Myxomas of the tricuspid valve are extremely rare, with only 13 cases reported in the world literature (1). We report the case of a 15-month old male with tricuspid valve myxoma and massive myxomatous pulmonary emboli discovered at autopsy.
Platelet-leukocyte interaction was observed in an asymptomatic woman. After incubation in the patient's EDTA-plasma, autologous and allogeneic platelets adhered to the surfaces of neutrophils, monocytes, macrophages and, rarely, eosinophils. Monocytes, macrophages, and occasionally neutrophils phagocytosed platelets. Degranulation of peroxidase-positive lysosomes into the platelet-containing phagosome was demonstrated ultrastructurally. Bone marrow studies indicated that bands and earlier neutrophilic precursors did not participate in the reaction, and that neutrophils adhered to, and were rarely engulfed by megakaryocytes. Sequential exposure of the patient's EDTA-plasma to platelets and leukocytes indicated that a nondialyzable factor(s) was first absorbed by platelets which then interacted with leukocytes. The reaction proceeded best in the presence of EDTA at 21 degrees C, and was inhibited or dissociated by divalent cations or at 37 degrees C. Metabolic integrity of both platelets and leukocytes was also essential for the reaction since each was inhibited by formalin fixation and partially inhibited by the metabolic inhibitor 2-deoxyglucose. Formalin-treated platelets continued to absorb the plasma factor(s). The plasma and the cell fractions were inactivated by periodate and nonspecific protease. Treatment of the platelets with trypsin or the leukocytes with neuraminidase diminished the interaction by 50%. The reaction was also interfered with by concanavalin A. Immunofluorescent and immunoabsorption studies failed to identify an immune component of this interaction. These findings indicate that the plasma factor(s) and the cell surface receptors are nonimmune glycoconjugates and consequently differ from previously documented cases of platelet-leukocyte interaction.
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