1. May Thyrotoxicosis Trigger Thrombocytopenia? ABSTRACT Introduction: Thyrotoxicosis is a frequent disease occurring in approximately 2% of women and 0.2% of men. Thyrotoxicosis can have many causes; such as Graves’ disease, and toxic nodular goiter. Autoimmune forms of thyrotoxicosis are more prevalent among smokers. Toxic nodular goiter is common in regions where dietary iodine is insufficient. Anti- thyroid therapy during thyrotoxicosis can affect the platelet count due to bone marrow suppression but also thyrotoxicosis itself can be associated with thrombocytopenia. For a better understanding of the pathogenesis of thrombocytopenia we evaluated thyrotoxicosis patients before and after drug therapy. Methods: We retrospectively analyzed the clinical records of 91 patients diagnosed to have thyrotoxicosis. The platelet counts during the hyperthyroid phase and after the treatment were evaluated. Therapy duration was depending on achieving the euthyroid status. Statistical analyses for comparison of the mean values were done with the Student’s t-test. p< 0,05 was considered as significant. Results: 26 male and 65 female patients were evaluated. The mean age of male patients were 48, 46±16, 4/year and 54, 41±19, 49/year for female patients. The platelet count before therapy 219,04±79,43 /x103 ul and 248,49±72,47/x103 ul after therapy ( p value was <0,001). The MPV (mean platelet volume) was 8, 73±1, 07 fl before therapy and 8, 68±1, 15 fl (p value was <0,001) when the patient became euthyroid. TSH levels and FT4 levels were 0,056±0, 1 mIU/L (normal 0.30–4.00) and 2,22± 1, 46 ng/dL (normal 1.00-1.60), respectively before therapy and TSH levels were 2, 87±8, 38 and FT4 levels were 1, 17±0, 5 after therapy (p values were <0,001). Discussion: The thyrotoxic state can affect the platelet numbers, but the effect of therapy on platelet numbers is controversial. Anti-thyroid drugs may have some suppressive effects on bone marrow and also normalization of the thyrotoxic status may lead to normalization of the thrombocytopenia. In our study the mean value of the platelet count was lower during the hyperthyroid status, which may depend on the increased turnover of the platelets. The platelet numbers in our study group increased after resolution of the thyrotoxic state suggesting the theory that elevation of thyroid hormones can diminish platelet numbers which seems to be reversible with appropriate therapy. Improvement in thyroid function with drugs may lead to the spontaneous recovery of the platelet count. Dr. Kevser Onbaşı 1, Dr. Lezan Keskin 2, Dr. Serdar Üçgün 3 Dumlupınar University Faculty of Medicine, Department of Endocrinology, Kütahya 1, Malatya State Hospital, Department of Endocrinology, Malatya 2, Dumlupınar University Faculty of Medicine, Department of Internal Medicine 3, Kütahya, Turkey. INTRODUCTION The prevalence of hyperthyroidism is 1,2%. The most common cause of thyrotoxicosis is Graves’ disease. Other common causes are toxic multinodular goiter (TMNG), solitary toxic adenoma, and thyroiditis. Graves’ disease is caused by an activating autoantibody that targets the TSH receptor. Patients typically present with goiter and hyperthyroidism symptoms (1). Activation of the reticuloendothelial system by thyroid hormones can increase clearance of platelets by the spleen in thyrotoxic states, and also the restoration of the platelet count can be observed when euthyroidism is reached. Anti- thyroid therapy during thyrotoxicosis can affect the platelet count due to bone marrow suppression but also thyrotoxicosis itself can be associated with thrombocytopenia (2). Shortened platelet survival and hypersplenism resulting from long-standing hyperthyroidism may also contribute to thrombocytopenia (3). For a better understanding of the pathogenesis of thrombocytopenia we evaluated thyrotoxicosis patients before and after drug therapy. METHODS: We retrospectively analyzed the clinical records of 91 patients diagnosed to have thyrotoxicosis. The platelet counts during the hyperthyroid phase and after the treatment were evaluated. Therapy duration was depending on achieving the euthyroid status. Statistical analyses for comparison of the mean values were done with the Student’s t-test. p values with less than p< 0,05 were considered as significant. RESULTS: 26 male and 65 female patients were evaluated. The mean age of male patients were 48, 46±16, 4/year and 54, 41±19, 49/year for female patients. The platelet count before therapy 219,04±79,43 /x103 ul and 248,49±72,47/x103 ul after therapy ( p value was <0,001). The MPV (mean platelet volume) was 8, 73±1, 07 fl before therapy and 8, 68±1, 15 fl (p value was <0,001) when the patient became euthyroid. TSH levels and FT4 levels were 0,056±0, 1 mIU/L (normal 0.30–4.00) and 2,22± 1, 46 ng/dL (normal 1.00-1.60), respectively before therapy and TSH levels were 2, 87±8, 38 and FT4 levels were 1, 17±0, 5 after therapy (p values were <0,001). DISCUSSION The association between thrombocytopenia and thyroid diseases has been reported. Thrombocytopenia has been attributed either to an excess of thyroid hormone or to an autoimmune mechanism. Some studies have shown that platelet count and platelet survival improved with treatment of hyperthyroidism (4). The thyrotoxic state can affect the platelet numbers, but the effect of therapy on platelet numbers is controversial. Anti-thyroid drugs may have some suppressive effects on bone marrow and also normalization of the thyrotoxic status may lead to normalization of the thrombocytopenia. In our study the mean value of the platelet count was lower during the hyperthyroid status, which may depend on the increased turnover of the platelets. The platelet numbers in our study group increased after resolution of the thyrotoxic state suggesting the theory that elevation of thyroid hormones can diminish platelet numbers which seems to be reversible with appropriate therapy. CONCLUSION Improvement in thyroid function with drugs may lead to the spontaneous recovery of the platelet count. REFERENCES 1.Nayak B, Hodak SP. Hyperthyroidism. Endocrinology and Metabolism Clinics of North America 2007; 36: 617–656. 2.Azar M, Frates A, Rajput V. Idiopathic Thrombocytopenic Purpura (ITP) and Hyperthyroidism: An Unusual But Critical Association for Clinicians. Journal of Hospital Medicine 2008; 3 (5):431-433. 3.Adrouny A, Sandler RM, Carmel R. Variable presentation of Thrombocytopenia in Graves’ Disease. Archives of Internal Medicine 1982; 142:1460-1464. 4.Cordiane I, Betterle C, Spadaccino CA. Soini B, Girolami A, Fabris F. Autoimmune thrombocytopenia (AITP) and thyroid autoimmune disease (TAD): overlapping syndromes? Clin Exp Immunol. 1998 Sep;113(3):373-8. MON-0527