Graves’ Disease and the Manifestations of Thyrotoxicosis
DeGroot LJ.
ncbi.nlm.nih.gov/books/NBK2...
HEMATOLOGIC CHANGES
In most patients the hemoglobin and hematocrit are in the normal or low range [360]. Blood volume is increased, and the red cell mass is actually increased in some patients. In severe thyrotoxicosis normocytic anemia with hemoglobin concentrations as low as 8 - 9 g/dl may be observed. Hyperthyroid patients with anemia may show impaired iron use [361, 362]. Malnutrition may play a role in this decrease. These anemias are unresponsive to hematinic therapy, but the blood picture returns to normal when the thyrotoxicosis is controlled [262]. Iron deficiency or megaloblastic anemia is exceptional and requires a search for some explanation other than thyrotoxicosis. It is possible that thyrotoxicosis may increase the need for vitamin B12, as shown experimentally, and perhaps for folic acid. Also, there is an increased incidence of antigastric antibodies and mild pernicious anemia in patients with Graves' disease.The glucose-6-phosphate dehydrogenase activity of red cells is increased in thyrotoxicosis [363].
A relative lymphocytosis is frequently found in the peripheral blood due to neutropenia [364]. A relative and an absolute increase in the number of monocytes was noted years ago [365]. The monocyte count was between 10 and 15%; in only 2 of the 30 cases was it less than 10%. Relative lymphocytosis and relative monocytosis, with a normal or slightly low total white cell count, constitute the characteristic blood findings of Graves' disease. There is also an increase in the percentage and number of B lymphocytes and, as discussed previously, an altered ratio of T lymphocyte subsets. Significant pancytopenia with leukocyte counts under 3x109/l and neutrophiles under 2x109/l occasionally occurs, and if unrelated to drug therapy, tend to recover during treatment (366).
Graves' disease is often associated with mild thrombocytopenia, and occasionally with idiopathic thrombocytopenic purpura [367]. This co-occurrence is thought to reflect the autoimmune pathogenesis of both diseases. Fourteen percent of patients with ITP are reported to have coincident Graves' disease. Mild thrombocytopenia may disappear spontaneously or with treatment of hyperthyroidism, or if severe, may respond to glucocorticoid therapy [368]. Other more severe cases are managed as typical cases of ITP. Bone marrow examination may show normal or increased megakaryocytes [368]. Hyperthyroidism also induces a shortened platelet life span, believed to be due to more rapid clearing of normal platelets by an activated reticulo-endothelial system. Both anti-platelet antibodies and shortened platelet life span could contribute to the low or low-normal levels of platelets found in Graves' patients. It is reported that all patients with Graves' disease have evidence of IgG bound to platelets.
Coagulation is usually normal in spite of mild prolongation of the prothrombin time. Antihemophilic factor is often elevated in level and returns to normal with treatment. Hyperthyroidism can be associated with increased coagulability, in part through elevation of factor VIII. Cerebral venous thrombosis has been reported in association with thyrotoxicosis, suggesting that occasionally the propensity for coagulation can lead to serious consequences(369). Capillary fragility is increased. Severe liver damage caused by thyrotoxicosis and secondary congestive heart failure may be associated with a hemorrhagic tendency.
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