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These are substances required in the formation of blood, and are used for treatment of anemia.

  1. Iron
  2. Maturation Factors: VIT. B12 and FOLIC ACID
  3. Growth Factors:
    1. Rbc: Eryhtropoitin, Darbepoitin Alfa
    2. Wbc: G-Csf, Gm-Csf
    3. Platelet: Thrombopoitin, Romiplostim, Eltrombopag, Oprelvekin                                           


Required for biosynthesis of heme and heme-containing proteins, including hemoglobin and myoglobin



  1. Iron is absorbed in the duodenum and proximal jejunum, although the more distal small intestine can absorb iron if necessary.
  2. Heme iron in meat hemoglobin and myoglobin can be absorbed intact without first having to be dissociated into elemental iron.
  3. Nonheme iron in foods and iron in inorganic iron salts and complexes must be reduced by a ferri-reductase to ferrous iron (Fe2+) before it can be absorbed by intestinal mucosal cells.
  4. Iron crosses the luminal membrane of the intestinal mucosal cell by two mechanisms: active transport of ferrous iron by the divalent metal transporter DMT1, and absorption of iron complexed with heme
  5. From basolateral membrane iron is transported by ferroportin and oxidized to ferric iron (Fe3+) by the ferroxidase hephaestin. The liver-derived hepcidin inhibits intestinal cell iron release by binding to ferroportin and triggering its internalization and destruction.
  6. Excess iron is stored in intestinal epithelial cells as ferritin, a water-soluble complex consisting of a core of ferric hydroxide covered by a shell of a specialized storage protein called apoferritin.


Iron is transported in the plasma bound to transferrin, a β-globulin that can bind two molecules of ferric iron


  1. In addition to the storage of iron in intestinal mucosal cells, iron is also stored, primarily as ferritin, in macrophages in the liver, spleen, and bone, and in parenchymal liver cells.
  2. The mobilization of iron from macrophages and hepatocytes is primarily controlled by Hepcidin.


  1. There is no mechanism for excretion of iron.
  2. Small amounts are lost in the feces by exfoliation of intestinal mucosal cells, and trace amounts are excreted in bile, urine, and sweat.




Ferrous Gluconate (36 mg of elemental iron )

Ferrous sulfate (65 mg of elemental iron)

Ferrous Fumarate (106 mg of elemental iron)

Iron dextran

Iron sucrose complex

Sodium ferric gluconate complex



  1. Microcytic, hypochromic anemia with MCV <80 fL and MCHC <30%.
  2. Low Serum Iron <30 mcg/dL with increased TIBC, resulting in a % transferrin saturation (SI/TIBC) of <10%.
  3. Low serum ferritin level (<20 mcg/L).

Adverse effects: Parenteral preparations can cause pain, hypersensitivity reactions.



Acute Iron Toxicity   

Chronic Iron Toxicity (Hemochromatosis)

Exclusively in young children who accidentally ingest iron tablets.

Necrotizing gastroenteritis, abdominal pain, bloody diarrhea, shock, lethargy, and dyspnea.

Whole bowel irrigation should be performed to flush out unabsorbed pills. Deferoxamine, a potent iron-chelating compound, can be given intravenously to bind iron that has already been absorbed and to promote its excre- tion in urine and feces.

Activated charcoal does not bind iron and thus is ineffective.

Most commonly occurs in patients with inherited hemochromatosis, and in patients who receive many red cell transfusions over a long period of time (eg, individuals with β-thalassemia).

Results in hemochromatosis, with damage to the heart, liver, pancreas, and other organs Organ failure and death can ensue

Most efficiently treated by Intermittent Phlebotomy. Iron chelation therapy using parenteral deferoxamine or the oral iron chelator deferasirox.


VIT. B12 and Folic Acid

VIT. B12


Cofactor required for essential enzymatic reactions that form tetrahydrofolate, convert homocysteine to methionine, and metabolize L-methylmalonyl-CoA

Precursor of an essential donor of methyl groups used for synthesis of amino acids, purines, and deoxynucleotide (DNA)

Vitamin B12 deficiency, which manifests as megaloblastic anemia and is the basis of pernicious anemia

Folic acid deficiency, which manifests as megaloblastic anemia, and prevention of congenital neural tube defects

Parenteral vitamin B12 is required for pernicious anemia and other malabsorption syndromes

No toxicity associated with excess vitamin B12


Toxicity: Folic acid is not toxic in overdose, but large amounts can partially compensate for vitamin B12 deficiency and put people with unrecognized B12 deficiency at risk of neuro- logic consequences of vitamin B12 deficiency, which are not compensated by folic acid



Folacin (pteroylglutamic acid)




  1. Macrocytic, normochromic with MCV >100 fL and normal or elevated MCHC
  2. FOLIC ACID: Low serum folic acid (<4 ng/mL)
  3. VIT. B12: Low serum cobalamin (<150 pmol/L) accompanied by increased serum homocysteine (>13 μmol/L), and increased serum (>0.4 μmol/L) and urine (>3.6 μmol/mol creatinine) methylmalonic acid.


Endogenous erythropoietin is primarily produced in the kidney in response to tissue hypoxia. In patients with renal disease, erythropoietin levels are usually low because the kidneys cannot produce the growth factor. These are the patients most likely to respond to treatment with exogenous erythropoietin.


  1. Patients with chronic renal failure
  2. HIV-infected patients treated with zidovudine
  3. Cancer patients treated with myelosuppressive cancer chemotherapy
  4. Patients scheduled to undergo elective, noncardiac, nonvascular surgery

Adverse effect: The most common adverse effects of erythropoietin are hypertension and thrombotic complications. Allergic reactions have been infrequent. There have been a small number of cases of pure red cell aplasia (PRCA)


Three preparations are available:

  1. EPOETIN ALPHA – Thrice a week s/c injection
  2. EPOETIN BETA – once a month s/c injection (longest acting)
  3. DARBEPOETIN ALFA – weekly s/c injection

Myeloid Growth Factors

Granulocyte-colony-stimulating factor (G-CSF; filgrastim)

Pegfilgrastim: Long-acting form of filgrastim that is covalently linked to a type of polyethylene glycol


  1. Stimulates G-CSF receptors expressed on mature neutrophils and their progenitors.
  2. Stimulates neutrophil progenitor proliferation and differentiation, activates phagocytic activity of mature neutrophils and extends their survival
  3. Mobilizes hematopoietic stem cells.


  1. Neutropenia associated with congenital neutropenia, cyclic neutropenia, myelodysplasia, and aplastic anemia
  2. Secondary prevention of neutropenia in patients undergoing cytotoxic chemotherapy
  3. Mobilization of peripheral blood cells in preparation for autologous and allogeneic stem cell transplantation.

Toxicity: Bone pain, rarely splenic rupture

GM-CSF (Sargramostim): Myeloid growth factor that acts through a distinct GM-CSF receptor to stimulate proliferation and differentiation of early and late granulocytic progenitor cells, and erythroid and megakaryocyte progenitors; clinical uses are similar to those of G-CSF, but it is more likely than GM-CSF to cause fever, arthralgia, myalgia, and capillary leak syndrome

Plerixafor: Antagonist of CXCR4 used in combination with G-CSF for mobilization of peripheral blood cells prior to autologous transplantation in patients with multiple myeloma or non-Hodgkin’s lymphoma who responded suboptimally to G-CSF alone.


Megakaryocyte Growth Factors

  1. Oprelvekin (interleukin-11; IL-11)
    Recombinant form of an endogenous cytokine, which activates IL-11 receptors

Action: Stimulates growth of multiple lymphoid and myeloid cells, including megakaryocyte progenitors • increases the number of circulating platelets and neutrophils

Uses: Secondary prevention of thrombocytopenia in patients undergoing cytotoxic chemotherapy for non-myeloid cancers

Toxicity: Fatigue, headache, dizziness, anemia, fluid accumulation in the lungs, and transient atrial arrhythmias

  1. Romiplostim:
  • Genetically engineered protein in which Fccomponents of a human antibody are fused to multiple copies of a peptide that stimulates the thrombopoitin receptors.
  • Approved for treatment of idiopathic thrombocytopenic purpura (ITP).
  1. Eltrombopag: Orally active.


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