Pseudothrombocytopenia Due to Agglutinins

Veenhoven, Wa; Vanderschans, Gs; Huiges, W; Mettingscherphuis, He; Halie,; Nieweg, H. O.

doi:10.1093/ajcp/72.6.1005

Cited by 50 publications

(30 citation statements)

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“…A spurious low platelet count due to platelet clumping or aggregation in EDTA-anticoagulated blood is an in vitro phenomenon known as EDTA-dependent pseudothrombocytopenia (EDTA-PTCP) (Gowland et al, 1969;Shreiner & Bell, 1973;Veenhoven et al, 1979;Onder et al, 1980). Recent studies have suggested that EDTA-PTCP is due to the presence of antiplatelet antibodies that recognize antigens on platelet membrane modified by EDTA (Mant et al, 1975;Robblee & Sherpro, 1976;Kunicki et al, 1981;Howard et al, 1982;Pegels et al, 1982;Ginsberg et al, 1986;van Vliet et al, 1986;Casonato et al, 1994;Bizzaro & Brandalisa, 1995).…”

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confidence: 99%

“…EDTA-PTCP is of practical importance because the lack of recognition of this clinical entity may result in unnecessary treatment, such as steroid therapy or splenectomy, of patients with a normal platelet count (Berkman et al, 1991). Although EDTA-PTCP has been reported both in apparently normal individuals and in association with a variety of disease states such as malignancies, liver diseases, cardiovascular diseases, or autoimmune diseases (Gowland et al, 1969;Shreiner & Bell, 1973;Mant et al, 1975;Veenhoven et al, 1979;Onder et al, 1980;Berkman et al, 1991), there is no clinical evidence that associates the presence of EDTA-PTCP with specific diseases or the use of specific drugs. Therefore it is important to exclude the diagnosis of EDTA-PTCP in patients with a low platelet count in routine testing, and the development of a suitable method to evaluate the platelet counts in patients with EDTA-PTCP is of consequence.…”

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confidence: 99%

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Aminoglycosides prevent and dissociate the aggregation of platelets in patients with EDTA‐dependent pseudothrombocytopenia

et al. 1997

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Summary.Although EDTA-dependent pseudothrombocytopenia (EDTA-PTCP) is of practical importance because failure to recognize this clinical entity may result in misdiagnosis and subsequent mismanagement of the patients, the pathophysiological nature of EDTA-PTCP remains unknown. To develop an effective way to evaluate the platelet counts in patients with EDTA-PTCP, we introduced aminoglycosidessupplemented anticoagulating agents. When kanamycin was pre-supplemented with EDTA for anticoagulating blood samples from EDTA-PTCP patients there was no significant change in the platelet counts and the morphology of blood cells after 150 min of incubation at room temperature. Furthermore, when kanamycin was added to EDTA-anticoagulated blood samples from EDTA-PTCP patients within 30 min after blood withdrawal, rapid dissociation of platelets without apparent morphological changes of blood cells was observed, and complete blood cell counts as well as the histogram patterns were almost the same as those examined immediately after blood sampling. The dissociation of aggregated platelets was also detected when other antibiotics were used, although it was associated with some extent of morphological changes of blood cells. These findings indicate that the supplementation of aminoglycosides either before or after blood sampling is a useful method for the diagnosis EDTA-PTCP and for the evaluation of platelet counts in patients with EDTA-PTCP.

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Aminoglycosides prevent and dissociate the aggregation of platelets in patients with EDTA‐dependent pseudothrombocytopenia

et al. 1997

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“…93 patients had antiplatelet antibodies (48 IgM, 30 IgG,3 IgA, and 12 had two different isotypes concomitantly). In 20% of patients, the presence of IgM antibodies characteristically accompanied platelet agglutination also at 37"C, and in citrated blood.…”

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EDTA‐dependent pseudothrombocytopenia: A clinical and epidemiological study of 112 cases, with 10‐year follow‐up

1995

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In the past 10 years, we have observed 112 cases of EDTA-dependent pseudothrombocytopenia (PTCP) due to in vitro platelet clumping at room temperature. 93 patients had antiplatelet antibodies (48 IgM, 30 IgG, 3 IgA, and 12 had two different isotypes concomitantly). In 20% of patients, the presence of IgM antibodies characteristically accompanied platelet agglutination also at 37 degrees C, and in citrated blood. The phenomenon was not age or sex related, nor was it associated with any particular pathology or use of specific drugs, and was present in both healthy subjects and patients with various diseases. Flow cytofluorimetric analysis of CD5-positive B cells, which are responsible for autoantibody production, did not demonstrate any changes in the percentage and absolute number of this lymphocyte subset. Average follow-up was 5 years (6 months-10 years); however, previous clinical records disclosed that PTCP was present for more than 15 years in four cases, and more than 20 years in three others, with no clinical manifestation of disease. This study confirms that EDTA-dependent PTCP is a phenomenon related to the presence of natural autoantibodies with antiplatelet activity, devoid of pathological significance. Its clinical interest resides in the need for its prompt and certain recognition in order to avoid unnecessary examinations and therapeutic interventions. The best and most rapid technique for obtaining accurate platelet counts in PTCP subjects is to collect and examine EDTA blood at 37 degrees C; however, clumping will still be present in about 20% of these cases, and even in citrated blood. To obviate this phenomenon, blood should be collected in ammonium oxalate, and platelets counted in a Burker chamber.

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“…It appeared to be an immunoglobulin molecule of unspecified class. A third type was recently described by Veenhoven et a1 [7], which shared features of both, in that it was not only EDTA dependent, but also most active at room temperature. In the six cases reported by these authors, the agglutinin was an IgM antiplatelet antibody.…”

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confidence: 80%

Spurious thrombocytopenia produced by the interaction of rheumatoid factor with antiplatelet antibody

Poskitt

1985

American J Hematol

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A patient had spurious thrombocytopenia resulting from a mechanism not previously described. Whereas in prior reports the in vitro phenomenon of platelet clumping has been effected by either EDTA-dependent or temperature-dependent antibodies capable of direct platelet agglutination, neither the IgG nor the IgM fractions of this patient's serum demonstrated such activity. However, agglutination was produced by incubating allogeneic platelets with the IgG fraction followed by a room temperature incubation with the rheumatoid factor-positive IgM fraction. The data support a new mechanism for spurious thrombocytopenia resulting from the interaction of a cold-reactive rheumatoid factor with antiplatelet antibody.

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Pseudothrombocytopenia Due to Agglutinins

Cited by 50 publications

References 0 publications

Aminoglycosides prevent and dissociate the aggregation of platelets in patients with EDTA‐dependent pseudothrombocytopenia

Aminoglycosides prevent and dissociate the aggregation of platelets in patients with EDTA‐dependent pseudothrombocytopenia

EDTA‐dependent pseudothrombocytopenia: A clinical and epidemiological study of 112 cases, with 10‐year follow‐up

Spurious thrombocytopenia produced by the interaction of rheumatoid factor with antiplatelet antibody

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