Nutritional Anemias

Spenser Parker, Katie Gardner, Juliette Soelberg, McKell Compton

Case Study Patient SH 31 yr. old female 23rd week of gestation, 3rd pregnancy Chief complaint:

Fell on ice and has had abdominal pain and vaginal spotting. Questioned if she was beginning premature labor

Dx: microcytic, hypochromic anemia 2o to iron deficiency

Discharged the following day on 40 mg ferrous sulfate TID

Basic terms Anemia: a deficiency in the size or number of

RBC or the amount of Hgb they contain that limits the exchange of oxygen and carbon dioxide

Macrocytic: larger-than-normal RBC Microcytic: smaller-than-normal RBC Megaloblastic: large, immature, abnormal, RBC Hypochromic: deficient Hgb content and pale

color of RBC Normochromic: sufficient Hgb content of RBC CBC: complete blood count

CBC Includes:

Total blood cell (TBC) count Hemoglobin Hematocrit RBC indices (measurements of the volume,

size, distribution and Hgb content of RBC) WBC count and differential count Blood smear Platelet count and mean platelet volume (MPV)

Iron Deficiency Anemia

Erythropoiesis Occurs in bone marrow Erythrocytes derived from precursor cells, erythroblasts/

normoblasts Abnormal erythroblasts called megaloblasts Erythropoietin stimulates uncommitted stem cells to

differentiate into proerythroblasts Hgb is apparent and increases in quantity as nuclear size

shrinks Reticulocyte matures into an erythrocyte within 24 to 48

hours Erythrocyte loses its capacity for Hgb synthesis and oxidative

metabolism

Hemoglobin Synthesis Hgb: the substance that reversibly binds oxygen Each hemoglobin molecule consists of two parts

1. a protein “globin” part, composed of four polypeptide chains2. Four disk-shaped pigment molecules called “hemes”. Each heme has an iron molecule in the center. Fe++(ferrous iron) + porphyrin= Heme

Each heme molecule is capable of carrying one molecule of oxygen

Ferric iron carries an extra positive charge and forms methemoglobin, forming an unstable type of hgb not capable of binding oxygen

Heme (Fe+porphyrin) Hemoglobin (globin+heme)

Iron Adult body contains 2 major pools of iron

1. functional iron in hgb, myoglobin, and enzymes

2. storage iron in ferritin, hemosiderin, and transferrin (transport protein in blood)

Iron is highly conserved by the body 90% is recovered and reused everyday The rest is excreted mainly in the bile Dietary iron must meet this 10% gap to

maintain iron balance or else iron deficiency result

Dietary iron exists in two chemical forms: heme and nonheme

Heme Iron Heme iron: in hemoglobin, myoglobin, and

some enzymes from animal sources absorbed across brush border after

digested from animal sources. the ferrous iron is enzymatically removed

from the ferroporphyrin complex the free iron ions combine with apoferritin

to form ferritin iron stores are moved into blood at the

basolateral membrane involving an active transport mechanism

Nonheme Iron Nonheme iron: mainly in plant foods but also in some

animal foods must be in a soluble (ionized) form to be

transferred across the brush border acid of gastric secretions enhance the solubility

and change the iron to the ionic state either as ferric (+3) or ferrous (+2) oxidation state

divalent metal transporter 1 (DMT1) transports ferrous iron across the border

the ferrous (+2) form is absorbed more readily, ferric iron (+3) has to be reduced by ferric reductase to be absorbed

the ferrous iron is then bound to apoferritin and goes through the same process as with heme iron to enter the blood

Absorption Efficiency of absorption is controlled by intestinal

mucosa allowing certain amounts of iron to enter blood from the ferritin pool according to the body’s needs

Hepcidin produced by liver acts on mucosa cells and inhibits absorption of iron.

Another signal from body to the absorbing cells may be transferrin saturation.

A low %TIBC of transferrin would stimulate absorbing cells to transport iron across the basolateral membrane to the blood. If iron concentration is excessive, absorbing cells would be down regulated and less iron would be absorbed

When circulating % transferrin saturation is low, the new intestinal cells (intestinal cells are sloughed off every 5 to 6 days) will have more receptors for iron absorption

Iron Deficiency Anemia World’s most common nutritional deficiency

disease Iron deficiency results in decreased production

of hemoglobin (Hgb) Which in turn results in microcytic,

hypochromic anemia This anemia is the last stage of iron

deficiency, representing a long period of iron deprivation

Etiology1. Inadequate ingestion2. Inadequate absorption 3. Inadequate utilization4. Increased requirement5. Increased blood loss or excretion6. Defects in release from stores

Inadequate Absorption Medications that cause GI bleeding (aspirin,

NSAIDS) Diarrhea (decreases intestinal transit

time/absorption) Achlorydria (production of gastric acid is not

present or low) Celiac disease Atrophic gastritis Partial or total gastrectomy Drug interference (antacids, cholestyramine,

cimedtidine [Tagamet], pancreatin, ranitidine [Zantac], tetrcycline, and antiretroviral medications [especially the necleoside reverse transcriptase inhibitors, Combivir, Epivir, Retrovir, Zerit and the protease inhibitor Crixivan])

Stages of Deficiency Stages of negative iron balance

I: Moderate depletion of iron stores; no dysfunctionII: Severe depletion of iron stores; no dysfunctionIII: Iron deficiency; dysfunctionIV: Iron deficiency; dysfunction and anemia

Measurements Of Iron Deficiency1. Plasma ferritin2. Plasma iron3. Total circulating transferrin4. Saturation of circulating transferrin5. Saturation of ferritin with iron6. Soluble serum transferrin receptor (STFR)

Diagnosis Diagnosis requires more than one method

of iron evaluation Preferably the first three measurements Should also include an assessment of cell

morphology Serum or plasma ferritin level is the most

sensitive parameter of negative iron balance (decreases only in presence of true iron deficiency, as with transferrin saturation)

Laboratory TestsNormal Levels:

Ferritin: Males:12-300 ng/mL Female:10-150 ng/mLSerum Iron: Male (80-180 mcg/dL) Female (60-160mcg/dL).Total Iron-Binding Capacity (TIBC): 250-460 mcg/dL.Transferrin: Male (215-365 mg/dL) Female (250-380 mg/dL) Transferrin Saturation: Male 20% to 50% Females 15% to 50%Hematocrit: Male 42%-52% Female 37%-47%Hemoglobin: Male14-18g/dL Female12-16g/dL

Laboratory Tests: Ferritin Most sensitive test to determine iron-deficiency

anemia Major iron-storage protein, normally present in the

serum in concentrations directly related to iron storage

Decreases in ferritin levels indicate a decrease in iron storage associated with iron deficiency anemia

Ferritin level below 10mg/100mL is diagnostic of iron deficiency anemia

Only when protein depletion is severe can ferritin be decreased by malnutrition

Ferritin can act as acute-phase reactant protein and may be elevated in conditions not reflecting iron stores

Laboratory Tests : Serum Iron

Serum iron: measurement of the quantity of iron bound to transferrin (globulin protein transporting absorbed iron from the plasma to the bone marrow to be incorporated into Hgb).

Decreased serum iron level is characteristic of iron-deficiency anemia.

Serum iron levels may vary significantly during the day

Blood specimen should be drawn in the morning Refrain from eating for appx. 12 hrs to avoid high iron

measurement by eating food with a high iron content

Laboratory Test: TIBC and Transferrin TIBC is a measurement of all proteins

available for binding mobile iron. Transferrin represents the largest quantity

of iron-binding proteins. Thus TIBC is an indirect yet accurate

measurement of transferrin. Ferritin not included in TIBC (binds only

stored iron) TIBC is increased in 70% of patients with

iron deficiency. During iron overload, TIBC is less reflective

of true transferrin levels

Laboratory Test: TIBC and Transferrin Saturation Transferrin saturation (%)= Serum iron level x

(100%) TIBC

Percentage of transferrin and other mobile iron-binding proteins saturated with iron is helpful in determining the cause of abnormal iron and TIBC levels.

Decreased TIBC saturation or transferrin saturation level is characteristic of iron-deficiency anemia (decreased below 15%)

Increased intake or absorption of iron leads to elevated iron levels (TIBC is unchanged and the percent of transferrin saturation increases)

Laboratory Tests: Iron-related CBC Hematocrit (Hct)-measure of the percentage of total blood volume

that is made up by the RBCs. Decreased levels of Hct indicate anemia. Hct can be altered by dehydration, increased RBC

size, pregnancy due to chronic hemodilution, living at high altitudes.

Hemoglobin (Hgb)-measure of the total amount of Hgb in the blood. Oxygen carrying capacity of the blood determined by the Hgb concentration

Decreased levels of Hgb indicate anemia Hgb levels can be altered during pregnancy, living in

high altitudes, being a heavy smokes. Red Blood Cell Count (RBC)- count of the number of circulating

RBCs in 1 mm3 of peripheral venous blood. When the value is decreased by more than 10% of the

expected normal value, the patient is said to be anemic. RBC alters with pregnancy, high altitudes, and

hydration status.

Laboratory Tests: Hemoglobin Hgb concentration by itself unsuitable as a

diagnostic tool in cases of suspected iron deficiency anemia

It is affected only late in the disease It cannot distinguish iron deficiency

from other anemias Hemoglobin values in normal

individuals vary widely

Laboratory Tests: protoporphyrin The iron-containing portion of the

respiratory pigments that combine with protein to form hemoglobin or myoglobin can be used to assess iron deficiency

The zinc protoporphryin (ZnPP)/heme ratio is measured

This can be affected by chronic infection Can produce a condition that mimics

iron deficiency anemia when iron is adequate

Pathophysiology Depleted iron stores, inadequate iron delivery to bone

marrow, impaired iron use within the marrow causes reduced hgb synthesis

Iron deficiency anemia present when the demand for iron exceeds the supply

Develops slowly through four overlapping stages Stage I: Early negative iron balance Stage II: Iron stores are depleted. Erythropoiesis

proceeds normally with the hgb content of RBCs remaining normal

Stage III: Decreased circulating iron levels; thus transportation of iron to bone marrow is diminished resulting in damaged metabolism and iron deficiency erythropoiesis (decreased levels of erythron iron)

Stage IV: more small hemoglobin-deficient cells enter the circulation in sufficient numbers to replace the normal mature erythrocytes that have been removed from the circulation

Signs and Symptoms Fatigue, shortness of breath Decreased work

performance/exercise tolerance

Anorexia Pica Pagophagia (ice eating) Slow cognitive and social

development in children Growth abnormalities Reduction in gastric acidity Reduced immunocompetence Mental confusion, memory

loss, disorientation in elderly population

More severe epithelial disorders: Red, sore, painful tongue Brittle, thin, spoon shaped

(koilonychia) nails Mouth: atrophy of lingual

papillae- glossitis; burning; redness; angular stomatitis; and a form of dysphagia

Stomach: gastritis, may result in achloryhdria

Skin may appear pale Inside of lower eyelid may be

light pink instead of red Cardiovascular and

respiratory changes can lead to cardiac failure

Screening Strategies Physical signs may not appear until stage III

or IV Important to screen those individuals who

are at risk Measurement of serum ferritin levels may

best reveal stages I and II negative iron balance

Serum TIBC may also be as good an indicator

Risk for Iron Deficiency Anemia Infants Adolescent girls Childbearing years/pregnancy for

women Older Adults Those living in chronic poverty Female athletes (esp. involve in

endurance sports)

Treatment of Iron Deficiency Anemia Treatment should focus on underlying disease leading

to the anemia. Repletion of the iron stores, not merely alleviation of the anemia

Chief treatment: oral administration of inorganic iron in the ferrous form Most widely used preparation is ferrous sulfate Other salts absorbed to about the same degree

are ferrous forms of lactate, fumarate, glycine sulfate, glutamate, and gluconate

Iron best absorbed when stomach is empty (although this can cause gastric irritation)

GI side effects: nausea, heartburn, diarrhea, constipation, epigastric discomfort and distention

If this happens, patients should take iron with meals, though this will reduce absorbability

Continued Health professional generally prescribe oral iron for

iron deficiency for 3 months (taken 3 times daily) Depending on the severity of the anemia and

tolerance of iron supplementation, a daily dose should be 50 to 200 mg for adults and 6 mg/kg for children

Ascorbic acid increases both iron absorption and iron gastric irritation

Absorption of 10 to 20 mg of iron per day permits RBC production to increase to about 3x the normal rate and increase hgb concentration .2g/dL

Increased reticulocytosis is seen within 2 to 3 days, hgb level will begin to increase by day 4 of treatment

Iron supplementation should be continued for 4 to 5 months to allow for repletion of body iron reserves

Continued If iron supplements don’t correct the anemia:

1. patient may not be taking the medication as prescribed, most likely because of side effects2. bleeding may be be continuing at a rate faster than erythroid marrow can replace the blood cells3. the supplemental iron may not be absorbed 2° to steatorrhea, celiac disease, or hemodialysis.

In these circumstances parenteral administration of iron in the form of iron-dextran may be necessary

Bioavailability of Iron Rate of absorption depends on iron status of

individual The lower the iron stores, the greater the

rate of absorption will be. Iron absorption averages about 5 to 15%

from diet of both heme and nonheme iron in a person with normal iron stores

Absorption in iron deficiency often increases iron absorption to about 20 to 30%

Absorption can be as high as 50% in iron deficiency anemia although not common

Bioavailability of Iron Efficiency of iron absorption determined somewhat by

food that it is derived from Heme iron is much better absorbed than nonheme

iron About 3 to 8% of nonheme iron is absorbed About 15% of heme iron is absorbed The ferrous form of nonheme iron is better absorbed

than ferric iron Not all ferrous compounds are equally available.

Ferrous pyrophosphate used in breakfast cereals is used often because it doesn’t add a gray color to food but it is poorly absorbed

Ascorbic acid improves iron absorption (reduces ferric to ferrous iron and forms a chelate with iron remaining soluble throughout lower SI)

Bioavailability of Iron Animal proteins enhance absorption by an

unknown mechanism Gastric acidity enhances solubility and

bioavailability of iron from foods; administration of alkaline substances can interfere with nonheme absorption

High phytate, oxalates, and tannin content in foods inhibit absorption of nonheme iron (avoid tea and coffee with meals)

Increased intestinal motility decreases contact time and removes chyme from highest intestinal acidity, decreasing absorption

Poor fat digestion leading to steatorrhea also decreases iron absorption

Food Sources of Iron Best source of dietary iron is liver. Followed by seafood, kidney, heart, lean

meat, and poultry Dried beans and vegetables are the best

plant sources Other foods: egg yolks, dried fruits, dark

molasses, whole grain and enriched breads, wine and cereal

Milk devoid of iron Corn poor source of iron Iron skillet used for cooking add to total iron

intake

Intake of Iron RDA:

Men and postmenopausal women: 8 mg/day Women of childbearing age: 18 mg/day Teenage boys: 11 mg/day

Median iron intakes of most women are lower than the RDA, and the median intakes of men generally exceed the RDA.

Foods that supply the greatest amount of iron in US diet include ready to eat cereals fortified with iron; bread, cakes, cookies, doughnuts, and pasta (all fortified with iron); beef; dried beans and lentils; and poultry.

Iron fortification of cereals, flours, and bread has added significantly to the total iron intake of the US.

Concern about potential iron overloading from fortified breakfast foods was raised because analyzed values of iron content were greater than labeled values

Iron OverloadConcern with excessive iron intake is related to its role in coronary heart disease and cancer

Excessive iron can contribute to an enriched oxidative environment that favors oxidation of LDL cholesterol arterial vessel damage other adverse effect affecting the cardiovascular

system

Iron OverloadMajor cause of iron overload is hereditary hemochromatosisOverload is linked to a distinct gene that favors excessive iron absorption when iron is available in the dietFrequent blood transfusions or long term ingestion of large amounts of iron can lead to abnormal accumulation of iron in the liverSaturation of tissue apoferritin with iron is followed by the appearance of hemosiderin (storage form for iron but contains more iron than ferritin and is very insoluble)Hemosiderosis (iron storage condition) associated with tissue damage is considered hemochromatosisThis tissue damage can result in progressive hepatic, pancreatic, cardiac, and other organ damageAbsorb 3x more iron from their food than normal

Iron overload Treatment/MNTTreatment for significant iron overload:

Weekly phlebotomy for 2 to 3 years may be required to eliminate all excess iron

May also involve iron depletion with intravenous desferrioxamine-B

Calcium disodium ethylenediaminetetraactic acid can also be used

MNT: Ingest less heme iron compared with nonheme

iron Avoid alcohol and vitamin C supplements because

both enhance iron absorption Avoid foods highly fortified with iron, iron

supplements, or multiple vitamins/mineral supplements that contain iron

RDA should not be exceeded

B12 Deficiency

Pathophysiology B12 is freed from protein (by way of gastric

secretions) B12 binds to R-protein R-protein hydrolyzed in sm. Intestine

Intrinsic factor bind to B12 IF binds to specific membrane receptor on

illeul brush border B12 is absorbed B12 binds to transcobalamins (TCI, TCII,

etc)

EtiologyNot enough B12 in diet strict vegan chronic alcoholism poverty religionInadequate use B12 antagonist enzyme deficiency abnormal binding proteins inadequate binding proteinsIncreased Requirement hyperthyroidism hematopoiesis infancyIncrease excretion  liver disease renal disease inadequate binding protein

Poor Absorption  Gastric disorders

Addisonian Pernicious Anemia hereditary, defective,

autoimmunity gastrectomy

total subtotal

antibody to IF blocking  binding

sm. intestine disorders celiac tropical sprue strictures, lesions, resection

specific malabsorptions competition for B12

bacteria(H. pylori) pancreatic disease HIV

S/SGastrointestinal Tract Decr. gastric secretions

decr. breakdown of protein-->lower amt of B12

incr. bac count

Other fatigue diarrhea shortness of breath nervousness

Central/peripheral nervous system paresthesia

(demylination) reduction of senses decr. muscle

coordination decr. memory incr. risk for

osteoporosis

Diagnosis Radio assays measure B12 and folate

together IF antibody dU suppression test serum homocysteine & serum

methionine anti-parietal cell antibodies low holoTCII (early sign)

Schillings TestNote: normal absorption of Vit B12 : Ileum

absorbs more vitamin than body needs and excretes excess in urine

Abnormal/impaired absorption: no vitamin will appear in urine

Stage 1: take radioactive B12 without IFStage 2: take radioactive B12 with IF

PA from lack of IF: abnormal results in 1st and normal in 2nd

PA from malabsorption (intestinal): abnormal in both

Not popular because... expensive complicated

Results altered by: renal insufficiency laxatives (alter absorption) elderly, diabetes,

hypothyroid (altered excretion)

inadequate collection of urine

stool in urine

Medical Treatment

Usual treatment     >/= 100mcg injected once a week (reduced

until maintenance of monthly injections)    

   ** 1000mcg orally (1% will absorb by diffusion--effective even without IF)

Nasal gel Sublingual tablets Initial dose increases when deficiency due to

illness

Medical Nutrition Therapy High protein diet (1.5g/kg) Green leafy vegetables (iron, folic acid) Liver Beef, pork, eggs,    DGA: over age 50 consume B12 in crystalline

(fortified cereals, supplements)

High Risk Groups Type 1 Diabetes, autoimmune thyroid

Pregnancy   Elderly HIV Eating Disorder vegans h. pylori disease/bariatric surgery

Supplementation oral supplements can increase amt of

B12 (no evidence of PA) Though absorbed mainly in Ileum, B12 is

passively absorbed throughout the entire intestine

rarely will oral supplementation not work

Folate Deficiency Anemia

Folate Deficiency Anemia A megaloblastic anemia Reflects a disturbed DNA synthesis

Results in changes in blood cell structures and functions

Pathophysiology Folate is absorbed in the SI It binds to protein and is transported as 5-

methyl tetrahydrofolate (THFA) Folate is activated when it donates its

methyl group to vitamin B12 Methylfolate Trap

Without B12 folate cannot be activated and is trapped as the inactive methyl THFA

B12 deficiency can result in a folate deficiency

Etiology Poor folate absorption Increased folate requirement Prolonged inadequate diet of folate

Poor Absorption Caused by

Medications Ex. Phenytoin, methotrexate, sulfasalazine,

barbituates Chronic alcoholism Disease

Crohn’s disease, celiac disease, tapeworm, tropical sprue and other digestion problems

Surgery affecting the upper third of the small intestine

Increased Requirement Pregnancy and lactation

Extra tissue demand, especially in 3rd trimester of pregnancy

Infancy Increased hematopoiesis

Hemolytic anemia

Symptoms

Same clinical signs as vitamin B12 deficiency

Fatigue Dyspnea Sore tongue Diarrhea Irritability Forgetfulness Anorexia Glossitis Weight loss

Diagnosis RBC Indices

Folate deficiency results in an increased Mean corpuscular volume (MVC)

Low serum folate and red blood cell folate level Serum folate (<3 ng/ml) RBC folate (<140-160 ng/ml)

Elevated formiminoglutamic acid in urine

Folate vs. B12 Deficiency Compare:

Serum folate Red blood cell folate Serum vitamin B12 Vitamin B12 bound to TCII

These are measured simultaneously

Course of Folate Deficiency Folate stores are depleted within 2-4

mo. of a deficient diet Folate deficiency occurs in four stages 2 involved in depletion, 2 marked by

deficiency

Stages of Folate Deficiency Stage 1: Serum folate depletion

<3 ng/ml) Stage 2: Cell (erythrocyte) folate depletion

< 160 ng/ml Stage 3: Damaged folate metabolism and

folate-deficient erythropoiesis Characterized by slowed DNA synthesis

Stage 4: Clinical folate deficiency anemia Manifested by and elevated MCV and anemia

Medical Treatment 1 mg folate to be taken orally every day

for 2-3 weeks to replenish stores This will correct megaloblastosis caused

by either folate deficiency OR B12 deficiency

50-100 mcg of folate daily will maintain stores

Symptomatic improvement is seen within 24-48 hrs of supplementation

MNT One fresh, uncooked fruit/vegetable or juice

daily Orange juice has 135 mcg of folate

Sources of folate with > 100 mcg Chicken or pork liver Black beans Soybean nuts Spinach Fortified cereals

RDA is 400 mcg daily for adults

Other Anemias

Copper-Deficiency Anemia

Copper is essential for the proper formation of hemoglobin

90% of copper in serum is incorporated into ceruloplasmin

Copper in ceruloplasmin has a role of oxidizing iron before it is transported in the plasma

Copper proteins are needed for the use of iron by developing erythrocyte

RDA’s for Copper Adolescents and adults for both genders

have been established at .9 mg/day 340 to 440 mcg/day for young children 200 to 220 mcg/ day for infants Net absorption of copper is 25% to 60%

Copper-Deficiency Anemia

Deficiency usually occurs in infants who are fed cow’s milk or a copper-deficient infant formula

Children or adults that have a malabsorption syndrome

Receiving long term TPN that does not supply copper

Copper deficiency leads to iron unable to be released leading to low serum iron and hemoglobin levels

Anemia of Protein-Energy Malnutrition Protein is essential for the proper production of

hemoglobin and red blood cells Protein-Energy Malnutrition (PEM)

Is a reduction in cell mass and thus a reduction in oxygen requirements

Fewer red blood cells are then required to oxygenate the tissue

Blood volume stays the same so there is a reduced number of red blood cells with a low hemoglobin level (hypochromic, normocytic anemia)

Anemia of Protein-Energy Malnutrition Can mimic an iron deficiency and is actually a

physiologic (non harmful) rather than harmful anemia

In acute PEM loss of active tissue mass may be greater than reduction in red blood cells then leading to polycythemia

The body responds to this red blood cell production which is not a reflection of protein and amino acid deficiency but an oversupply of red blood cells

Anemia of Protein-Energy Malnutrition Iron released from normal red blood cell

destruction is not reused but stored Iron deficiency anemia can reappear with

rehabilitation A diet lacking in protein usually is

deficient in iron, folic acid, and less frequently vitamin B12

Dietitian plays a key role in assessing the diet for typical amounts of these nutrients

Sideroblastic (Pyridoxine-Responsive) Anemia

Has four primary characteristics Mircrocytic and hypochromic red blood cells High serum and tissue iron levels Presence of an inherited defect in the

formation of sigma-aminolevulinic acid synthetase (enzyme involved in heme synthesis)

Buildup of iron containing immature red blood cells (sideroblasts)

Sideroblastic (Pyridoxine-Responsive) AnemiaPatients will have:

Cardiovascular problems Iron overload Respiratory problems Splenomegaly Hepatomegaly Occasionally seen is bronze colored

skin

Sideroblastic (Pyridoxine-Responsive) Anemia

Diagnosis is confirmed when finding sideroblasts in the bone marrow

The anemia responds to administration of pharmacologic doses of pyridoxine or vitamin B6

Treatment consists of 25 to 100 times the RDA of pyridoxine phosphate

Blood transfusions are given which is then done with deferoxamine an iron-chelating agent is given to eliminate iron stores

Vitamin E-Responsive Anemia Hemolytic anemia occurs when defects in red

blood cell membranes lead to oxidative damage and results in lysis Vitamin E is involved in protecting the

membrane against oxidative damage Vitamin E intake in developing countries are

limited, results from multiple studies suggest that poor overall nutritional status and higher prevalence of other oxidative stressors, such as malaria or HIV, predispose populations for deficiency

Vitamin E-Responsive Anemia

Signs of Vitamin E deficiency Early hemolysis of red blood cells Peripheral neuropathy Ataxia Muscle weakness Retinal damage leading to blindness

(retinitis pigmentosa) Infertility Dementia

Vitamin E-Responsive Anemia

Children and the elderly are more vulnerable age groups

Men may be at higher risk for deficiency than women

Premature Infants need vitamin E since the production of Vitamin E doesn’t happen for a baby until right before scheduled birth

Vitamin E-Responsive Anemia Since iron is a biologic oxidant a diet high in either iron or

PUFA’s increases the risk of vitamin E deficiency PUFA’s are incorporated into the red blood cell

membranes and are more susceptible to oxidative damage

This anemia is becoming more and more uncommon since there is a ratio of Vitamin E to PUFA given in infant formula

Recommendation is .7 IU per 100 kcal and at least 1 IU of Vit. E per gram of linoleic acid

Supplemental vitamin E appears to be most highly bioavailable when finely dispersed in a fortified food source or as a powder

High doses of Vitamin E results in intraventricular hemorrhage, sepsis, necrotizing enterocolitis, liver and renal failure, and death

Non-Nutritional Anemias

Sports Anemia Hypochromic Microcytic Transient Anemia First thought the cause was soldiers as a

result of mechanical trauma to the erythrocytes during long marches and was called march hemoglobinuria

There is an increased red blood cell destruction, decreased hemoglobin, serum iron, and ferritin concentrations in the early stages of vigorous training

Sports Anemia Athletes that have low hemoglobin

concentrations would benefit from Iron rich foods Protein Avoiding

Coffee Tea antacids H2 blockers Tetracycline

Sports Anemia No athlete should take iron

supplements unless there is a true iron deficiency

Female athletes who are vegetarian involved in endurance sports or undergoing growth are at a risk for iron deficiency and should be periodically monitored

Anemia of Pregnancy

Related to increase blood volume Usually resolves itself at the end of

pregnancy Demands of iron do increase during

pregnancy so inadequate iron intake could play a role

Anemia of Chronic Disease Pro-inflammatory cytokines have a negative effect

on erythropoiesis development leading to anemia in multiple diseases including:

Chronic infections Chronic inflammatory diseases Myelodysplastic syndromes Malignancy

Mechanisms unclear but thought to be related to inflammatory cytokine-mediated pathogenesis, which includes

Defective production of erythropoietin Reduced bone marrow response to erythropoietin Defective reticulo-endothelial release of iron causing

iron-deficit erythroblast by IL-1 and TNF

Anemia of Chronic Disease

Important to not confuse this with iron deficiency since this is mild and normocytic, so not to give iron supplements when inappropriate

Recombinant erythropoietin therapy usually corrects this anemia

Sickle Cell Anemia

Chronic hemolytic anemia also known as hemoglobin S disease affects 1 of 600 blacks in US as a result of homozygous inheritance of hemoglobin S

Results in defective hemoglobin synthesis and produces sickle shaped red blood cells that get caught in capillaries and do not carry oxygen

Sickle Cell Anemia Characterized by episodes of pain resulting

from occlusion of small blood vessels by the abnormally shaped erythrocytes

Hemolytic anemia & vasoocclusive disease results in: Impaired liver function JaundiceGallstonesDeteriorating renal function

Frequently occur in abdomen causing acute severe abdominal pain

Sickle Cell Anemia Important not to mistake this with

iron deficiency since patients with sickle cell have usually excessive iron stores

Zinc can increase oxygen affinity of both normal and sickle shaped erythrocytes so supplements are usually beneficial

Sickle Cell Anemia Special care and attention should be given to the diet for those

with sickle cell anemia: Dietary intake is usually low since there is pain in the abdomen Children need to make sure they have adequate amounts of

calories to maintain growth and development Also have metabolic increase rate since the constant

inflammation and oxidative stress Diets must have enough calories and provide foods high in folate,

zinc, copper, and even vitamins A,C,D, and E Multivitamin that containing 50 to 150% RDA of folate, zinc, and

copper is recommended 2 to 3 quarts of water each day is very important Also patients may need higher than RDA of protein Low in absorbable iron, so iron rich foods should be excluded Alcohol and ascorbic acid should be avoided since they increase

iron absorption

Thalassemais Affects most people in Mediterranean

region Severe inherited anemia’s characterized

by microcytic, hypochromic, and short lived red blood cells resulting in defective hemoglobin synthesis

The ineffective erythropoiesis leads to an increase in plasma volume, progressive splenomegaly, and bone marrow expansion thus resulting in facial deformities, osteomalacia, and bone changes

Thalassemais There is an increase in iron absorption

which causes iron to be deposited into tissues which results in oxidative damage Accumulation of iron causes dysfunction of the heart,

liver, and endocrine glands Patients require transfusions to stay alive, they must

also have regular chelation therapy to prevent buildup of iron from damaging their tissues

Malnutrition is common and an important factor in the stunted growth in patients

Sources Kheansaard W, Mas-Oo-di S, Nilganuwong S,

Tanyong DI. Interferon-gamma induced nitric oxide-mediated apoptosis of anemia of chronic disease in rheumatoid arthritis. Available at: http://www.springerlink.com.erl.lib.byu.edu/content/h36027236338n15l/fulltext.pdf. Accessed January 25, 2012.

Dror DK, Allen LH. Vitamin E deficiency in developing countries.Food and Nutrition Bulletin. 2011;32:124-143

Krause Chapter 31

Case Study

Nutritional assessment Anthropometric:

Current: 5’5” 145 lbs (165 cm 65.9 kg) Prepregnancy: 135 lbs (61.4 kg) Prepregnancy: BMI 22.5%

Nutritional assessment Biochemical:

Low Hgb, RBC and hematocrit Low red blood cell indices Low ferritin High transferrin High total iron binding capacity (TIBC)

Nutritional assessment Clinical:

Vaginal bleeding and some abdominal pain

Tired, shortness of breath Skin pale without rash Everything else was non remarkable

Nutritional assessment Dietary:

Patient states that appetite is good Hasn’t taken prenatal vitamins because

they make her nauseous

*Women require an extra 1000 mg of Iron during pregnancy (Nutrition through the life cycle textbook)

Nutritional assessment Genetic:

Mother had cancer Father had heart problems and high blood

pressure Grandmother had arthritis

Nutritional assessment History:

Two pregnancies Smokes (.5/day for 15 years) Has had routine prenatal care She is more tired with this pregnancy Shortness of breath is common with

pregnancies but has started earlier this time

Nutritional Diagnosis PES Statement

Increased iron requirement related to pregnancy as evidenced by low ferritin values.

One-day Sample diet

Diet Rationale