Therapeutic activities of naringenin on efavirenz-induced sleep-like disorder in the midbrain of white albino mice.

OBJECTIVES: Efavirenz, has proven to be effective in suppressing human immunodeficiency virus (HIV) viral load; however, complaints of sleep disorders including hallucination, and insomnia have greatly contributed to non-adherence to antiretroviral therapy. This study aimed at investigating therapeutic activities of naringenin on efavirenz-induced sleep disorder. MATERIALS AND METHODS: Sixty mice were divided into six groups of control, combination antiretroviral therapy (cART), efavirenz, naringenin, naringenin/efavirenz and naringenin/cART. Efavirenz, cART, and naringenin were administered orally and daily at 15 mg/kg, 24 mg/kg and 50 mg/kg, respectively for 28 days. Post neurobehavioral test, oxidative stress, histology and immunohistochemistry for dopamine were carried out after administration process. RESULTS: Efavirenz (P<0.0001) and cART (P<0.01) significantly increased immobility during open field (P<0.01), escape time in seconds (sec) in Morris water maze (P<0.001) and numbers of head-twitch response (HTR) (P<0.0001). Similarly, there was a significant increase in malondialdehyde (MDA) (P<0.0001) and decreased superoxide dismutase (SOD) (P<0.001) and reduced glutathione (GSH) (P<0.001); however, naringenin-treated groups potentiated anti-oxidant function by reducing oxidative stress (P<0.01). Histological evaluation demonstrated severe neurodegeneration, vacuolization and pyknosis in efavirenz and cART compared to naringenin groups. Dopaminergic neurons using immunohistochemial antibody (tyrosine hydroxylase) staining showed poor immunoreactivity in efavirenz and cART in contrast to naringenin groups. CONCLUSION: Efavirenz and cART have the potential of inducing sleep disorder possibly due to their capability to trigger inflammation and deplete dopamine level. However, naringenin has proven to be effective in ameliorating these damages.

Urine methylmalonic acid levels in HIV-infected adults with peripheral neuropathy.

BACKGROUND: Cobalamin deficiency and peripheral neuropathy (PN) are commonly seen in HIV-infected adults. The level of urine methylmalonic acid (UMMA), a reliable indicator of tissue cobalamin status, was determined in HIV infected subjects with and without PN to establish this association. METHODS: One hundred and ninety-eight (198) consenting HIV infected subjects with and without PN were recruited for the study. UMMA level was determined by Cation Exchange High Performance Liquid Chromatography (HPLC) with Ultraviolet detector in 165 subjects. Simple proportions of patients with raised UMMA (defined as value> 3.4 mg in 24hr) were determined for each arm. RESULTS: Among the 198 subjects studied, 146 had PN and 52 had no PN. From the 165 subjects whose UMMA was studied, raised UMMA was found in 76.6% (36 of 47) of subjects with no PN as compared with 53.4% (63 of 118) of those with PN (p=0.018). CONCLUSION: Cobalamin deficiency (measured by UMMA level) even though common in HIV infected subjects, may not be the cause of peripheral neuropathy in these subjects.

Plasma folate studies in HIV-positive patients at the Lagos university teaching hospital, Nigeria.

INTRODUCTION: In various studies globally, the prevalence of anemia in persons with HIV infection range from 10 to 20% at initial presentation, and anemia is diagnosed in 70 to 80% of these patients over the course of HIV disease. The etiology of anemia in this group of patients has not been fully established, thus a need to evaluate the role of plasma folate as a possible etiological factor. OBJECTIVE: This study was set to determine plasma folate levels in newly diagnosed, treatment naïve, HIV-positive patients, and relate this to other hematological changes. MATERIALS AND METHODS: A total of 200 participants were recruited for this study, of which 100 were HIV positive, treatment naive patients who were recruited at the point of registration and 100 were HIV-negative subjects (controls). 5 ml of venous blood was collected and plasma extracted for folic acid estimation by HPLC. A full blood count, CD4 and Viral load were estimated. RESULTS: Mean ages for control and study group were 38 ± 2.3 and 32 ± 1.7 years, respectively. Mean plasma folate concentration among the study group (5.04 µg/l) was significantly lower than that for the control group (15.89 µg/l; P = 0.0002). Prevalence of anemia among the study group was 72% (144 of 200), with a mean hemoglobin (Hb) concentration of 9.5 g/dl compared with mean Hb of 13.0 g/dl among the control group (P = 0.002). Plasma folate correlated positively with CD4 cell count (r = 0.304, P<0.05) and inversely with the viral load (r = -0.566; P<0.05). CONCLUSION: Plasma folate level is a predictor of anemia in early HIV infections.