Hubungan Kadar Viral Load, Cluster Of Differentiation 4 dan Homosistein Serum Terhadap Neuropati Perifer Terkait Human Immunodeficiency Virus

Abstract

Background: Peripheral neuropathy is the most common neurological complication of human immunodeficiency virus infection, with a prevalence of approximately 19–42%. Elevated viral load is associated with an increased risk of peripheral neuropathy, partly through direct and indirect neurotoxic effects on peripheral nerves. Decreased CD4 counts lead to immune dysregulation and macrophage activation, which trigger the release of pro inflammatory cytokines and result in axonal degeneration. Increased serum homocysteine levels, which are frequently observed in HIV infection, can cause neuronal injury through excitotoxicity, oxidative stress, and DNA damage, leading to distal axonal degeneration. Purpose: To determine the association between viral load levels, CD4, and serum homocysteine levels with peripheral neuropathy related to human immunodeficiency virus. Method: This study was an observational analytic study with a cross sectional design conducted 50 HIV patients at Adam Malik Hospital in Medan. Peripheral neuropathy was diagnosed using the Brief Peripheral Neuropathy Screening (BPNS) tool and nerve conduction studies, while serum viral load, CD4 count, and homocysteine levels were measured using real time PCR, flow cytometry, and enzymatic assays, respectively. The associations of viral load, CD4 count, and serum homocysteine levels with HIV associated peripheral neuropathy were analyzed using chi square and Mann–Whitney tests, followed by multivariate logistic regression analysis to obtain odds ratios and 95% confidence intervals. Results: Based on the BPNS, there was a significant association between viral load (p<0.001), CD4 count (p<0.001), and serum homocysteine levels (p<0.001) with peripheral neuropathy. According to nerve conduction studies, there was a significant association between viral load (p=0.003), CD4 count (p=0.018), and serum homocysteine levels (p=0.003) with peripheral neuropathy. With respect to sural nerve amplitude, there was a significant association between viral load (p=0.003), CD4 count (p=0.001), and serum homocysteine levels (p<0.001). In multivariate analysis, only viral load remained significantly associated with peripheral neuropathy as defined by BPNS (p=0.010; OR 9.643; 95% CI 1.722–54.015) and nerve conduction studies (p=0.038; OR 5.361; 95% CI 1.097–26.195). For sural nerve amplitude, viral load (p=0.048; OR 9.629; 95% CI 1.017–91.206) and CD4 count (p=0.037; OR 5.732; 95% CI 1.106–29.691) showed a significant association with abnormal amplitude. Conclusion: Viral load showed the most consistent association with HIV related peripheral neuropathy, based on both BPNS and nerve conduction studies, and together with CD4 was significantly associated with sural nerve amplitude. In the bivariate analysis, CD4 and serum homocysteine were also associated with HIV related peripheral neuropathy.