ABSTRACT
Both HIV and Tuberculosis infections are associated with lipid peroxidation and antioxidant imbalance. The Pathology of the two diseases produced free radicals which lead to lipid peroxidation indices one of which is Malondialdehyde (MDA) and to disease progression due to CD4 cells apoptosis. The current study was carried out with the objective of determining Serum MDA, Vitamin E, CD4, CD8 and lipid peroxidation index (LPI) in four different subgroups comprising of HIV, Tuberculosis and HIV/TB co-infected patients and the Controls respectively with a view to assessing the interaction between oxidants and antioxidants in the course of HIV/TB co-infection. Lipoperoxides, as Malondialdehyde by thiobarbituric acid reaction and Vitamin E in serum from all the four subgroups were measured spectrophotometrically. Lipid Peroxidation Index (LPI) was determined by obtaining the ratio of MDA and Vitamin E in these cohorts, while CD4 and CD8 cells count was obtained by flowcytometry. A total of 186 [HIV/TB co-infected patients, 44 (23.66%); HIV patients 57 (30.64%); Tuberculosis patients 44 (23.66%) and apparently normal controls 41 (22.04%)] were evaluated in this study. There were 105 men (56.5%) and 81 women (43.5%). The median values were compared among the four subgroups. Results showed the following patients/controls median values respectively for 1. MDA (HIV/TB co-infection = 3.81 umol/l, HIV patients = 4.60 umol/l, Tuberculosis patient = 3.73 umol/l vs 0.55 umol/l for controls), 2. CD4 (HIV/TB co-infection =200.5 cell/mm3, HIV patients = 356.0 cell/mm3, Tuberculosis patient = 571.0 cell/mm3 vs 743.0 cell/mm3 for controls), 3. Vitamin E (HIV/TB co-infection = 3.85 ug/mL, HIV patients = 7.99 ug/mL, Tuberculosis patient = 8.29 ug/mL vs 18.65 ug/mL for controls) and 4. LPI (HIV/TB co-infection = 0.99, HIV patients = 0.58, Tuberculosis patient = 0.45 vs 0.03for controls). The differences viii between patients and controls were statistically significant (p<0, 05). There was a negative correlation between CD4 counts and MDA levels (rho = -0.144, p= 0.350); duration of treatment and MDA level (rho = -0.003, p=0.985) and Vitamin E concentration and CD4 cell counts (rho= - 0,144; p>0, 05) in the HIV/TB co-infection group. The estimated reference limits for MDA (0.025 and 0.975 fractals) were: HIV =1.99 μmol/L - 10.16 μmol/L; TB=1.55 μmol/L - 7.26 μmol/L; HIV/TB co-infection = 4.22 μmol/L - 4.57μmol/L and normal controls = 1.06 μmol/L - 3.29μmol/L lower and upper limits respectively. The higher MDA result from the subjects supports the assertion that HIV/TB co-infection is associated with increased lipid peroxidation and lower antioxidant potential. It can therefore be concluded that co-infection with Tuberculosis exacerbates oxidative stress in HIV patients, while treatment enhances their anti-oxidant status and ameliorates the oxidative stress.