The total amount of iron in the body varies by age and sex. Iron deposition decreases during the growing period. After adolescence need iron drops, men showing a gradual increase iron stores throughout life (have a minimum of 50 mg Fe / kg). In contrast, women show a loss continue until menopause iron (Fe have ~ 35mg / kg); women after menopause iron accumulates in a linear fashion, reaching a level similar to that of men.
Most of the iron in the body is found in heme compounds, especially hemoglobin and myoglobin. Most non-hemic iron is stored as ferritin or hemosiderin in macrophages and hepatocytes. Only a very small fraction (~ 0.1%) circulates in plasma in the form of Fe 3+ bound to a carrier protein – transferrin.
Iron is absorbed in the proximal small intestine as hemic iron and ferrous iron (Fe 2+), its absorption is influenced by gastric acidity (decrease in aclorhidia or gastrectomy), enhancers and inhibitors food factors. Absorption is achieved by means of transport proteins and using enzymes ferirreductase that converts Fe3 + from food into Fe2 + transfer in cells lining the gut, and ferrioxidase (hefaestina), which converts Fe2 + to Fe3 + on the membrane basolateral to transfer plasma.
Since the human body does not possess a physiological mechanism for removing excess iron, its absorption is very well controlled. Iron excretion occurs by cell loss in the gastrointestinal, skin, urinary and menstrual losses in women. Most functional iron in the body comes from reuse of existing iron derived from senescent erythrocytes destroyed in the reticuloendothelial system, mainly the spleen.
Recommendations for determination of serum iron (in combination with transferrin / transferrin saturation and ferritin):
• Differential diagnosis of microcytic anemia in particular and / or hypochromic;
• Evaluation of iron deficiency anemia, thalassemia, sideroblastic anemia;
• The diagnosis of iron overload and hemochromatosis;
• Diagnosis of iron poisoning
60-158 mg / dL
Interpretation of results:
• thalassemia, sideroblastic anemia •, • hemolytic anemia, idiopathic hemochromatosis • (increased serum iron may indicate iron overload earlier than increasing ferritin) and secondary (multiple transfusions, iron inadequate treatment are porto-hollow, chronic dialysis, etc.) • acute iron intoxication (in children), • severe hepatic necrosis (acute viral hepatitis, can achieve> 1000μg / dL) and some chronic liver disease, • Destruction ineffective erythropoiesis increased marrow erythroid progenitors (relapse pernicious anemia, congenital dyserythropoietic anemias ).
• iron deficiency anemia: poor diet; Poor absorption of iron: achlorhydria, gastrectomy, celiac disease, duodenal bypass; Chronic blood loss; increased iron needs: pregnancy, lactation, growth period.
• Anemia of chronic disease (inflammatory disease, chronic infections, kidney disease, etc.).
• nephrotic syndrome (urinary loss of iron binding protein).
• remission after pernicious anemia.