RESEARCH ARTICLE


Detrimental Impact of Interferon-Based Regimens for Chronic Hepatitis C on Vitamin D/Parathyroid Hormone Homeostasis



Livia Salmi1, *, Matteo Nazzareno Barbaglia1, Carlo Smirne1, 2, Sara Bianco1, 2, Giulia Guaschino1, 2, Maria Grazia Stella Crobu3, Rosalba Minisini1, Mario Pirisi1, 2
1 Department of Translational Medicine, Università del Piemonte Orientale UPO, Novara, Italy
2 Division of Internal Medicine, “AOU Maggiore della Carità”, Novara, Italy
3 Laboratory of Molecular Virology,“AOU Maggiore della Carità”, Novara, Italy


© 2018 Salmi et al.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: (https://creativecommons.org/licenses/by/4.0/legalcode). This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Department of Translational Medicine, Università del Piemonte Orientale UPO, via Solaroli 17, Novara (NO), 28100, Italy; Tel: +3903213733690; E-mail: livia.salmi@uniupo.it


Abstract

Background:

Both the anti-infective and anti-inflammatory properties of vitamin D, an essential hormone of calcium homeostasis, have ample support in the literature. The high rates of vitamin D deficiency among patients with chronic hepatitis C are also well known. That supplementation with vitamin D may boost sustained viral response rates in vitamin D deficient, hepatitis C virus (HCV) infected patients undergoing Interferon-alpha (IFN) treatment, on the other hand, is controversial. Surprisingly, studies considering in this latter setting what are the effects of IFN treatment (with or without vitamin D supplementation) on the other major regulator of mineral metabolism, i.e. the Parathyroid hormone (PTH), are lacking.

Aim:

Evaluate the impact of interferon-based treatment against HCV (±cholecalciferol supplementation) on vitamin D and PTH homeostasis.

Methods:

A series of 40 consecutive patients received pegylated IFN plus ribavirin to treat chronic hepatitis C. At the discretion of their physician, some of them (N. = 27) received vitamin D supplementation while others did not (N. = 13). All had measured plasma 25-hydroxycholecalciferol and PTH concentrations at baseline, at completion of the 4th (TW4) and 12th treatment week (TW12) and at 24 weeks after the end of therapy (SVR24).

Results:

Plasma PTH concentration increased significantly from baseline during treatment, raising to 44.8 [30.7-57.2] pg/mL at TW4 (p=0.01), 47.0 [37.1-63.2] pg/mL at TW12 (p=0.006) to return to baseline levels in the follow-up (34.5 [27.6-43.0]; p=0.16). The proportion of patients who satisfied criteria for hyperparathyroidism was higher at TW12 (N=10, 25%) than at TW4 (N=6, 15%). There was no statistical correlation between vitamin D and PTH blood levels (ρ=-0.07; p=0.65).

Conclusion:

An increase in plasma PTH occurs systematically during IFN treatment of HCV patients and cannot be prevented by vitamin D supplementation.

Keywords: INF, HCV therapy, Vitamin D supplementation, Secondary hyperparathyroidism, PTH, FGF23.