General Hospital, University of Vienna Währinger Gürtel, Austria A-1090
An association between thrombocytopenia with hyperthyroidism has been observed previously. In an earlier study we have shown that, in hyperthyroidism, platelet life-span is shorter than in controls, platelet turnover is increased in about 50% of patients, and as a consequence, platelet counts are lower during the hypermetabolic state (1). These changes of platelet parameters are reversed upon achievement of euthyroidism. To date, the possibility that hyperthyroidism is associated with an increased rate of platelet production has not been addressed directly, mainly because the determination of thrombopoiesis was considered too invasive.
The number of reticulated platelets in the peripheral blood reflects thrombopoietic activity in the bone marrow (2). We therefore determined reticulated platelets in 12 patients with recently diagnosed hyperthyroidism (Graves disease, n = 6; toxic adenoma, n = 6), and again after achievement of euthyroidism according to the previously described methods (3). Patients with platelet reactive auto-antibodies were excluded from the study.
At the time of hyperthyroidism 11 out of 12 patients had significantly higher percentages of reticulated platelets than after achievement of euthyroidism (hyperthyroidism, median 2.8%, range 0.811.8%; euthyroidism, median 0.8%, range 0.31.8%, P < 0.001). Likewise, the absolute number of reticulated platelets declined significantly at the time of euthyroidism (hyperthyroidism, median 5.2 x 109/L, range 1.435.6 x 109/L; euthyroidism, median 1.8 x 109/L, range 0.56.4 x 109/L; P < 0.001). During the observation period peripheral platelet counts were normal in all patients except one. This latter patient was thrombocytopenic at the time of hyperthyroidism and had normal platelet counts after achievement of euthyroidism.
Our data indicate that hyperthyroidism leads to an increase of platelet production, even in patients with a normal platelet count. The increased thrombopoiesis may result from the shortened platelet life-span (1) to maintain a normal platelet count. Therefore, we hypothesized in our previous paper that the thrombocytolytic state is compensated in these patients (1). Alternatively, platelet life-span is reduced as a consequence of increased thrombopoiesis to prevent thrombocythaemia. Our current investigation indicates that platelet turnover is increased in hyperthyroidism. In our previous study, however, we were able to demonstrate such an increase of platelet turnover in only 8 out of 15 patients, possibly because the turnover rate is calculated by an equation from platelet life-span and counts. The latter were not reduced in the majority of patients. In contrast, the estimation of reticulated platelets can be considered a superior indicator of thrombopoiesis, because an increase of reticulated platelets was discernible even if the total number of platelets was not significantly altered because of hyperthyroidism. The determination of reticulated platelets demonstrates directly the influence of hyperthyroidism on the fine regulation on thrombopoiesis.
Footnotes
Address correspondence to: Simon Panzer, MD, Clinic for Blood Group Serology and Transfusion Medicine, University of Vienna, A-1090 Wien, Währinger Gürtel 18-20, Austria.
Received January 29, 1998.
References
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