HIV-associated sensory neuropathy (HIV-SN) is a common, and frequently painful complication of HIV, but factors that determine the presence of pain are unresolved. We investigated: (i) if psychological factors associated with painful (n = 125) versus non-painful HIV-SN (n = 72), and (ii) if pain and psychological factors affected quality of life (QoL). We assessed anxiety and depression using the Hopkins Symptoms Checklist-25. Pain catastrophizing and QoL were assessed using the Pain Catastrophizing Scale and Euroqol-5D, respectively. Presence of neuropathy was detected using the Brief Neuropathy Screening Tool, and pain was characterised using the Wisconsin Brief Pain Questionnaire. Overall, there was a high burden of pain, depression and anxiety in the cohort. None of the psychological variables associated with having painful HIV-SN. Greater depressive symptoms and presence of pain were independently associated with lower QoL. In those participants with painful HIV-SN, greater depressive symptom scores were associated with increased pain intensity. In conclusion, in a cohort with high background levels of psychological dysfunction, psychological factors do not predict the presence of pain, but both depression and presence of pain are associated with poor quality of life.

Background Sensory neuropathy (SN) is a common and often painful neurological condition associated with HIV‐infection and its treatment. However, data on the incidence of SN in neuropathy‐free individuals initiating combination antiretroviral therapies (cART) that do not contain the neurotoxic agent stavudine are lacking. Aims We investigated the 6‐month incidence of SN in ART naïve individuals initiating tenofovir (TDF)‐based cART, and the clinical factors associated with the development of SN. Methods 120 neuropathy‐free and ART naïve individuals initiating cART at a single center in Johannesburg, South Africa were enrolled. Participants were screened for SN using clinical signs and symptoms at study enrolment and approximately every 2‐months for a period of ~6‐months. Diagnostic criteria for symptomatic SN was defined by the presence of at least one symptom (pain/burning, numbness, paraesthesias) and at least two clinical signs (reduced vibration sense, absent ankle reflexes or pin‐prick hypoaesthesia). Diagnostic criteria for asymptomatic SN required at least two clinical signs only (as above). Results A total of 88% of the cohort completed three visits within the 6‐month period. The 6‐month cumulative incidence of neuropathy was 140 cases per 1000 patients (95% CI: 80‐210) at an incidence rate of 0.37 (95% CI: 0.2‐0.5) per person year. Height and active tuberculosis (TB) disease were independently associated with the risk of developing SN (P < .05). Interpretation We found that within the first 6 months of starting cART, incident SN persists in the post‐stavudine era, with 11 (9%) of individuals developing asymptomatic SN, and 9 (8%) developing symptomatic SN.

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HIV-associated sensory neuropathy (HIV-SN) is a disabling complication of HIV disease and antiretroviral therapies (ART). Since stavudine was removed from recommended treatment schedules, the prevalence of HIV-SN has declined and associated risk factors have changed. With stavudine, rs1799964*C (TNF-1031) associated with HIV-SN in Caucasians and Indonesians but not in South Africans. Here, we investigate associations between HIV-SN and rs1799964*C and 12 other polymorphisms spanning TNF and seven neighboring genes (the TNF-block) in Indonesians (n = 202; 34/168 cases) and South Africans (n = 75; 29/75 cases) treated without stavudine. Haplotypes were derived using fastPHASE and haplotype networks built with PopART. There were no associations with rs1799964*C in either population. However, rs9281523*C in intron 10 of BAT1 (alternatively DDX39B) independently associated with HIV-SN in Indonesians after correcting for lower CD4 T-cell counts and >500 copies of HIV RNA/mL (model p = 0.0011, Pseudo R 2 = 0.09). rs4947324*T (between NFKBIL1 and LTA) independently associated with reduced risk of HIV-SN and shared haplotype 1 (containing no minor alleles) associated with increased risk of HIV-SN after correcting for greater body weight, a history of tuberculosis and nadir CD4 T-cell counts (model: p = 0.0003, Pseudo R 2 = 0.22). These results confirm TNF-block genotypes influence susceptibility of HIV-SN. However, critical genotypes differ between ethnicities and with stavudine use.

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HIV-associated sensory neuropathy (HIV-SN) is a common and often painful neurological condition associated with HIV-infection and its treatment. However, data on the incidence of HIV-SN in neuropathy-free individuals initiating combination antiretroviral therapies (cART) that do not contain the neurotoxic agent stavudine are lacking. We investigated the six-month incidence of HIV-SN in ART naïve individuals initiating tenofovir (TDF)-based cART, and the clinical factors associated with the development of HIV-SN. 120 neuropathy-free and ART naïve individuals initiating cART at a single centre in Johannesburg, South Africa were enrolled. Participants were screened for HIV-SN at study enrolment and then approximately every two- months for a period of approximately six-months. Symptomatic HIV-SN was defined by the presence of at least one symptom (pain/burning, numbness, paraesthesias) and at least two clinical signs (reduced vibration sense, absent ankle reflexes or pin- prick hypoaesthesia). Asymptomatic HIV-SN required at least two clinical signs only. A total of 88% of the cohort completed three visits within the six-month period. Eleven individuals developed asymptomatic HIV-SN and nine developed symptomatic HIV-SN, giving a six-month cumulative incidence of neuropathy of 140 cases per 1000 patients (95% CI: 80 - 210) at an incidence rate of 0.37 (95% CI: 0.2 - 0.5) per person year. Increasing height and active tuberculosis (TB) disease were independently associated with the risk of developing HIV-SN (p << 0.05). We found that within the first six months of starting cART, incident SN persists in the post- stavudine era, but may be asymptomatic.

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