Iron therapy

D Constipation related to adverse reaction to iron therapy... 

In patients with iron-deficiency anemia, appropriate oral iron therapy that delivers sufficient elemental iron should be administered before giving parenteral iron. 

The initial treatment of iron-deficiency anemia is oral iron therapy with 200 mg of elemental iron daily for those who are able to tolerate the oral route. In order to attain this amount of elemental iron daily, many different iron products and salt forms are available. Table 63-3 lists the various salt forms of oral iron available, the amount of elemental iron in each product, and the approximate daily dose of the salt to attain 200 mg of elemental iron daily. 

What changes to this patient s iron therapy do you recommend ... 

Parenteral iron therapy may be appropriate in cases where patients are unable to tolerate the oral formulation because of toxicities or compliance. In addition, those who have documented iron-deficiency anemia and have not responded to... 

Parenteral iron therapy currently is available in three different formulations, which are listed in Table 63-3. Iron dex-tran was the first parenteral iron formulation to be approved, followed by ferric gluconate, and then iron sucrose. Although these newer agents are only approved by the Food and Drug Administration (FDA) to treat anemia associated with CKD in patients receiving erythropoietin products, they are effective in treating iron-deficiency anemia as well. Iron dextran is FDA approved for treating documented iron deficiency in patients who are unable to tolerate the oral formulation. 

Because the patient is not able to tolerate oral iron therapy (constipation and nausea), changing to intravenous iron therapy is appropriate. 

What formulation of intravenous iron therapy should the patient receive ... 

Although EPO deficiency is the primary cause of CKD anemia, iron deficiency is often present, and it is essential to assess and monitor the CKD patient s iron status (NKF-K/DOQI guidelines). Iron stores in patients with CKD should be maintained so that transferrin saturation (TSAT) is greater than 20% and serum ferritin is greater than 100 ng/mL (100 mcg/L or 225 pmol/L). If iron stores are not maintained appropriately, epoetin or darbepoetin will not be effective, and most CKD patients will require iron supplementation. Oral iron therapy can be used, but it is often ineffective, particularly in CKD patients on dialysis. Therefore, intravenous iron therapy is used extensively in these patients. Details of the pharmacology, pharmacokinetics, adverse effects, interactions, dose, and administration of erythropoietin and iron products have been discussed previously. 

Silverstein SB, Rodgers GM. Parenteral iron therapy options. Am J Hematol 2004 76(l) 74-78. 

Iron-deficiency anemia in chronic PN patients may be due to underlying clinical conditions and the lack of iron supplementation in PN. Parenteral iron therapy becomes necessary in iron-deficient patients who cannot absorb or tolerate oral iron. Parenteral iron should be used with caution owing to infusion-related adverse effects. A test dose of 25 mg of iron dextran should be administered first, and the patient should be monitored for adverse effects for at least 60 minutes. Intravenous iron dextran then may be added to lipid-free PN at a daily dose of 100 mg until the total iron dose is given. Iron dextran is not compatible with intravenous lipid emulsions at therapeutic doses and can cause oiling out of the emulsion. Other parenteral iron formulations (e.g., iron sucrose and ferric gluconate) have not been evaluated for compounding in PN and should not be added to PN formulations. 

Geisser, P. (1998). Iron Therapy with Special Emphasis on Oxidative Stress, Vifor International Inc, St Gallen, Switzerland. 

Oral iron therapy with soluble ferrous iron salts, which are not enteric coated and not slow- or sustained-release, is recommended at a daily dosage of200 mg elemental iron in two or three divided doses (Table 33-3). 

Diet plays a significant role because iron is poorly absorbed from vegetables, grain products, dairy products, and eggs iron is best absorbed from meat, fish, and poultry. Administration of iron therapy with a meal decreases absorption by more than 50% but may be needed to improve tolerability. 

Parenteral iron may be required for patients with iron malabsorption, intolerance of oral iron therapy, or noncompliance. Parenteral administra-... 

Treatment of anemia of chronic disease is less specific than that of other anemias and should focus on correcting reversible causes. Iron therapy is... 

In iron-deficiency anemia, iron therapy should cause reticulocytosis in 5 to 7 days and raise Hb by 2 to 4 g/dL every 3 weeks. The patient should be reevaluated if reticulocytosis does not occur or if Hb does not increase by 2 g/dL within 3 weeks. Iron therapy is continued until iron stores are replenished, which usually requires at least 3 to 6 months. 

Iron supplementation is necessary to replete iron stores (Fig. 76-5). Parenteral iron therapy improves response to erythropoietic therapy and reduces the dose required to achieve and maintain target indices. In contrast, oral therapy is often inadequate. 

Peritoneal dialysis Attempt oral iron therapy, 200 mg/day elemental iron. Change to IV if necessary. 

FIGURE 76-5. Guidelines for iron therapy in the management of the anemia of chronic kidney disease (CKD). (CHr, content of hemoglobin in the reticulocytes ESA, erythropoietic-stimulating agent Hb, hemoglobin HD, hemodialysis PD, peritoneal dialysis TSat transferrin saturation.)... 

Gordeuk VR et ah Garhonyl iron therapy for iron deficiency anemia. Blood 61-J45-152, 1986... 

The length of iron therapy depends upon the cause and severity of the iron deficiency. In general, approximately 4 to 6 months of oral iron therapy is required to reverse uncomplicated iron deficiency anemias. Iron therapy should increase hemoglobin levels by 1 g/week. 

The parenteral use of complexes of iron and carbohydrates has resulted in anaphylactic-type reactions. Deaths associated with such administration have been reported therefore, use iron dextran injection only in those patients in whom the indications have been clearly established and laboratory investigations confirm an iron-deficient state not amenable to oral iron therapy. Because fatal anaphylactic reactions have been reported after administration of iron dextran injection, administer the drug only when resuscitation techniques and treatment of anaphylactic and anaphylactoid shock are readily available. 

Iron replacement for blood loss Direct iron therapy in these patients toward replacement of the equivalent amount of iron represented in the blood loss. The table and formula described under Iron deficiency anemia are not applicable for simple iron replacement values. 

Monitoring Exercise caution to withhold iron administration in the presence of evidence of tissue iron overload. Periodically monitor hematologic and hematinic parameters (hemoglobin, hematocrit, serum ferritin, and transferrin saturation). Withhold iron therapy in patients with evidence of iron overload. Transferrin saturation values increase rapidly after IV administration of iron sucrose thus, serum iron values may be reliably obtained 48 hours after IV dosing. 

Rimon E, Kagansky N, Kagansky M, Mechnick L, Mashiah T, Namir M, Levy S. Are we giving too much iron Low-dose iron therapy is effective in octogenarians. Am J Med 2005 118 1142-7. 

Stools may become black during iron therapy this side effect is harmless unless accompanied by abdominal cramping or pain and red streaking or sticky consistency of stool... 

After confirmation of iron deficiency iron therapy can be given by oral or parenteral route. Generally oral iron therapy is given unless the patient is suffering from severe anaemia, malabsorption syndrome, gastrectomy or patient is showing adverse effects to oral iron therapy. 

The challenge with parenteral iron therapy is that parenteral administration of inorganic free ferric iron produces serious dose-dependent toxicity, which severely limits the dose of that can be administered. However, when the ferric iron is formulated as a colloid containing particles with a core of iron oxyhydroxide surrounded by a core of carbohydrate, bioactive iron is released slowly from the stable colloid particles. In the USA, the three available forms of parenteral iron are iron dextran, sodium ferric gluconate complex, and iron sucrose. 

For patients who are treated chronically with parenteral iron, it is important to monitor iron storage levels to avoid the serious toxicity associated with iron overload. Unlike oral iron therapy, which is subject to the regulatory mechanism provided by the intestinal uptake system, parenteral administration, which bypasses this regulatory system, can deliver more iron than can be safely stored. Iron stores can be estimated on the basis of serum concentrations of ferritin and the transferrin saturation, which is the ratio of the total serum iron concentration to the total iron-binding capacity ( ). 

For mild anemia, the determination of red cell indices has some value in diagnosis however, it should be realized that these indices may appear to be entirely normal and that they are subject to errors. Patients with statistically normal hemoglobin values may show a positive hemoglobin response to iron therapy. A woman with hemoglobin concentration of 13g (100 ml)-1 may be iron deficient through excessive menstrual flow for her a hemoglobin concentration of 15g (100 ml)-1... 

The effective oral doses of mifepristone are 100-600 mg, and at any dose the bulk of recipients abort. Of 150 healthy women who received the higher dose, 131 attained a complete abortion. Three women reported bleeding for more than 2 weeks after abortion 16 women had a reduced hemoglobin concentration of under 11 g/dl, justifying iron therapy. Other adverse effects were uterine contractions and pelvic pain (n = 4), transient asthenia (n = 3), and nausea (n = 2) (5). These findings seem to be typical, even though dosage schemes have varied as little as 100 mg orally has been used successfully with similar adverse effects (SED-12,1037 6). 

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