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Dr. этот участник имеет превосходную репутацию на форумеDr. этот участник имеет превосходную репутацию на форумеDr. этот участник имеет превосходную репутацию на форумеDr. этот участник имеет превосходную репутацию на форумеDr. этот участник имеет превосходную репутацию на форумеDr. этот участник имеет превосходную репутацию на форумеDr. этот участник имеет превосходную репутацию на форумеDr. этот участник имеет превосходную репутацию на форумеDr. этот участник имеет превосходную репутацию на форумеDr. этот участник имеет превосходную репутацию на форумеDr. этот участник имеет превосходную репутацию на форуме
Failure to respond to oral iron therapy*—*On occasion, a patient may not respond to oral iron therapy. The potential causes for this situation include the following (show table 2): Incorrect diagnosis (eg, thalassemia, myelodysplastic syndrome) Presence of a coexisting disease interfering with response (eg, anemia of chronic inflammation, renal failure). (See "Anemia of chronic disease (anemia of chronic inflammation)", section on Differential diagnosis). Patient is not taking the medication Medication is not being absorbed for physical reasons (eg, enteric coated tablets, concomitant use of antacids). Iron (blood) loss or need is in excess of the amount ingested (eg, severe continuous GI bleeding, dialysis patient, idiopathic pulmonary hemosiderosis). (See "Idiopathic pulmonary hemosiderosis" and see "Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)"). The patient has malabsorption for iron. In one study, for example, refractoriness to oral iron treatment was noted in all patients with celiac disease and approximately 70 percent of those with autoimmune atrophic gastritis or Helicobacter pylori infection [4]. (See "Pathogenesis, epidemiology, and clinical manifestations of celiac disease in adults", section on Iron deficiency and see "Metaplastic (chronic) atrophic gastritis", section on Helicobacter pylori).

The appropriate treatment depends upon the cause for failure to respond.

Pregnancy*—*Treatment of iron deficiency in pregnancy is the same as that in nonpregnant, postpartum, premenopausal, and postmenopausal women; indications for the use of parenteral iron are also the same [5].

PARENTERAL IRON THERAPY

Indications*—*Parenteral iron, which can be given IM but preferably IV, is used in the rare patient who is unable to tolerate even modest doses of oral iron (see "Side effects" above), or in patients whose level of continued gastrointestinal bleeding exceeds the ability of the gastrointestinal tract to absorb iron (eg, hereditary hemorrhagic telangiectasia, iron malabsorption in sprue).

Other uses include: Occasional patients with inflammatory bowel disease and iron deficiency may give a history of severe intolerance to oral iron preparations, making therapy with parental iron necessary. (See "Nutritional considerations in inflammatory bowel disease", section on Iron). Parenteral iron is routinely employed in dialysis patients because of ongoing blood loss associated with the procedure, the need for adequate iron to respond to the administration of erythropoietin, and the frequent inability to utilize iron administered orally [6]. (See "Iron balance in predialysis, peritoneal dialysis, and home hemodialysis patients", section on Iron therapy). Parenteral iron has also been employed in anemic cancer patients receiving treatment with erythropoiesis-stimulating agents (eg, erythropoietin, darbepoetin). (See "Role of erythropoiesis-stimulating agents in the treatment of anemia in patients with cancer", section on Supplemental iron).

Available preparations*—*There are currently three parenteral iron preparations approved for use in the United States: Iron dextran (INFeD, Dexferrum) preparations contain 50 mg of elemental iron/mL, and can be given either IM or IV. INFeD and Dexferrum differ in that they are "low" and "high" molecular weight dextran preparations, respectively.

Both local and systemic side effects can occur following use of iron dextran, with an anticipated frequency of reactions of 4.7 percent [7]. High molecular weight dextran preparations, including Imferon which is no longer manufactured in the United States, are associated with a considerably higher incidence of adverse events than are the low molecular weight preparations [8].

Local reactions include pain, muscle necrosis, and phlebitis in adjacent vessels. Anaphylactic reactions occur in about 1 percent of patients and are thought to be caused by the free iron present in the preparation [7]. Other systemic effects include fever, urticaria, and a flare in arthritis in patients with rheumatoid arthritis. Ferric gluconate complex (Ferrlecit, 12.5 mg iron/mL) Iron sucrose (Venofer, iron saccharate, 20 mg iron/mL)

Ferric gluconate complex and iron sucrose are only approved for IV use. (See "Iron balance in predialysis, peritoneal dialysis, and home hemodialysis patients" and see "Use of iron preparations in hemodialysis patients").

Data from Europe and the United States indicate that, in comparison with iron dextran, sodium ferric gluconate complex in sucrose has a reduced incidence of adverse allergic reactions (3.3 versus 8.7 allergic events per one million doses per year), including death (case fatality rate of zero versus 16 percent for allergic/anaphylactic events) [9].

One group has reported on the efficacy and safety of 125 mg of ferric gluconate complex given either undiluted by slow IV push at a rate of 12.5 mg/minute or diluted in 100 mL isotonic saline and infused over 30 to 60 minutes, in 74 patients with iron deficiency anemia and normal levels of serum creatinine [10]. Of 639 infusions, 11 reactions (1.7 percent) were documented; no reaction was considered severe or anaphylactic. Two reactions were moderately severe (eg, dyspnea, severe urticaria, neck and back spasm), causing the infusion to be stopped. All other reactions were minor (eg, pruritus, palpitations, dizziness), causing the infusion to be temporarily stopped, following which all patients were able to continue the infusion. When measured in 56 of the 74 patients, all efficacy end points (eg, increases in hemoglobin, hematocrit, mean corpuscular volume, serum ferritin) showed significant improvement. (See "Iron balance in predialysis, peritoneal dialysis, and home hemodialysis patients" and see "Use of iron preparations in hemodialysis patients").

Iron sucrose also appears to be safe, even among those with a prior history of sensitivity to iron dextran. (See "Iron balance in predialysis, peritoneal dialysis, and home hemodialysis patients" and see "Use of iron preparations in hemodialysis patients").

Intramuscular iron*—*Mobilization of iron from intramuscular sites is slow and occasionally incomplete. As a result, the rise in the hemoglobin concentration is only slightly faster then that which occurs following the use of oral iron preparations.

Patients who have very brisk continuing bleeding (as with gastrointestinal angiodysplasia) are difficult to treat with an intramuscular (IM) regimen because repeated courses of IM iron are painful, and the utilization of iron given IM is variable. Patients with severe malabsorption and/or malnutrition may not be candidates for IM treatment if they have a markedly reduced muscle mass into which the iron preparation can be injected.

For all of the above reasons, including the fact that IM administration of iron dextran has not been shown to be safer or less toxic than the IV route, the most appropriate parenteral route is the intravenous one [11].

Intravenous iron*—*Intravenous iron is commonly administered to hemodialysis patients because of ongoing blood loss associated with the procedure, the need for adequate iron to respond to the administration of erythropoietin, and the frequent inability to utilize iron administered orally [6].

When ferric gluconate complex is used for this purpose (Ferrlecit®, Schein Pharmaceutical), a test dose of 2 mL of ferrlecit (25 mg elemental iron) is diluted in 50 mL of normal saline and infused IV over 60 minutes. If there is no reaction, up to 125 mg is administered (10 mL) at any one setting, diluted in 100 mL of normal saline, and infused over one hour. The remainder of the calculated dose of iron is given at subsequent dialysis sessions at this rate [12]. (See "Iron balance in predialysis, peritoneal dialysis, and home hemodialysis patients", section on Iron therapy).

Calculation of the dose*—*In selecting the dose of parenteral iron required, one calculates the iron deficit based upon the fact that 1 gm of hemoglobin contains 3.3 mg of elemental iron (show table 3).

Assume, for example, that a 60 kg woman with a hemoglobin concentration of 8 g/dL due to iron deficiency needs parenteral iron replacement, which will be given intravenously in the form of iron sucrose (20 mg iron/mL). The normal blood volume is approximately 65 mL/kg. Thus, her total blood volume is approximately 3900 mL or 39 deciliters (65 mL/kg x 60 kg). A normal hemoglobin concentration would be 14 g/dL. Thus, her hemoglobin deficit is 6 g/dL with a total deficit of 234 g (6 g/dL x 39 dL). Each gram of hemoglobin contains 3.3 mg of iron. Thus, her total red cell iron deficit is 772 mg (234 g of hemoglobin x 3.3 mg Fe per gram of hemoglobin). At an iron concentration of 20 mg/mL, this would require a total of 38.6 mL of iron sucrose. The product information sheet, as well as institutional guidelines, should be consulted for the need for a test dose, proper dilution, rate of infusion, and maximal allowable dose per infusion