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  • Anemia due to endocrine disease is generally mild to moderate; however, a decreased plasma volume in some of these disorders may mask the severity of the decrease in red cell mass.

  • The pathophysiologic basis of the anemia seen in endocrine disorders is often multifactorial.


  • Anemia in hypothyroidism may be normocytic, macrocytic, or microcytic; coexisting deficiencies of iron, B12, and folate may explain some of this heterogeneity.

  • Iron deficiency often occurs in hypothyroidism as a result of increased predisposition to menorrhagia, an associated achlorhydria, or because a deficit of thyroid hormone may decrease iron absorption.

  • In patients with coexisting iron-deficiency anemia and subclinical hypothyroidism, the anemia often does not adequately respond to oral iron therapy.

  • The mechanism underlying the association of hypothyroidism and pernicious anemia is unknown.

  • The mean corpuscular volume cannot be used to differentiate hypothyroid patients with low vitamin B12 levels from those with uncomplicated hypothyroidism.

  • Anemia is also a direct consequence of thyroid hormone deficiency; thyroid hormones have been shown to potentiate the effect of erythropoietin on erythroid colony formation.

  • Patients with hyperthyroidism have increased red cell mass, but the hematocrit and hemoglobin concentration are usually not elevated because the plasma volume is also increased.

  • Autoimmune hemolytic anemia and pancytopenia responsive to treatment of hyperthyroidism have also been reported.


  • The red cell mass is decreased in primary adrenal insufficiency (Addison disease), but it may not be reflected in the hematocrit or hemoglobin measurements because of a concomitant reduction in plasma volume.

  • The pathophysiologic basis of the anemia and any influence of adrenal cortical hormones on erythropoiesis are not well defined.

  • Some patients with Addison disease develop a transient fall in hematocrit and hemoglobin concentration after initiation of hormone replacement therapy (presumably secondary to an increased plasma volume).

  • Pernicious anemia occurs in patients with autoimmune adrenal insufficiency, but is seen primarily in patients with type I polyglandular autoimmune syndrome, whose other manifestations include mucocutaneous candidiasis and hypoparathyroidism.

  • Polycythemia has been reported in Cushing syndrome, primary aldosteronism, Bartter syndrome, and congenital adrenal hyperplasia secondary to 21-hydroxylase deficiency.

  • Conversely, some males with Cushing syndrome are anemic; this finding is correlated with a low testosterone level.

  • Some individuals with congenital polycythemia develop recurrent pheochromocytomas, paragangliomas, and somatostatinomas that are heterozygous for a gain-of-function mutation of hypoxia-inducible factor 2α. However, the association of these tumors with polycythemia is unknown.


  • Decrease in androgen production due to orchiectomy or medical androgen blockade causes anemia.

  • Androgen therapy has been used for the treatment of various anemias, especially before the development of recombinant erythropoietin.

  • The mechanism of androgen action appears to be complex, with evidence for stimulation of erythropoietin secretion and a direct effect on the marrow erythroid progenitors.

  • Estrogens in large doses cause moderately severe anemia by a mechanism not clearly defined.

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