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CHAPTER 44 deficiency represents a public health problem among infants, school-
Surveys conducted in developing countries suggest that vitamin A
ANEMIA RESULTING FROM children and women of childbearing age. 10,11 The prevalence of vitamin
A deficiency closely coincides with the prevalence of iron deficiency in
OTHER NUTRITIONAL this demographic setting. However, there is no known causal relation-
ship between the two nutrients beyond both occurring in a setting of
generalized malnutrition. Although vitamin A deficiency is recognized
DEFICIENCIES to occur in the United States, the relationship between it and anemia is
not known.
DEFICIENCIES OF MEMBERS OF THE
Ralph Green
VITAMIN B GROUP
Isolated nutritional deficiencies of members of the vitamin B group,
SUMMARY with the exception of folic acid and vitamin B , are very uncommon
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in humans. Evidence linking isolated nutritional deficiencies of pyri-
The anemia that results from deficiencies of vitamin B , folic acid (Chap. 41) doxine, riboflavin, pantothenic acid, and niacin to anemia in patients is
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or iron (Chap. 43) are, in general, clearly defined and are relatively common. inconclusive. In animals, experimentally induced deficiency states are
more commonly associated with hematologic abnormalities.
In contrast, characteristics of anemia that may occur with deficiencies of the
other vitamins and minerals are poorly defined and relatively rare in humans. Vitamin B Deficiency
When present, they usually exist not as isolated deficiencies of one vitamin or Vitamin B includes pyridoxal, pyridoxine, and pyridoxamine. These
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one mineral, but rather, as a combination of deficiencies resulting from malnu- components are converted to pyridoxal 5-phosphate, which acts as a
trition or malabsorption. In this context, it is difficult to deduce which abnor- coenzyme in decarboxylation and transamination of amino acids and
malities are the result of which deficiency. Studies in experimental animals synthesis of aminolevulinic acid, the porphyrin precursor (Chap. 58).
may not accurately reflect the role of micronutrients in humans. Accordingly, Vitamin B deficiency induced in infants is associated with a hypochro-
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our knowledge of the effects of many micronutrients on hematopoiesis is mic microcytic anemia. A malnourished patient with a hypochro-
fragmentary and based on clinical observations and interpretations that may mic anemia who failed to respond to iron therapy but subsequently
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be flawed. Inborn metabolic errors that affect single micronutrient pathways responded to administration of vitamin B has been described. In
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may shed light on specific effects of those micronutrients on hematopoiesis. some anemic pregnant women who did not respond to iron supplemen-
tation alone, vitamin B administration resulted in subsequent improve-
Daily requirements of some micronutrients are available at: http://www.nal. ment in hemoglobin level. Occasionally, patients receiving therapy
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usda.gov/fnic/dga/rda.pdf, and levels normally found in serum, red cells, and with antituberculosis agents, such as isoniazid, which interfere with
leukocytes are shown in Table 44–1. vitamin B metabolism, develop a microcytic anemia that can be cor-
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rected with large doses of pyridoxine. Pyridoxine is usually prescribed
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with isoniazid to prevent such an effect. Some patients with siderob-
lastic anemias (Chap. 59) respond to administration of large doses of
VITAMIN-DEFICIENCY ANEMIAS pyridoxine, but these patients are not deficient in this vitamin. A review
of more than 200 patients with acquired sideroblastic anemia reported
VITAMIN A DEFICIENCY that fewer than 7 percent showed greater than 1.5 g/dL improvement
Chronic deprivation of vitamin A results in anemia similar to that in hemoglobin concentration with pyridoxine treatment. Pyridoxine
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observed in iron deficiency. Mean corpuscular volume (MCV) and is involved in many metabolic processes. Derangements in these path-
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mean corpuscular hemoglobin concentration (MCHC) are reduced. ways, sometimes involving anemia, are usually the result of inborn
Anisocytosis and poikilocytosis may be present, and serum iron levels errors affecting the pathways of vitamin B metabolism and specific
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are low. Unlike iron-deficiency anemia, but similar to anemia of chronic pyridoxal phosphate-dependent enzymes or inborn errors that lead to
disease, iron stores in the liver and marrow are increased, serum trans- accumulation of small molecules that react with pyridoxal phosphate
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ferrin concentration usually is normal or decreased, and administration and inactivate it. Other acquired conditions that may influence pyr-
of medicinal iron does not correct the anemia. However, there is some idoxine metabolism include drugs that react with pyridoxal phosphate
evidence to suggest that vitamin A deficiency may result in impaired or affect metabolism, malabsorptive states such as celiac disease, and
iron absorption or utilization and this may be mediated through effects renal dialysis which leads to increased loss of vitamin B vitamers from
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on the expression of genes involved in the regulation of intestinal iron the circulation as these vitamers are bound to plasma albumin. 18
absorption. The suggestion that vitamin A may facilitate iron absorp-
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tion was not confirmed. Supplementation with vitamin A alone may Riboflavin Deficiency
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ameliorate the anemia, although coadministration of vitamin A and Riboflavin deficiency results in a decrease in red cell glutathione reduc-
iron resulted in a better response than with either nutrient alone. 9 tase activity because this enzyme requires flavin adenine dinucleotide
for activation. Glutathione reductase deficiency, induced by riboflavin
deficiency, is not associated with hemolytic anemia or increased suscep-
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tibility to oxidant-induced injury (Chap. 47). Human volunteers main-
Acronyms and Abbreviations: MCHC, mean corpuscular hemoglobin concentra- tained on a semisynthetic riboflavin-deficient diet and fed the riboflavin
tion; MCV, mean corpuscular volume; RDW, red cell distribution width; T , triiodothy- antagonist, galactoflavin, developed pure red cell aplasia. Vacuolated
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ronine; T , thyroxine. erythroid precursors are evident prior to the development of aplasia.
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This anemia is reversed specifically by administration of riboflavin. It
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