Table 98-6 Diagnosis of Hypoproliferative Anemias
Iron Deficiency tion
Hypometa bolic States
Mild to severe
MCV (fL) 90
Morphol ogy mo-
Internal iron exchange.
Normally about 80% of iron passing through the plasma transferrin pool is recycled from broken-down red cells. Absorption of about 1 mg/d is required from the diet in men, 1.4 mg/d in women to maintain homeostasis.
As long as transferrin saturation is maintained between 20–60% and erythropoiesis is not increased, iron stores are not required. However, in the event of blood loss, dietary iron deficiency, or inadequate iron absorption, up to 40 mg/d of iron can be mobilized from stores. RE, reticuloendothelial.
Stages of Iron Deficiency Iron-deficiency anemia is the condition in which there is anemia and clear evidence of iron lack. The progression to iron deficiency can be divided into three stages (Fig. 98-2). The first stage is negative iron balance, in which the demands for (or losses of) iron exceed the body's ability to absorb iron from the diet.
Clinical Presentation of Iron Deficiency Certain clinical conditions carry an increased likelihood of iron deficiency. Pregnancy, adolescence, periods of rapid growth, and an intermittent history of blood loss of any kind should alert the clinician to possible iron deficiency. A cardinal rule is that the appearance of iron deficiency in an adult male means gastrointestinal blood loss until proven otherwise. Signs related to iron deficiency depend on the severity and chronicity of the anemia in addition to the usual signs of anemia—fatigue, pallor, and reduced exercise capacity.
Anemia of Acute and Chronic Inflammation/Infection (the Anemia of Chronic Disease)
The anemia of chronic disease—which encompasses inflammation, infection, tissue injury, and conditions (such as cancer) associated with the release of proinflammatory cytokines—is one of the most common forms of anemia seen clinically and probably the most important in the differential diagnosis of iron deficiency, since many of the features of the anemia are brought about by inadequate iron delivery to the marrow, despite the presence of normal or increased iron stores.
The second condition is the anemia of chronic inflammation with inadequate iron supply to the erythroid marrow. The distinction between true irondeficiency anemia and the anemia associated with chronic inflammation is among the most common diagnostic problems encountered by clinicians (see below). Usually the anemia of chronic inflammation is normocytic and normochromic. The iron values usually make the differential diagnosis clear, as the ferritin level is normal or increased and the percent transferrin saturation and TIBC are typically below normal.
Nutritional Iron Balance The balance of iron in humans is tightly controlled and designed to conserve iron for reutilization. There is no regulated excretory pathway for iron, and the only mechanisms by which iron is lost from the body are blood loss (via gastrointestinal bleeding, menses, or other forms of bleeding) and the loss of epithelial cells from the skin, gut, and genitourinary tract.
Normally, the only route by which iron comes into the body is via absorption from food or from medicinal iron taken orally.
Table 98-3 Iron Store Measurements
Iron Stores 4+
Marrow Iron Stain, 0– µg/L
Red Cell Protoporphyrin Levels
Protoporphyrin is an intermediate in the pathway to heme synthesis. Under conditions in which heme synthesis is impaired, protoporphyrin accumulates within the red cell.
Of the complications of oral iron therapy, gastrointestinal distress is the most prominent and is seen in 15–20% of patients. Abdominal pain, nausea, vomiting, or constipation may lead to noncompliance. Although small doses of iron or iron preparations with delayed release may help somewhat, the gastrointestinal side effects are a major impediment to the effective treatment of a number of patients.
The response to iron therapy varies, depending on the erythropoietin (EPO) stimulus and the rate of absorption.
Protein Starvation Decreased dietary intake of protein may lead to mild to moderate hypoproliferative anemia; this form of anemia may be prevalent in the elderly. The anemia can be more severe in patients with a greater degree of starvation. In marasmus, where patients are both protein- and calorie-deficient, the release of EPO is impaired in proportion to the reduction in metabolic rate; however, the degree of anemia may be masked by volume depletion and becomes apparent after refeeding.
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The safe upper limit for vitamin B6 has been set at 100 mg/d, although no adverse effects have been associated with high intakes of vitamin B 6 from food sources only. When toxicity occurs, it causes a severe sensory neuropathy, leaving patients unable to walk. Some cases of photosensitivity and dermatitis have also been reported.
Folate, Vitamin B12 See Chap. 90.
Vitamin C Both ascorbic acid and its oxidized product dehydroascorbic acid are biologically active.