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

• Published in: BMC infectious diseases Vol. 16; no. 1; p. 507
• Main Authors: Hoan, Nghiem Xuan, Khuyen, Nguyen, Binh, Mai Thanh, Giang, Dao Phuong, Van Tong, Hoang, Hoan, Phan Quoc, Trung, Ngo Tat, Anh, Do Tuan, Toan, Nguyen Linh, Meyer, Christian G, Kremsner, Peter G, Velavan, Thirumalaisamy P, Song, Le Huu
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 23-09-2016; BioMed Central
• Subjects: Deoxyribonucleic acid; Development and progression; DNA; Hepatitis; Hepatitis B; Hepatitis B virus; Infectious diseases; Liver; Liver diseases; Regression analysis; Risk factors; Vitamin D; Vitamin D deficiency; Vitamin D deficiency; Hepatocellular carcinoma; Chronic liver disease; Liver cirrhosis; HBV infection
• ISSN: 1471-2334; 1471-2334
• DOI: 10.1186/s12879-016-1836-0

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.
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.
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).
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.