Abstract
Hepcidin is a protein responsible for maintaining iron (Fe) homeostasis. Data regarding the role of hepcidin in the pathomechanism of Fe balance disturbances associated with acromegaly (AG) are scarce. The aim of the study was to assess the impact of alterations in complete blood count parameters, Fe homeostasis, gonadal status and GH/IGF-1 on the level of hepcidin in AG patients. The study evaluated the differences in hepcidin concentration and iron homeostasis between patients newly diagnosed with AG in comparison to healthy control subjects (CS). We prospectively enrolled 25 adult patients newly diagnosed with AG and 25 healthy volunteers who served as CS. The level of hepcidin was measured using the Hepcidin 25 (bioactive) hs ELISA, which is a highly sensitive enzyme immunoassay for the quantitative in vitro diagnostic measurement (DRG Instruments GmbH, Germany). The median of hepcidin concentration in the serum of patients with AG was significantly lower 9.8 (6.2–18.2) ng/ml as compared to CS 21.3 (14.3–34.0) ng/ml (p = 0.003). In the AG group, a statistically significant negative correlation between hepcidin and IGF-1 (rho = −0.441) was observed. Our study demonstrated a decreased hepcidin level in AG patients in comparison to CS what may have a potentially protective effect against anemia through an increased bioavailability of Fe. Additionally, GH may have a positive direct or indirect effect on erythropoiesis. Further studies on larger patient groups are necessary in order to clarify the exact role of hepcidin in the regulation of erythropoiesis in the excess of GH/IGF-1.
Highlights
Hepcidin constitutes an acute phase liver-derived protein, responsible for maintaining iron (Fe) homeostasis through both local and systemic impact [1, 2]
The objective of the study was to assess the impact of alterations in complete blood count parameters, Fe homeostasis, gonadal status and growth hormone (GH)/IGF-1 on the level of hepcidin in AG patients
We found a slight difference in age between the two groups (p = 0.04), a correlation between hepcidin and age was not observed
Summary
Hepcidin constitutes an acute phase liver-derived protein, responsible for maintaining iron (Fe) homeostasis through both local and systemic impact [1, 2]. Hepcidin triggers the internalization and degradation of ferroportin (the major Fe transporter) which results in a decrease in serum Fe level [3]. Iron metabolism is controlled by hepcidin on three levels: absorption in the duodenum, release from macrophages, and from hepatocytes [2]. Hepcidin was first identified in 2000 [8], it has recently been evaluated in view of the various endocrine disorders associated with an increase in acute-phase proteins or with concomitant disturbances in Fe homeostasis [9,10,11]. As a result of such reports, a growing awareness of the hormonal influence on Fe metabolism and hepcidin levels has emerged
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