الفهرس 
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Abstract
The discovery of hepcidin, as a key regulator of iron homeostasis, has advanced the current knowledge of this field. It was initially reported as LEAP-1, for Liver-Expressed Antimicrobial Protein and later became known as Hepcidin. Hepcidin has been shown to prevent the absorption of iron from the digestive tract, and also inhibit the release of stored iron from macrophages and hepatocytes.
Anemia of chronic disease is immune driven; cytokines and cells of the reticuloendothelial system induce changes in iron homeostasis, the proliferation of erythroid progenitor cells, the production of erythropoietin, and the life-span of red cells, all of which contribute to the pathogenesis of anemia.
This study included 50 subjects, 40 patients, who had anemia associating chronic liver disease excluding hepato-renal affection and HCC patients, and 10 age- and sex-matched healthy controls. The patients were attending Ain-Shams University Hospitals [Internal Medicine Department and Tropical Medicine Department].The study was conducted during 2012.
Both groups were subjected for clinical history, examination, complete blood picture, liver function tests, hepatitis markers, renal function tests, ESR and serum Hepcidin level using ELISA technique.
In the present work, regarding the serum hepcidin level, there was a statistically non-significance difference on comparing patients (mean: 133.85 ± 58.366 ng/ml) versus controls (mean of 106 ± 28.94 ng/dl).
Considering the serum Hepcidin levels and gender among the patients’ group, the study showed a statistically non-significant difference between both sexes, as male patients showed a mean of 136.18 ± 56.303 ng/ml versus female patients who showed a mean of 131 ± 62.317 ng/ml, and P value was > 0.01. While in the controls, a statistically significant difference in the serum Hepcidin level was documented, as male controls showed a mean of 121.67 ± 15.81 ng/ml versus female controls who had a mean of 82.5 ± 29.94 ng/ml.
Correlating between serum Hepcidin levels and HCV infection in the patients’ group, revealed a statistically non-significant correlation: as HCV positive patients had a mean of 132.19 ± 52.699 ng/ml, while HCV negative patients had a mean of 137.31 ± 70.956 ng/ml.
As regards to serum Hepcidin levels in patients with and without manifestation of blood loss (hematemesis, melena, etc.), the study showed a statistically significant lower mean serum Hepcidin level in the patients with bleeding symptoms (106.05 ± 21.549 ng/ml) versus patients without these symptoms (161.65 ± 70.007 ng/ml).
Correlating serum Hepcidin with the studied parameters in the patients’ group, the study showed that total bilirubin, direct bilirubin and PT were highly significantly positively correlated to serum Hepcidin level. Hemoglobin and albumin were significantly inversely correlated with serum Hepcidin level. The INR was significantly positively correlated with serum Hepcidin level. Meanwhile, the other parameters showed statistically non-significant correlation.
Finally, the present study documented that serum Hepcidin level was higher in normal males than normal females. There was no statistically significant difference in serum Hepcidin level between patients with anemia of chronic liver disease and the controls. Serum Hepcidin level was lower in patients who have blood loss associating anemia of chronic liver disease versus patient without blood loss. There is positive correlation between total bilirubin and direct bilirubin with serum Hepcidin.
The present study recommends further studies, on a larger scale, for confirmation of the results of this study, correlating serum Hepcidin level with the degree of liver de-compensation, serum hepcidin level and elements of iron profile, in patients with anemia of chronic liver disease, with or without iron deficiency anemia.