Evidence has been presented that the gonads, thyroid, adrenal cortex and pituitary glands have a definite influence on blood formation. The normal sex difference in erythrocyte levels in animals, and probably in man, can be obliterated by castration and restored by appropriate replacement therapy. Hypothyroidism results in a moderately severe anemia in animals. In the uncomplicated form, the anemia is slightly macrocytic and associated with a hypoplastic bone marrow. In clinical experience the anemia may be complicated by the secondary effects of achylia gastrica leading either to iron deficiency or to a deficiency in the antipernicious anemia factor. Hyperthyroidism causes some alterations in the white blood cells, but has little effect on the red blood cell series. Hyperactive states of the adrenal cortex may be associated with a mild polycythemia. Adrenal steroids also have a marked lymphocytic effect, causing the release of beta and gamma globulins from lymphoid tissue. A mechanism involving the anterior pituitary and adrenal seems to exist, controlling the release of antibodies under certain conditions. It is suggested that other mechanisms also exist which control the number of circulating lymphocytes.
Deficiency of the anterior pituitary secretions results in anemia in animals and man. The anemia in animals is usually microcytic and hypochromic and may respond to several types of replacement therapy. In man anemia develops slowly and is rarely severe. Moderate reductions in the red blood cell count occur and the color index varies. There is hypoplasia of the bone marrow. The anemia in man does not respond uniformly well to the therapy now available, but improvement often occurs with the replacement of "end-organ" hormones.
The preponderance of evidence indicates that the regulation of blood formation is not primarily under hormonal control. The effects noted in various glandular disorders are due to alterations in metabolism produced in the bone marrow as well as all other body tissues.