CD4 Count and Routine Laboratory Parameters in Neurological Manifestations of HIV: A Secondary Analysis of Their...

Background Neurological manifestations are a significant cause of morbidity among individuals living with HIV. In many clinical settings, particularly where access to advanced neuroimaging and cerebrospinal fluid diagnostics is limited, risk stratification often relies on CD4 count and routinely available laboratory parameters. In clinical practice, these parameters are frequently used as surrogate indicators of disease severity; however, their role as triage tools for identifying neurological involvement remains uncertain. This study evaluated whether CD4 count and routine laboratory parameters (haematological, renal, and hepatic) are independently associated with the presence of neurological manifestations in HIV-infected adults. A secondary objective was to assess their ability to distinguish between infectious and non-infectious neurological aetiologies. Methodology We performed a hypothesis-driven secondary analysis of a prospective observational cohort study conducted at a tertiary care teaching hospital in India between June 2016 and July 2017. Adults with confirmed HIV infection were evaluated for neurological manifestations based on clinical assessment, neuroimaging, and cerebrospinal fluid findings. CD4 count and routinely available laboratory parameters, including haemoglobin, total leucocyte count, renal and hepatic functions (aspartate and alanine aminotransferase and bilirubin), and serum sodium, were analysed. Multivariable logistic regression adjusted for age, sex, and antiretroviral therapy status was used to assess independent associations. Model discrimination was evaluated using receiver operating characteristic (ROC) curve analysis. Primary and subgroup analyses assessed neurological and infectious versus non-infectious outcomes. Results Among 100 adults with HIV infection, neurological manifestations were present in 44 (44%) patients. Of these, 27 (61.4%) were opportunistic central nervous system infections, while 17 (38.6%) were non-infectious neurological diagnoses. Mean CD4 count did not differ significantly between patients with and without neurological involvement (100.27 ± 48.20 vs. 102.00 ± 44.28 cells/µL; p = 0.85). Similarly, routinely measured haematological, renal, and hepatic parameters were not independently associated with neurological manifestations (all p > 0.05). In contrast, on multivariable analysis within the neurological subgroup, lower CD4 count was independently associated with infectious etiology (adjusted odds ratio = 4.30 per 50-cell decrease; 95% confidence interval = 1.18-15.63; p = 0.027). ROC analysis demonstrated poor discrimination for predicting overall neurological involvement (area under the curve (AUC) = 0.60), but moderate discriminative ability for distinguishing infections from non-infectious aetiologies (AUC = 0.73). Conclusions CD4 count was not an independent predictor of overall neurological involvement in adults living with HIV, although it remained significantly associated with infectious neurological aetiologies. Therefore, CD4 count reflects the degree of immunosuppression but may not be sufficient as a standalone triage marker for overall neurological involvement. Routine laboratory parameters have limited discriminating value for neurological risk certification when used in isolation. These findings highlight the need for a more integrated clinical approach rather than reliance on single laboratory markers, particularly in resource-constrained settings.