- Emmanuel Ifeanyi Obeagu
- Department of Biomedical and Laboratory Science, Africa University, Zimbabwe
Sickle cell disease (SCD) and HIV are chronic conditions with overlapping pathophysiological mechanisms that can significantly impact patient outcomes. Vaso-occlusive crises (VOCs), a hallmark of SCD, result from inflammation, endothelial dysfunction, and microvascular occlusion. HIV, through chronic immune activation, endothelial injury, and hematologic alterations, may influence the frequency and severity of VOCs. The interaction between these two diseases creates a complex clinical scenario that warrants further investigation. HIV-induced chronic inflammation and endothelial dysfunction may exacerbate VOCs by increasing oxidative stress, promoting coagulation abnormalities, and altering red blood cell adhesion properties. Additionally, hematologic complications such as anemia and bone marrow suppression due to HIV further complicate SCD progression. While antiretroviral therapy (ART) has improved HIV outcomes, its impact on VOCs remains unclear, with some regimens potentially exacerbating vascular complications while others may reduce systemic inflammation and endothelial damage.