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
]. 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 [12
]. 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
Considering the persisting risk of HIV-SN despite optimizing therapy for HIV, we explored the determinants of occurrence of HIV-SN and found one nonmodifiable independent predictor, that is, advancing age above 40 years, and most importantly, a modifiable risk factor, that is, the use of stavudine-based therapy. Gender, height, lower CD4 count, use of HAART, and duration on HAART were not associated with increased risk. Ellis in the Central Nervous System HIV Antiretroviral Therapy Effects Research (CHARTER) study [10
] had documented lower nadir CD4 count and the use of HAART, in addition to advancing age, as risk factors. He speculated that HAART is neurotoxic as it was associated with higher SN prevalence. Maritz and colleagues also documented use of HAART in addition to age as risk factors of SN.
Age has remained a consistent independent risk factor in almost every published cohort, both before and after the introduction of HAART [15
]. This is consistent with the known vulnerability of the aging peripheral nervous system to most types of polyneuropathies, HIV-SN inclusive. Height has also been identified as a risk factor for sensory neuropathy in HIV infection on HAART. The pathology involves a length-dependent degeneration of both small and large peripheral nerve fibers making taller individuals more prone to the development of SN. Cherry et al. [18
] had documented that the risk of HIV-SN was 65% higher among the older (>40 years) and taller (>170
cm) HIV patients exposed to stavudine. They proposed that age and height measurements represent an effective way of identifying individuals at higher risk for neuropathy and prioritizing them to alternative HAART therapy rather than neurotoxic HAART. Height was not found to be an independent risk factor in this study probably due to the small number of patients that were above 1.7
Previously reported literature assessing immune status and HIV-SN is mixed, with some reports linking neuropathy to increased viral load levels, while others have reported no relationship. Several studies from the highly active antiretroviral therapy (HAART) era show a lack of association between distal painful sensorimotor polyneuropathy and the degree of immunosuppression, including low CD4 counts and high HIV viral load [19
]. Morgello and colleagues speculate that this difference in findings may relate to a difference in patient populations. Other reasons may include residual axonal injury even with restoration of immune function, immune reconstitution disorders or even the presence of other confounding neurotoxins such as nutritional or vitamin deficiencies. Also the association between neuropathic pain and a higher CD4 nadir may suggest that a functional immune system may contribute to the stimulation of pain.
Limitations of our study include a cross-sectional design as a longitudinal follow-up would provide further insight into the incidence of HIV-SN in Nigerians. Furthermore, the nonavailability of electrophysiological studies limited diagnostic accuracy.