Effect of vitamin D supplementation in patients with chronic hepatitis C after direct-acting antiviral treatment: a randomized, double-blind, placebo-controlled trial
Autor: | Nunthiya Srisoonthorn, Sukanya Sittisomwong, Supachaya Sriphoosanaphan, Piyawat Komolmit, Kessarin Thanapirom, Yong Poovorawan, Bundit Chaopathomkul, Kanokwan Sonsiri, Natthaporn Tanpowpong, Nicha Teeratorn, Stephen J. Kerr, Sirinporn Suksawatamnuay, Panarat Thaimai, Sombat Treeprasertsuk |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Liver fibrogenesis
medicine.medical_specialty Liver fibrosis Placebo-controlled study lcsh:Medicine Gastroenterology and Hepatology Placebo Gastroenterology General Biochemistry Genetics and Molecular Biology 03 medical and health sciences 0302 clinical medicine Chronic hepatitis Fibrosis Internal medicine medicine Vitamin D and neurology Internal Medicine Clinical Trials Vitamin D 030304 developmental biology Nutrition 0303 health sciences business.industry General Neuroscience lcsh:R General Medicine Hepatitis C medicine.disease Confidence interval 030211 gastroenterology & hepatology Direct-acting agent General Agricultural and Biological Sciences business Hepatic fibrosis Translational Medicine |
Zdroj: | PeerJ PeerJ, Vol 9, p e10709 (2021) |
ISSN: | 2167-8359 |
Popis: | Background Replacement of vitamin D (VD) among patients with chronic hepatitis C (CHC) before viral eradication has demonstrated a protective effect on serum markers associated with hepatic fibrogenesis. We therefore hypothesized that VD may facilitate further fibrosis amelioration following curative treatment with direct-acting antivirals (DAA). Methods This study was a randomized, double-blind, placebo-controlled trial conducted between February 2018 and August 2018. Patients with CHC and VD deficiency were randomized in a 1:1 ratio to either receive ergicalciferol or placebo over 6 weeks. Biochemical analysis indicators, including 25-hydroxyvitamin D (25(OH)D), fibrogenic markers [(transforming growth factor beta 1 (TGF-β1) and tissue inhibitors of matrix metalloproteinases 1 (TIMP-1)], and fibrolytic markers [matrix metalloproteinase 9 (MMP-9) and amino terminal type III procollagen peptide (P3NP)], were assessed at baseline and at 6 weeks. Serum 25(OH)D was analyzed by a chemiluminescence immunoassay. Serum hepatic fibrogenesis markers were measured using a quantitative sandwich enzyme-linked immunosorbent assay. Results Seventy-five patients with CHC and VD deficiency were randomly assigned to VD (n = 37) and placebo (n = 38) groups. At the end of the study, the mean serum 25(OH)D level had risen to a normal level in the VD group, but was still deficient in the placebo group (41.8 ± 9.1 vs. 18.1 ± 4.6 ng/mL, p < 0.001). Upon restoration of the VD level, there were no significant mean differences in the change from baseline for TGF-β1 (−0.6 ng/mL (95% confidence interval (95% CI) [−2.8–1.7]), p = 0.63), TIMP-1 (−5.5 ng/mL (95% CI [−26.4 –15.3]), p = 0.60), MMP-9 (122.9 ng/mL (95% CI [−69.0 –314.8]), p = 0.21), and P3NP (−0.1 ng/mL (95% CI [−2.4 –2.2]), p = 0.92) between the VD and placebo groups. Conclusion Short-term VD supplementation after DAA treatment in patients with CHC does not improve serum fibrogenesis markers and may not expedite the residual liver fibrosis healing process. Future studies are warranted to evaluate the long-term effect of VD supplementation on hepatic fibrosis regression. |
Databáze: | OpenAIRE |
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