Neutrophilic phagocytosis in autoimmune thrombocytopenia purpura
In vivo neutrophil phagocytosis was demonstrated by transmission electron microscopy (TEM) in the peripheral blood of two half-sibs with hereditary thrombocytopenia. These sibs have had a lifetime documented history of thrombocytopenia. Light microscopy morphology and histochemistry studies of blood and marrow were normal, similar studies of blood from available members of the kinship were also normal. Scanning electron microscopy (SEM) of platelets from each member of the kinship showed normal dendritic and spreading formation. In the TEM thin sections of platelet buffy coats, neutrophil ingestion of platelets was common and all stages of the phagocytic process were noted--from platelet-neutrophil intimacy to the formation of myelin bodies in phagosomes. The clinical courses over a 10-year period were mild, requiring rare therapeutic interventions. The chronic thrombocytopenia, lengthy mild course, modestly elevated platelet-associated immune globulin, normal aggregation and survival studies, and autoimmune neutrophil reaction to platelets allowed classification of these patients as hereditary thrombocytopenia purpuras.
In vivo neutrophil phagocytosis was demonstrated by transmission electron microscopy (TEM) in the peripheral blood of two half-sibs with hereditary thrombocytopenia. These sibs have had a lifetime documented history of thrombocytopenia. Light microscopy morphology and histochemistry studies of blood and marrow were normal, similar studies of blood from available members of the kinship were also normal. Scanning electron microscopy (SEM) of platelets from each member of the kinship showed normal dendritic and spreading formation. In the TEM thin sections of platelet buffy coats, neutrophil ingestion of platelets was common and all stages of the phagocytic process were noted--from platelet-neutrophil intimacy to the formation of myelin bodies in phagosomes. The clinical courses over a 10-year period were mild, requiring rare therapeutic interventions. The chronic thrombocytopenia, lengthy mild course, modestly elevated platelet-associated immune globulin, normal aggregation and survival studies, and autoimmune neutrophil reaction to platelets allowed classification of these patients as hereditary thrombocytopenia purpuras.
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