Ebada Said, Waleed El Agawy, Rehab Ahmed, Mohamed Hassany, Amal Ahmed, Hanan Fouad and Hosam Baiumy
Background and Objectives
According to the demographic health survey conducted in 2015, Egypt had 10% documented prevalence of anti-HBc positive patients aged 1-59 and 1% viremic patients amongst the population in the same age group, with a domination of genotype D. Several studies claimed the possible role of vitamin D deficiency in hepatitis B virus (HBV) replication and disease progression.
Patients and Methods
Serum vitamin D levels [25(OH D3] were assessed in 96 HBeAg negative non-cirrhotic chronic HBV patients and 25 healthy subjects classified as following: Group I: 48 chronic HBV patients with persistently normal ALT levels and HBV DNA level < 2000 IU/mL for ≥ 6 months; Group II: 48 chronic HBV patients with CHB with persistently elevated ALT and HBV DNA level ≥ 2000 IU/mL for ≥ 6 months; and Group III: 25 apparently healthy subjects with normal liver enzymes and negative hepatitis viral markers were taken as the control group.
Vitamin D was much more deficient in group II than in group I and group III being 11.55 ± 3.97 ng/mL, 15.03 ± 3.45, 27.00 ± 6.76 ng/mL (P < 0.001), respectively, and a strong negative correlation was observed between vitamin D levels and HBV DNA levels (P = 0.043) in groups I and II.
The current study showed high HBV DNA replication in patients with vitamin D deficiency suggesting the antimicrobial immunomodulatory role of vitamin D.
Amal Ahmed Mohamed, Eman R. Abd Almonaem, Amira I. Mansour, HebatAllah Fadel Algebaly, Rania Abdelmonem Khattab and Yasmine S. El Abd
Background and Objective
Hepcidin is the key regulator of iron metabolism and is a significant biomarker for systemic inflammatory states. Vitamin D is a powerful immunomodulator and plays a significant role in the inflammatory responses and fibrosis occurring due to hepatitis C virus (HCV) infection. This study assessed the level of vitamin D and serum hepcidin and its expression in peripheral blood of children with chronic hepatitis C (CHC) and correlated them with other serum markers to reflect iron metabolism and liver disease severity.
A total of 100 children were included in this study: 50 with HCV infection and 50 healthy controls. Biochemical parameters together with vitamin D, hepcidin, and its expression were all measured.
The level of hepcidin and its expression together with vitamin D and hepcidin-to-ferritin (H/F) ratios were significantly reduced in patients, but the iron and ferritin levels were higher (P<0.001). Serum hepcidin level showed significant positive correlation with hepcidin expression, HCV titer, iron, ferritin, and H/F ratio (r = 0.43, 0.31, 0.34, 0.28, and 0.91, respectively) but significant negative correlation with vitamin D (r = −0.37). Both hepcidin and ferritin were higher in patients with Child Pugh scores B and C than those with score A (P<0.001).
Measuring serum hepcidin and its expression together with vitamin D levels in patients may have a prognostic value and is promising in the follow-up of the severity of liver disease.