Abstract

HIV-associated sensory neuropathy (HIV-SN) remains common in HIV patients receiving anti- retroviral therapy (ART). Neuropathies resulting from HIV infection itself and toxic side effects of ART have similar presentations and include neuropathic pain, tingling and numbness. Some nucleoside analogue reverse transcriptase inhibitors used to treat HIV were strongly associated with HIV-SN. The prevalence of HIV-SN in patients receiving stavudine at Cipto Mangunkusumo Hospital was 34% and had strong association with age and height. As stavudine has been phased out recently, some patients still have HIV-SN. In 2016, the prevalence of HIV-SN had been significantly reduced became 14.2% and associated factors was viral load >500 copies HIV RNA/mL. It is an evidence that lack of stavudine exposure is central to the lower neuropathy prevalence. One of clinical manifestation of HIV-SN is neuropathic pain. Neuropathic pain can be found as solely symptom without other sensory neuropathy symptoms (numbness) and signs (decreased physiological reflex and vibration). Prevalence of neuropathic pain (NP) of HIV patients was 6.6% at Cipto Mangunkusumo Hospital, smaller than HIV-SN. Our study showed that HIV patients with NP had shorter duration of ART than patients with HIV-SN, and may be an early symptom of small fiber neuropathy in HIV patients. Some evidences indicate that HIV-SN is immune-mediated. Intra-epidermal fiber density of HIV-SN patients is lower than HIV-noSN and healthy control. Low fiber density in HIV-SN seems to be corelated with low nadir CD4+ counts. CD14+ macrophages were evident at surrounding intra-epidermal nerve of HIV-SN and HIV-noSN patients. Some chemokine receptors such as CX3CR1, CCR2 and CCR5 was more common in HIV-SN patients. These evidences showed that inflammatory macrophages expressing chemokine receptors may participate in peripheral nerve damage leading to HIV-SN in HIV patients treated without stavudine.

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