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J Thorac Cardiovasc Surg 1994;107:316-317
© 1994 Mosby, Inc.
LETTERS TO THE EDITOR |
Departments of Cardiothoracic Surgery and Hematology
Walsgrave Hospital
Coventry, England
To the Editor:
A 69-year-old man with severe proximal left anterior descending coronary artery disease was referred for a coronary artery operation after two attempted angioplasties resulted in early restenosis. Preadmission screening revealed severe thrombocytopenia (platelet count 63 x 109 cells/L). Current medications were atenolol, isosorbide mononitrate, nifedipine, frusemide, and amiloride. The patient was referred for hematologic investigation.
Bone marrow aspiration revealed active normal marrow with plentiful megakaryocytes, consistent with peripheral platelet destruction. Results of indirect platelet antibody tests and assay for antinuclear factor were negative. A presumptive diagnosis of idiopathic thrombocytopenic purpura was made. Therapy with prednisolone (1 mg/kg per day) was commenced in an attempt to obtain remission before operation, but this regimen resulted in only small, transient increases in the platelet count. Because of this complication, the patient was admitted to the hospital and intravenously given monomeric immunoglobulin (Sandoglobulin) at a dose of 0.4 gm/kg daily for 5 days, commencing 5 days before the proposed date of operation. The patient's platelet counts before and after operation were as follows: preoperative day 5, 7 x 109 cells/L;preoperative day 3, 37 x 109 cells/L;day of operation, 64 x 109 cells/L;postoperative day 1, 157 x 109 cells/L;postoperative day 2, 140 x 109 cells/L;and postoperative day 10, 141 x 109 cells/L.
At operation, full cardiopulmonary bypass was used with aortic crossclamping and crystalloid cardioplegia. Saphenous vein was used to graft the left anterior descending coronary artery. Bypass time was 30 minutes and clamp time was 14 minutes. From the time the sternum was wired to the time the mediastinal drain was removed (20 hours), remarkably there was no drainage.
Adult idiopathic thrombocytopenia purpura is an autoimmune condition arising from antibody binding to the glycoprotein IIb-IIIa complex on the platelet membrane. Antibody-coated platelets are prematurely removed from the circulation by attachment to macrophage Fc receptors, followed by phagocytosis. Reduced platelet life span results in an increase in the megakaryocyte mass and the platelet turnover (two to eight times normal).
1 The mechanism of action of intravenously administered immunoglobulin is not entirely clear, but a major effect is likely to be the blockade of macrophage Fc receptors so that the antibody-coated platelets are not recognized or destroyed.
2 The increased platelet production is thus unopposed and large, young platelets, which are highly effective in hemostasis, are released into the circulation. This case serves as a further illustration of the effectiveness of the intravenous administration of monomeric immunoglobulin in the management of patients with idiopathic thrombocytopenia purpura refractory to steroid treatment.
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