Platelet satellitism, spurious neutropenia, and cutaneous vasculitis: Casual or causal association?

Lazo‐Langner, Alejandro; Piedras, J; Romero-Lagarza, Penélope; Lome-Maldonado, Carmen; Sánchez‐Guerrero, Jorge; López‐Karpovitch, Xavier

doi:10.1002/ajh.10141

Cited by 15 publications

(14 citation statements)

References 12 publications

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“…PLT satellitism, or satellitosis or rosetting, is an in vitro phenomenon related to the adherence of PLT to mature polymorphonuclear neutrophils (PMN; Figure 1b), and occasionally to other cells (Figure 3), PLT surrounding WBC in EDTA‐anticoagulated blood samples (Zeigler, 1974; Mende, Doring & Thomas, 1975). This phenomenon is rare (1 of 12 000 blood counts; Bizzaro, Goldschmeding & von dem Borne, 1995), sometimes related to an autoimmune process, but in most instances unrelated to any specific disease (Lazo‐Langner et al. , 2002).…”

Section: Situations Leading To Spuriously Low Plt Countsmentioning

confidence: 99%

Spurious counts and spurious results on haematology analysers: a review. Part I: platelets

Zandecki

Geneviève

Gérard

et al. 2007

Int J Lab Hematology

180

140

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Summary The widespread use of haematology analysers (HA) has led to a major improvement of cellular haematology, because of quick and accurate results found in most instances. However, in several situations, spurious results are observed. Inadequate blood samples, situations induced by the anticoagulant(s) used, peculiar changes related to the pathology in the patient, and technical considerations about performances of the various HA must be considered. Spurious thrombocytopenia occurs in several circumstances related to the presence of ethylenediamine tetra‐acetic acid (EDTA) used as the anticoagulant. Mechanism of EDTA‐dependent platelet (PLT) agglutination is related to circulating (auto)antibodies directed against normally hidden epitope(s) in the glycoprotein alpha IIb/beta IIIa complex from PLT membrane exposed only in the presence of EDTA. Other spuriously low PLT counts may be related to EDTA, including PLT rosetting around white blood cells (WBC; satellitism) and PLT‐WBC aggregates, but mechanisms responsible for those latter phenomena are less well known. Spurious increase of PLT count may be related to several situations, including fragmented red blood cells, cytoplasmic fragments of nucleated cells, cryoglobulins, bacteria or fungi, and lipids. Flags generated in several of these situations alert the operator on possible abnormal findings and may identify the problem. Analysing only PLT parameters is not sufficient: in many situations the WBC differential scattergram is of crucial help for flagging. Flags generated depend on the software version on the HA used, the performance in detecting the same anomalies may differ according to which analyser is used, even those from the same manufacturer. Operators must be aware of the characteristics of their analyser and be able to recognize and circumvent anomalous results.

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Section: Situations Leading To Spuriously Low Plt Countsmentioning

confidence: 99%

Spurious counts and spurious results on haematology analysers: a review. Part I: platelets

Zandecki

Geneviève

Gérard

et al. 2007

Int J Lab Hematology

180

140

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“…The mean platelet volume (MPV) was 3–fold higher in the rabbit with the lowest platelet counts (Alice), which is consistent with platelet activation and platelet destruction (immune thrombocytopenia) and new platelet production (Coban et al, 2008). Adherence of platelets on neutrophils and monocytes, known as satellitism, was observed (not shown), which is frequently associated with sporadic thrombocytopenia (Lazo-Langner et al, 2002). …”

Section: Resultsmentioning

confidence: 99%

A putative role for platelet-derived PPARγ in vascular homeostasis demonstrated by anti-PPARγ induction of bleeding, thrombocytopenia and compensatory megakaryocytopoiesis

Simpson-Haidaris

Seweryniak

Spinelli

et al. 2010

Journal of Biotechnology

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Widely known for its role in adipogenesis and energy metabolism, PPARγ also plays a role in platelet function. To further understand functions of platelet-derived PPARγ, we produced rabbit polyclonal (PoAbs) and mouse monoclonal (MoAbs) antibodies against PPARγ 14mer/19mer peptide-immunogens. Unexpectedly, our work produced two key findings. First, MoAbs but not PoAbs produced against PPARγ peptide-immunogens displayed antigenic crossreactivity with highly conserved PPARα and PPARβ/δ. Similarly, Santa Cruz PoAb sc-7196 was monospecific for PPARγ while MoAb sc-7273 crossreacted with PPARα and PPARβ/δ. Second, immunized rabbits and mice exhibited unusual pathology including cachexia, excessive bleeding, and low platelet counts leading to thrombocytopenia. Spleens from immunized mice were fatty, hemorrhagic and friable. Although passive administration of anti-PPARγ PoAbs failed to induce experimental thrombocytopenia, megakaryocytopoiesis was induced 4-8-fold in mouse spleens. Similarly, marrow megakaryocytopoiesis was enhanced 1.8-4-fold in immunized rabbits. These peptide-immunogens are 100% conserved in human, rabbit and mouse; thus, immune-mediated platelet destruction via crossreactivity with platelet-derived PPARγ likely caused bleeding, thrombocytopenia, and compensatory megakaryocytopoiesis. Such overt pathology would cause significant problems for large-scale production of anti-PPARγ PoAbs. Furthermore, a major pitfall PJS-H developed the concept, designed and performed experiments, analyzed data, prepared figures and wrote the manuscript; KES designed and performed experiments, analyzed data and edited the paper; SLS, TMG-B, TIM, and SJP performed experiments and edited the manuscript; PJS and RPP made substantial contributions to interpretation of the data, critical revisions to the manuscript for important intellectual content and supplied critical reagents.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript associated with MoAb production against closely related molecules is that monoclonicity does not guarantee monospecificity, an issue worth further scientific scrutiny.

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“…Pseudothrombocytopenia is a well-known and solvable problem, unlike a rare phenomenon of platelet satellitism which is still fairly unknown among laboratory staff and therefore often not even recognized as a crucial finding. Cases of platelet satellitism due to urinary tract infection have been already reported in the literature ( 2 , 15 ) and observed in patients with vasculitis, lupus ( 12 ) and mantle cell lymphoma ( 13 ), marginal zone B-cell lymphoma ( 9 , 17 ), hepatocelular carcinoma ( 24 ), chronic lymphocytic leukemia ( 25 ), thrombocytopenic purpura ( 26 ), squamous cell carcinoma ( 22 ), cryofibrinogenemia ( 27 ), chronic alcoholism ( 28 ) as well as in healthy individuals ( 5 - 7 ). Cryofibrinogenemia may be primary (essential) or secondary to other underlying disorders, such as carcinoma, infection, vasculitis, collagen disease, or associated with cryoglobulinemia ( 29 ).…”

Section: Discussionmentioning

confidence: 97%

“…Adhesion of platelets to neutrophils is possible by existence of an active stimulus presented on the surface of platelets ( 11 , 12 , 17 ). …”

Section: Introductionmentioning

confidence: 99%

Platelet satellitism in infectious disease?

et al. 2015

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BackgroundPlatelet satellitism is a phenomenon of unknown etiology of aggregating platelets around polymorphonuclear neutrophils and other blood cells which causes pseudothrombocytopenia, visible by microscopic examination of blood smears. It has been observed so far in about a hundred cases in the world.Case subject and methodsOur case involves a 73-year-old female patient with a urinary infection. Biochemical serum analysis (CRP, glucose, AST, ALT, ALP, GGT, bilirubin, sodium, potassium, chloride, urea, creatinine) and blood cell count were performed with standard methods on autoanalyzers. Serum protein fractions were examined by electrophoresis and urinalysis with standard methods on autoanalyzer together with microscopic examination of urine sediment. Erythrocyte sedimentation rate, blood culture and urine culture tests were performed with standard methods.ResultsDue to typical pathological values for bacterial urinary infection, the patient was admitted to the hospital. Blood smear examination revealed phenomenon, which has persisted for three weeks after the disease has been cured. Blood smears with EDTA as an anticoagulant had platelet satellitism whereas the phenomenon was not observed in tubes with different anticoagulants (Na, Li-heparin) and capillary blood.DiscussionWe hypothesize that satellitism was induced by some immunological mechanism through formation of antibodies which have mediated platelets binding to neutrophil membranes and vice versa. Unfortunately we were unable to determine the putative trigger for this phenomenon. To our knowledge this is the second case of platelet satellitism ever described in Croatia.

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Platelet satellitism, spurious neutropenia, and cutaneous vasculitis: Casual or causal association?

Cited by 15 publications

References 12 publications

Spurious counts and spurious results on haematology analysers: a review. Part I: platelets

Spurious counts and spurious results on haematology analysers: a review. Part I: platelets

A putative role for platelet-derived PPARγ in vascular homeostasis demonstrated by anti-PPARγ induction of bleeding, thrombocytopenia and compensatory megakaryocytopoiesis

Platelet satellitism in infectious disease?

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