Plasma and Breast Milk Pharmacokinetics of Tenofovir Disoproxil Fumarate in Nursing Mother with Chronic Hepatitis B-Infant Pairs.

Tenofovir use is associated with lower risk of mother-to-infant transmission of the virus, and discontinuation of the treatment is not safe. However, the safety of the drug during pregnancy and breastfeeding is not clear. In this study, we aimed to determine the tenofovir concentration in plasma of mother-infant pairs along with breast milk in chronic hepatitis B patients during the lactation period. A total of 11 mother-infant pairs were enrolled in the study. All the mothers received tenofovir disoproxil fumarate (TDF) 245 mg/day for at least 1 month because of chronic hepatitis B infection. Maternal blood, breast milk, and infant blood samples were obtained concomitantly. Tenofovir concentrations were determined by liquid chromatography-tandem mass spectrometry. The median concentrations of tenofovir in maternal plasma and breast milk samples were 88.44 (interquartile range [IQR], 62.47 to 116.17) ng/ml and 6.69 (IQR, 4.88 to 7.03) ng/ml, respectively. Tenofovir concentrations were undetectable (<4 ng/ml) in all of the infant plasma samples. The ratio of tenofovir concentration in breast milk to that in maternal plasma was 0.07. Tenofovir disoproxil fumarate passes through the breast milk in a small amount. Infants had no detectable tenofovir level in their plasma. Our study suggests that tenofovir disoproxil fumarate treatment is safe during the breastfeeding period in chronic hepatitis B patients.

A potential role for nitric oxide pathway in tuberculous pleural effusion.

SETTING: Tuberculous pleural effusion leads to an immune response involving mainly immune and mesothelial cells. Nitric oxide (NO) produced by these cells may have antimycobacterial effects against Mycobacterium tuberculosis. OBJECTIVE: To investigate the possible role of NO in connection with the arginase enzyme, which controls the synthesis of NO through arginine depletion. DESIGN: Pleural fluid samples from 20 patients with tuberculous pleural effusion were used for arginase activity and NO level determination. Results were compared with those from 12 lung cancer, 12 pneumonia and 12 congestive heart failure (CHF) patients. RESULTS: Pleural arginase activity in tuberculosis patients was found to be significantly decreased compared to lung cancer and pneumonia groups, while the NO level was higher in tuberculosis patients. All groups except the CHF group had significant correlations between NO level and white blood cell count. Arginase activity and red blood cell count correlated significantly in lung cancer and CHF groups. CONCLUSION: The arginine-NO pathway seems to be involved in the pathogenesis of tuberculous pleural effusion. Decreased arginase activity may cause arginine accumulation, which may then lead to increased NO synthesis by immune and mesothelial cells, reflecting a host defence mechanism.