Neurocognitive impairment in HIV-infected patients with past syphilis.

Type: Poster
Title: Neurocognitive impairment in HIV-infected patients with past syphilis.
Authors: Marra C, Deutsch R, Collier A, Morgello S, Letendre S, Clifford D, Gelman B, McArthur J, McCutchan A, Grant I, and the CHARTER Group
Date: 02-28-2011
Abstract:Background: Treponema pallidum causes syphilis. It invades the CNS early in disease and may be more difficult to eradicate in HIV-infected individuals. Our goal was to determine if HIV-infected persons with prior syphilis performed more poorly on a comprehensive neuropsychological (NP) test battery than HIV-infected persons without prior syphilis. Methods: 82 of 1574 enrollees in the CHARTER cohort had reactive serum rapid plasma reagin (RPR) tests at their local site. They were matched to 84 controls by age, gender, race, ethnicity and HIV risk factor. Serum RPR and fluorescent treponemal antibody absorbed (FTA-ABS) tests were performed in a single research laboratory; 69 serum RPR tests were confirmed as reactive. All subjects underwent detailed NP testing; NP analysis excluded 30 with significant confounding factors. Results: The 166 subjects (41 (25%) women, 101 (61%) Black, mean (SD) age 41.6 (9.1) yr, median (IQR) current and nadir CD4 418 (260-560) and 200 (84-319) cells/ul) were divided into three groups: recent syphilis (serum RPR > 1:8, FTA-ABS reactive, n=35), past syphilis (serum RPR < 1:8 and FTA-ABS reactive, n=66) and no syphilis (serum FTA-ABS nonreactive, n=65). Age, current and nadir CD4 did not differ between the 3 groups. There were no differences in the number of globally impaired patients, Global Deficit Score (GDS), or number of impaired NP test domains in patients with recent (N=31) vs. past (N=53) syphilis. However, patients with prior syphilis (current and past, N=84) had a higher mean (SD) GDS (0.47 (0.46) vs. 0.31 (0.33), p=0.03) and a higher number of impaired NP test domains (1.9 (1.8) vs. 1.3 (1.5), p=0.03) than those without (n=52). Nadir CD4, but not current CD4, was higher in patients with prior syphilis compared to those without (mean (SD) 260 (246) vs 189 (161) cells/ul, p=0.04). Controlling for nadir CD4, mean GDS and mean number of impaired NP domains remained higher in patients who had prior syphilis (F=6.5, p=0.01 and F=6.2, p=0.01). There were no differences in current or past antiretroviral use, plasma or CSF HIV RNA levels, or CSF white blood cell count between the two groups. Conclusions: HIV-infected individuals with serologic evidence of previous syphilis performed more poorly on a battery of NP tests than those who never had syphilis. Longitudinal studies of the relationships between syphilis, its treatment, and neurocognitive function may clarify pathogenic mechanisms.