U

Figure 5.4 Microcytic and hypochromic red cells.

Causes of Iron Deficiency

There are many populations that are vulnerable to IDA. Infants and pregnant women may suffer from nutritional deficiency, young children may develop IDA when their growth and development rate outstrip their iron intake, and young women who have increased iron need due to menstruation or pregnancy may develop IDA (see Table 5.6). But the primary cause of iron deficiency in the Western world is GI bleeding for males and excessive menses for females. In both of these cases, blood is lost from the body. External blood loss presents a significant challenge to the body because millions of shed red cells can never be used for recycling new red cells. Slow GI bleeds and dysfunctional uterine bleeding over time will lead to a depletion of iron stores and IDA will commence. Storage iron, represented by ferritin, represents a primary reservoir of iron that can be used as other iron sources are depleted. The average ferritin concentrations in males are 135 pg/L, females, 43 pg/L, and children, 30 pg/L.7 Barring any other external loss of blood, iron deficiency solely due to lack of dietary sources would develop over a protracted period of time.

Treatment for Iron Deficiency

Treatment for iron deficiency is given orally in the form of drops (good for infants and children) or tablets. Iron preparations are in the form of ferrous sulfate, ferrous gluconate, and ferrous fumerate and are readily available over the counter in most places.8 Side effects from oral iron therapy may include constipation, stomach discomfort, or diarrhea. Most side effects can be overcome with consultation from the pharmacist for a gentler preparation. What is essential is to remain compliant and to continue on iron therapy despite side effects. Laboratory evaluations such as the CBC and the reticulocyte count should show marked improvement in a few weeks. Additionally, the microcytosis and hypochromia seen in the peripheral smear will eventually be replaced by normocytic and normochromic red cells. Although oral iron will normalize the hematologi-cal picture, an investigation should commence as to the source of the anemia and whether there are any underlying causes that are contributory. Table 5.7 provides recommendations to prevent and control iron deficiency in the United States.

ANEMIA OF CHRONIC DISEASE AND INFLAMMATION: PATHOPHYSIOLOGY, DIAGNOSIS, AND TREATMENT

The anemia of chronic disease or the anemia of inflammation is one of the most common anemias in hospital

Table 5.7 O Recommendations to Prevent and Control Iron Deficiency in the United States

For infants (0 to 12 months) and children (1 to 5 years)

• Encourage breastfeeding or

• Iron-fortified formula

• Serve one serving of fruits, vegetables, juice by 6 months

• Screen children for anemia every 6 months

School-age children (5 to 12 years) and adolescent boys (12 to 18 years)

• Screen only those with history of IDA or low iron intake groups

Adolescent girls (12 to 18 years) and nonpregnant women of childbearing age

• Encourage intake of iron-rich food and foods that increase iron absorption

• Screen nonpregnant women every 5 to 10 years through childbearing years

Pregnant women

• Start oral doses of iron at first prenatal visit

• Screen for anemia at first prenatal visit

• If hemoglobin is <9 g/dL, provide further medical attention

Postpartum women

• Risk factors include continued anemia, excessive blood loss, and multiple births

Males older than 18 years/postmenopausal women

• No routine screening is recommended

Modified from Centers for Disease Control and Prevention. Recommendations to Prevent and Control Iron Deficiency in the United

States. April 1998. Available at http://www.cdc.gov/mmnr/preview/

mmwrhtml/100051880.htm. Accessed September 24, 2006.

populations and second only to iron deficiency in terms of frequency

Many individuals with chronic disorders such collagen vascular disease, chronic kidney disease, thyroid disorders, malignancies, and so on may show an anemia that will eventually develop into a microcytic anemia (Table 5.8). When this occurs, most physicians will order laboratory testing to establish whether there is also an iron deficiency process. This is termed differential diagnosis. Differential diagnosis is a process by which a physician examines a group of laboratory values and symptoms and tries to correlate them to a particular physiology. Patients with the anemia of chronic disease will show a borderline low red cell count, hemoglobin, and hematocrit, a slightly low MCV, and a nor-

Table 5.8 O Conditions Leading to

Anemia of Inflammation or Anemia of Chronic Disease

• Rheumatoid arthritis

Chronic renal disease

• Thyroid disorders

• Malignancies

• Inflammatory bowel disease mal MCHC. The peripheral smear will be essentially normal with slight variation in size and chroma. Serum iron will be low, serum ferritin will be normal or increased, and serum TIBC will be decreased. Although this is NOT the profile for a patient with IDA, in both conditions the patient will have a low serum iron. There are several theories to account for these data. In the anemias of inflammation, iron is blocked from reaching erythroid precursors because of impaired release from macrophages; there is impaired EPO production; and the pronormoblasts are not as responsive to EPO from patients with chronic disease.9 Few individuals require a blood transfusion for treatment of their anemia. On most occasions, once the underlying disease is successfully managed, symptoms of anemia seem to resolve. Recently, a new hormone, hepcidin, was discovered. Hepcidin is linked to the immune response and has been identified as a regulator of iron transit. As more information unfolds, undoubtedly this discovery will have major implications for iron use and the inflammatory process.10

ANEMIAS RELATED TO IRON OVERLOAD CONDITIONS, THE SIDEROBLASTIC ANEMIAS

The disorders in this category are either inherited or acquired. There is an excessive accumulation of iron in the mitochondria. This leads to the presence of iron deposits in the red cell precursors in the marrow called ringed sideroblasts (Fig. 5.5), a dimorphic blood picture, as well as increased serum ferritin. If the iron loading is an acquired process, it may result from diseases such as thalassemia major or sickle cell anemia that require a high transfusion protocol. Additionally, acquired iron loading may occur from alcoholism, lead poisoning, or chloramphenicol use. Inherited sideroblastic anemias will be the result of inherited abnormal genes, which is discussed later in the chapter.

72 Part II • Red Cell Disorders

Figure 5.5 Ringed sideroblast in the bone marrow.

In any case, the patient's peripheral smear will show a microcytic process, with dimorphism (some microcytes and some normal cells, some hypochromic and some normochromic) (Fig. 5.6) and the presence of Pappenheimer bodies (Fig. 5.7), red cells with precipitated iron inclusions that look like grape clusters in the periphery of the red cell. An iron profile will reveal an increased serum ferritin and an increased serum iron. As can be expected, once the underlying condition is successfully managed, the iron overload conditions will be resolved.

Hereditary Hemochromatosis

Hereditary hemochromatosis (HH) is one of the most common genetic disorder in persons with European ancestry and a major inherited sideroblastic anemia. More than a million persons are affected in the United States.11 Caucasians, African Americans, and Hispanics are particularly at risk. Yet this disorder has a low profile, relative to other blood disorders, partially because

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