Annals of Hepatology
March-April, Vol. 12 No.2, 2013: 199-204
ORIGINAL ARTICLE
José M. Ladero,* María J. Torrejón,† Pilar Sánchez-Pobre,‡ Avelina Suárez,§ Francisca Cuenca,† Virginia de la Orden,|| María J. Devesa,† María Rodrigo,¶ Vicente Estrada,¶ Gustavo López-Alonso,† José A. Agúndez**
* Service of Gastroenterology, Hospital Clínico San Carlos, Department of Medicine, Medical School, Universidad Complutense, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain. † Clinical Laboratory Department, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain. ‡ Service of Gastroenterology, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain. § Service of Clinical Microbiology, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain.
|| Genomics Unit, Clinical Laboratory Department, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain. ¶ Infectious Diseases Unit, Service of Internal Medicine, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain. **Department of Pharmacology, University of Extremadura, Cáceres, Spain.
ABSTRACT
Background. Vitamin D has immunomodulatory properties, exerts an anti-hepatitis C virus (HCV) effect in vitro and improves response to interferon-based therapy in patients with chronic hepatitis C (CHC). Low serum levels of 25(OH) vitamin D [25(OH)D] are frequently found in CHC patients and seem to be related to more advanced stages of liver fibrosis. The study aims to establish the incidence of vitamin D deficiency in Spanish patients with CHC, its possible relation with features of liver damage and with the IL28B gene polymorphism, and the immediate effect of vitamin D therapy on CHC-related analytical variables. Materials and methods. Baseline serum 25(OH)D levels were measured in 108 consecutive CHC patients (60 men, age 54.3 ± 10.5 yrs). Results of transient elastography and of IL28B rs12979860C/T genotype were available in 89 and 95 patients, respectively. Forty one patients with insufficient levels of 25(OH)D received vitamin D supplements and were re-evaluated thereafter. Results. Deficiency of vitamin D (< 20 µg/dL) and suboptimal levels (20-30 µg/mL) were detected in 36.1% and 40.9% of patients, respectively. No relationships were found between 25(OH)D levels and biochemical liver tests, fibrosis stage and IL28B genotype. Vitamin D therapy normalized 25(OH)D levels in all treated patients, but did not modify significantly HCV-NA serum levels or biochemical tests. Conclusions. Vitamin D deficiency is common in Spanish patients with CHC but it is related neither to biochemical and virological variables nor with the fibrosis stage and IL28B polymorphism. Vitamin D therapy has no immediate effect on HCV-RNA serum levels.
1) It would be worth checking the dosage form in these sorts of studies, occasional high doses (55,000iu typically) might not be as beneficial as regularly taking 4,000-8,000iu per day.
ReplyDelete2) What was the time frame? It may take years for the anti-inflammatory effect of optimal vitamin D to influence fibrosis scores.
3) there are significant racial differences in responses to and requirements for vitamin D (other than those those directly related to skin colour). The ethnicity of the subjects is relevant.