EDTA-dependent Pseudothrombocytopenia Research Articles

IgG platelet antibodies in EDTA-dependent pseudothrombocytopenia bind to platelet membrane glycoprotein IIb.

EDTA-dependent pseudothrombocytopenia (PTCP) consists of an inappropriate low platelet count caused by autoantibodies present in the serum samples reacting with platelets only in EDTA-anticoagulated blood. By using immunoprecipitation and Western blot techniques, we studied the immunochemical specificity of platelet agglutinating autoantibodies in the serum samples of 10 patients with PTCP. Furthermore, to evaluate a possible role of PTCP-associated IgG autoantibodies in increased platelet turnover, we assayed the plasma glycocalicin (GC) level and calculated the GC index for every patient. Our results provide direct evidence that an epitope located on platelet membrane glycoprotein IIb is recognized by PTCP-associated IgG antibodies; moreover GC levels in patients with EDTA-dependent PTCP were similar to control levels, thus excluding an increased platelet turnover. We conclude that antiplatelet antibodies directed against platelet cryptantigens are unlikely to have a major role in the increased removal of cells from circulation.

Ethylenediaminetetraacetic Acid-Dependent Pseudothrombocytopenia in a Cardiac Surgical Patient

Ethylenediaminetetraacetic Acid-Dependent Pseudothrombocytopenia in a Cardiac Surgical Patient

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

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 aminoglycosides-supplemented 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.

Guillain-Barre Syndrome and Ethylene Diamine Tetraacetic Acid-Dependent Pseudothrombocytopenia Associated with Mumps.

A 35-year-old man with Guillain-Barré syndrome and ethylene diamine tetraacetic acid (EDTA)-dependent pseudothrombocytopenia associated with serologically-confirmed mumps is presented. A polyneuropathy developed 18 days after the onset of mumps, that improved with plasmapheresis. A decreased platelet count was observed 25 days after the onset of mumps attributed to platelet agglutination in blood anticoagulated with EDTA, and the agglutination was prevented by other anticoagulants. Guillain-Barré syndrome associated with mumps is rare and EDTA-dependent pseudothrombocytopenia following mumps has never been documented. This represents the first report of Guillain-Barré syndrome and EDTA-dependent pseudothrombocytopenia following mumps. Furthermore, our findings suggest activation of the humoral immune response as a potential pathogenesis.

More on False Thrombocytopenias: EDTA-Dependent Pseudothrombocytopenia Associated with a Congenital Platelet Release Defect

We report herein the case of a 54-year-old woman with a moderate bleeding tendency, diagnosed as an EDTA-dependent pseudothrombocytopenia associated with a congenital platelet release defect. The patient, at the age of 12, had a misleading diagnosis of idiopathic thrombocytopenic purpura and all the recurrent bleeding problems she had during her life were referred to that disease. The recent correct diagnosis of a false thrombocytopenia stimulated further laboratory investigation on the cause of the patient’s bleeding tendency with the consequent identification of a congenital platelet deficiency of the arachidonic acid pathway. This finding is of relevant importance for the management of the patient in case of elective surgery or hemorrhagic emergency.

EDTA-dependent pseudothrombocytopenia: a clinical and epidemiological study of 112 cases, with 10-year follow-up.

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.

EDTA-dependent Pseudothrombocytopenia:Association with Antiplatelet and Antiphospholipid Antibodies

In a study of 88 patients with EDTA-dependent pseudothrombocytopenia (PTCP), EDTA-dependent antiplatelet antibodies were seen in the sera of 72 (81.8%) patients (44 IgM, 25 IgG, and 3 IgA). The same sera also were tested for anticardiolipin antibodies (aCL), and 56 (63.6%) patients had sera that also were reactive for aCL (33 IgM, 21 IgG, and 2 IgA). The 16 patients who were negative for antiplatelet antibodies also were negative for aCL antibody. Overall concordance between antiplatelet and aCL antibodies was 82.9%; the correlation between antiplatelet and aCL antibody isotype distribution was 82.1%. Following cardiolipin absorption, most of the PTCP-sera were negative for antiplatelet activity, and no longer reproduced platelet clumping when incubated with normal blood. This finding showed that the antiplatelet antibodies cross-reacted with negatively charged phospholipids. However, after absorption on normal platelets, complete inhibition of aCL activity was observed in 34 (60.7%), and partial inhibition in 14 of the 56 patients who were aCL positive. These findings support the hypothesis that antibody subpopulations (naturally occurring autoantibodies) directed against negatively charged phospholipids can bind to antigens modified by EDTA on the platelet membrane, and may be responsible for PTCP genesis.

Incidence and Diagnosis of EDTA-Dependent Pseudothrombocytopenia in a Consecutive Outpatient Population Referred for Isolated Thrombocytopenia

Incidence and Diagnosis of EDTA-Dependent Pseudothrombocytopenia in a Consecutive Outpatient Population Referred for Isolated Thrombocytopenia

Studies of Platelet Aggregation in Six Cases of EDTA-dependent Pseudothrombocytopenia

Studies of Platelet Aggregation in Six Cases of EDTA-dependent Pseudothrombocytopenia

Diagnosis of EDTA-dependent pseudothrombocytopenia in a horse

Diagnosis of EDTA-dependent pseudothrombocytopenia in a horse

Edta‐dependent pseudothrombocytopenia: A clinical study of 18 patients and a review of the literature

EDTA-dependent pseudothrombocytopenia (EDTA-PTCP) is the phenomenon of a spurious low platelet count due to the appearance of antibodies that cause platelet agglutination in blood anticoagulated with EDTA. We review here the clinical features of 18 patients with EDTA-PTCP treated in our hospital from 1984 to 1987 as well as those of 34 patients reported in the literature. This phenomenon appears more frequently in severely ill patients, in association with autoimmune, neoplastic, atherosclerosis-related, and liver diseases. In the majority of our patients, EDTA-PTCP appeared during hospitalization, indicating that the antibody is an acquired one. Neither splenomegaly nor the presence of autoimmune markers were features of this entity. Unlike true thrombocytopenias, EDTA-PTCP is associated with a normal mean platelet volume. Awareness of this entity is essential since EDTA-PTCP is frequently misdiagnosed and therefore incorrectly treated.

A CASE REPORT OF EDTA-DEPENDENT PSEUDOTHROMBOCYTOPENIA

We report a case of hepatolithiasis with EDTA-dependent pseudothrombocytopenia in a 69-year-old female.On admission ultrasound and computed tomography revealed many stones in the anterior-lateral segment and anterior inferior segment of the liver and two stones in the common bile duct.The platelet count was low with agglutination in a peripheral-blood smear, in addition to the EDTA, however, it was normal in citrated blood. A diagnosis of EDTA-dependent pseudothrombocytopenia was made, surgical treatment being performed immediately. She is alive and well one year after the operation. In this disease a number of platelets is seemingly fewer, because platelets are agglutinated by EDTA which acts as an anticoagulant, and autocounter measures them as red or white blood cells. According to earlier studies, it has been reported that the incidence of this disease was 0.07% of all reported blood examination cases in Japan, while it was 0.09% of all reported cases and 1.94% of those in hospital in Europe and North America. If thrombocytopenia occurs without any clinical symptom, a possible diagnosis of EDTA-dependent pseudothrombocytopenia should be considered.

Studies on A Case of EDTA-Dependent Panagglutination and on Its Relationship to EDTA-Dependent Pseudothrombocytopenia

Studies on A Case of EDTA-Dependent Panagglutination and on Its Relationship to EDTA-Dependent Pseudothrombocytopenia

Analysis of Antigens Against Anti-Platelet Antibody Detected in Patients with EDTA-Dependent Pseudothrombocytopenia

Analysis of Antigens Against Anti-Platelet Antibody Detected in Patients with EDTA-Dependent Pseudothrombocytopenia