Date Published: April 17, 2012
Publisher: Hindawi Publishing Corporation
Author(s): Olajumoke Oshinaike, Akinsegun Akinbami, Oluwadamilola Ojo, Anthonia Ogbera, Njideka Okubadejo, Frank Ojini, Mustapha Danesi.
Background. Sensory neuropathy (SN) is one of the most common AIDS-associated neurologic disorders especially in the era of highly active antiretroviral therapy (HAART). The aim of this study was to determine the prevalence of SN among highly-active-antiretroviral-therapy- (HAART-) experienced and HAART-naïve HIV-positive individuals and to investigate the relationship to demographic, clinical, and laboratory factors. Methods. 323 patients with HIV infection (142 on HAART and 181 HAART naïve) were enrolled in a cross-sectional neuropathy screening program. Data was collected using structured questionnaires which contained the brief peripheral neuropathy screening tool of AIDS Clinical Trial Group protocol. Neuropathy was defined by the presence of at least 1 clinical sign in a distal, symmetrical pattern. Patients were classified as symptomatic if they described aching, stabbing, or burning pain, paresthesia, or numbness in a similar distribution. Demographic, clinical, and laboratory details were documented as risk factors. Result. The prevalence of sensory neuropathy was 39.0% (126/323), (of which 29/126 (23%)) were symptomatic. Amongst those on HAART, 60/142 (42.3%) had SN compared to 66/181 (36.5%) HAART-naïve individuals (P = 0.29). On multivariate analyses, the independent associations with SN were increasing age (P = 0.03) and current exposure to stavudine (P = 0.00). Gender (P = 0.99) height (P = 0.07) use of HAART (P = 0.50), duration of HAART treatment (P = 0.10), and lower CD4 count (P = 0.12) were not associated with an increased SN risk.
Conclusion. HIV SN remains common despite improved immunologic function associated with HAART and decreased neurotoxic HAART use. In this cross-sectional analysis, age and stavudine-based therapies were the independent risk factors.
Peripheral neuropathy is common at all stages of human immunodeficiency virus (HIV) infection and causes considerable morbidity. The manifestations include focal mononeuropathies (particularly cranial neuropathies) polyneuropathies such as the inflammatory demyelinating polyneuropathies (acute, subacute, and chronic subtypes), and sensory neuropathy, which is the most common. In the pre-HAART era, HIV sensory neuropathy (HIV-SN) was documented in as high as 35% of patients with AIDS . With the advent of HAART, the prevalence has increased, a situation partially attributable to the emergence of antiretroviral-induced toxic neuropathy, particularly with the nucleoside analogue reverse transcriptase inhibitors (NRTIs) [2, 3].
This cross-sectional study on the burden of HIV-sensory neuropathy has added to existing body of evidence that HIV-SN occurs frequently in people with HIV/AIDS, with a frequency of 39% overall and 36.5% on cases on HAART. Recent estimates of HIV-SN prevalence among cohorts with access to HAART ranges from 20 to 50% irrespective of whether there is additional risk such is conferred by the use of established neurotoxic antiretroviral drugs [11, 12]. Also, available evidence suggests that HIV-SN prevalence remains high among HAART-treated patients, even in regions where known neurotoxic antiretroviral drugs such as stavudine are no longer commonly used . In this study, only 12/323 cases were on stavudine-based HAART suggesting that other risk factors should be considered and the aetiology of HIV-SN is clearly beyond that attributable to use of neurotoxic HAART. Host genotype has been associated with HIV-SN risk among neurotoxic HAART-exposed patients in several groups. Consistent with pathogenic mechanisms of HIV-SN, the associations include mitochondrial haplogroups and genes associated with inflammation. Associations with hemochromatosis gene polymorphisms have also been reported [13, 14].
This study has confirmed the high prevalence of SN in HIV/AIDS patients on HAART. SN persists despite improved immunologic function associated with HAART and decreased neurotoxic HAART use. With these high prevalent rates and majority experiencing debilitating neuropathic pain, HIV-SN represents a huge and potentially worsening source of world morbidity. There is need to develop more effective preventative strategies and treatments to control the symptoms associated with existing cases of HIV-SN.