Iron Restricted anemias  When the iron in the diet is

Iron-Restricted Anemias  Iron Deficiency anemia consistently inadequate, over time the
-Iron Deficiency Anemia body’s stores of iron become
-Anemia of Chronic Inflammation depleted.
Sideroblastic Anemias  Ultimately, RBC production slows to
-Acquired: Lead Poisoning manage the iron needs for other body
-Hereditary: Porphyrias cells.
Iron Overload  With approximately 1% of cells dying
-Etiology naturally each day, the anemia
-Pathogenesis becomes apparent when the
-Laboratory Diagnosis production rate is insufficient to
-Treatment replace lost cells.
General Concepts in Iron-Related Disorders - Increased need relative to iron supply
 Anemia may result whenever red blood cell (RBC) Etiology  Iron deficiency can also develop when the
production is impaired, RBC life span is shortened, or - Iron deficiency anemia develops: level of iron intake is inadequate to meet
there is frank loss of RBCs from the body -When the intake of iron is inadequate to meet the needs of an expanding erythron. This is
 The anemias associated with iron and heme typically a standard level of demand the case in periods of rapid growth, such as
are categorized as anemias of impaired production -When the need for iron expands without infancy (especially in prematurity),
resulting from the lack of raw materials for compensated intake childhood, and adolescence.
hemoglobin assembly -When there is impaired absorption  For example, although both infants and
 When iron is the limiting factor, the anemias are -When there is chronic loss of hemoglobin from adult men need about 1 mg/day of iron,
called iron restricted. the body that corresponds to a much higher amount
- Important iron-restricted anemias: - Inadequate intake per kilogram of body weight for the infant.
Iron deficiency anemia and anemia of chronic  Iron deficiency anemia can develop Pregnancy and nursing place similar
inflammation when the erythron is slowly starved demands on the mother’s body to provide
 Inadequate production of protoporphyrin also leads for iron iron for the developing fetus or nursing
to diminished production of heme and thus  Each day, approximately 1 mg of iron infant in addition to her own iron needs. In
haemoglobin is lost from the body, mainly in the each of these instances, what had
 Blockages of protoporphyrin production at various mitochondria of desquamated skin previously been an adequate intake of iron
stages in the heme synthetic pathway lead to and sloughed intestinal epithelium. for the individual becomes inadequate as
accumulations of various porphyrins. Because the body tenaciously the need for iron increases.
 Iron metabolism can be perturbed, resulting in conserves all other iron from  Treatment with erythropoietin is another
senescent cells, including RBCs, daily instance when there is rapid expansion of
excess accumulations of iron, usually without anemia
replacement of 1 mg of iron from the the erythron
 There is another group of anemias with impaired iron
diet maintains iron balance and  The demand for iron is often so great that
kinetics called iron-loading anemias, it involve
supplies the body’s need for RBC even individuals with adequate stores of
chronic erythroid hyperplasia as is seen in the
production as long as there is no other iron will experience iron-restricted
hemoglobinopathies and thalassemias. These are
source of loss. erythropoiesis because it cannot be
diseases caused by heritable mutations affecting
mobilized fast enough. This is called
globin chain structure or their production.

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PART IV: CHAPTER
ERYTHROC 17: Disorders
functional iron deficiency because iron  Individuals with chronic intravascular  The hemoglobin content of reticulocytes begins to
stores are adequate but the iron is not hemolytic processes, such as paroxysmalCHAPTER decrease, which reflects the onset of iron-restricted
available to support normal erythropoiesis nocturnal hemoglobinuria, can develop17: Disorders erythropoiesis, but because the bulk of the
- Impaired absorption. iron deficiency as a result of the loss of iron circulating RBCs were produced during the period of
 Even when the diet is adequate in iron, the in hemoglobin passed into the urine adequate iron availability, the overall haemoglobin
inability to absorb that iron through the Pathogenesis concentration is still within the reference interval, as
enterocyte into the blood will, over time, - Iron deficiency anemia develops slowly, progressing are the mean cell volume (MCV), mean cell
result in a deficiency of iron in the body through stages that physiologically blend into one hemoglobin (MCH), and mean cell hemoglobin
 The impairments may be pathologic, as another but are useful delineations for concentration (MCHC).
with malabsorption caused by celiac understanding disease progression  An individual’s hemoglobin may begin dropping, and
disease. - Iron is distributed among three compartments: the RBC distribution width (RDW) may begin
 Others may be inherited mutations of iron 1. the storage compartment, principally as increasing as some smaller RBCs are released from
regulatory proteins, like the mutations of ferritin in the bone marrow macrophages the bone marrow, without multiple measurements
the matriptase-2 protein that lead to a and liver cells over time, these changes will not be detected.
persistent production of hepcidin, causing 2. the transport compartment of serum  The serum iron and serum ferritin levels decrease,
ferroportin in the enterocyte to be transferrin whereas total iron-binding capacity (TIBC), an
inactivated, thus preventing iron 3. the functional compartment of indirect measure of transferrin, increases.
absorption in the intestine hemoglobin, myoglobin, and cytochromes  Transferrin receptors increase on the surface of iron-
 diseases that decrease stomach acidity - Hemoglobin iron and intracellular ferritin and starved cells as they try to capture as much available
impair iron absorption by decreasing the hemosiderin constitute nearly 90% of the total iron as possible. The receptors are also shed into the
conversion of dietary ferric iron to the distribution of iron blood, so the soluble transferrin receptor (sTfR)
absorbable ferrous form - For a time, as an increase in demand or increased levels increase measurably. Prussian blue stain of the
 Some loss of acidity accompanies normal loss of iron exceeds iron intake, essentially normal bone marrow in stage 2 shows essentially no stored
aging, but gastrectomy or bariatric iron status continues. iron, and iron-restricted erythropoiesis is evident.
surgeries can impair iron absorption - The body strives to maintain iron balance by STAGE 3
dramatically. Medications such as stomach accelerating absorption of iron from the intestine  Stage 3 of iron deficiency is frank anemia. The
acid reducers can inhibit iron absorption by through a decrease in the production of hepcidin in haemoglobin concentration and hematocrit are low
decreasing gastric acidity, whereas other the liver. This state of declining body iron with relative to the reference intervals.
drugs may even bind the iron in the increased absorption is not apparent in routine  Depletion of storage iron and diminished levels of
intestine, preventing its absorption laboratory test results or patient symptoms. transport iron prevent normal development of RBC
- Chronic blood loss. - The individual appears healthy. As the negative iron precursors.
 A fourth way iron deficiency develops is balance continues, however, a stage of iron depletion  In this phase the patient experiences the nonspecific
with repeated blood donations, chronic develops. symptoms of anemia are typically: fatigue, weakness,
hemorrhage, or hemolysis that results in STAGE 1 and shortness of breath, especially with exertion.
the loss of small amounts of heme iron  Stage 1 of iron deficiency is characterized by a Pallor is evident in light-skinned individuals but also
from the body over a prolonged period. progressive loss of storage iron. RBC production and can be noted in the conjunctivae, mucous
 Anemia develops when the iron loss development are normal throughout this phase. membranes, or palmar creases of dark skinned
exceeds iron intake over time and the  Serum ferritin levels drop over time, which indicates individuals.
storage iron is exhausted. the decline in stored iron, and this also could be
 In women, prolonged menorrhagia (heavy detected in an iron stain of the bone marrow. EPIDEMIOLOGY
menstrual bleeding) or conditions such as STAGE 2 - Menstruating women are at especially high risk. Their
uterine fibroid tumors or uterine  Stage 2 of iron deficiency is defined by the monthly loss of blood increases their routine need
malignancies can also lead to heme iron exhaustion of the storage pool of iron. for iron, which often is not met with the standard US
loss. diet.

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PART IV: CHAPTER
ERYTHROC 17: Disorders
- Growing children also are at high risk. Growth  Polychromasia may be apparent early, although it is  Measuring the hemoglobin content of reticulocytes
requires iron for the cytochromes of all new cells, not a prominent finding CHAPTER enables detection of iron-restricted erythropoiesis
myoglobin for new muscle cells, and hemoglobin in  Poikilocytosis, including occasional target cells and17: Disorders within days as the first iron-deficient cells leave the
the additional RBCs needed to supply oxygen for a elliptocytes, may be present, although no particular bone marrow.
larger body. The increasing need for iron as the child shape is characteristic or predominant. Specialized test of iron status
grows can be coupled with dietary inadequacies,  Thrombocytosis may be present, particularly if the  In the absence of iron, FEP may be preferentially
especially in circumstances of poverty or neglect. iron deficiency results from chronic bleeding, but this chelated with zinc to form zinc protoporphyrin (ZPP).
- Iron deficiency is relatively rare in men and is not a diagnostic parameter.  The FEP and zinc chelate can be assayed
postmenopausal women because the body conserves  White blood cells are typically normal in number and fluorometrically, although they are not particularly
iron so tenaciously, and these individuals lose only appearance. valuable in the diagnosis of iron deficiency.
about 1 mg/day  Iron deficiency should be suspected when the CBC  Soluble transferrin receptors (sTfR) can be assayed
- Elderly individuals, particularly those living alone, findings show a hypochromic, microcytic anemia with using immunoassay. Levels increase as the disease
may not eat a balanced diet, so pure dietary an elevated RDW but no consistent shape changes to progresses, and individual cells seek to take in as
deficiency is seen among these individuals. the RBCs. much iron as possible.
- Soldiers subjected to prolonged maneuvers and long- Diagnostic testing for iron deficiency Treatment and its effects
distance runners also can develop iron deficiency.  Biochemical iron studies remain the backbone for Treatment
Exercise-induced hemoglobinuria, also called march diagnosis of iron deficiency, though some argue that  The first therapy for iron deficiency is to treat any
hemoglobinuria, develops when RBCs are hemolyzed modern automated blood cell analyzers can supplant underlying contributing cause, such as hookworms,
by foot-pounding trauma and iron is lost as the biochemical studies. tumors, or ulcers.
hemoglobin in the urine  The biochemical analyses include assays of serum  Oral supplements of ferrous sulfate are the standard
Laboratory Diagnosis iron, TIBC, transferrin saturation, and serum ferritin prescription. The supplements should be taken on an
 The early stages of iron deficiency can be detected  Serum iron is a measure of the amount of iron bound empty stomach to maximize absorption.
with tests such as ferritin, but those tests are not to transferrin in the serum.  Vigilance on the part of the health care providers is
likely to be ordered because there is virtually no  TIBC (total iron-binding capacity) is an indirect important to ensure that patients complete the
physiologic evidence suggesting a declining iron measure of transferrin and the available binding sites course of iron replacement, which usually lasts 6
state. for iron. months or longer.
 Early iron deficiency might be suspected in an  Instrument manufacturers have developed  The intestinal side effects are reduced compared
individual in a high-risk group, and appropriate parameters that can be reported with a CBC to with ferrous sulfate while being equally effective in
testing can be ordered. enhance detection of latent iron indicators of correcting iron deficiency.
Screening for iron deficiency anemia impending anemia, they can provide an early alert  Because of the risks associated with RBC
 When iron-restricted erythropoiesis is underway, the Reticulocyte parameters also support the diagnosis transfusions, they are rarely warranted for the
CBC results begin to show evidence of anisocytosis, of iron deficiency. correction of uncomplicated iron deficiency unless
microcytosis, and hypochromia  A low absolute reticulocyte count confirms a the patient’s hemoglobin level has become
 As the hemoglobin concentration continues to fall, diminished rate of effective erythropoiesis because dangerously low
microcytosis and hypochromia become more this is a nonregenerative anemia. Response to treatment
prominent, with progressively declining values for  The MCH is the average weight of hemoglobin per  When optimal treatment with iron is initiated, the
the MCV, MCH, and MCHC. cell across the entire RBC population. effects are quickly evident.
 Automated measures of microcytosis and  If iron deficiency is developing, the MCH does not  The hemoglobin content of reticulocytes will correct
hypochromia may detect these changes before they change until a substantial proportion of the cells are within 2 days.
are noticeable on the peripheral blood film. iron deficient, and the diagnosis is effectively delayed  Reticulocyte counts (relative and absolute) begin to
 The RBC count ultimately becomes decreased, for weeks or months after iron-restricted increase within 5 to 10 days. The anticipated rise in
though lagging behind the drop in indices, as does erythropoiesis begins. hemoglobin appears in 2 to 3 weeks, and levels
the hematocrit.

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PART IV: CHAPTER
ERYTHROC 17: Disorders
should return to normal for the individual by about 2 the amount of iron absorbed into the blood from the  The hemoglobin content of reticulocytes will be
months after the initiation of adequate treatment. intestine. CHAPTER decreased, demonstrating the iron-restricted
 The peripheral blood film and indices still reflect the  Conversely, when systemic body iron levels decrease,17: Disorders erythropoiesis, but the sTfR will be normal, reflecting
microcytic RBC population for several months, with a hepcidin production by hepatocytes decreases, and normal intracellular iron.
biphasic enterocytes export more iron into the blood.  The iron deficiency may be missed because of the
 If the patient has been adherent to the therapeutic  When systemic iron levels are high, hepcidin increase in serum ferritin levels associated with the
regimen, the failure to respond to iron treatment increases, enterocytes export less iron into the inflammation.
Anemia of Chronic Inflammation blood, and macrophages and hepatocytes retain iron.  Iron deficiency anemia and anemia of chronic
 Anemia is commonly associated with systemic  During inflammation, the liver increases the synthesis inflammation may be distinguished in such situations,
diseases, including chronic inflammatory of hepcidin in response to interleukin produced by or their coexistence can be verified, by measuring
conditions such as rheumatoid arthritis, chronic activated macrophages. This increase occurs sTfRs in the serum. These receptors are sloughed
infections such as tuberculosis or human regardless of systemic iron levels in the body. from cells into the blood.
immunodeficiency virus infection, and  As a result, during inflammation, there is a decrease  Additional modifications to the use of the sTfR assay
malignancies.
in iron absorption from the intestine and iron release have been developed to better distinguish iron
 Cartwright was the first to suggest that although
from macrophages and hepatocytes although there is deficiency, latent iron deficiency, and anemia of
the underlying diseases seem quite disparate, the
plenty of iron in the body, it is unavailable to chronic inflammation.
associated anemia may be from a single cause,
proposing the concept of anemia of chronic developing RBCs because it is sequestered in the  It is expected that the sTfR/ log ferritin will rise most
disease. macrophages and hepatocytes. dramatically in iron deficiency as the numerator rises
 This anemia ranks only behind iron deficiency Diminished erythropoiesis and the denominator falls; in anemia of chronic
anemia in incidence worldwide and is common  Production of inflammatory cytokines also impairs inflammation, both remain essentially normal, and
among hospitalized patients. proliferation of erythroid progenitor cells, diminishes thus a normal ratio results.
Etiology their response to erythropoietin, and decreases Treatment
 Although the anemia associated with chronic production of erythropoietin by the kidney  Therapeutic administration of erythropoietin can
systemic disorders was originally called anemia of Shortened red blood cell life span correct anemia of chronic inflammation, but iron
chronic disease, chronic blood loss is not among the  A third factor contributing to the anemia of chronic must be administered concurrently because stored
conditions leading to the anemia of chronic disease. inflammation is a shortened RBC life span. body iron remains sequestered and
Chronic blood loss results in quantitative iron  The cause appears to be an extracellular mechanism  The anemia is typically not severe, however, and this
deficiency. but without clear identification to date. costly treatment is warranted only in select patients.
 Anemia of chronic disease is more correctly termed  Inflammation appears to induce increased SIDEROBLASTIC ANEMIA
anemia of chronic inflammation, because production of hemophagocytic macrophages. Ring sideroblast
inflammation is the unifying factor among the three Although inflammatory suppression and shortened
aforementioned general types of conditions in RBC life span contribute to the anemia of chronic
which this anemia is seen. inflammation, the impaired ferrokinetics is the most
 The central feature of anemia of chronic significant cause of the anemia.
inflammation is sideropenia in the face of abundant Laboratory diagnosis
iron stores.  The peripheral blood picture in anemia of chronic
Impaired ferrokinetics inflammation is that of a mild anemia, with
 Body iron levels, particularly absorption of iron in the hemoglobin concentration usually 8 to 10 g/dL and
intestine and release of iron from macrophages and without reticulocytosis.
hepatocytes.  The serum ferritin level, as an acute phase reactant,
 Hepcidin interacts with and causes degradation of is usually increased beyond the value that would be
transmembrane protein ferroportin, which exports expected for the same patient in the absence of the
iron from enterocytes into the blood, thus reducing inflammatory condition.

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PART IV: CHAPTER
ERYTHROC 17: Disorders
 As in iron deficiency, the anemia may be microcytic chronic exposure to lead, a microcytic, hypochromic - In both cases the toxic effects of excess iron lead to
and hypochromic. blood picture may be seen. CHAPTER serious health problems as lipids, proteins, nucleic
 A Prussian blue stain of the bone marrow shows  The reticulocyte count in acute poisoning may be17: Disorders acids, and heme iron become oxidized.
erythroblasts with iron deposits in the mitochondria quite elevated, which suggests that the anemia has a
surrounding the nucleus. hemolytic component.
 The sideroblastic anemias are a diverse group of  Although the bone marrow may show erythroid Etiology
diseases that include hereditary and acquired hyperplasia, consistent with the elevated reticulocyte  Excess accumulation of iron results from acquired or
conditions. count, in some patients it may be hypoplastic. hereditary conditions in which the body`s rate of iron
 Some patients experience at least modest  Disorders Included in Sideroblastic Anemias acquisition exceeds the rate of loss, which is usually
improvement of anemia with pharmacologic doses of Hereditary X-linked Autosomal Acquired Primary about 1 mg/day.
pyridoxine to stimulate heme synthesis. sideroblastic anemia (refractory) Secondary  It occurs when there is a need for repeated
Acquired: lead poisoning sideroblastic anemias caused by drugs and bone transfusions, as in the treatment of anemias such as
 Adults may be exposed to leaded compounds at marrow toxins Antitubercular drugs Chloramphenicol sickle cell anemia and b-thalassemia major The iron
work if proper safety precautions are not in place. Alcohol Lead Chemotherapeutic agents poisoning is present in the transfused RBCs exceeds the usual 1
 Adults and children living in older homes can be typically large, so the stippling is heavier than that mg/day of iron typically added to the body`s stores
exposed to lead from paints produced before the seen in many anemias and thus represents truly by a healthy diet.
1970s. punctate basophilia.  Some chronic anemias, usually hereditary hemolytic
 They are at risk if dust is created during renovations Hereditary: Porphyrias anemias, are innately iron loading, even without
or paint is permitted to peel.  Lead poisoning is an example not only of an acquired transfusion therapy.
 Toddlers and crawling infants are at special risk from sideroblastic anemia but also of an acquired  Although this is seen most often with hereditary
getting dust on their hands and placing them in their porphyria. hemolytic anemias, the iron loading is secondary to
mouths.  The porphyrias are diseases characterized by the hereditary condition that causes the hemolysis.
 Although anyone can experience lead poisoning, it is impaired production of the porphyrin component of  On the other hand, hemochromatosis may develop
of special concern in children because the metal heme. as a result of mutations in genes for proteins
affects the central nervous system as well as the  The impairments to heme synthesis may be acquired, controlling iron kinetics so that feedback regulation
hematologic system, leading to impaired mental as with lead poisoning, or hereditary. of iron is impaired and the body continues to absorb
development and anemia.  The term porphyria is most often used to refer to the iron, even when stores are full.
 In children and adults with lead poisoning, a hereditary conditions that impair production of  Trying to explain their diseases led to discovery of
peripheral neuropathy can be seen with abdominal protoporphyrin. the other proteins that are now known to be
cramping and vomiting or seizures.  When an enzyme in heme synthesis is missing, the involved in iron kinetics.
 Lead interferes with porphyrin synthesis at several products from earlier stages in the pathway  What has emerged is a picture of hereditary
steps. The most critical are as follows: accumulate in cells that actively produce heme, such hemochromatosis as a general phenotype that can
1. The conversion of aminolevulinic acid (ALA) to as erythrocytes and hepatocytes. be produced by various genotypes when a gene for
porphobilinogen (PBG) by ALA dehydratase (also  Accumulation during childhood leads to fluorescence an iron regulatory protein is mutated.
called PBG synthase); the result is the accumulation of developing teeth and bones.  Failure of normal regulation as a result of mutations
of aminolevulinic acid.  Only three of the porphyrias have hematologic leads to excessive absorption and storage, causing
2. The incorporation of iron into protoporphyrin IX by manifestations; the others have a greater effect on the diseases collectively known as the hereditary
ferrochelatase (also called heme synthase); the result liver cells. hemochromatoses.
is accumulation of iron and protoporphyrin in the Iron overload  Because mutations of the HFE gene remain the most
mitochondria. - Iron overload may be primary, as in hereditary common, that form of the disease will be discussed
 Anemia, when present in lead poisoning, is most hemochromatosis, or secondary to chronic anemias here with some references to differences seen in
often normocytic and normochromic; however, with and their treatments. other forms of the disease.

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PART IV: CHAPTER
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 Other iron overload conditions, such as  In the juvenile forms of the disease associated with elevations in these values are among the earliest
hemochromatosis type 5 and hypotransferrinemia, mutations to the hepcidin or hemojuvelin genes, theCHAPTER findings in most forms of hemochromatosis.
involve mutations of proteins involved in iron kinetics process of iron accumulation is accelerated, so these17: Disorders  Genetic testing for known mutations provides
but not the hepcidin ferroportin axis. effects may appear as early as the teenage years. confirmation of the diagnosis for most patients with
 Homozygous hereditary hemochromatosis involving  In the slower-developing diseases, phenotypic hereditary hemochromatosis.
the HFE gene occurs in approximately 5 of 1000 expression of the tissue damage in hereditary  Whether hemochromatosis is acquired or hereditary,
northern Europeans. Heterozygosity approaches hemochromatosis is more common in men, although the serum ferritin level provides an assessment of
13%. the gene frequency of HFE mutations is not higher in the degree of iron overload and can be monitored
 The first two mutations known to produce the men. after treatment is initiated to reduce iron stores.
hereditary hemochromatosis phenotype involve HFE,  This is because the blood loss associated with
a gene on the short arm of chromosome 6 that menstruation and childbirth forestalls the effects of
encodes an HLA class I-like molecule that is closely excess iron in affected women, and they usually Treatment
linked to HLA-A. develop clinical symptoms later in life than affected  Treatment of the underlying condition leading
 The mutated HFE molecule either does not bind b2- men. to excess iron accumulation is also needed.
microglobulin and thus does not reach the cell  The amount of iron available in the diet for  In forms of hereditary hemochromatosis,
surface or, if it does reach the cell surface, does not absorption affects the rate at which disease can withdrawal of blood by phlebotomy provides a
bind TfR1 or associate properly with TfR2. In any case develop. simple, inexpensive, and effective means of
the result is that when HFE protein is mutated, the  In transfusion-related hemosiderosis, the frequency removing iron from the body.
BMP-BMPR mediated signal to produce hepcidin is of transfusions over time affects the rate of  Hemoglobin levels are monitored, and a mild
diminished. development of clinical disease. anemia is sought and maintained.
Pathogenesis Laboratory Diagnosis  Individuals who rely on transfusions to maintain
 When cells exhaust the capacity to store iron as  It can be used to screen for the condition, diagnose hemoglobin levels and prevent anemia cannot
hemosiderin, free iron (ferrous) accumulates the cause of organ damage, pinpoint the mutation be treated with phlebotomy.
intracellularly. for family genetic counseling, and monitor  Although they also have side effects, the
 The ultimate result is cell death caused by treatment. convenience of oral administration with the
irreversible membrane damage.  Elevations of transferrin saturation or serum ferritin potential for improved patient outcomes may
 The tissues most obviously affected are the skin, can be used as a screening test for hereditary lead to a greater reliance on this form of
where deposition of hemosiderin gives the skin a hemochromatosis. treatment.
golden color; the liver, where cirrhosis-induced  Individuals with undiagnosed hereditary
jaundice and subsequent cancer may develop; and hemochromatosis may come to medical attention
the pancreas, where damage results in diabetes because of organ function problems leading to
mellitus. nonspecific physical complaints or the disease may
 The disease is rarer than the C282Y gene frequency be discovered incidentally with routine laboratory
predicts, so the penetrance of the genes is not testing.
complete. Other factors also affect the development  Abnormal results on common tests of liver function
of clinical disease, including the particular mutation, may be among the first laboratory findings that lead
zygosity, presence of other physiologic conditions, a care provider to order further testing to identify
diet, and other environmental influences. the cause.
 In classic hereditary hemochromatosis (HFE  If hereditary hemochromatosis is among the
mutations), individuals usually harbor 20 to 30 g of disorders being considered to explain organ
iron by the time their disease becomes clinically dysfunction, serum iron, transferrin saturation, and
evident at the age of 40 to 60 years. serum ferritin testing are warranted because

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PART IV: CHAPTER
ERYTHROC 17: Disorders
CHAPTER
17: Disorders

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