Erythropoiesis and erythropoietin in hypo- and hyperthyroidism.
Qualitative and quantitative studies of erythropoiesis in 23 patients with hypothyroidism and 21 patients with hyperthryoidism included routine hematologic evaluation, bone marrow morphology, status of serum iron, B12 and folate red blood cell mass and plasma volume by radioisotope methods, erythrokinetics and radiobioassay of plasma erythropoietin. A majority of patients with the hypothyroid state had significant reduction in red blood cell mas per kg of body weight. The presence of anemia in many of these patients was not evident from hemoglobin and hematocrit values due to concomitant reduction of plasma volume. The erythrokinetic data in hypothyroid patients provided evidence of significant decline of the erythropoietic activity of the bone marrow. Erythroid cells in the marrow were depleted and also showed reduced proliferative activity as indicated by lower 3H-thymidine labeling index. Plasma erythropoietin levels were reduced, often being immeasurable by the polycythemic mouse bioassay technique. These changes in erythropoiesis in the hypothyroid state appear to be a part of physiological adjustment to the reduced oxygen requirement of the tissues due to diminished basal metabolic rate. Similar investigations revealed mild erythrocytosis in a significant proportion of patients with hyperthyroidism. Failure of erythrocytosis to occur in other patients of this group was associated with impaired erythropoiesis due to a deficiency of hemopoietic nutrients such as iron, vitamin B12 and folate. The mean plasma erythropoietin level of these patients was significantly elevated; in 4 patients the levels were in the upper normal range whereas in the rest, the values were above the normal range. The bone marrow showed erythyroid hyperplasia in all patients with hyperthyroidism. The mean 3H-thymidine labeling index of the erythroblasts was also significantly higher than normal in hyperthyroidism; in 8 patients the index was within the normal range whereas in the remaining 13 it was above the normal range. Erythrokinetic studies also provided evidences of increased erythropoietic activity in the bone marrow. It is postulated that thyroid hormones stimulate erythropoiesis, sometimes leading to erythrocytosis provided there is no deficiency of hemopoietic nutrients. Stimulation of erythropoiesis by thryoid hormones appears to be mediated through erythropoietin.
D001681:Biological Assay; D001856:Bone Marrow Examination; D002455:Cell Division; D004912:Erythrocytes / Q000378:metabolism; D004920:Erythropoiesis; D004921:Erythropoietin / Q000378:metabolism*; D005492:Folic Acid / Q000097:blood; D006400:Hematocrit; D006452:Hemoglobinometry; D006801:Humans; D006980:Hyperthyroidism / Q000503:physiopathology*; D007037:Hypothyroidism / Q000503:physiopathology*; D007501:Iron / Q000097:blood; D007527:Isoenzymes; D007770:L-Lactate Dehydrogenase / Q000097:blood / Q000378:metabolism; D010953:Plasma Volume; D011086:Polycythemia / Q000209:etiology; D013936:Thymidine / Q000378:metabolism; D014805:Vitamin B 12 / Q000097:blood
D007527:Isoenzymes; D004921:Erythropoietin; D005492:Folic Acid; D007501:Iron; D007770:L-Lactate Dehydrogenase; D014805:Vitamin B 12; D013936:Thymidine