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Nutritional anemias


Overview

Nutritional anemias result from deficiencies of micronutrients that are essential for hematopoiesis and clinically defined by the presence of anemia with an inappropriately low reticulocyte count response by the marrow to the degree of anemia. Nutritional anemias are often grouped by size or mean corpuscular volume (MCV), with microcytic most commonly resulting in iron-deficiency anemia (IDA) and macrocytic or megaloblastic anemia due to either vitamin B 12 or folate deficiency.

Iron-deficiency anemia

Introduction

Iron deficiency is the most common nutritional deficiency in children and is worldwide in distribution, affecting 2 billion people, predominantly women and children. While patients of any age may be affected, pediatric patients are characteristically between 6 months and 3 years or 11 and 17 years of age because of the rapid growth that occurs during these periods.

Prevalence

The incidence of IDA is high in young children. It is estimated that 40–50% of children under age 5 years in low- and low middle–income countries are iron deficient. In the United States, approximately 3% of children age 1–2 years have IDA. Prevalence rates are twice as high in high-risk groups such as Latino children. Iron deficiency typically occurs during this age-group due to a combination of rapid growth and insufficient dietary iron ( Table 4.1 ). A second peak is seen during adolescence with up to 16% of adolescent girls being iron deficient, with African-American and Latino girls disproportionately affected. Adolescents also experience rapid growth and occasionally suboptimal iron intake. Such risk factors are exacerbated in females due to the onset of menarche, particularly in the context of abnormal uterine or heavy menstrual bleeding.

Table 4.1
Causes of iron-deficiency anemia.
Modified from Lanzkowsky, P. Lanzkowsky’s Manual of Pediatric Hematology and Oncology, sixth ed. Elsevier (2016).
Deficient intake
  • 1.

    Breastfeeding without supplemental iron

  • 2.

    Excessive cow milk intake

  • 3.

    Low iron diet (vegan, vegetarian diet without appropriate supplementation)

Inadequate/impaired absorption
  • 1.

    Antacid therapy or high gastric pH

  • 2.

    Gastrointestinal disorder (inflammatory bowel disease, celiac disease)

  • 3.

    Intestinal failure (malabsorption) /resection

  • 4.

    Infection (prolonged diarrhea; Helicobacter pylori infection-associated gastritis)

Increased demand
  • 1.

    Low birth weight, prematurity, twins

  • 2.

    Growth (infancy, adolescence, and pregnancy)

  • 3.

    Cyanotic congenital heart disease

Blood loss
  • 1.

    Perinatal

    • a.

      Placental

    • b.

      Umbilicus

    • c.

      Postnatal

  • 2.

    Gastrointestinal tract

    • a.

      Hypersensitivity to whole cow’s milk? Due to heat-labile protein, resulting in blood loss and exudative enteropathy (leaky gut syndrome) ( Table 3.4 )

    • b.

      Anatomic gut lesions, including substantial intestinal resection

    • c.

      Gastritis

    • d.

      Intestinal parasites [e.g., hookworm ( Necator americanus or Ancylostoma duodenale ) and whipworm ( Trichuris trichiura )]

  • 3.

    Menstrual

  • 4.

    Other

    • a.

      Recurrent epistaxis

    • b.

      Idiopathic pulmonary hemosiderosis

    • c.

      Renal disease: infectious cystitis, microangiopathic hemolytic anemia, nephritic syndrome (urinary loss of transferrin), Berger disease, Goodpasture syndrome, and chronic intravascular hemolysis (hemoglobinuria)

    • d.

      Extracorporeal (hemodialysis, trauma)

Inadequate presentation to erythroid precursors (atransferrinemia; antitransferrin receptor antibodies)

Etiology

Growth

Growth during childhood is particularly rapid during infancy and puberty. Blood volume and body iron are directly related to body weight throughout life. IDA can occur at any time when rapid growth outstrips the ability of diet and body stores to supply iron requirements. In the first year of life, body weight triples and circulating hemoglobin mass doubles. Each kilogram gain in weight requires an increase of 35- to 45-mg body iron. The amount of iron in the newborn is 75 mg/kg. If no iron is present in the diet or blood loss occurs, the iron stores present at birth will be depleted by 6 months in a full-term infant and by 3–4 months in a premature infant.

Diet

The commonest cause of IDA is inadequate intake during the rapidly growing years of infancy and childhood ( Table 4.2 ).

Table 4.2
Infants at high risk for iron deficiency.
Modified from Lanzkowsky, P. Lanzkowsky’s Manual of Pediatric Hematology and Oncology, sixth ed. Elsevier (2016).
Increased iron needs
  • 1.

    Low birth weight

  • 2.

    Prematurity

  • 3.

    Multiple gestation

  • 4.

    High growth rate

  • 5.

    Chronic hypoxia—high altitude, cyanotic heart disease

  • 6.

    Fetal anemia/anemia at birth

Blood loss
  • 1.

    Perinatal bleeding

  • 2.

    Iatrogenic

Dietary factors
  • 1.

    Early cow’s milk intake

  • 2.

    Early solid food intake

  • 3.

    Rate of weight gain greater than average

  • 4.

    Low-iron formula

  • 5.

    Frequent tea intake a

  • 6.

    Low vitamin C intake b

  • 7.

    Low meat intake

  • 8.

    Breastfeeding >6 months without iron supplements

a Tea inhibits iron absorption.

b Vitamin C enhances iron absorption

Iron requirements of infancy

In normal infants, 1 mg/kg/day (assuming 10% absorption) is required to support normal growth. In premature or low-birth-weight infants, infants with anemia during the neonatal period, and those who have experienced significant blood loss, 2 mg/kg/day initiated by 2 weeks of age is recommended.

Dietary iron content and requirements

Newborn infants predominantly receive breast milk or iron-fortified formula as their primary source of nutrition. Breast milk and cow’s milk each contain less than 1.5-mg iron per 1000 calories (0.5–1.5 mg/L). Although both forms of milk are equally poor in iron, the bioavailability of iron in breast milk is greater. Breastfed infants absorb 20–80% of the iron, in contrast to about 10% absorbed from cow’s milk. After 6 months of age, however, breastfeeding does not provide sufficient iron to support ongoing growth, and a supplemental source of dietary or medicinal iron is required for optimal iron nutrition. Full-term, formula-fed infants do not need additional iron as infant formulas for over the last two decades in the United States contain 12 mg of iron/L. Table 4.3 lists iron content of infant foods.

Table 4.3
Iron content of infant foods.
Modified from Lanzkowsky, P. Lanzkowsky’s Manual of Pediatric Hematology and Oncology, sixth ed. Elsevier (2016).
Food Iron, mg Unit
Milk 0.5–1.5 Liter
Eggs 1.2 Each
Cereal, fortified 3.0–5.0 Ounce
VEGETABLES (STARCHED)
Yellow 0.1–0.3 Ounce
Green 0.3–0.4 Ounce
MEATS (STRAINED)
Beef, lamb, liver 0.4–2.0 Ounce
Pork, liver, bacon 6.6 Ounce
FRUITS (STRAINED)
0.2–0.4 Ounce

Young children, 1–3 years of age, should have an intake of iron of 7 mg/day. In the transition from infant foods to more standard table foods, infants may take less iron-fortified formula and cereal, but gain a variety of naturally iron-containing foods, such as meats and some vegetables. During this time period, children with excessive cow milk intake are at particularly high risk for developing iron deficiency. In severe cases, cow milk can result in an exudative enteropathy associated with chronic gastrointestinal (GI) blood loss resulting in iron deficiency. Long-standing iron deficiency may also induce an enteropathy or leaky gut syndrome. In this condition a number of blood constituents, in addition to red cells, are lost in the gut ( Table 4.4 ). Whole cow’s milk should be considered the cause of IDA under the following clinical circumstances:

  • 1.

    ≥24 ounces or more of whole cow’s milk consumed per day

  • 2.

    Iron deficiency accompanied by hypoalbuminemia (with or without edema), which is associated with hypotransferrinemia due to gut leakage of this similarly sized protein

  • 3.

    IDA unexplained by low birth weight, poor iron intake, or excessively rapid growth

  • 4.

    Suboptimal response to oral iron in IDA or IDA recurring after a satisfactory hematologic response following iron therapy

  • 5.

    Positive stool guaiac tests in the absence of gross bleeding and other evidence of intestinal lesions; return of GI function and prompt correction of anemia on cessation of cow’s milk

Table 4.4
Classification of iron-deficiency anemia (IDA) in relationship to gut involvement.
Modified from Lanzkowsky, P. Lanzkowsky’s Manual of Pediatric Hematology and Oncology, sixth ed. Elsevier (2016).
Mild or severe Severe a
Pathogenesis Cow’s milk Cow’s milk Anatomic lesions or inflammation
Gut changes None Leaky gut syndrome Malabsorption syndrome
Effect No blood loss Loss of: Red cells only Loss of:Red cellsPlasma proteinAlbuminImmune globulinCopperCalcium Impaired absorption of iron only Impaired absorption of xylose, fat, and vitamin A
Duodenitis
Result IDA IDA, guaiac-positive IDA, exudative enteropathy IDA, refractory to oral iron IDA, transient enteropathy
Treatment Oral ironModify diet Oral ironDiscontinue cow milk Oral ironDiscontinue cow milk Intravenous iron Intravenous iron

a Can occur in severe chronic IDA from any cause.

School-age children, 4–13 years of age, should have an intake of at least 8–10 mg/day of iron. Transitioning to adolescence increases iron requirements as this group has an increase in hemoglobin mass, increase in muscle mass, and menstrual loss in adolescent girls. For these reasons the recommended daily allowance for iron in the adolescent age-group is 11 mg for males and 15 mg for females.

Most environmental iron exist as insoluble salts and gastric acidity assists in converting it to an absorbable form. Any factors reducing gastric acidity (e.g., drugs—histamine-2 blockers, acid pump blockers; surgical procedures) impair iron absorption from nonheme sources. The iron present in plant products is limited both by low solubility and the presence of natural chelators, for example, phytates. Heme iron derived from animal sources is the most readily absorbed iron and is independent of gastric pH. The exact mechanisms of heme iron absorption are unknown.

Menstrual blood loss

Post menarche, girls have increased iron requirements to maintain overall iron balance. In this age-group, menstrual blood loss is an important cause of iron deficiency. Menstrual blood loss may average approximately 40 mL (20-mg iron) per cycle or more in adolescents with abnormal uterine or heavy menstrual bleeding. Adolescent girls with underlying bleeding disorders are at even higher risk for the development of iron-deficiency and/or severe anemia.

Gastrointestinal blood loss and impaired absorption

While blood loss from the GI tract can occur at any age, it should be formally evaluated and ruled out in any child presenting with IDA outside the typical young child and adolescent female patient populations. School-age children and adolescent males should have stool guaiac assessments performed and be considered for referral to gastroenterology to assess for underlying pathology (i.e., inflammatory bowel disease). Impaired iron absorption due to a generalized malabsorption syndrome (e.g., celiac disease) occurs at higher rates in adults but should be considered a cause for IDA in children, particularly when poor growth or other GI symptoms are present.

Iron-refractory iron-deficiency anemia

Iron-refractory iron-deficiency anemia (IRIDA) is an extremely rare autosomal recessive disorder caused by a mutation of TMPRSS6 , the gene encoding transmembrane protease, serine 6, also known as matriptase-2, which inhibits the signaling pathway that activates hepcidin, the iron regulatory hormone. It is characterized by striking microcytosis, extremely low transferrin saturation, normal or borderline-low ferritin levels, and high hepcidin levels. The diagnosis is confirmed by sequencing of TMPRSS6 . IRIDA occurs in less than 1% of cases of IDA seen in medical practice. Most cases of iron resistance are due to an uncorrected underlying etiology, poor adherence to prescribed oral iron administration, or disorders in the GI tract (see Table 4.1 ).

Stages of iron depletion

  • 1.

    Iron depletion: this occurs when tissue stores are decreased without a change in hematocrit or serum iron levels; serum ferritin levels will be first marker to decrease.

  • 2.

    Iron-deficient erythropoiesis : this occurs when reticuloendothelial macrophage iron stores are depleted. Serum iron level drops, and the total iron-binding capacity increases without a change in the hematocrit. Erythropoiesis begins to be limited by a lack of available iron and soluble transferrin receptor (STfR) levels increase. Reticulocyte hemoglobin content or equivalent (Ret-He, CHr) will become low.

  • 3.

    IDA: this is associated with erythrocyte microcytosis, hypochromia, increased red cell distribution width (RDW), and elevated levels of free erythrocyte protoporphyrin (FEP). It is detected when iron deficiency has persisted long enough that a large proportion of circulating erythrocytes were produced after iron became limiting. Anemia is the final stage in iron deficiency.

Note that initiation of iron therapy will result in improvement of iron and hematologic parameters in the reverse order to which they initially developed (i.e., anemia will resolve first).

Nonhematological manifestations of iron deficiency

Iron deficiency is a systemic disorder involving multiple systems rather than exclusively a hematologic condition associated with anemia. Table 4.5 lists important iron-containing compounds in the body and their function and Table 4.6 lists the tissue effects of iron deficiency.

Table 4.5
Important iron-containing compounds and their function.
From Lanzkowsky, P. Lanzkowsky’s Manual of Pediatric Hematology and Oncology, sixth ed. Elsevier (2016).
Compound Function
α-Glycerophosphate dehydrogenase Work capacity
Catalase RBC peroxide breakdown
Cytochromes ATP production, protein synthesis, electron transport
Ferritin Iron storage
Hemoglobin Oxygen delivery
Hemosiderin Iron storage
Mitochondrial dehydrogenase Electron transport
Monoamine oxidase Catecholamine metabolism
Myoglobin Oxygen storage for muscle contraction
Peroxidase Bacterial killing
Ribonucleotide reductase Lymphocyte DNA synthesis, tissue growth
Transferrin Iron transport
Xanthine oxidase Uric acid metabolism
Abbreviation: RBC , Red blood cell.

Table 4.6
Tissue effects of iron deficiency.
Modified from Lanzkowsky, P. Lanzkowsky’s Manual of Pediatric Hematology and Oncology, sixth ed. Elsevier (2016).
Gastrointestinal tract

  • Anorexia: common and an early symptom

  • Atrophic glossitis with flattened, atrophic, lingual papillae, which makes the tongue smooth and shiny

  • Dysphagia

  • Esophageal webs (Kelly–Paterson syndrome)

  • Exudative enteropathy/leaky gut syndrome

  • Generalized malabsorption

    • Beeturia

    • Decreased cytochrome oxidase activity, succinic dehydrogenase

    • Decreased disaccharidases

    • Increased absorption of cadmium and lead

    • Increased intestinal permeability index

Central nervous system

  • Irritability

  • Fatigue and decreased activity

  • Reduced cognitive performance; lower mental/motor developmental test scores

  • Decreased attentiveness, shorter attention span

  • Breath-holding spells

  • Papilledema

Cardiovascular system

  • Increase in exercise and recovery heart rate and cardiac output

  • Cardiac hypertrophy

  • Increase in plasma volume

  • Increased minute ventilation values

  • Increased tolerance to digitalis

Musculoskeletal system

  • Deficiency of myoglobin and cytochrome C

  • Decreased physical performance in both brief, intense exercise and prolonged endurance work

  • Rapid development of tissue lactic acidosis on exercise

Immunologic system

  • Impaired rate of recovery from illness; increased frequency of respiratory infections

  • Impaired leukocyte transformation; impaired granulocyte killing and nitroblue tetrazolium reduction by granulocytes

  • Decreased myeloperoxidase in leukocytes and small intestine

  • Decreased cutaneous hypersensitivity

  • Transferrin inhibition of bacterial growth by binding iron so that no free iron is available for growth of microorganisms

Cellular changes

  • Red cells

    • Ineffective erythropoiesis; decreased red cell survival

    • Increased autohemolysis; increased red cell rigidity

    • Increased susceptibility to sulfhydryl inhibitors

    • Decreased heme production; decreased globin and α-chain synthesis

    • Precipitation of α-globin monomers to cell membrane

    • Decreased glutathione peroxidase and catalase activity

    • Inefficient H 2 O 2 detoxification; greater susceptibility to H 2 O 2 hemolysis

    • Oxidative damage to cell membrane; increased cellular rigidity

    • Increased rate of glycolysis-glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, 2,3-DPG, and glutathione

    • Increase in NADH-methemoglobin reductase

    • Increase in erythrocyte glutamic oxaloacetic transaminase

    • Increase in free erythrocyte protoporphyrin

    • Impairment of DNA and RNA synthesis in bone marrow cells

  • Other tissues

    • Reduction in heme-containing enzymes (cytochrome C, cytochrome oxidase) and iron-dependent enzymes (succinic dehydrogenase, aconitase)

    • Reduction in monoamine oxidase

    • Increased excretion of urinary norepinephrine

    • Reduction in tyrosine hydroxylase (enzyme converting tyrosine to dihyroxyphenylalanine)

    • Alterations in cellular growth, DNA, RNA, and protein synthesis

    • Reduction in plasma zinc

2,3-DPG , 2,3-Diphosphoglycerate.

Clinical features

IDA is chronic, frequently asymptomatic, and likely undiagnosed. In mild anemia, minimal symptoms may be reported until treatment initiation and response occurs. In severe deficiency, pallor, irritability, anorexia, listlessness, fatigue, and pica (craving for nonfood items such as sand, dirt, ice, and clay) may occur. Symptoms of pica are often reversed in a few days on iron treatment before the anemia corrects itself. Restless leg syndrome, a condition that causes discomfort of the lower extremities that is relieved with movement, has been associated with iron deficiency, with a subset of patients having symptomatic improvement in response to iron therapy. It is theorized that this condition results from tissue iron deficiency within parts of the central nervous system related to movement.

Differential diagnosis

Although iron deficiency is one of the most common causes of microcytic anemia, other conditions should be considered, particularly in patients with a suboptimal response to a trial of oral iron therapy or history without significant risk factors for iron deficiency. Note that in patients with iron deficiency, hemoglobin A2 is decreased. Therefore the diagnosis of β-thalassemia trait/minor (in which hemoglobin A2 is increased) cannot typically be made until after the iron deficiency is corrected, if present. In patients with refractory or persistent microcytic anemia, it may be necessary to do additional investigations, such as determination of serum ferritin, STfR levels, hemoglobin analysis, and, rarely, the examination of the bone marrow for stained iron, in order to establish the cause of the hypochromia. Table 4.7 lists the investigations employed in the differential diagnosis of microcytic anemias.

Table 4.7
Summary of laboratory studies in microcytic anemias.
Modified from Lanzkowsky, P. Lanzkowsky’s Manual of Pediatric Hematology and Oncology, sixth ed. Elsevier (2016).
Ethnic origin Hb MCV RDW FEP Ferritin Serum iron TIBC Bone marrow iron Hb analysis Other features
Iron deficiency Any ↓ ↓ ↑ ↑ ↓ ↓ ↑ ↓ N Dietary deficiency
β-Thalassemia β + trait (heterozygous) Mediterranean Slight↓ ↓ N N N or↑ N N N A 2 raised F N or↑ Normal examination
β 0 (Homozygous) Mediterranean ↓ ↓ N ↑ ↑ ↑ ↑ ↑ F raised (60–90%) Transfusion dependent
Trait (α-thal-1) Asians, Blacks, Mediterranean N or slightly↓ ↓ N N N or↑ N N N N
Hemoglobin H disease ↓ ↓ ↑ N N or↑ N or↑ N ↑ Hgb H (2–40%) Variable hemolytic anemia; RBC inclusion bodies
Anemia of chronic infection Any ↓ N N ↑ N or ↑ ↓ N or ↑ N or ↑ N
Sideroblastic Any ↓ N ↑ N or↑ N or↑ N or↑ N or↓ ↑ N
Abbreviations: FEP , Free erythrocyte protoporphyrin; Hb , hemoglobin; MCV , mean corpuscular volume; N , normal; RBC , red blood cell; RDW , red cell distribution width; TIBC , total iron-binding capacity, ↑, abnormally high; ↓, abnormally low.

Laboratory parameters consistent with iron-deficiency anemia

  • 1.

    Hemoglobin : below the acceptable level for age ( Appendix 1 ); final stage of iron deficiency.

  • 2.

    Red cell indices : lower than normal MCV; widened RDW. In general, though not absolute, the RDW is high (>14.5%) in iron deficiency and normal in thalassemia (<13%). Decrease in MCV generally parallels decreases in hemoglobin.

  • 3.

    Reticulocyte count : relative number of reticulocytes often increased, but when corrected for anemia the reticulocyte count is usually normal. In severe IDA associated with bleeding, a reticulocyte count of 3–4% may occur.

  • 4.

    Reticulocyte hemoglobin content/equivalent (Ret-He, CHr): low, occurs prior to a drop in hemoglobin; one of the first parameters to correct with initiation of iron therapy.

  • 5.

    Platelet count : varies from thrombocytopenia to thrombocytosis; thrombocytopenia more common in severe IDA.

  • 6.

    Blood smear : red cells are hypochromic and microcytic with anisocytosis and poikilocytosis; thrombocytosis may also be noted.

  • 7.

    Bone marrow : not indicated to diagnose iron deficiency. If performed, shows hypercellularity of red cell precursors; distortion of normoblast nuclei may occur. Little or no iron is shown in normoblast and reticulum cells by Prussian blue staining.

  • 8.

    FEP : incorporation of iron into protoporphyrin represents the ultimate stage in the biosynthetic pathway of heme; failure of iron supply will result in an accumulation of free protoporphyrin not incorporated into heme synthesis and the release of erythrocytes into the circulation with high FEP levels. This process occurs prior to the development of microcytic anemia:

    • a.

      Normal FEP level is 15.5±8.3 mg/dL (upper limit 40 mg/dL).

    • b.

      Elevated in both iron deficiency and lead poisoning but much higher in lead poisoning; normal in thalassemia trait.

    • c.

      Elevated FEP level, an indication for iron therapy even when anemia and microcytosis have not yet developed.

  • 9.

    Red blood cell (RBC) zinc protoporphyrin/heme ratio : increased when there is disruption of normal heme production. Nonspecific—raised in iron deficiency, lead poisoning; markedly raised in protoporphyria, congenital erythropoietic porphyria. In these conditions, zinc substitutes for iron in protoporphyrin IX and the concentration of zinc protoporphyrin relative to heme increases. False-positive results may occur in hyperbilirubinemia and falsely low results if the specimen is not protected from light.

  • 10.

    Serum ferritin : reflects the level of body iron stores; it is quantitative, reproducible, specific, and sensitive and requires only a small blood sample. A concentration of less than 15 ng/mL is considered diagnostic of iron deficiency. Low serum ferritin is always consistent with iron deficiency. Normal ferritin levels, however, can exist in iron deficiency when bacterial or parasitic infection, malignancy, or chronic inflammatory conditions coexist because ferritin is an acute-phase reactant and its synthesis increases in acute or chronic infection or inflammation.

  • 11.

    Serum iron and iron saturation percentage : marker of circulating iron; limitations as diagnostic tool for iron deficiency. Reflects balance between several factors, including iron absorbed, iron used for hemoglobin synthesis, iron released by red cell destruction, and size of iron stores. Wide range of normal, varies significantly with age (see Appendix 1 ) and is subject to marked circadian changes (as much as 100 mg/dL during the day) and recent ingestion of iron. May be helpful to assess iron absorption.

  • 12.

    S oluble transferrin receptor (STfR) levels : sensitive measure of iron deficiency; correlates with hemoglobin and other laboratory parameters of iron status. STfR is increased in instances of hyperplasia of erythroid precursors such as IDA and thalassemia. It is unaffected by infection and inflammation, unlike serum ferritin. It is, therefore, of great value in distinguishing iron deficiency from the anemia of chronic disease and in identifying iron deficiency in the presence of chronic inflammation or infection. With erythroid hypoplasia or aplasia, for example, aplastic anemia, red cell aplasia, or chronic renal failure, the STfR concentration is decreased.

  • 13.

    STfR/log ferritin ratio : calculating the ratio of STfR to the logarithm of serum ferritin concentration provides the highest sensitivity and specificity in the presence of chronic inflammation or infection. Values of less than 2.2 mg/L exclude iron deficiency and values of more than 2.9 mg/L confirm iron deficiency.

  • 14.

    Serum hepcidin : may help identify patients in whom a response to oral iron is probable (those with low hepcidin levels) and those in whom it is not probable (those with normal or elevated hepcidin levels); not readily accessible as a diagnostic tool.

Treatment

Correct underlying etiology

In addition to correctly diagnosing IDA, its etiology must be addressed to ensure treatment success. The history should include conditions resulting in low iron stores at birth, dietary history, and consideration of all factors leading to blood loss. In adolescent girls a detailed menstrual history is imperative, and hormone therapy may be indicated to support recovery of anemia and prevention of recurrence. Aside from menstrual blood loss the most common site of bleeding is into the bowel. If examination of the stool for occult blood is positive, its cause should be evaluated further. Negative guaiac tests may occur if occult blood loss is intermittent or in very small amounts (<5 mL). For this reason, occult bleeding should be tested multiple times when GI bleeding is suspected.

Epistaxis, renal blood loss (hematuria or hemoglobinuria from paroxysmal nocturnal hemoglobinuria), and, on rare occasions, bleeding into the lung (idiopathic pulmonary hemosiderosis and Goodpasture syndrome) may all be causes of IDA. Bleeding into these areas requires specific investigations designed to detect the underlying cause.

Dietary counseling

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