25-OH Vitamin D Xpress ELISA Kit

Background: Vitamin D (VD) is important in hepatic fibrogenesis in animal models and human studies. VD deficiency is associated with liver fibrosis progression. Metabolic dysfunction of the liver, as an intermediate organ for VD metabolism, contributes partly to this deficiency. We hypothesized that improving hepatic fibrosis and inflammation in chronic hepatitis C (CHC) patients after eradication with direct-acting antivirals (DAA) would increase 25-hydroxyVD [25(OH)VD] levels. Methods: Eighty CHC patients (17 chronic hepatitis, and 63 cirrhosis) were enrolled. Baseline characteristics, hepatitis C viral load (VL), genotypes, liver enzymes and liver stiffness measurements (LSM) were assessed at baseline. Blood samples for 25(OH)VD and the procollagen type III N-terminal peptide (P3NP) were collected at baseline, 24 and 48 weeks. LSMs were re-evaluated at 48 weeks. Serum 25(OH)VD levels < 30 ng/mL were defined as VD insufficiency/deficiency. Pairedt-tests were used for statistical analyses. Results: Among 80 patients, the mean age was 57.7 +/- 10.5 years, and 52.5% were men. The mean VL was 6.1 +/- 0.7 logIU/mL with genotype 1 predominance (55%). All patients achieved sustained virological response. The alanine aminotransferase levels decreased from 79.9 +/- 53.3 U/L at baseline to 25.7 +/- 17.2 and 22.3 +/- 11.0 U/L at 24 and 48 weeks, respectively (p < 0.001). The mean LSM decreased from 19.2 +/- 15.3 to 11.7 +/- 8.0 kPa at 48 weeks (p < 0.001). The P3NP levels decreased from 43.6 +/- 22.0 ng/mL before treatment to 35.7 +/- 21.1 and 29.4 +/- 15.0 ng/mL at 24 and 48 weeks, respectively (p < 0.001). The proportions of VD insufficiency/deficiency were 72.5%, 91.3%, and 86.5% at baseline, 24 and 48 weeks, respectively. The 25(OH)VD levels decreased from 26.3 +/- 10.7 ng/mL at baseline to 20.8 +/- 8.1 and 20.8 +/- 8.5 ng/mL at 24 and 48 weeks, respectively (p < 0.001). Conclusions: Curative treatment with DAA attenuated the liver stiffness and inflammation but did not improve VD levels. Over 80% of patients remained VD insufficient/deficient. Whether VD replacement during and after DAA therapy can improve hepatic fibrosis remains unclear. Trial registrationThe Thai Clinical Trial Registry as TCTR20161025001 (31 October 2016)..

Objective To assess whether increment of vitamin D daily intake results in improved serum25(OH) vitamin D levels and reduced respiratory morbidity in premature infants. Methods A randomized double-blind clinical pilot trial, including preterm infants born at 32 + 6 to 36 + 6 weeks of gestation. The control group received 400 international units (IU) of cholecalciferol daily compared to 800 IU daily in the intervention group. Levels of 25(OH) vitamin D were measured at birth and 6 and 12 months of age. Respiratory morbidity was followed until 1 year of age. Results Fifty subjects were recruited during the study period; the median measured 25(OH) vitamin D levels in the control vs intervention groups were: 26.5 vs 34 nmol/L (P = .271) at birth, 99 vs 75.5 nmol/L (P = .008) at 6 months and 72.5 vs 75 nmol/L (P = .95) at 12 months of age. Infants with insufficient vitamin D (<75 nmol/L) levels had higher respiratory morbidity. Serum vitamin 25(OH) D is a fair predictor for respiratory symptoms (area under the curve [AUC], 0.697; 95% confidence interval [CI], 0.509-0.885;P = .047) and for recorded acute respiratory illnesses (AUC, 0.745; 95% CI, 0.569-0.922;P = .012). Conclusion Doubling the daily intake of vitamin D in premature infants did not increase serum 25(OH) vitamin D level, due to poor compliance in the intervention group. We found an inverse association between serum 25(OH) vitamin D and respiratory symptoms, indicating vitamin D deficiency is a fair predictor for respiratory morbidity.