Potential for Riboflavin in minimizing adverse effects associated with the use of Nucleoside Reverse Transcriptase Inhibitors

Abstract

Background: Nucleoside analogues represent the cornerstone of antiretroviral regimens, but their long-term use is associated with a range of deleterious effects. However, due to their potency and cost-effectiveness compared to other antiretroviral agents, strategies to minimise the toxicities should be explored.

Objective: To investigate the influence of riboflavin in minimising adverse effects induced by nucleoside analogue reverse transcriptase inhibitors.

Method: Adult Swiss albino mice weighing between 28-30 g were orally given stavudine, lamivudine and riboflavin alone and in various dose combinations calculated on weight basis with reference to 70kg normal human dose: In absence of fatality/toxicity drugs were given at three dose levels for up to four months. Blood glucose was assessed periodically, followed by animal sacrifice after four months or earlier if signs of toxicity manifested, and blood was collected by cardiac puncture. Lipid and haematological profiles were measured. Categorical variables were summarised using proportions, means, standard deviations, and 95% upper and lower limits. One-way ANOVA was used in the data analysis.

Results: Elevated blood glucose levels, prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT) accompanied by deranged lipid profiles were noted in the stavudine and stavudine plus lamivudine treated groups given at standard and double standard doses. The adipose tissue content ranged from diminished to totally depleted in stavudine- and stavudine plus lamivudine-treated groups given at standard and double standard dose levels, respectively. Skin wounds, rashes, red eyes, and pale liver were noted in mice treated with stavudine or stavudine plus lamivudine standard doses. Riboflavin was found to protect against these derangements.

Conclusion: Riboflavin has a protective effect against adverse effects associated induced by stavudine and lamivudine.