New Insights on Iron Study in Myelodysplasia

Abstract

Objective: Hepcidin plays a pivotal role in iron homeostasis. It is predominantly produced by hepatocytes and inhibits iron release from macrophages and iron uptake by intestinal epithelial cells. Competitive ELISA is the current method of choice for the quantification of serum hepcidin because of its lower detection limit, low costs, and high throughput. This study aims to discuss the role of hepcidin in the pathogenesis of iron overload in recently diagnosed myelodysplasia (MDS) cases. Materials and Methods: The study included 21 recently diagnosed MDS patients and 13 healthy controls. Ferritin, hepcidin, and soluble transferrin receptor (sTFR) were measured in all subjects. Results: There were 7 cases of hypocellular MDS, 8 cases of refractory cytopenia with multilineage dysplasia, and 6 cases of refractory anemia with excess blasts. No difference was observed among the 3 MDS subtypes in terms of hepcidin, sTFR, and ferritin levels (p>0.05). Mean hepcidin levels in the MDS and control groups were 55.8±21.5 ng/mL and 19.9±2.6 ng/mL, respectively. Mean sTFR was 45.7±8.8 nmol/L in MDS patients and 31.1±5.6 nmol/L in the controls. Mean ferritin levels were significantly higher in MDS patients than in controls (539.14±83.5 ng/mL vs. 104.6±42.9 ng/mL, p<0.005). There was a statistically significant correlation between hepcidin and sTFR (r=0.45, p=0.039). No difference in hepcidin levels between males and females was observed, although it was lower in males in comparison to females (47.9±27.6 vs. 66.7±35.7, p>0.05). Conclusion: Hepcidin may not be the main cause of iron overload in MDS. Further studies are required to test failure of production or peripheral unresponsiveness to hepcidin in MDS cases.

The Role of Hepcidin in Myelodysplastic Syndromes (MDS): A Systematic Review of Observational Studies

“…The remaining 53 citations were subjected to a thorough full-text investigation. Ultimately, 12 references were included in this systematic review [20][21][22][23][24][25][26][27][28][29][30][31]. The primary reason for excluding full-text citations was a lack of complete data on hepcidin levels in patients with MDS.…”

“…Our specific search terms were: "hepcidin" and "myelodysplastic syndromes" with no limitations on language or publication type. We also conducted manual searches of the bibliographies of all included studies [20][21][22][23][24][25][26][27][28][29][30][31] and reviewed articles to identify any remaining studies. We utilized Zotero version 6.0.4 (Corporation for Digital Scholarship, Vienna, VA, USA) to extract duplicate research.…”

“…A variety of works concentrating on hepcidin levels and MDS have been published [20][21][22][23][24][25][26][27][28][29][30][31]. Nonetheless, these studies do not present a unified concept regarding the role of hepcidin in MDS; hence, there is a need to systematize our knowledge in this field.…”

Flaming and fanning: The Spectrum of inflammatory influences in myelodysplastic syndromes

“…Iron can inhibit osteoblast formation [115] and would be expected to affect macrophage phagocytosis activity. Hepcidin levels are quite variable in MDS [116,117] and there is evidence that iron chelation can lead to hematologic improvement in some patients [118].…”

Effect of the Ginger Derivative, 6-Shogaol, on Ferritin Levels in Patients With Low to Intermediate-1–Risk Myelodysplastic Syndrome—A Small, Investigative Study

“…In intestinal epithelial cells, it is believed to downregulate divalent metal transporter 1, which is involved in the transfer of iron across the intestinal wall. 3 It has been reported that ineffective erythropoiesis enhances iron absorption in MDS through downregulation of hepcidin and its prohormones such that SF rises. 4 Plants of the ginger family have been credited with hepatoprotective activity.…”