Sensory polyneuropathy in human immunodeficiency virus-infected patients receiving tuberculosis treatment
| Autor: | Chad M. Centner, Michael Benatar, Taylor B. Harrison, Jeannine M. Heckmann, H. Carrara |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Adult
Male Pulmonary and Respiratory Medicine medicine.medical_specialty Time Factors Tuberculosis Genotype Sensory Receptor Cells Arylamine N-Acetyltransferase Antitubercular Agents HIV Infections Pathogenesis Polyneuropathies Risk Factors Internal medicine medicine Humans Longitudinal Studies Prospective Studies Prospective cohort study Tuberculosis Pulmonary Genotyping Survival analysis business.industry Hazard ratio Isoniazid Acetylation Vitamins Pyridoxine medicine.disease Vitamin B 6 Phenotype Treatment Outcome Infectious Diseases Dietary Supplements Immunology Female Vitamin B 6 Deficiency business medicine.drug |
| Zdroj: | The International Journal of Tuberculosis and Lung Disease. 18:27-33 |
| ISSN: | 1815-7920 1027-3719 |
| DOI: | 10.5588/ijtld.13.0375 |
| Popis: | SETTING: Human immunodeficiency virus (HIV) infection and treatments for HIV infection and tuberculosis (TB) are associated with the risk of developing sensory polyneuropathy (SPN). Vitamin B6 and genetically determined slow isoniazid (INH) acetylation are believed to play key roles in the development of SPN in a TB treatment setting. OBJECTIVE: To investigate slow acetylation and risk factors for SPN in HIV-infected patients receiving TB treatment, and establish vitamin B6 status and its association with SPN. METHODS: HIV-infected in-patients were prospectively assessed after initiating TB treatment and vitamin B6 supplementation, and monthly during hospitalisation. SPN was defined as ≥1 symptom plus ≥1 sign. NAT2 genotyping predicted acetylation status, and plasma high performance liquid chromatography estimated vitamin B6 status. A survival analysis estimated hazard ratios (HRs) for SPN during TB treatment. RESULTS: Of 116 participants, 56% had SPN at study entry. Participants developed SPN at a rate of 26/100 person-months (95%CI 18-35) during TB treatment, which was independently associated with slow acetylation (HR 2.5; 95%CI 1.1-5.9), as well as black race, previous TB and extra-pulmonary/disseminated TB. Vitamin B6 status was normal, irrespective of SPN. CONCLUSIONS: Risk factors for SPN suggest a multi-factorial pathogenesis related to INH and other potential nervous system insults. SPN developed despite normal vitamin B6 status, suggesting other mechanisms of injury. |
| Databáze: | OpenAIRE |
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