The patient was a 66 year old male with past medical history significant for obesity, hypertension, and type II diabetes mellitus, who was found to have hematochezia thought to be secondary to diverticulosis. The white blood cell count was 9,100 K/mL, hemoglobin 13.7 g/dL, mean corpuscular volume 92 fL, and platelet count 207,000 K/mL. There was a reported history of thrombocytopenia, however, and a peripheral smear was obtained from an EDTA (lavender-top) tube.
A peripheral blood smear showed prominent ‘rosetting’ of platelets around polymorphonuclear neutrophils, an in vitro phenomenon known as platelet satellitism (Figure 1). Unfortunately, no citrate tube was drawn to verify if clumping dissipated, due to presumed platelet satellitism.
Platelet satellitism is a rare morphologic variant of pseudo-thrombocytopenia, which is thought to be due to the in vitro effects of room temperature ethylenediamine tetra-acetic acid (EDTA), a common anti-coagulant added to CBC tubes. This phenomenon is not seen in samples collected using alternative anticoagulants, such as heparin or citrate, so these may be used if clumping is suspected (Chakrabarti 2014). Of note, in blood smears displaying platelet satellitism, automated platelet analyzers may or may not display normal platelet counts. Importantly, severe satellitism may lead to a misdiagnosis of thrombocytopenia if the peripheral blood smear is not examined (Chakrabarti 2014).
Some studies have suggested this phenomenon results from circulating IgG autoantibodies against the FcγRIII expressed by neutrophils, and an EDTA-induced epitope of platelet glycoprotein IIb/IIIa (Bizzaro et al, 1995). Such autoantibodies may result in direct ‘bridge formation’ between the two cell types, leading to the rosetting observed on the blood smear.
Results of both in vivo and in vitro platelet function are normal, although some have argued that platelet satellitism may occur as a result of a non-immunologic mechanism, from either platelet or neutrophil activation in vivo, due expression of CD62P (P-selectin) or CD11b/CD18 (B2 integrin), respectively (Shahab et al 1998; Peters et al, 1998). These markers are both involved in cell adhesion and leukocyte diapedesis and extravasation.
Platelet satellitism has been documented in patients with vasculitis, lupus, lymphomas, and also in cirrhosis, as well as in healthy patients; a precise etiologic mechanism in these disease states remains to be discovered (Bobba et al 2012; Yoshikawa et al 2006). Regardless of etiology, clinically, when this phenomenon is seen on the blood smear, it is important to instruct clinicians to redraw a sample using a collection tube containing non-EDTA anticoagulants (i.e citrate), for evaluation of ‘true’ platelet count and ruling out of this known cause of pseudo-thrombocytopenia.