Fig. 5.

Overview of alcohol-induced alterations in iron parameters. The figure shows alcohol-induced alterations in iron parameters, as indicated via red upward and downward arrows. Essentially, alcohol decreases hepcidin synthesis, which causes decrement in serum hepcidin. This allows excessive iron absorption into the circulation via the duodenal enterocytes and increased iron egress from the iron storing macrophages and hepatocytes leading to elevation in serum iron levels. Serum iron is also partly elevated due to alcohol-induced upregulations of duodenal DMT-1 and ferroportin that facilitate iron entry and exit into and from the enterocyte, respectively. Resultantly, intracellular and serum ferritin levels increase and so does the iron saturation of serum transferrin. Interestingly, ferritin is elevated by both increased iron levels and inflammation, the latter often found in heavy or chronic alcohol consumers. Inflammation also reduces transferrin synthesis. Alongside, alcohol can decrease hematopoietic activity in the bone marrow leading to reduction in the number of functional red blood cells (RBCs), thereby contributing to the many causes of anemia, as observed in some ALD cases. Carbohydrate-deficient transferrin (CDT) levels increase, but alcohol does not seem to alter soluble transferrin receptor (sTfR) levels. Distinct from the depiction in this figure, serum iron levels may decrease or remain unaltered in ALD. Also, levels of transferrin and transferrin saturation may remain unaltered. Hemoglobin levels (not shown in the figure) may increase, decrease, or remain unaltered. The figure was created with BioRender.com