LETTER
Hyperthyroidism
Brian J. Bohlmann
1 March 1995 | Volume 122 Issue 5 | Pages 393-394
TO THE EDITOR:
A review article on hyperthyroid disease [1] described immune-mediated leukopenia associated with Graves disease. I describe a patient with thrombocytopenia that complicated Graves disease.
A 24-year-old pregnant Hispanic woman had Graves disease at 14 weeks gestation and was treated with propylthiouracil. Three weeks later, a routine complete blood count showed a platelet count of 20 000 cells/mm3. Examination of a bone marrow biopsy specimen showed increased megakaryocytes, and platelet-associated IgG and IgM antibodies were elevated. She was treated successfully with prednisone, 100 mg daily.
In one series [2], five patients with Graves disease and thrombocytopenia were described. As was the case with our patient, two patients had idiopathic thrombocytopenic purpura-like illnesses that responded to prednisone. Four of the five patients were Latin American, which raises the interesting possibility of a heritable component in Hispanic patients.
Autoimmunity is one mechanism to explain the thrombocytopenia sometimes seen in hyperthyroid states, and it may be responsible for the extremely low platelet counts seen in patients with idiopathic thrombocytopenic purpura-like illnesses [2]. The underlying derangement in immune function that results in autoantibody formation may lead separately to the production of antithyroid and antiplatelet antibodies. Cross-reaction between antithyroid antibodies and the thyrotropin receptors on leukocytes has been postulated to account for the leukopenia sometimes seen in Graves disease, although no similar mechanism has been proposed for platelet destruction.
Increased activation of the reticuloendothelial system in hyperthyroid states is found in humans and in animal models, and this mechanism may account for the more mild cases of thrombocytopenia that are seen with hyperthyroidism. Platelet survival curves were shortened in all patients with hyperthyroidism whom we studied [3], and 43% of patients with untreated hyperthyroidism were frankly thrombocytopenic [4]. Conversely, 14% of patients with unexplained thrombocytopenia had hyperthyroidism [5].
Clinicians need to be alert for thrombocytopenia that complicates Graves disease. Recommendations to check thyroid function in patients with unexplained thrombocytopenia [2] seem appropriate.
1. Klein I, Becker D, Levey G. Treatment of hyperthyroid disease. Ann Intern Med. 1994; 121:281-8.
2. Adrouny A, Sandler RM, Carmel R. Variable presentation of thrombocytopenia in Graves disease. Arch Intern Med. 1982; 142:1460-4.
3. Lamberg BA, Kivikangas V, Pelkonen R. Thrombocytopenia and decreased life-span of thrombocytes in hyperthyroidism. Ann Clinic Res. 1971; 3:98-102.
4. Kurata Y, Nishioeda Y, Tsubakio T. Thrombocytopenia in Graves disease: effect of T3 on platelet kinetics. Acta Haemotol. 1980; 63:185-90.
5. Marshall JS, Weisberger AS, Levy RP. Coexistent idiopathic thrombocytopenic purpura and hyperthyroidism. Ann Intern Med. 1967; 67:411-4.
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