Platelets in Hyperthyiroidism: Studies on Platelet Counts, Mean Platelet Volume, 111-Indium-Labeled Platelet Kinetics, and Platelet-Associated Immunoglobulins G and M*

Abstract

We compared in 15 patients with hyperthyroidism (11 with Graves' disease, 3 with toxic adenoma, and 1 with multinodular goiter) platelet counts (PC) and mean platelet volume (MPV) before and 3 weeks after initiation of antithyroid drug therapy when the patients were euthyroid. In addition, platelet kinetic studies of autologous 111-indium-labeled platelets and platelet-associated immunoglobulins G and M (PAIgG and PAIgM, respectively) were investigated. The control group for the platelet kinetic studies consisted of 2 patients with diffuse nontoxic goiter and 86 patients who were studied for evaluation of their arteriosclerotic vascular disease. After 3 weeks of antithyroid drug therapy there was a significant increase in PC and a decrease in MPV compared with the pretreatment values (pretreatment PC median, 215 X 10(9)/L; range, 96-350 X 10(9)/L; PC median 3 weeks later, 248 X 10(9)/L; range, 157-384 X 10(9)/L; P less than 0.005; pretreatment MPV median, 10.6 fL; range, 9.1-13.2 fL; MPV 3 weeks later, 9.9 fL; range, 8.4-11.0 fL; P less than 0.005). 111-Indium platelet recovery was normal in all subjects. Platelet lifespan was significantly shortened in the patients with hyperthyroidism compared with the control group (median, 163.8 h; range, 128.5-206 h; vs. 180.0 h; range, 138.3-231.5 h; P less than 0.05). Platelet turnover averaged 45.6 (range, 25.6-71.9) X 10(9)/L.day; values above the limit of normal were found in 7 of 15 patients with hyperthyroidism. Three patients with Graves' disease had elevated levels of PAIgG; 1 of these patients had elevated levels of PAIgM and was the only patient with thrombocytopenia (PC, 96 X 10(9)/L). Various combinations of statistical correlations between the degree of hyperthyroidism, pretreatment PC and MPV, platelet kinetic studies, levels of PAIg, and serum levels of antithyroid antibodies revealed no significant differences. These findings suggest that the platelet changes observed in hyperthyroidism, such as lower PC and increased MPV, together with the shortened platelet lifespan reflect metabolically rather than immunologically mediated phenomena, although these may be involved in cases with marked thrombocytopenia.

Age-Related Prevalence of Platelet-Associated Immunoglobulins G in Nonthrombocytopenic Patients with Autoimmune Thyroid Disease and Autoimmune Polyglandular Syndrome

“…These associations are regarded, nowadays, as autoimmune polyglandular syndrome (APS; types 1–3) [7], characterized by the association between endocrine and nonendocrine autoimmune disease, either during the clinical or the subclinical phase. Several morphological and functional changes in platelets have been described in patients with thyroid disorders [8, 9]. Isolated or familial autoimmune idiopathic thrombocytopenia (AITP) has been described in patients with Graves’ disease (GD) in the presence of platelet-associated IgG (paIgG) [10, 11].…”

“…Isolated or familial autoimmune idiopathic thrombocytopenia (AITP) has been described in patients with Graves’ disease (GD) in the presence of platelet-associated IgG (paIgG) [10, 11]. However, paIgG has been reported both in GD and Hashimoto’s thyroiditis (HT) also in the absence of AITP [8, 11]. Unfortunately, the criteria used in these studies were not homogeneous and based mainly on the thyroid function; indeed, the routine diagnostic use of antiperoxidase antibodies [3, 12]has apparently led to an increase, over the last few years, in the diagnoses of AITD, whilst still in an early, subclinical phase [1, 3, 13].…”

Thrombin Activatable Fibrinolysis Inhibitor Antigen Levels Are Inversely Correlated with Plasminogen Activator Inhibitor-1 Antigen Levels in Hyperthyroid Patients

“…Although hyperthyroid patients are prone to developing thromboembolism, bleeding due to various coagulation defects are also reported [11][12][13]. Increased levels of a specific fragment of fibrinogen, which is degraded by plasmin, suggest hyperfibrinolysis in hyperthyroid patients [14].…”

Idiopathic thrombocytopenic purpura (ITP) and hyperthyroidism: An unusual but critical association for clinicians

“…Panzer et al reported the presence of antiplatelet IgG in patients with Grave's as well as improved platelet counts and increased mean platelet volume after successful antithyroid therapy. 8 In addition to the coexistence of thyroidstimulating immunoglobulins (TSIs) and antiplatelet antibodies as a potential mechanism for Grave's-associated thrombocytopenia, some have postulated that in Grave's patients, TSIs and other thyroid antibodies might actually bind to the platelets themselves. The postulated site for binding would be a truncated actin-binding protein on the platelets that would link the high-affinity Fc receptor of immunoglobulin G to the platelets' cytoskeleton, thereby accelerating their destruction.…”

“…Early recognition and treatment of the hyperthyroid state with antithyroid medications can lead to significant improvement in the platelet count. 1,8 We report this rare but critical clinical relationship.…”