Vitamin D supplementation did not significantly increase levels from insufficient or deficient to sufficient in chronic hepatitis C patients after treatment with direct-acting antivirals, according to a paper published in PeerJ.
Investigators from Thailand conducted a randomized trial of 75 patients with chronic hepatitis C and vitamin D deficiency in order to determine whether a treatment with vitamin D for 6 weeks would be effective in fibrosis amelioration. Half of the patients were treated with vitamin D (ergicalciferol) and the other half received placebo for 6 weeks between February and August 2018. The investigators used various biochemical analysis indicators detected from blood samples at baseline and after 6 weeks in order to make their observations.
Additionally, the patients were asked to refrain from using vitamin D supplements or multivitamin supplements that came from outside the trial for the duration of the study period, and were told to maintain their normal activity. The patients had a mean age of 60 years, were mostly female, and 60% of them had cirrhosis. There were no significant differences in any biochemical factor between the two groups, the investigators noted.
The mean serum 25-hydroxyvitamin D (25(OH)D) level increased from 17.2 ng/mL at baseline in the vitamin D group to a normal level, 41 ng/mL, by the end of the 6-week study, the authors said. Notably, though, 3 patients in the vitamin D group still had a 25(OH)D level less than 30 ng/mL after 6 weeks of therapy, they said, including 2 patients who changed from an initial deficient state to an insufficient state after supplementation.
However, the placebo group only saw a slight increase, which was still deficient, by the end of the 6 weeks (from 16.6 ng/mL to 23 ng/mL), the authors observed. All of the placebo patients had a vitamin D insufficiency or deficiency by the end of the 6 week study period.
There was no significant difference in the mean change from baseline to 6 weeks between the vitamin D and placebo groups in terms of serum transforming growth factor beta 1 (TGF-β1) levels or the tissue inhibitors of matrix metalloproteinases 1 (TIMP-1) levels, the study authors said. There was also no significant difference between the 2 groups after 6 weeks in terms of mean fibrolytic markers likematrix metalloproteinase 9 (MMP-9) levels, which were slightly increased in the vitamin D group, or mean amino terminal type III procollagen peptide (P3NP) levels, which were slightly decreased among both groups.
“Short-term vitamin D replacement after hepatitis C eradication by direct-acting antivirals did not improve serum hepatic fibrogenesis marker levels and, thus, might not clinically facilitate the amelioration of residual liver fibrosis,” the study authors concluded, while adding that overall, vitamin D supplementation did not vary according to baseline serum 25(OH)D levels or liver fibrosis severity.
The study authors said their findings seem to indicate that vitamin D may regulate and influence hepatic fibrogenesis through its immunomodulatory rather than its anti-fibrotic property, where it is not strong enough to affect the associated serum markers.
“Nevertheless, further investigation to determine whether a higher dose (vitamin D derivative) for a longer period could potentially help ameliorate liver fibrosis is warranted,” they wrote.
Source: HCPLive
