Hadar Moran-Lev1,2, Yosef Weisman3, Shlomi Cohen4, Varda Deutsch5, Michal Cipok5, Ekaterina Bondar6, Ronit Lubetzky3, Dror Mandel7. 1. Department of Pediatrics, Dana Dwek Children Hospital and The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. hadarm@tlvmc.gov.il. 2. Department of Pediatric Gastroenterology, Dana Dwek Children Hospital and The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. hadarm@tlvmc.gov.il. 3. Department of Pediatrics, Dana Dwek Children Hospital and The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. 4. Department of Pediatric Gastroenterology, Dana Dwek Children Hospital and The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. 5. Department of Hematology Laboratories, Tel Aviv Sourasky Medical Center and The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. 6. Preclinical Research Pulmonary Laboratory, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. 7. Department of Neonatology, Dana Dwek Children Hospital and The Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Abstract
BACKGROUND: Hepcidin is a master regulator of iron metabolism. Recently, it has been shown that vitamin D suppresses hepcidin expression. Our hypothesis was that hepcidin levels inversely correlate with vitamin D levels in anemic children during acute infection. METHODS: A prospective study was performed on 90 patients (45 females, 45 males, mean age 7.3 ± 5 years) who were admitted to the pediatric ward. Sixty-two patients had infectious disease (32 with coexisting anemia, 30 without anemia), and 28 patients were hospitalized for noninfectious causes. Blood samples for IL-6, hepcidin, iron status parameters, and 25-hydroxyvitamin D (25-OHD) were obtained within 72 h after admission. RESULTS: Serum concentrations of IL-6 and hepcidin were significantly higher and 25-OHD, iron, and transferrin were significantly lower in anemic children with infectious disease compared with controls. Children with a serum 25-OHD level < 20 ng/ml had significantly increased odds of having anemia than those with a level > 20 ng/ml (OR: 6.1, CI: 1.15-32.76). Correlation analyses found positive associations between hepcidin levels and ferritin (R2 = 0.47, P < 0.001) and negative associations between hepcidin and transferrin (R2 = 0.57, P < 0.001). CONCLUSION: Higher IL-6 and lower 25-OHD levels may lead to higher hepcidin levels and subsequently to hypoferremia and anemia in children with acute infection.
BACKGROUND:Hepcidin is a master regulator of iron metabolism. Recently, it has been shown that vitamin D suppresses hepcidin expression. Our hypothesis was that hepcidin levels inversely correlate with vitamin D levels in anemicchildren during acute infection. METHODS: A prospective study was performed on 90 patients (45 females, 45 males, mean age 7.3 ± 5 years) who were admitted to the pediatric ward. Sixty-two patients had infectious disease (32 with coexisting anemia, 30 without anemia), and 28 patients were hospitalized for noninfectious causes. Blood samples for IL-6, hepcidin, iron status parameters, and 25-hydroxyvitamin D (25-OHD) were obtained within 72 h after admission. RESULTS: Serum concentrations of IL-6 and hepcidin were significantly higher and 25-OHD, iron, and transferrin were significantly lower in anemicchildren with infectious disease compared with controls. Children with a serum 25-OHD level < 20 ng/ml had significantly increased odds of having anemia than those with a level > 20 ng/ml (OR: 6.1, CI: 1.15-32.76). Correlation analyses found positive associations between hepcidin levels and ferritin (R2 = 0.47, P < 0.001) and negative associations between hepcidin and transferrin (R2 = 0.57, P < 0.001). CONCLUSION: Higher IL-6 and lower 25-OHD levels may lead to higher hepcidin levels and subsequently to hypoferremia and anemia in children with acute infection.