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NEUROLOGY 1997;48:13-18
© 1997 American Academy of Neurology

Myelopathy Among Brazilians Coinfected with Human T-cell Lymphotropic Virus Type I and HIV

L. H. Harrison, MD, B. Vaz, MD, D. M. Taveira, MD, T. C. Quinn, MD, C. J. Gibbs, PhD, S. H. de Souza, MD, J. C. McArthur, MBBS, MPH and M. Schechter, MD, PhD

From the Departments of International Health (Dr. Harrison), Medicine (Drs. Harrison and Quinn), and Neurology (Dr. McArthur), The Johns Hopkins University Schools of Hygiene and Public Health and Medicine, Baltimore, MD; Infectious Diseases (Dr. Schechter) and Neurology (Drs. Vaz, Taveira, and de Souza) Services, Hospital Universitario Clementino Fraga Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil; and National Institute of Allergy and Infectious Diseases (Dr. Quinn) and National Institute of Neurological Disorders and Stroke (Dr. Gibbs), National Institutes of Health, Bethesda, MD.
Supported in part by grants from Petrobras, S.A. and NIH NINDS NS26643.
Received December 8, 1995. Accepted in final form June 11, 1996.
Address correspondence and reprint requests to Dr Harrison, Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, 521 Parran Hall, 130 DeSoto Street, Pittsburgh, PA 15261, or to LHARRISO+@PITT.EDU.

Objective: To determine whether subjects coinfected with HTLV-I and HIV have a higher frequency of myelopathy than subjects singly infected with HIV. Design: A prospective, nested case-control study of HTLV-I and HIV coinfected (cases) and HIV singly infected adults (controls) participating in a prospective HIV cohort study at a university hospital outpatient HIV clinic in Rio de Janeiro, Brazil. Measurements: Subjects were evaluated for evidence of myelopathy by a neurologist unaware of their HTLV serologic status. Patients with at least two pyramidal signs, such as paresis, hypertonicity or spasticity, hyperreflexia, clonus, diminished or absent superficial reflexes, or the presence of pathologic reflexes (e.g., Babinski or Hoffmann), were defined as having myelopathy. Myelopathy severity was quantified using the Kurtzke Functional Disability Scale (FDS); patients with FDS scores >or=to4 were considered to have significant myelopathy. Selected patients with myelopathy underwent lumbar puncture for the evaluation of intrathecal synthesis of HTLV-I antibodies. Results: Of 15 coinfected subjects, 11 (73%) had evidence of myelopathy versus 10 of 62 subjects (16%) with HIV single infection (adjusted odds ratio [OR] = 13.0, p = 0.00002). When only myelopathy patients with FDS scores of >or=to2 or >or=to4 were included, the association between coinfection and the presence of myelopathy remained (OR = 7.3, p = 0.0003 for scores >or=to2; and OR = 8.9 for scores >or=to4, p = 0.04). In addition, a higher proportion of coinfected subjects had peripheral neuropathy (40%) than controls (16%) (OR = 3.5, p = 0.07). Conclusion: Coinfection with HTLV-I was strongly associated with myelopathy among subjects infected with HIV. The relative contribution of HTLV-I versus HIV in the pathogenesis of coinfection-associated myelopathy is not known. Coinfection may also be associated with peripheral neuropathy. Further studies are needed to elucidate the mechanisms of coinfection-associated neurologic conditions.

NEUROLOGY 1997;48: 13-18







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