Assessment of serum soluble intercellular adhesion molecule-1 and albumin in human immuno-deficiency virus-infected individuals with or without malaria parasite infection in Nauth, Nnewi, Nigeria
DOI:
https://doi.org/10.18203/2320-6012.ijrms20240196Keywords:
HIV, Malaria, Co-infection, Bystander effects and Inflammation, Endothelial dysfunction, Borderline hypertension/PrehypertensionAbstract
Background: Human immunodeficiency virus (HIV) co-infection with malaria is the main cause of morbidity and mortality in developing countries, including Nigeria. Both infections have impact on the disease severity and progression.
Methods: This was a cross-sectional study aimed to determine the serum soluble intracellular adhesion molecule-1 (sICAM-1) and albumin in HIV/malaria-infected individuals attending the antiretroviral therapy (ART) clinic at Nnamdi Azikiwe Teaching Hospital, (NAUTH) Nnewi, Nigeria. 168 randomly selected individuals aged 18-65 years grouped into 42 HIV-infected individuals on ART, 42 HIV-malaria c-o-infected individuals on ART, 42 malaria-infected individuals, and 42 apparently healthy individuals (control) were included in the study. Serum sICAM-1 and albumin were determined using enzyme linked immunosorbent assay (ELISA) and bromocresol green technique respectively while CD4 T-cell count was obtained from the patients’ records.
Results: The mean serum sICAM-1, albumin and systolic blood pressure (SBP) levels were significantly higher in HIV individuals with and without malaria infection when compared with control participants (p<0.05) respectively. The mean CD4 T-cell count was significantly lower in HIV/malaria co-infected individuals when compared with HIV infected individuals (p <0.05). A significant negative correlation was observed between CD4 count and sICAM-1 both in HIV infected individuals and HIV-malaria co-infection (p<0.05).
Conclusions: The increased sICAM-1, SBP with decreased albumin levels suggests inflammatory and vascular changes with reduced hepatic synthesis which may result in endothelial dysfunction, adverse cardiovascular conditions, and disease progression.
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References
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