Platelet satellitism: experimental studies.
Platelet satellitism (PS), the in vitro phenomenon of platelets rosetting about nonlymphocytic leukocytes, is an uncommon and poorly understood finding reported in the ethylenediaminetetra-acetic acid (EDTA)-anticoagulated blood of patients with a wide variety of clinical conditions. This report presents experimental studies investigating the nature of this phenomenon by utilizing the blood of patients with platelet satellitism. Wet preparation studies and electron microscopy (transmission and scanning) demonstrated the morphologic sequences involved in the phenomenon, including eventual phagocytosis of platelets by neutrophils. The results of varying conditions such as time, temperature, and anticoagulant are described. All of five patients tested were found to have cryofibrinogenemia. Certain blood components from all of three patients tested were capable of inducing PS in normal whole blood, whereas components from normal subjects usually were not. In one patient (A), the PS-inducing capability appeared to be present in both plasma and platelets. In another patient (B) the PS-inducing capability was present in platelets (in both 1966 and 1975) and also in the cryosupernate of serum and plasma; among various antisera, antifibrinogen had the greatest ability to reduce the degree of PS in patient blood; addition of moderate amounts of CaCl2 and/or MgCl2 did not diminish the phenomenon; and two sisters and two daughters demonstrated no PS. In a third patient (C) the PS-inducing capability appeared to be largely concentrated in the cryoprecipitable fraction of plasma. These studies suggest that there are different factors in the patients' blood resulting in PS. Further studies showed PS could be induced in normal blood by adding certain nonprimate antihuman antisera (anti-IgM, antialbumin or antifibrinogen) and also by adding some preparations of normal washed platelets to the same individuals's normal whole blood. This indicates that the phenomenon of PS can be produced by factors other than those specifically present in patients with PS. Antigen-antibody complexes, either formed in vivo (mixed cryoglobulinemia) or in vitro, did not result in PS when mixed with normal blood. These and other studies suggest that PS can result from the presence of several different factors, usually proteins (in conjunction with EDTA), which probably attach to the surface of platelets apparently resulting in some alteration (such as change in surface charge) causing the platelets to be attracted to and phagocytosed by neutrophils.
D001791:Blood Platelet Disorders / Q000097:blood*; D001792:Blood Platelets / Q000502:physiology* / Q000648:ultrastructure; D001796:Blood Protein Disorders / Q000097:blood; D003080:Cold Temperature; D004492:Edetic Acid; D005340:Fibrinogen; D006801:Humans; D008855:Microscopy, Electron, Scanning; D009504:Neutrophils / Q000502:physiology* / Q000648:ultrastructure; D010587:Phagocytosis; D012397:Rosette Formation
D005340:Fibrinogen; D004492:Edetic Acid