Liver steatosis and fibrosis in people with human immunodeficiency virus in West Africa and the relationship with hepatitis B virus coinfection.

There is a heavy burden of liver disease in West Africa. While the role of hepatitis B virus (HBV) infection is well recognized, less is known about the contributing role of liver steatosis and how the two interact in the context of human immunodeficiency virus (HIV) infection. Adults with HIV in Ghana underwent FibroScan measurements to determine prevalence of liver steatosis (expressed as controlled attenuation parameter [CAP]) and fibrosis (expressed as liver stiffness [LS]). We explored contributing factors in linear regression models, including demographics, lifestyle characteristics, medical history, HIV and HBV status, and measurements of metabolic syndrome. Among 329 adults (72.3% women; median age, 47 years), 322 (97.9%) were on antiretroviral therapy (median duration, 8.9 years). CD4 counts were preserved (median, 619 cells/mm3 ); plasma HIV RNA was fully suppressed in 162 (50.3%) of the treated participants. Cigarette smoking, excessive alcohol consumption, and use of traditional or herbal remedies were uncommon (6.1%, 1.8%, 3.3%, respectively). Largely undiagnosed metabolic syndrome was detected in 87 (26.4%) participants. We obtained readings indicative of ≥S2 steatosis and ≥F2 fibrosis in 43 (13.1%) and 55 (16.7%) participants, respectively. Higher CAP values were associated with metabolic syndrome and longer prior stavudine exposure. Higher LS values were associated with male sex, higher HIV RNA, and higher CAP values. Relative to people without HBV, those with HBV (n = 90) had a similar prevalence of ≥S2 steatosis but a higher prevalence of ≥F2 fibrosis (36.7% vs. 9.2%, p < 0.0001) and concomitant ≥S2 steatosis and ≥F2 fibrosis (9.1% vs. 1.3%, p < 0.001). Conclusion: Both HBV and liver steatosis pose a threat to long-term liver health among people with HIV in West Africa. Urgently required interventions include improving HIV suppression and diagnosing and managing determinants of the metabolic syndrome.

No Effect of Coenzyme Q10 on Cognitive Function, Psychological Symptoms, and Health-related Outcomes in Schizophrenia and Schizoaffective Disorder: Results of a Randomized, Placebo-Controlled Trial.

BACKGROUND: Cognitive impairments, negative symptoms, affective symptoms, and low energy are highly prevalent features of schizophrenia. Mitochondrial dysfunction has been hypothesized as one of the numerous factors to underlie the manifestation of these symptoms. The objective of this study was to evaluate whether Coenzyme Q10 (CoQ10) has a role in the treatment of schizophrenia and schizoaffective disorder. METHODS: A double-blind, randomized, placebo-controlled trial was conducted to assess the effects of CoQ10 supplementation (300 mg/day) on the co-primary outcomes of attention and working memory performance after 3 and 6 months. Secondary outcomes included plasma CoQ10 levels, mitochondrial function, energy, depression, anxiety, negative symptoms, and quality oflife. FINDINGS: In total, 72 patients were randomized to intervention groups. Overall, there was no effect of CoQ10 supplementation on the primary outcome measures at 3 or 6 months. Further, with the exception of plasma CoQ10 levels, CoQ10 supplementation also had no effect on the secondary outcomes. At 3 months, CoQ10 concentration was significantly higher in the CoQ10 group (3.85 µg/mL) compared with placebo (1.13 µg/mL); this difference was not present at 6 months. CONCLUSIONS: The results of the study suggest that CoQ10 supplementation at 300 mg/day for 6 months is unlikely to be beneficial for cognitive, psychological and health-related outcomes in schizophrenia and schizoaffective disorder. However, a number of limitations including low adherence, modest sample size, and attrition, likely reduce estimates of effects. As such, results should be considered preliminary.