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Diagnosis of Glanzmann thrombasthenia by whole blood impedance analyzer ( MEA ) vs . light transmission aggregometry
Author(s) -
Albanyan A.,
AlMusa A.,
AlNounou R.,
Al Zahrani H.,
Nasr R.,
AlJefri A.,
Saleh M.,
Malik A.,
Masmali H.,
Owaidah T.
Publication year - 2015
Publication title -
international journal of laboratory hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.705
H-Index - 55
eISSN - 1751-553X
pISSN - 1751-5521
DOI - 10.1111/ijlh.12320
Subject(s) - thrombasthenia , ristocetin , platelet , glanzmann's thrombasthenia , whole blood , chemistry , platelet membrane glycoprotein , bleeding time , chromatography , platelet poor plasma , phosphotungstic acid , medicine , platelet aggregation , biochemistry , platelet rich plasma , catalysis
Summary Background Glanzmann thrombasthenia ( GT ) is a rare inherited platelet disorder that is characterized by spontaneous or postprocedural bleeding. The diagnosis of GT depends on identifying the dysfunction of the platelets. Aim The aim of this study was to compare a whole blood impedance Multiplate analyzer ( MEA ) with the standard method, light transmission aggregometry ( LTA ) in diagnosis of GT . Methods Fifteen patients with GT were assessed on MEA and LTA using arachidonic acid ( ASPI : 15 m m ), ( TRAP : 1 m m ), collagen (100 μ g/mL), ADP (0.2 m m ), and ristocetin (Risto: 10 mg/mL). Whole blood samples were collected in sodium citrate and hirudin vacuum, blood collection tubes and tested within 4 h. Platelet‐rich plasma was used for LTA using platelet agonists (ristocetin 1.5 mg/mL) (arachidonic acid 0.5 mg/mL) ( ADP 2.5 mg/mL) and (collagen 1 mg/mL). Results The platelet count and PFA ‐100 results were (average and SD ) 319 ± 93 × 10 9 L and 252 ± 34 s, respectively. Flow cytometry analysis showed that all samples are positive for CD 42a and CD 42b, whereas 9/15 samples were negative for CD 61 and CD 41. The other six patients had either partial or full expression of CD 61/ CD 41. Aggregation analysis using both methods showed that all samples had no aggregation response to any of the agonists used apart from six samples which, using only the MEA , showed minimal aggregation in response to collagen (average = 14.3 ± 7 μ g, which may suggest ability to detect qualitative abnormality of GPII b/ III a). Conclusion These results suggest that the MEA is sensitive for the detection of Glanzmann thrombasthenia. Furthermore, MEA may also be able to differentiate between the subtypes of Glanzmann thrombasthenia.