The challenge of early tuberculosis (TB) infection among rural patients accessing highly active antiretroviral therapy (HAART) in a resource-limited setting with high HIV and TB burden has not been fully quantified.
This is a retrospective study nested within a prospective study of 969 patients consecutively initiated onto HAART at the CAPRISA AIDS Treatment programme in rural KwaZulu-Natal between January 2007 and December 2010. Patients were screened for clinical symptoms consistent with TB using a standardized checklist, and routine clinical investigations that included sputum microscopy and chest x-ray diagnosis.
Of 969 HIV-infected patients initiated on HAART, 173 [17.9%; 95% confidence interval (CI): 15.5 to 20.4] had active TB at HAART initiation. TB incidence rates were 3-fold higher in the first 3 months (early incident TB) after HAART initiation [11.5/100 person-years (py); 95% CI: 7.1 to 17.5] compared with 4–24 months (late incident TB) post-HAART initiation (3.2/100 py; 95% CI: 2.2 to 4.5; incidence rate ratio: 3.6; 95% CI: 2.0 to 6.4; P < 0.001). Immune status of patients at HAART initiation did not impact TB incidence rates in patients with CD4+ counts of <50 (5.3/100) and >200 (4.9/100 py; P = 0.81) cells per cubic millimeter. CD4+ count gains achieved 12 months post-HAART initiation were significantly different in patients with early incident TB versus late incident TB; P = 0.03.
Rural HIV treatment programmes in TB-endemic settings experience high rates of TB irrespective of immunologic status of patients at HAART initiation, or duration on HAART.
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*Centre for the AIDS Programme of Research in South Africa (CAPRISA), University of KwaZulu-Natal, Durban, South Africa;
†Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY; and
‡Oxford Department of Public Health, University of Oxford, Oxford, United Kingdom.
Correspondence to: Kogieleum Naidoo, MBChB, Centre for the AIDS Program of Research in South Africa (CAPRISA), 2nd Floor Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Private Bag X7, Congella, 4013, South Africa (e-mail: firstname.lastname@example.org).
Presented as an oral abstract at the Seventh IAS Conference on HIV Pathogenesis, Treatment and Prevention (IAS 2013), June 30, 2013 to July 3, 2013, Kuala Lumpur, Malaysia; Abstract no. A-581-0078-00125.
K.N. conceived the study. K.N. and A.B. designed and conducted the study. K.N., Q.A.K., S.S.A.K., A.B., N.Y-Z., and K.N. prepared, extracted, and analyzed the data. J.F., M.U., F.K., and P.K. provided ongoing support, management of clinical care, and study co-ordination. K.N., Q.A.K., S.S.A.K., A.B., and K.N. wrote the article. K.N., Q.A.K., S.S.A.K., A.B., K.N., and N.Y-Z. interpreted the data. All authors approved submission of this article.
Patient care in the CAPRISA AIDS Treatment project is supported by the KwaZulu-Natal Department of Health, the Global Fund to fight AIDS, Tuberculosis and Malaria, and the U.S. President's Emergency Plan for AIDS Relief (PEPFAR). The research infrastructure to conduct this trial, including the data management, laboratory, and pharmacy cores were established through the US National Institutes for Health's Comprehensive International Program of Research on AIDS Grant (CIPRA, Grant AI51794). K.N. was supported by the Columbia University-South Africa Fogarty AIDS International Training and Research Program (AITRP, Grant D43 TW000231). A.B. was supported by funds from the Oxford University Department of Public Health.
The funding sources listed here did not have any role in the analysis or preparation of the data in this article, nor was any payment received by these or other funding sources for this article.
The authors have no conflicts of interest to disclose.
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Received July 28, 2013
Accepted November 02, 2013