IDA is the most common form of anemia worldwide, affecting approximately 50% of anemia cases. It results from prolonged negative iron balance in the body due to factors like inadequate iron intake, decreased absorption, increased demand, or blood loss. Diagnosis involves a complete history, physical exam, and lab tests showing low indicators of iron stores like serum ferritin and iron, along with an elevated TIBC. Treatment aims to replenish iron stores and typically consists of oral iron supplementation of 200mg elemental iron per day for 3-6 months.
Anemia Causes, Types, Symptoms, Diet, and Treatment Dr Medical
https://userupload.net/0gv9ijneu7hf
Anemia is a condition that develops when your blood lacks enough healthy red blood cells or hemoglobin. Hemoglobin is a main part of red blood cells and binds oxygen. If you have too few or abnormal red blood cells, or your hemoglobin is abnormal or low, the cells in your body will not get enough oxygen.
Megaloblastic anaemia is a type of anaemia characterized by the formation of unusually large, abnormal and immature red blood cells called as megaloblasts by the bone marrow, which are released into the blood. To know more visit here: www.lazoi.com
Megaloblastic anaemia is a red blood cell disorder due to the inhibition of DNA synthesis during erythropioesis.
Mitotically, the inhibition of the DNA synthesis impaires the progression of the cell cycle development from G2 to (M) stage.
Aplastic anemia is one of the stem cell disorder which leads to pancytopenia in the peripheral blood and decrease production of all cell line in bone marrow. it require bone marrow transplantation to cure the patient.
Anemia Causes, Types, Symptoms, Diet, and Treatment Dr Medical
https://userupload.net/0gv9ijneu7hf
Anemia is a condition that develops when your blood lacks enough healthy red blood cells or hemoglobin. Hemoglobin is a main part of red blood cells and binds oxygen. If you have too few or abnormal red blood cells, or your hemoglobin is abnormal or low, the cells in your body will not get enough oxygen.
Megaloblastic anaemia is a type of anaemia characterized by the formation of unusually large, abnormal and immature red blood cells called as megaloblasts by the bone marrow, which are released into the blood. To know more visit here: www.lazoi.com
Megaloblastic anaemia is a red blood cell disorder due to the inhibition of DNA synthesis during erythropioesis.
Mitotically, the inhibition of the DNA synthesis impaires the progression of the cell cycle development from G2 to (M) stage.
Aplastic anemia is one of the stem cell disorder which leads to pancytopenia in the peripheral blood and decrease production of all cell line in bone marrow. it require bone marrow transplantation to cure the patient.
A decrease in red blood cells when the body can't absorb enough red blood cells.It is an organ specific autoimmune diseases in which the body’s immune system attacks the lining of the stomach.
It was considered as a deadly disease due to the lack of available treatment.
Pernicious anemia is most common in caucasian persons of north European ancestry than in other racial groups.
A decrease in red blood cells when the body can't absorb enough red blood cells.It is an organ specific autoimmune diseases in which the body’s immune system attacks the lining of the stomach.
It was considered as a deadly disease due to the lack of available treatment.
Pernicious anemia is most common in caucasian persons of north European ancestry than in other racial groups.
White paper "Iron Therapy without problems"Michael Collan
This white paper will discuss iron therapy in general, why it is sometimes problematic,mainly due to tolerance and practical issues for those suffering from iron deficiency.
Important groups that are discussed in this aspect are children, young girls, fertile females, seniors and people with chronic diseases such as IBD, CHF, CKD that affect the iron metabolism and how Heme‐Iron supplementation change this situation.
The target is to inform the medicinal and pharmaceutical communities of this relatively new form of therapy and why it has great benefits compared to the traditional methods.
Educational and therapeutic topic on asthma for MBBS and MD pharmacology students. other students like BDS , BHMS, BAMS etc can use for knowledge. and academic purpose.
Iron deficiency anemia is the most advanced stage of iron deficiency which is characterized not only by low hemoglobin and Hematocrit levels but also by a reduction or depletion of iron stores, by low serum iron levels and decreased transferrin saturation.
Iron deficiency is an extremely common comorbidity in patients with heart failure, affecting up to 50% of all ambulatory patients. It is associated with reduced exercise capacity and physical well-being and reduced quality of life. Cutoff values have been identified for diagnosing iron deficiency in heart failure with reduced ejection fraction as serum ferritin, <100 μg/l, or ferritin, 100 to 300 μg/l, with transferrin saturation of <20%. Oral iron products have been shown to have little efficacy in heart failure, where the preference is intravenous iron products. Most clinical studies have been performed using ferric carboxymaltose with good efficacy in terms of improvements in 6-min walk test distance, peak oxygen consumption, quality of life, and improvements in New York Heart Association functional class. Data from meta-analyses also suggest beneficial effects for hospitalization rates for heart failure and reduction in cardiovascular mortality rates. A prospective trial to investigate effects on morbidity and mortality is currently ongoing. This paper highlights current knowledge of the pathophysiology of iron deficiency in heart failure, its prevalence and clinical impact, and its possible treatment options
Small Linear/ Cyclic Bioactive/Synthetic peptides for the treatment of Iron Deficiency Anaemia. Softwares used were licenced versions. Method is specific for laboratory scale only, for fine crystals, Glycine / Alanine are better starting materials.
1.
Tauhid Ahmed Bhuiyan, PharmD
Pharmacy Practice Resident (PGY-1)
King Faisal Specialist Hospital & Research Center
2. Explain background, definition, epidemiology, and etiology of
iron deficiency anemia (IDA)
Outline diagnostic algorithm of IDA
Identify key laboratory findings to diagnose IDA
Discuss available therapeutic management of IDA
3. Anemia is a group of disease characterized by a decrease in either
hemoglobin (Hb) or circulating red blood cells (RBCs)
o Results in reduced oxygen-carrying capacity of the blood
According to World Health Organization (WHO)
o ̴1.6 billion people (1/4 of world’s population ) are anemic
Not an innocent bystander; affects both length and quality of life
(QOL)
IDA occurs across all populations and is associated with
o Diminished QOL
o Physical and cognitive performance, and
o Unfavorable clinical outcomes
http://www.who.int/nutrition/publications/en/ida_assessment_prevention_control.pdf
4. DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011
Anemia
Macrocytic Normocytic Microcytic
Megaloblastic Non-megaloblastic IDA Genetic
Anomaly
1. Vitamin B12
deficiency
2. Folic acid
deficiency
1. Sickle cell
2. Thalassemia
1. Recent blood loss
2. Hemolysis
3. Bone marrow failure
4. Anemia of chronic disease
1. Hepatic disease
2. Drug-induced
anemia
3. Hypothyroidism
4. Reticulocytosis
5. According to WHO
o Anemia is defined as Hb <130 g/L in men or <120 g/L in female
IDA is the result of long-term negative iron balances
o Progressive loss of iron stores in the form of hemosiderin and ferritin
IDA is defined as
o Anemia with biochemical evidence of iron deficiency based on
following laboratory findings
• Serum ferritin, total iron binding capacity (TIBC), transferrin saturation, or
transferrin receptor
DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011
6. IDA is the most common nutritional deficiency in developing and
developed countries
IDA is considered to be the leading cause of anemia worldwide,
accounting for as many as 50% of cases
Prevalence of IDA greatly varies according to age, gender,
physiological, pathological, environmental, and socioeconomic
conditions
Data from NHANES*, prevalence of IDA
o Young children 1.2%
o Women of childbearing age 4.5%
*National Health and Nutrition Examination Survey http://www.who.int/nutrition/publications/en/ida_assessment_prevention_control.pdf
7. RBC production
DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011
Iron + Hb
8. Normal iron content of the body
o ̴3-4 g (Hb, myoglobin, and cytochromes)
Iron is best absorb as ferrous (Fe2+) form in the duodenum, and to a smaller
extent in jejunum
Daily recommended allowance
o Adult males/postmenopausal females: 8 mg
o Menstruating female: 18 mg
Iron sources
o Heme iron (2-3X more absorbable): meat, fish, and poultry
o Non-heme iron: vegetables, fruits, dried beans, nuts, grain products, and dietary
supplements
Gastric acid/ascorbic acid increases non-heme iron absorption whereas
phytates (in bran), tannins/polyphenols (in tea), and calcium (in dairy product)
form insoluble complexes
DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011
9. ̶ Iron stores are reduced without reducing serum iron levels and can be
assessed with serum ferritin measurement
̶ Iron stores can be depleted without causing anemia
Iron deficiency occurs; Hb falls just above the lower limit normal
Considered as IDA and occurs because of Hb falls to less than normal values
Initial
Stage
Second
Stage
Third
Stage
Once iron stores are depleted, there still is adequate iron from daily RBC turnover
for Hb synthesis
10. IDA results from prolonged negative iron balance
Mainly due to following factors:
1. Inadequate iron intake
2. Decreased iron absorption
3. Increased iron demand or hematopoiesis
4. Increased iron loss
Matthew W. et al. Am Fam Physician. 2013;87(2):98-104
11. Females in the reproductive period of life
Menstruation
Pregnancy
Pathological blood loss
Deficient diet
Adult males and postmenopausal females
Pathological blood loss
Infants and children
Deficient diet
Diminished iron stores at birth
Firkin F. Hypochromic anemia. In: de Gruchy’s Clinical Hematology in Medical Practice, 1989Etiology
12. IDA adversely effects
o Cognitive performance, behavior, and physical growth of infants,
preschool, and school-aged children
o The immune status and morbidity from infections of all age groups
o The use of energy sources by muscle and thus the physical capacity
and work performance of adolescents and adults of all age groups
o Increase perinatal risks for mothers and neonates and overall infant
mortality during pregnancy
http://www.who.int/nutrition/publications/en/ida_assessment_prevention_control.pdf
14. Chief Complaints
Fatigue, lassitude, palpitation, and generalized weakness
History
Chronic blood loss, deficient diet
Clinical Features
1. Palor skin, nailbed, conjunctiva
2. Koilonychia (brittle, spoon shaped nails)
3. Atrophic glossitis (atrophy of tongue papilla; making the tongue
smooth and shiny)
4. Pica (compulsive eating of nonfood items) or pagophagia
(compulsive eating of ice)
Firkin F. Hypochromic anemia. In: de Gruchy’s Clinical Hematology in Medical Practice, 1989
15. Symptoms Signs
Decreased exercise tolerance Tachycardia
Fatigue
Pale appearance (most prominent in
conjunctiva)
Dizziness Decreased mental acuity
Irritability
Increased intensity of some cardiac valvular
murmurs
Weakness
Palpitations
Vertigo
Shortness of breath
Chest pain
DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011
16. Complete blood count (CBC), erythrocyte sedimentation rate
(ESR), and peripheral blood film (PBF)
Serum Iron profile
Bone marrow study (if needed)
Investigations to determine other causes of IDA (e.g. fecal
occult blood test, colonoscopy, urine examination)
17. Hematologic Indices Normal Range IDA
Hb 70—160 g/L Low
Hematocrit (Hct) 0.320—0.47 L/L Low
Mean corpuscular volume (MCV) 75—95 fL Low
Mean corpuscular hemoglobin (MCH) 24—30 pg Low
Mean corpuscular hemoglobin
concentration (MCHC) 290—370 g/L Low
Red cell distribution width (RDW) 11—15% High (early)
DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011c
18. Lab Exams Comments In IDA
Serum Fe
(50-100 mcg/dL)
1. It is the concentration bound to transferrin
2. Approximately one-third transferrin bound to iron
3. Levels are decreased by infection and inflammation
4. Best interpreted in conjunction with TIBC
Low
Serum ferritin
(>10-20 mcg/L)
1. Ferritin (storage iron) is proportional to total iron
stores
2. Best indicator of iron deficiency or overload
3. Infection or inflammation can increase the
concentration, independent of iron status
Low
Total iron binding capacity (TIBC)
(250-410 mcg/dL)
1. Indirect measurement of the iron-binding capacity of
serum transferrin (protein)
2. Levels don’t fluctuate over hours or days unlike serum
iron
High
% Saturation of transferrin (>20%)
1. Ratio of serum iron level to TIBC in percentage
2. Reflects the extent to which iron-binding sites are
occupied on transferrin and indicates the availability
of iron for erythropoiesis
3. Less sensitive and specific for IDA than ferritin
Low
DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011c
19. Matthew W. et al. Am Fam Physician. 2013;87(2):98-104
21. Short term
o Resolution of symptoms
o Replenish iron stores
Long term
o Improve quality of life (QOL)
o Prevention of recurrences
o Better growth and development (children)
24. Matthew W. et al. Am Fam Physician. 2013;87(2):98-104
25. Recommended dosage requirements
o 200 mg elemental iron per day for 3-6 months
o 2-3 divided doses to maximize tolerability
o Administration should be 1 hour before meals or on empty
stomach
Absorption of all oral preparations are similar
DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011
http://www.pharmapacks.com/product_images/g/220/a1174335_2761__43287.jpg
26. DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011
27. Gastrointestinal (GI) intolerance
o Nausea, vomiting, heartburn, and diarrhea or constipation
o Slow release or sustained release preparations may be used
o Combination products, e.g. Ferro-DDS (ferrous fumarate/docusate),
may be advantageous for certain patient population
Cause discoloration of stool
DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011
28. DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011
29. Indications for therapy
o Intolerance to oral route
o Malabsorption
o Long-term nonadherence
o Patient with significant blood loss who refuse transfusion and are
intolerant to oral therapy
o Chronic kidney disease (CKD)
Currently available formulations include
o Dextran, sodium ferric gluconate, iron sucrose, and ferumoxytol
Formulations differ in their molecular size, degradation kinetics,
bioavailability, and side effects profile
All preparations carry a risk for anaphylactic reactions but likely
to a lesser extent than iron dextran
DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011
30. Formulation
Amount of
elemental
iron
(mg/mL)
Warning Treatment Common adverse effects
Iron Dextran
(INFeD)
50
Black Box
Warning (BBW):
anaphylactic type
reactions
10 doses x 100 mg
= 1,000 mg
Pain and brown staining
at injection site, flushing,
hypotension, fever, chills,
myalgia, anaphylaxis
Sodium Ferric
Gluconate
(Ferrlecit)
62.5
No BBW:
Hypersensitivity
reaction
8 doses x 125 mg =
1,000 mg
Cramps, nausea and
vomiting, flushing,
hypotension, rash, pruritis
Iron Sucrose*
(Ferosac®) 20
BBW:
anaphylactic type
reactions
Up to 10 doses x
100 mg = 1,000 mg
Leg cramps, hypotension
Ferumoxytol
(Feraheme)
30
No BBW:
Hypersensitivity
reaction
2 doses x 510 mg =
1,020 mg
Diarrhea, constipation,
dizziness, hypotension,
peripheral edema
DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011*KFSH&RC Formulary
31. Hb-iron deficiency (in mg) = body weight (kg) x (normal Hb - actual Hb in g/L) x 0.24 §
Above calculation is based on:
A normal Hb 150 g/L for body weights >35 kg and 130 g/L ≤34 kg body weight
respectively
The iron-content of hemoglobin (0.34%)
The blood volume (∼7% of the body weight) and the requirements of depot iron
(∼15 mg/kg up to a weight of about 34 kg, total of 500 mg >34 kg)
§Factor 0.24 = 0.0034 x 0.07 x 1000
Total iron deficiency in mg =
Hb-iron deficiency + depot iron
KFSH&RC Formulary
http://online.lexi.com/lco/action/doc/retrieve/docid/faisal_f/289383
*Iron sucrose
32. • Total vials of iron requirement for SA:
• 1508 mg elemental iron / (20 mg/mL)
• Total iron sucrose = 75 mL
• Iron sucrose (5 mL / ampule)
• (75 mL / 5) = 15 ampules
SA, 60 kg woman with a hemoglobin concentration of 80 g/L due to
iron deficiency needs parenteral iron replacement, which will be
given intravenously in the form of iron sucrose (20 mg iron/mL).
Calculate total iron deficiency and amount of iron sucrose
(ampules) for SA? [Injection: 5 mL/ampule]
Solution:
o Step 1: calculating elemental iron deficiency in Hb of SA
• 60 kg X (150 g/L – 80 g/L) X 0.24 = 1008
o Step 2: depot iron
• 500 mg (since SA >34 kg)
o Step 3: total iron deficiency
• Step 1 + Step 2 = 1008 + 500 = 1508 mg elemental iron
35. Decision to manage anemia is based on the evaluation of risk and
benefit
Transfusion is generally not indicated if Hb >100 g/L whereas
transfusion of RBCs should be considered when Hb is <70 to 80 g/L
in hospitalized, stable patient
Transfusion of allogeneic blood is indicated in acute situations (e.g.
severe blood loss)
Transfusions may also be necessary for patient with cardiac
instability
DiPiro J. Anemia. In: Pharmacotherapy: A Pathophysiological Approach, 2011
Szczepiorkowski Z. et al. ASH Education Book 2013;1:638-644 or
http://asheducationbook.hematologylibrary.org/content/2013/1/638.full
KFSH&RC Transfusion Guideline: http://ig.kfshrc.edu.sa/wps/portal/
36. Positive response in reticulocytosis is seen in few days of oral
therapy
Hb should reach to normal level after 2 months
A Hb response of <20 g/L over a 3-week period warrants therapy
evaluation
Iron profile should be measure in the first week for oral therapy and
2 weeks after large intravenous doses
Hb and Hct should be measured weekly, and serum iron and ferritin
levels should be measured monthly
37. Provide education on healthy lifestyle
Identify high risk population for necessary preventative measures
Select appropriate medication therapy based on patient and drug
related factors
Provide medication counseling and adherence
Monitor therapeutic outcome and minimize adverse drug reactions
38. IDA is the most common form of anemia and is usually the result of
prolonged negative iron balance in the body
Four main factors contributing to IDA include
o Inadequate iron intake
o Decreased iron absorption
o Increased iron demand or hematopoiesis
o Increased iron loss
Clinical diagnosis of IDA should include complete patient history
and physical exams, followed by laboratory investigations
Abnormal laboratory investigations generally include low MCV,
serum iron, and ferritin; and high TIBC
39. Treatment of IDA usually consists of dietary supplementation and
administration of oral iron preparations
General recommendation for oral iron replacement is ̴200 mg
elemental iron/day, divided into 2-3 doses to maximize tolerability
Parenteral therapy is usually not indicated unless patient is
intolerant to oral therapy, having malabsorption, or in the case of
CKD
Anaphylactic reaction should be considered for all parenteral
formulation along with strictly monitoring adverse drug reaction
40. Decision to manage anemia with blood transfusion is based
on the evaluation of the risk and benefit and is only
considered when Hb is <70 to 80 g/L
Complete therapeutic response requires iron
supplementation for up to 2-6 months, however, symptoms
may improve within few days after oral therapy
41.
42. Q1: Which of the following is one of the common cause of IDA
in young male?
A. Deficient diet
B. Menstruation
C. Pathological blood loss
D. None of the above
43. Q2: Microcytic hypochromic anemia can be due to the
following factor(s):
A. Folic Acid
B. Vitamin B12
C. Iron deficiency
D. Hemolysis
44. Q3: Which of the following statement is false regarding iron in
our body?
A. It is best absorb in ferrous (Fe2+) form in the duodenum
B. Heme iron is found in meat, fish, and poultry
C. Gastric acid/ascorbic acid increases non-heme iron absorption
D. Non-heme iron is 2-3X more absorbable than heme iron
45. Q4: Identify the following laboratory investigations for
diagnosing IDA as high/low:
Hb
MCV
Serum iron
TIBC
Serum ferritin
Transferrin saturation
Low
Low
Low
High
Low
Low
46. Q5: For oral iron products, the following statements are true
except:
A. Ferrous sulfate tablet contains 65 mg elemental iron
B. Administration of oral iron should be 1 hour before meals or on
empty stomach preferably
C. Can cause GI intolerance and discoloration of stools
D. Percent elemental iron of all oral preparations is roughly the same
Editor's Notes
3rd bullet: Retrospective observational studies of hemodialysis and HF patients suggest that anemia is independent risk factor for mortality
- Anemia can be classified on the basis of the morphology of the RBCs, etiology, or pathophysiology
- This scheme of classification is based on the size of RBC which is measured by Mean cell volume (MCV). As per MCV, cells are considered macrocytic if they are larger than normal, microcytic if hey are smaller than normal, and normocytic if their size falls within normal limits
RBC production: The hormone EPO, 90% of which is produced in the kidneys, initiates and stimulates the production of RBCs. The main mechanism of EPO is preventing apoptosis of erythoid precursor cells and allowing their proliferation and subsequent maturation. Additionally, a decrease of tissue oxygen concentration can trigger the kidney to increase the production and release of EPO into the plasma.
RBC maturations: In normal RBC formation, a pluripotent stem cells give rise to erythroid burst forming unit which is then stimulated by GM-CSF, IL-3, and EPO to become erythoid colony forming unit. This unit is sensitive to EPO which then yields to proerythroblast. Proerythroblast further divides and finally forms into reticulocyte. In the bone marrow, this immature retuculocyte gradually gets matured by incorporation of Hb and iron, which is eventually released to the circulation. The maturation process of RBC occurs in circulation and it takes about a week.
- Approximate 2 g of iron exist in the form of Hb, and 3 mg of iron is bound to transferrin in plasma, and 1000 mg of iron exists as storage iron in the form of ferritin or hemosiderin
Hepcidine is a regulator o intestinal iron absorption, iron-recycling, and iron mobilizatin from hepatic stores. It is a peptide made in the liver, distributed in plasma, and excreted in urine. Hepcidin synthesis is increased by iron loading and decreased in hypoxia. Hepcidin is an important mediator of Anemia of chronic disease.
Normal western daily diet contains appox. 12-15 mg of iron, mainly in the ferric form.
Iron is ionized by the stomach acid and reduced to ferrous form to get absorbed by the small intestine
WHO NHD 01.3
Lassitude: lack of energy
Anemia of rapid onset is most likely to present with cardio respiratory symptoms such as tachycardia, palpitattions, angina, hypotension, lightheadedness, and breathlessness due to decreased oxygen delivery to tissues or hypovolemia in those with acute bleeding
If onset is more chronic, presenting symptoms may include fatigue, weakness, headache, symptoms of heart failure, vertigo, faintness, sensitivity to cold, palor, or loss of skin tone
Possible manifestations of IDA include glossal pain, smooth tongue, reduced salivary flow, pica (compulsive eating of nonfood items), and pagophagia (compulsive eating of ice)
PBF: Provide information on the functional status of the bone marrow and defects in RBC production. Additionally, it provides variation in the cell size (anisocytosis) and shape (poikilocytosis).
Higher values of Hb seen in males are due to stimulation of RBC production by androgenic steroids, whereas the lower values in females are due to decrease in Hb as a result of blood loss during menstruation
Hct expressed as a percentage because of the measurement of actual volume of RBCs in a unit volume of whole blood. In general, Hct is 3X the Hb values
MCH is the amount of hb in a RBC. Two morphologic changes, microcytosis and hypochromia, can reduce MCH whereas the most common cause of an elevated MCH is macrocytosis
MCHC (Hb/Hct) is the concentration of Hb per volume of cells. Because MCHC is independent of cell size, it is more useful than MCH in distinguishing between microcytosis and hypochromia.
Another investigation is total reticulocyte count, which is an indirect measurement of new RBC production. It reflects how quickly immature RBCs (reticulocyte) are produced by the bone marrow and released into the blood. Reticulocytes circulate in the blood approx. 2 days before maturing into RBCs. A lack of reticulocytosis in anemia indicates impaired RBC production (e.g. IDA, b12 deiciency, ACD, malabsorption, renal deficiency, and malignancy) whereas a high reticulocyte count may be seen in acute blood loss or hemolysis. Multiplying the reticulocyte percentage by the patient’s Hct and then dividing the product by an average normla Hct (for men or women) produces a corrected percentage of reticulocytes. When the reticulocyte count is >2.5%, hemolysis may be present.
Wintrobe indices describe the size and Hb content of the RBCs
The higher the RDW is, the more variable is he size of the RBCs. RDW increased in early IDA because of the release of large, immature, mucleated RBC to compensate for the anemia, but this change is not speicific for IDA
Serum Fe level show diurnal variation (higher in the morning, lower in the afternoon), but this variation is probably not clinically significant in timing of levels.
Serum Fe level decreases with IDA and ACD and increases with hemolytic anemias and iron overload
Each transferrin molecule can carry two iron atoms. The finding of low serum iron level and high TIBC suggest IDA. Patients with infection, inflammation, malignancy, liver disease, and uremia may have a decreased TIBC and a decreased iron level, which are consistent with the diagnosis of ACD. Oral contraceptive use and pregnancy can increase TIBC because serum transferrin production is increased with a variety of other protiens
In IDA, transferrin saturation of 15% or lower is commonly seen
Ferritin levels indicated the amount of iron stored in the liver, spleen, and bone marrow cells. Low serum ferritin levels are virtually indicative of IDA because they decrease only in association with IDA.
Another factor or investigation is soluble transferrin receptor assay. It is considered sensitive, early, highly quantitative marker of iron depletion. The concentration of sTfR is inversely proportional to tissue iron storage and if high indicative of iron deficiency.
fL= femtoliters (10-15L)
Exsiccate: to remove moisture or dry.
Iron is absorbed in the duodenum and upper jejunum; in persons with normal serum iron stores, 10% of an oral dose is absorbed; this is increased to 20% to 30% in persons with inadequate iron stores
- Antacids and tetracycline mostly chelate whereas the PPI/H2blocker reduces gastric acid which in turn decrease the absorption
- A concern with IV iron is that iron may be released too quickly and overload the ability of transferrin to bind it, leading to free iron reactions that can interfere with neutrophil function.
IV iron formulations generally consist of an iron core surrounded by a stabilizing carbohydrate shell to encapsulate the bioactive iron, to ensure release of iron within the cells of the reticuloendothelial system, and to limit side effects. The first-generation iron dextrans had the advantage of permitting administration of larger doses of iron by slow infusion over several hours, but the risk of anaphylaxis, consequent requirement of a test dose, and other side effects have led to a decline in use in most developed countries. Second-generation iron formulations such as iron sucrose and iron gluconate are associated with a lower incidence of allergic reactions compared with iron dextrans, but are administered only in small doses because of dose-related side effects such as hypotension (13,14). Ferumoxytol is a novel iron oxide nanoparticle with a polyglucose sorbitol carboxymethylether coating designed to minimize immunological sensitivity.
Iron Dextran: a complex of Ferric hydroxiide and carbohydrate dextran which can be given IV or IM. Different brands are not interchangable because they differ in their molecular weight. Iron dextran must be processed by macrophages for the iron to be biologically active. The benefit of iron dextran is it can be given as the total dose infusion.
Sodium ferric gluconate: complex of iron bound to one gluconate and four sucrose molecules. Must be taken up by mononuclear phagocytic system and has half life of 1 hour in the blood stream
Iron sucrose: polynuclear iron (III) hydroxide in sucrose complex. Following IV administration,, the iron is released directly from the circulating iron sucrose to transferrin and is taken up by the mononuclear system and metabolized. The half-life is 6 hours and should not be used concomitantly with oral iron preparations because it will reduce the absorption of oral iron. Overall, safe and efficacy analysis, it has been shown to the most safe and efficacious.
Ferumoxytol: approved by FDA in june 2009. approved to treat IDA in adults with CKD who are on or off dialysis. Feromoxytol can be administered at a quicker rate than other parenteral iron products at a rate of 30mg/s. Typical dosing is 510 mg IV followed by a second dose 3-8 days later.
Each unit of PRBCs contains approximately 200 mg of iron and will raise the hemoglobin by about 1 g/dL. side effects of blood transfusion, with the most common being fever, chills, and mild shortness of breath.
