As the roll-out of antiretroviral therapy continues to drive downwards morbidity and mortality in people living with HIV/AIDS (PLWHAs), organ toxicities (especially the liver) are frequently becoming a major concern for researchers, scientists and healthcare planners.This study was conducted to investigate the possible protective effect of Hypoxis hemerocallidea (AP) against highly active antiretroviral therapy (HAART)-induced hepatotoxicity. A total of 63 pathogen-free adult male Sprague-Dawley rats were divided into 9 groups and treated according to protocols.While no mortality was reported, animals treated with adjuvant HAART and AP recorded least% body weight gain. Significant derangements in serum lipid profiles were exacerbated by treatment of with AP as LDL (increased p < 0.03), triglycerides (increased p < 0.03) with no change in total cholesterol levels. Adjuvant AP with HAART caused reduction in LDL (p < 0.05 and 0.03), increased HDL (p < 0.05) and TG (p < 0.05 and 0.001 for AP100 and AP200 doses respectively). Markers of liver injury assayed showed significant increase (p < 0.003, 0.001) in AST in AP alone as well as HAART+ vitamins C and E groups respectively. Adjuvant HAART and AP and vitamins C and E also caused significant declines in ALT and ALP levels. Serum GGT was not markedly altered. Disturbances in histopathology ranged from severe hepatocellular distortions, necrosis and massive fibrosis following co-treatment of HAART with vitamins C and E as well as HAART alone. These results warrant caution on the adjuvant use of AP with HAART by PLWHAs as implications for hepatocellular injuries are suspect with untoward cardiometabolic changes.

Amoebiasis, a disease of worldwide distribution, is endemic in tropical countries with suboptimal sanitation facilities. Isolated amoebic appendicitis (IAA) is regarded as a rare manifestation of the disease globally. Because there are no defined clinical features that distinguish IAA from bacterial appendicitis, diagnosis is usually dependent on histopathological examination. A 9-year retrospective study was undertaken to investigate the clinicopathological aspects of IAA. The main complaints were fever and abdominal pain. None of the patients had dysentery. The pre-operative clinical diagnosis was acute appendicitis and acute abdomen in 13 and 8 patients, respectively. In all cases the intra-operative diagnosis was acute appendicitis. Gross pathological appraisal revealed peritonitis and perforation in 19 and 17 cases, respectively. Histopathological examination of these appendices demonstrated appendiceal ulceration, transmural mixed inflammation, haematophagous amoebic trophozoites and necrosis in all cases. Vascular pathology comprised venous and capillary luminal plugging (11 cases), necrotising small vessel vasculitis (11 cases), thrombophlebitis of medium sized veins (9 cases) and arteritis with associated thrombosis (1 case). Organising fibrinopurulent peritonitis was present in 19 cases. Two appendices that appeared normal macroscopically demonstrated ulceration and inflammation that were confined to the mucosa and submucosa. All of 18 patients who were treated with metronidazole survived without further surgery, while three patients who were untreated succumbed to the disease. Appendicectomy, accurate histopathological appraisal thereof and optimal, timely management of IAA were critical to the favourable outcome in the present study.

Background: There is paucity of literature regarding the nephrotoxicity of antiretroviral drugs and its interaction with plantbased adjuvants. This study investigates the attenuating effect of kolaviron in nevirapine-therapy on the histological structure of the kidneys of adult male Sprague-Dawley rats. Objective: To determine the attenuating influence of anti-oxidant status of kolaviron on the kidneys of experimental animals following nevirapine administration. Methods: Forty eight pathogen-free adult male Sprague-Dawley rats were used for this study. The animals were divided into 8 groups (A-H) with 6 animals in each group. Group A was given normal saline as the control; group B was given nevirapine; group C was given kolaviron; group D was given vitamin C; group E was given nevirapine and kolaviron; group F was given nevirapine and vitamin C; Group G was given nevirapine and kolaviron (kolaviron withdrawn after day 28) and group H was given corn oil. The experiment lasted 56 days after which the animals were sacrificed, blood samples were collected through cardiac puncture for serum analysis and the kidneys were harvested and prepared for H& E histological examination. Results: Nevirapine caused histoarchitectural damage in the glomerular apparatus with resultant increase in kidney/body weight ratio (p<0.001). Adjuvant treatment with kolaviron attenuated these nephrotoxic effects. Serum anti-oxidant enzyme (SOD and CAT) activities were significantly reduced in kolaviron and vitamin C treated animals, whereas in the nevirapine group these parameters were significantly elevated (P<0.05). However, co-administration of nevirapine and vitamin C did not improve the histoarchitecture of the kidney. Conclusion: Adjuvant treatment with kolaviron (an anti-oxidant) for 56 days appears to attenuate the nephrotoxicity of nevirapine in this model. Sci. 2017;17(1): 164-174. https://dx.doi.org/10.4314/ahs.v17i1.21