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Association of Hyperthyroidism with Idiopathic Thrombocytopenic Purpura and Haemolytic Anaemia
22
Citations
27
References
1979
Year
Short Platelet SurvivalThrombosisHaemolytic AnaemiaBone Marrow FailureBlood PlateletThyroid DiseaseHematologyParathyroid HormonePathologyPlatelet PathobiologyThyroid DisordersSurgeryParathyroid GlandMedicineEarly StageBone Marrow Sections
ABSTRACT. Two cases of thyrotoxicosis associated with acute idiopathic thrombocytopenic purpura and haemolytic anaemia are reported. The underlying cause of the hyperthyroidism was lymphoid thyroiditis and the severe thrombocytopenia was due to an extremely short platelet survival as determined with the 51 Cr‐labelling technique. The amount of megakaryocytes was increased in bone marrow sections, indicating increased platelet production. Treatment with high doses of corticosteroids did not increase the platelet count, which remained at critical levels below 10times10 9 /1, and there were still signs of increasd bleeding tendency. Splenectomy was therefore considered at an early stage after diagnosis and was performed when the thyrotoxicosis had been brought under control with corticosteroids and β‐blocking agents. A method which has proven useful in minimizing bleeding during surgery in patients with low platelet counts is described. This method takes advantage both of the fact that normally 30% (in cases with splenomegaly even more) of the total body platelets are harboured in the spleen and can be expelled with i.v. epinephrine, and of the good haemostatic effect of small amounts of platelet concentrates given at appropriate times during the operation. It is proposed that splenectomy should be performed early if large doses of corticosteroids do not raise the platelet count above critical levels or if the bleeding continues. Partial control of the thyrotoxic state should be obtained with β‐blocking agents and corticosteroids and measures should be undertaken to minimize the bleeding risks during surgery. Underlying immunologic mechanisms responsible for the development of this disease combination are discussed. It is suggested that despite the great array of antibodies present, the basic abnormality is confined to immunocompetent T lymphocytes.
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