The role of hepcidin and haemojuvelin in the pathogenesis of iron disorders in patients with severe malnutrition.

INTRODUCTION AND OBJECTIVE

The clinical consequences of malnutrition are multi-directional and result in dysfunctions of the majority of internal organs and systems. The results of recent studies suggest that a significant role is played by malnutrition in pathophysiology of iron homeostasis disorders, but the underlying mechanism is unclear. The study describes the potential role of hepcidin and hemojuvelin in the pathogenesis of disorders of iron metabolism during malnutrition.

STATE OF KNOWLEDGE

The participation of hepcidin in regulating iron homeostasis encompasses inhibiting the absorption of food iron from enterocytes and inhibiting the release of stored iron from the reticuloendothelial system cells. One of the factors that increases the post-translational level is the expression of hepcidin is IL-6. In studies focused on malnutrition it was observed that in persons with protein and energy deficits the level of proinflammatory cytokine, i.e. interleukin-6, in the serum, increased. The involvement of haemojuvelin in the overall iron homeostasis is related with the regulation of expression of the hepcidin coding gene on the transcription level. The highest haemojuvelin expression was observed in humans in skeletal muscles. Observations and analyses conducted in vivo allowed the conclusion that soluble HJV and cell-related haemojuvelin regulate hepcidin expression in response to changes in iron concentration. The research also demonstrated that soluble HJV neutralizes the inductive effect of IL-6 action on hepcidin expression.

SUMMARY

It can be claimed that in persons with protein and/or protein-energetic malnutrition the muscle mass deficit may lead to insufficient production of haemojuvelin and sideropenia.