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gPosted by Crisha Alyziah Miller -When you have iron-deficiency, your cells can’t get enough oxygen. How can you tell if your levels are a little low? Be on the lookout for these 10 warning signs.
Iron is crucial to biologic functions, including respiration, energy production, DNA synthesis, and cell proliferation. Although the prevalence of iron-deficiency anemia has declined somewhat recently, iron deficiency continues to be the top-ranking cause of anemia worldwide.
The human body has evolved to conserve iron in several ways, including the recycling of iron after the breakdown of red cells and the retention of iron in the absence of an excretion mechanism.
However, since excess levels of iron can be toxic, its absorption is limited to 1 to 2 mg daily, and most of the iron in the body (about 25 mg per day) is recycled by macrophages that phagocytose senescent erythrocytes. The latter two mechanisms are controlled by the hormone hepcidin, which maintains total-body iron within normal range, avoiding both iron deficiency and excess.
Hepcidin is a peptide hormone that is synthesized primarily in the liver. It functions as an acute-phase reactant that adjusts fluctuations in plasma iron levels by binding to and inducing the degradation of ferroportin, which exports iron from cells. In iron deficiency, the transcription of hepcidin is suppressed. This adaptive mechanism facilitates the absorption of iron and the release of iron from body stores.
In most cases, iron resistance is due to disorders of the gastrointestinal tract. Partial or total gastrectomy or any surgical procedure that bypasses the duodenum can cause resistance to oral iron. Laparoscopic Roux-en-Y gastric bypass, which is performed in selected obese patients to reduce caloric intake and to correct diabetes, is an emerging cause of iron deficiency and anemia because the procedure effectively removes an active iron absorption site from the digestive process and increases gastric pH. Helicobacter pylori infection decreases iron absorption because the microorganism competes with its human host for available iron, reduces the bioavailability of vitamin C, and may lead to microerosions that cause bleeding. Since it is estimated that half the world’s population is infected with H. pylori, clinicians should be aware of the possibility of infection and provide treatment in order to eradicate this source of iron-resistant iron-deficiency anemia.
Patients with malabsorption and genetic iron-refractory iron-deficiency anemia may require intravenous iron. Intravenous administration is also preferred when a rapid increase in hemoglobin level is required or when iron-deficiency anemia caused by chronic blood loss cannot be controlled with the use of oral iron, as is the case in patients with hereditary hemorrhagic telangiectasia. Active inflammatory bowel disease is an emerging indication for the use of intravenous iron; oral iron is not only ineffective but may also increase local inflammation. Intravenous iron is essential in the management of anemia in patients with chronic kidney disease who are receiving dialysis and treatment with erythropoiesis-stimulating agents.
