun and the anti-TB drugs were subsequently reintroduced. During the 18 mo of the study, 22 patients developed DIH. The relative risk of developing DIH if the patient was hepatitis C or HIV positive was fivefold and fourfold, respectively (p < 0.05). If a patient was coinfected with both hepatitis C and HIV the relative risk of developing DIH was increased 14.4-fold (p < 0.002). In the treatment part, four patients were treated with alpha-interferon, and all were able to undergo the reintroduction of anti-TB therapy without reoccurrence of DIH. Infection with hepatitis C and HIV are independent and additive risk factors for the development of DIH during TB therapy. The treatment of hepatitis C with alpha-interferon may allow the reintroduction of anti-TB agents in those who previously developed DIH when exposed to these drugs.
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