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HIV neuropathy natural history cohort study

Assessment measures and risk factors

From Mount Sinai Hospital (D.M.S.), New York, NY; Harvard School of Public Health (D.K., S.R.E.), Boston, MA; Johns Hopkins School of Medicine (J.C.M.), Baltimore, MD; University of California, Davis Medical Center (D.M.A.), Sacramento, CA; Northwestern University Medical Center (B.C.), Chicago, IL; University of Miami School of Medicine (K.G.), Miami, FL; University of Hawaii School of Medicine (M.G.), Honolulu, HI; Stanford University Medical Center (Y.S.), Palo Alto, CA; University of Washington School of Medicine (C.M.M.), Seattle, WA; University of Texas Southwestern Medical Center (R.D.-A.), Dallas, TX; AACTG Operations Office (S.S.), Silver Spring, MD; Frontier Science and Technology Research Foundation (L.M.), Amherst, NY; and Washington University School of Medicine (D.B.C.), St. Louis, MO.

Address correspondence and reprint requests to Dr. David M. Simpson, Department of Neurology, Mount Sinai School of Medicine, One Gustave Levy Place, Box 1052, New York, NY 10029; e-mail: david.simpson{at}mssm.edu

Background: Distal sensory polyneuropathy (DSP) is the most common neurologic complication of human immunodeficiency virus (HIV) infection. Risk factors for DSP have not been adequately defined in the era of highly active antiretroviral therapy.

Methods: The authors evaluated 101 subjects with advanced HIV infection over 48 weeks. Assessments included a brief peripheral neuropathy (PN) screen (BPNS), neurologic examination, nerve conduction studies, quantitative sensory testing (QST), and skin biopsies with quantitation of epidermal nerve fiber density. Data were summed into a Total Neuropathy Score (TNS). The presence, severity, and progression of DSP were related to clinical and laboratory results.

Results: The mean TNS (range 0 to 36) was 8.9, with 38% of subjects classified as PN-free, 10% classified as having asymptomatic DSP, and 52% classified as having symptomatic DSP. Progression in TNS from baseline to week 48 occurred only in the PN-free group at baseline (mean TNS change = 1.16 ± 2.76, p = 0.03). Factors associated with progression in TNS were lower current TNS, distal epidermal denervation, and white race. As compared with the TNS diagnosis of PN at baseline, the BPNS had a sensitivity of 34.9% and a specificity of 89.5%.

Conclusions: In this cohort of advanced human immunodeficiency virus (HIV)–infected subjects, distal sensory polyneuropathy was common and relatively stable over 48 weeks. Previously established risk factors, including CD4 cell count, plasma HIV RNA, and use of dideoxynucleoside antiretrovirals were not predictive of the progression of distal sensory polyneuropathy (DSP). Distal epidermal denervation was associated with worsening of DSP. As compared with the Total Neuropathy Score, the brief peripheral neuropathy screen had relatively low sensitivity and high specificity for the diagnosis of DSP.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the June 13 issue to find the title link for this article.

*See the Appendix for a list of contributors.

Supported by the AIDS Clinical Trials Group (ACTG) funded by the NIAID, AI38858, AI03855, AI25903, AI27664, AI046376, AI34853, AI27658, AI27670, AI 46386, AI-25859, AI46370, AI32770, AI27668, and the Neurologic AIDS Research Consortium funded by the National Institute of Neurologic Diseases and Stroke, NS032228, NS44807, K24 NS002253 (D.M.S.), and GCRC Units funded by the NCRR, RR00522, RR016467, RR00044, RR-00071, RR00051.

Disclosure: The authors report no conflicts of interest.

Received September 26, 2005. Accepted in final form February 21, 2006.

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