Nejm 1999;341:1986; in infancy and childhood—Nejm 1993;329:190

Cause: Insufficient Fe for heme and related coenzyme synthesis because of gi blood loss from cancers, benign diseases like ulcers, eg, chronic H. pylorigastritis (Jama 1997;277:1135); or in runners (Ann IM 1984;100:843); or from cow's milk-induced giGI bleeding in infants <1 yr old; or because of absorptive defects in mucosa, as in sprue

Pathophys:Fe absorption is a balance between the reticuloendothelial system storage and gi mucosal cells' shedding of ferritin, a storage form (Nejm 1971;284:1413)

Prevalence in US (Jama 1997;277:973): children age q1-2yr = 3%, adolescent girls = 2%, childbearing women = 5%

Increased prevalence in

• Areas of low dietary Fe (Maritime Provinces)
• Children age <1 with Fe-deficient mother and/or diet (e.g., exclusively breastfed)
• Adult women with heavy menses, pregnancy, nursing, or dieting
• Adult men with occult gi bleed, esp cancers
• Pica eaters, since starch, clay, etc, absorb Fe
• Post-gastric surgery, 50% at 10 yr due to rapid transit and absent H⁺, which is necessary for Fe absorption
• Any patient with colon, esophageal, or other gi cancer

Sx: of anemia—sore mouth or tongue; pica, eating of starch, clay, etc (cause or effect? Ann IM 1968;69:435)

Si:Angular stomatitis, glossitis, nail spooning (r/o hyperthyroidism)

With rx, reticulocytes increase in 5 d, Hgb increases 0.2 gm/d

Plummer-Vinson syndrome, seen in women, with esophageal webbing between cricoid and arch of aorta causing dysphagia. In children, Fe % saturations <10% w anemia, even if corrected, correlate w poor later school performance (Nejm 1991;325:687), restless leg syndrome (Restless Leg Syndrome)

r/o COLON CANCER ALWAYS, w colonoscopy or unless UGI sx, in which case w EGD 1st. Hypoproliferative normochromic normocytic ANEMIA OF CHRONIC DISEASE (Nejm 2005;352:1011) caused by depressed erythropoietin (<100) (Nejm 1990;322:1689) and its activity as well as impaired iron utilization. Treatable w po Fe and erythropoietin 150 U sc biw (Nejm 1996;334:619) and rx of underlying disease. Also other microcytic anemias: thalassemia, lead intoxication, inherited hemoglobin E, paroxysmal nocturnal hemoglobinuria

Lab:

Chem:Serum iron <120 mg %, TIBC >340 mg %, % saturation <8% (between 8% and 20% may be hypoproliferative low reticuloendothelial system Fe release). Ferritin <100 and often <15 µgm/L (reflects marrow Fe but can be falsely elevated with inflammation). Erythropoietin levels elevated >500

Hem:Anemia w Hgb <11%, hct <32%; diagnostic trial of iron should lead to normal crit in <2 mo

Platelets increased (Nejm 1970;282:492) due to thrombopoietin effect of erythropoietin

Polys decreased in severe disease

Rbc's show microcytes, hypochromia, targets, pencil forms; indices show MCHC <30 mg %, decreased MCH and MCV (r/o ß-thalassemia, hemoglobin C or D disease, spherocytosis, lead poisoning, and chronic aluminum toxicity (Nejm 1997;336:1556)

Path:Marrow shows no intracellular iron

Rx:

FeSO₄ or ferrous gluconate 300 mg tid po, or qd if no rush; use elixir if rapid transit causes poor absorption; with vitamin C to increase absorption in elderly or unusual, esp achlorhydric, conditions; avoid taking w tea, which decreases absorption by 75%.

FeSO₄ in all exclusively breastfed infants beginning at 4 mos until Fe-containing foods added to diet (Peds 2010;126:1040), controversy re possible slowed growth with Fe supplemented kids with nl Hb (Nejm 2002;132:3249)

FeSO₄ 30 mg po (15 mg elemental iron) is adequate for replacement in elderly w fewer side effects (Am J Med 2005;118:1142)

Fe dextran iv only (not im), rarely need