Knut A Hestad1,2,3, Jonathan Chinyama4, Menon J Anitha4, Mary S Ngoma5, J Allen McCutchan6, Donald R Franklin7, Robert K Heaton8. 1. Department of Research, Innlandet Hospital Trust, Brumunddal, Norway. 2. Department of Psychology, Faculty of Social Sciences and Technology Management, Norwegian University of Science and Technology, Trondheim, Norway. 3. Department of health science, Faculty of Health and Social Sciences, Inland Norway University of Applied Sciences, Elverum, Norway. 4. Department of Psychology, University of Zambia, Lusaka, Zambia. 5. Department of Paediatrics and Child Health, University of Zambia, Lusaka, Zambia. 6. Division of Infectious Diseases, School of Medicine, University of California, San Diego. 7. HIV Neurobehavioral Research Program, University of California, San Diego, CA. 8. Department of Psychiatry, University of California, San Diego, CA.
Abstract
BACKGROUND: HIV infection may result in neurocognitive deficits, but the effects of pulmonary tuberculosis (TB+), a common comorbid condition in HIV infection, on cognition in HIV infections are unknown. Accordingly, we examined the effects of TB+, on neurocognitive functioning in HIV-infected (HIV+) Zambian adults. SETTING: All participants were drawn from HIV clinics in and around Lusaka, the capital of Zambia. METHODS: Participants were 275 HIV+, of whom 237 were HIV+ and TB-negative (HIV+/TB-), and 38 also had pulmonary TB+ (HIV+/TB+). Controls were 324 HIV- and TB-uninfected (HIV-) healthy controls. All HIV+ participants were prescribed combination antiretroviral treatment (cART). Published, demographically corrected Zambian neuropsychological norms were used to correct for effects of age, education, sex, and urban/rural residence. RESULTS: Neuropsychological deficits, assessed by global deficit scores, were more prevalent in this order: 14% (46 of 324) of HIV- controls, 34% (80 of 237) of HIV+/TB-, and 55% (21 of 38) of HIV+/TB+ group. Thus, both HIV-infected groups evidenced more impairment than HIV- controls, and the HIV+/TB+ group had a higher rate of neurocognitive impairment than the HIV+/TB- group. HIV+/TB+ patients were more likely to be male, younger, less-educated, and have lower CD4 counts and detectable HIV RNA in blood compared with the HIV+/TB- patients. CONCLUSIONS: In HIV infection, TB may contribute to cognitive impairment, even after controlling for lower CD4 counts and viral load. Thus, systemic inflammation from HIV and TB and more advanced immune deficiency at diagnosis of HIV may contribute to impaired cognition in HIV+/TB+ patients.
BACKGROUND:HIV infection may result in neurocognitive deficits, but the effects of pulmonary tuberculosis (TB+), a common comorbid condition in HIV infection, on cognition in HIV infections are unknown. Accordingly, we examined the effects of TB+, on neurocognitive functioning in HIV-infected (HIV+) Zambian adults. SETTING: All participants were drawn from HIV clinics in and around Lusaka, the capital of Zambia. METHODS:Participants were 275 HIV+, of whom 237 were HIV+ and TB-negative (HIV+/TB-), and 38 also had pulmonary TB+ (HIV+/TB+). Controls were 324 HIV- and TB-uninfected (HIV-) healthy controls. All HIV+ participants were prescribed combination antiretroviral treatment (cART). Published, demographically corrected Zambian neuropsychological norms were used to correct for effects of age, education, sex, and urban/rural residence. RESULTS: Neuropsychological deficits, assessed by global deficit scores, were more prevalent in this order: 14% (46 of 324) of HIV- controls, 34% (80 of 237) of HIV+/TB-, and 55% (21 of 38) of HIV+/TB+ group. Thus, both HIV-infected groups evidenced more impairment than HIV- controls, and the HIV+/TB+ group had a higher rate of neurocognitive impairment than the HIV+/TB- group. HIV+/TB+patients were more likely to be male, younger, less-educated, and have lower CD4 counts and detectable HIV RNA in blood compared with the HIV+/TB- patients. CONCLUSIONS: In HIV infection, TB may contribute to cognitive impairment, even after controlling for lower CD4 counts and viral load. Thus, systemic inflammation from HIV and TB and more advanced immune deficiency at diagnosis of HIV may contribute to impaired cognition in HIV+/TB+patients.
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