Serum levels of antioxidant vitamins and mineral elements of human immunodeficiency virus positive subjects in Sokoto, Nigeria

Background: Undernourishment and micronutrient deficiencies exacerbate immunosuppression, oxidative stress, acceleration of human immunodeficiency virus (HIV) replication and CD4 T-cell depletion in HIV-infected individuals.Materials and Methods: The current work reports the serum levels of antioxidant vitamins (vitamins A, C and E) and minerals (Zn, Fe, Cu) in 90 HIV positive subjects attending the Usmanu Danfodiyo University Teaching Hospital (UDUTH), Sokoto, Nigeria. The serum levels of the micronutrients were correlated with the CD4 count of the subjects.Results: The results showed that the HIV positive subjects have  significantly lower (P 0.05) difference. Vitamins A, E and C and Zn and Fe showed positive correlation with CD4 count of the HIV positive subjects.Conclusion: The results suggest that the HIV subjects in the study area have lowered serum levels of antioxidant micronutrients and that the levels decrease with increase in the severity of the infection. These may increase the chances of the symptomatic and asymptomatic subjects progressing into full-blown Acquired Immunodeficiency Syndrome

Potential protective effect of sunitinib after administration of diclofenac: biochemical and histopathological drug-drug interaction assessment in a mouse model

Sunitinib is a tyrosine kinase inhibitor for GIST and advanced renal cell carcinoma. Diclofenac is used in cancer pain management. Coadministration may mediate P450 toxicity. We evaluate their interaction, assessing biomarkers ALT, AST, BUN, creatinine, and histopathological changes in the liver, kidney, heart, brain, and spleen. ICR mice (male, n = 6 per group/dose) were administered saline (group A) or 30 mg/kg diclofenac ip (group B), or sunitinib po at 25, 50, 80, 100, 140 mg/kg (group C) or combination of diclofenac (30 mg/kg, ip) and sunitinib (25, 50, 80, 100, 140 mg/kg po). Diclofenac was administered 15 min before sunitinib, mice were euthanized 4 h post-sunitinib dose, and biomarkers and tissue histopathology were assessed. AST was 92.2 ± 8.0 U/L in group A and 159.7 ± 14.6 U/L in group B (p < 0.05); in group C, it the range was 105.1-152.6 U/L, and in group D, it was 156.0-209.5 U/L (p < 0.05). ALT was 48.9 ± 1.6 U/L (group A), 95.1 ± 4.5 U/L (p < 0.05) in group B, and 50.5-77.5 U/L in group C and 82.3-115.6 U/L after coadministration (p < 0.05). Renal function biomarker BUN was 16.3 ± 0.6 mg/dl (group A) and increased to 29.9 ± 2.6 mg/dl in group B (p < 0.05) and it the range was 19.1-33.3 mg/dl (p < 0.05) and 26.9-40.8 mg/dl in groups C and D, respectively. Creatinine was 5.9 pmol/ml in group A; 6.2 pmol/ml in group B (p < 0.01), and the range was 6.0-6.2 and 6.2-6.4 pmol/ml in groups C and D, respectively (p < 0.05 for D). Histopathological assessment (vascular and inflammation damages) showed toxicity in group B (p < 0.05) and mild toxicity in group C. Damage was significantly lesser in group D than group B (p < 0.05). Spleen only showed toxicity after coadministration. These results suggest vascular and inflammation protective effects of sunitinib, not shown after biomarker analysis