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BMC Infect Dis. 2016 Sep 23;16(1):507.

Association of vitamin D deficiency with hepatitis B virus - related liver diseases.

Author information

1
Institute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
2
Vietnamese-German Center for Medical Research (VG-CARE), Hanoi, Vietnam.
3
Department of Infectious Diseases, Duc Giang Hospital, Hanoi, Vietnam.
4
Department of Molecular Biology, 108 Military Central Hospital, Hanoi, Vietnam.
5
Department of Infectious Diseases, Vietnam Military Medical University, Hanoi, Vietnam.
6
Department of Pathophysiology, Vietnam Military Medical University, Hanoi, Vietnam.
7
Fondation Congolaise pour la Recherche Medicale, Brazzaville, Republic of Congo.
8
Vietnamese-German Center for Medical Research (VG-CARE), Hanoi, Vietnam. lehuusong@108-icid.com.
9
Institute of Clinical Infectious Diseases, 108 Military Central Hospital, Tran Hung Dao Street N1, Hai Ba Trung District, Hanoi, Vietnam. lehuusong@108-icid.com.

Abstract

BACKGROUND:

As an immune modulator, vitamin D is involved in various pathophysiological mechanisms in a plethora of diseases. This study aims to correlate the vitamin D deficiency status and clinical progression of liver diseases associated with hepatitis B virus (HBV) infection in patients in Vietnam and to compare it to healthy controls.

METHODS:

We quantified the levels of total vitamin D [25-(OH) D2 and D3] in serum samples from 400 HBV patients (chronic hepatitis B infection [CHB], n = 165; HBV-associated liver cirrhosis [LC], n = 127; HBV-associated hepatocellular carcinoma [HCC], n = 108) and 122 unrelated healthy controls (HC). Univariate and multivariate analyses were performed in order to determine the association between vitamin D levels and distinct clinical parameters.

RESULTS:

The prevalence of vitamin D inadequacy (<30 ng/mL) was high among healthy individuals (81.7 %) as well as in HBV patients (84.3 %). Vitamin D deficiency (<20 ng/ml) or severe deficiency (<10 ng/ml) was observed more frequently among HBV patients (52 %) and subgroups (CHB, 47.8 %; LC, 54.4 %; HCC, 55.3 %) compared to the control group (32.5 %) (P < 0.001). Vitamin D levels and HBV-DNA load were strongly and inversely correlated (rho = -0.57, P < 0.0001). Multivariate regression analysis also revealed an independent association of HBV-DNA loads with low vitamin D levels (P = 0.0004). In addition, reduced vitamin D levels were associated with significant clinical progression of LC (Child-Pugh C versus Child-Pugh A, P = 0.0018; Child-Pugh C versus Child-Pugh B, P = 0.016).

CONCLUSIONS:

Vitamin D deficiency was observed in the majority of HBV-infected patients and associated with adverse clinical outcomes. Our findings suggest that substitution of vitamin D may be a supportive option in the treatment of chronic liver diseases, in particular of HBV-associated disorders.

KEYWORDS:

Chronic liver disease; HBV infection; Hepatocellular carcinoma; Liver cirrhosis; Vitamin D deficiency

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