Isoniazid exposure and pyridoxine levels in human immunodeficiency virus associated distal sensory neuropathy.

Autor:	van der Watt JJ; Division of Neurology, Department of Medicine, University of Cape Town, Observatory, South Africa., Benatar MG; Departments of Neurology and Public Health Sciences, University of Miami, Miami, Florida, USA., Harrison TB; Department of Neurology, Emory University, Atlanta, Georgia, USA., Carrara H; School of Public Health and Family Medicine, University of Cape Town, Observatory, South Africa., Heckmann JM; Division of Neurology, Department of Medicine, University of Cape Town, Observatory, South Africa.
Jazyk:	angličtina
Zdroj:	The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease [Int J Tuberc Lung Dis] 2015 Nov; Vol. 19 (11), pp. 1312-9.
DOI:	10.5588/ijtld.15.0467
Abstrakt:	Setting: Distal sensory polyneuropathy (DSP) may manifest in human immunodeficiency virus (HIV) infected individuals before or after antiretroviral therapy (ART). DSP can also occur in response to isoniazid (INH); this can be prevented by pyridoxine supplementation. N-acetyltransferase 2 (NAT2) polymorphisms influence drug acetylation and possibly the risk for INH-associated DSP. Objective: To investigate the relationship between previous/current TB, pyridoxine deficiency and DSP in HIV-infected individuals enrolled in a government-sponsored HIV programme. Design: Neuropathy assessments were performed among 159 adults pre-ART and 12 and 24 weeks thereafter. DSP was defined as ⩾1 neuropathic symptom and sign. NAT2 genotypes predicted acetylation phenotype. Serum pyridoxine levels (PLP) were quantified at baseline and week 12. Results: DSP was present in 16% of individuals pre-ART and was associated with previous/current TB (P = 0.020). Over 50% were pyridoxine deficient (PLP < 25 nmol/l), despite supplementation with vitamin B complex supplements (2-4 mg/day pyridoxine). Those with a history of TB and pre-ART DSP were more likely to be pyridoxine deficient (P = 0.029), and slow/intermediate NAT2 phenotypes impacted on their PLP levels. Incident/worsening DSP after ART developed in 21% of the participants. PLP levels remained low after ART, particularly among those with prior TB, but without an association between DSP or NAT2 phenotypes. Conclusion: Adequate pyridoxine supplementation before ART initiation should be prioritised, particularly in those with a history of TB or current TB.
Databáze:	MEDLINE
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