Platelet Sequestration in Man. II. Immunological and Clinical Studies*

Abstract

The mechanisms of platelet destruction and their sites of sequestration in disease states are poorly understood. Although recent studies have emphasized the importance of platelet isoantibodies in certain clinical situations (1-3), little is known of the effects of antibodies on platelets in vivo. In conditions such as idiopathic thrombocytopenic purpura, there is debate as to whether immune mechanisms are involved, and sites of platelet sequestration are unknown.The availability of a method for labeling platelets with Cr5' that allows most of the transfused platelets to remain viable and reduces the initial deposition of nonviable platelets in the liver and spleen (4) permits study of some of these aspects of platelet pathophysiology. We investigated the survival and sites of sequestration of platelets exposed to isoantibodies in vivo. Included in this paper are observations of pyrogenic reactions after immune platelet destruction. Studies in patients with idiopathic thrombocytopenic purpura and other platelet disorders are also described. MethodsPreparation and transfusion of Cr51-!abeled "citrate platelets" and determination of the percentage of platelet survival were as described in the preceding report (4). In "extracting" Cr51-labeled platelets from blood samples taken from thrombocytopenic persons, nonradioactive platelets were added to the platelet-rich plasma to facilitate recovery of platelet Cr51. For isologous transfusions, only platelets from donors compatible with the recipients' ABO and Rh blood types were used.Methods of scintillation scanning over organs to evaluate sites of platelet sequestration have been described

A platelet and granulocyte membrane defect in paroxysmal nocturnal hemoglobinuria: usefulness for the detection of platelet antibodies

“…This finding is particularly surprising in view of the exquisite sensitivity manifested by platelets in vivo to a variety of antibodies (11,41,42). We have found that serum and plasma taken from two of the patients with PNH were as effective as normal plasma as a source of C' for platelet lysis, a finding suggesting that failure of PNH platelets to lyse in vivo is not due to deficiency of a plasma factor required for lysis.…”

Pooling of platelets in the spleen: role in the pathogenesis of "hypersplenic" thrombocytopenia.

“…A significant deviation from these values after transfusion of platelets indicated that platelet-5Cr was concentrated (relative to erythrocytes) in a particular site. Previous studies have suggested that actual total radioactivity in normal-sized organs can be crudely estimated from external scanning with various standards for comparison (12,(16)(17)(18). Direct assay of 'Cr in three surgically removed normal-sized spleens (idiopathic thrombocytopenic 1 Nuclear-Chicago DS-301 scintillation detector with 3-inch diameter crystal and collimator 3 inches wide and 3 inches deep and 132B spectrometer-scaler with window at 100 kv.…”

Cyclic 3′,5′-adenosine monophosphate in human blood platelets

“…J.) and polyvinyl chloride tubing into polypropylene tubes containing 1/10 vol of 3.8 g/100 ml of trisodium citrate dihydrate or 1/6 vol of the acid citrate anticoagulant of Aster and Jandl (18) or sodium heparin (final concentration 5 U/ml). Platelet-rich plasma (PRP) was prepared by centrifugation at 150-200 g for 15-20 min at room temperature.…”