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Association between HIV distal symmetric polyneuropathy and Mycobacterium avium complex infection
  1. IAN WOOLLEY,
  2. MARK FARAGHER,
  3. DENIS SPELMAN
  1. Departments of Infectious Diseases and Neurology, Alfred Hospital, Commercial Road, Prahran, 3081, Victoria, Australia
  1. Dr I Woolley, Division of Infectious Diseases, University Hospital of Cleveland Case Western Reserve University, Euclid Avenue, Cleveland, Ohio 44106, USA.

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We read with interest the paper by Norton et al 1 showing an association between distal symmetric polyneuropathy and Mycobacterium avium complex (MAC) infection but not between distal symmetric polyneuropathy and cytomegalovirus (CMV) infection. This confirms our findings presented in Sydney in 1994,2 to be published later this year.3

In our study a cohort of 94 consecutive patients with HIV were examined for evidence of peripheral neuropathy. Thirteen had distal symmetric polyneuropathy. We then performed a multivariate analysis of possible associated clinical factors including CD4 count, age, means of HIV acquisition, ddI (didanosine) and ddC (zalcitabine) treatment, opportunistic infections including CMV, Pneumocystis carinii pneumonia, and MAC and candidal infections. No factor reached significance but a history of MAC infection had borderline significance (P=0.051).

Surprisingly, homosexual transmission of HIV was the next most significant factor (P=0.089). Other factors including CMV and other opportunistic infections were not significant.

Distal symmetric polyneuropathy probably has heterogeneous causes, sometimes drug related and sometimes possibly multifactorial. We doubt that MAC itself is the cause of distal symmetric polyneuropathy given most of our patients (seven of 13) did not have overt MAC infections as was the case with five of 17 definite cases of distal symmetric polyneuropathy in the study by Norton et al. We also considered the possible role of isoniazid, although only three of our patients had taken isoniazid in the past, and concluded that cytokines such as tumour necrosis factor and interleukin-6, known to be raised in MAC infections,4 5 may be involved.

We agree with Norton et al that further investigation of (1) the mechanisms by which MAC may help produce peripheral neuropathy and (2) whether treatment and prophylaxis of MAC will alter the natural history of this condition will be of future interest.

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