Diagnosis of Glanzmann thrombasthenia by whole blood impedance analyzer (MEA)vs. light transmission aggregometry
Autor: | H. Al Zahrani, H. Masmali, Abdulmajeed Albanyan, Tarek Owaidah, Randa Alnounou, A. Malik, A. AlJefri, Mahasen al Saleh, Abdulrahman Al-Musa, R. Nasr |
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Rok vydání: | 2014 |
Předmět: |
Adult
Blood Platelets medicine.medical_specialty Adolescent Light Platelet Aggregation Platelet Function Tests Clinical Biochemistry Hirudin Gene Expression Platelet Glycoprotein GPIIb-IIIa Complex chemistry.chemical_compound Adenosine Triphosphate Thrombasthenia Antigens CD Nephelometry and Turbidimetry Internal medicine Electric Impedance medicine Humans Platelet Child Ristocetin Whole blood Arachidonic Acid Platelet Count Platelet-Rich Plasma Biochemistry (medical) Hematology General Medicine Collagen type I alpha 1 Endocrinology chemistry Child Preschool Platelet-rich plasma Immunology Receptors Thrombin Collagen Biomarkers medicine.drug |
Zdroj: | International Journal of Laboratory Hematology. 37:503-508 |
ISSN: | 1751-5521 |
DOI: | 10.1111/ijlh.12320 |
Popis: | 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.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.Fifteen patients with GT were assessed on MEA and LTA using arachidonic acid (ASPI: 15 mm), (TRAP: 1 mm), collagen (100 μg/mL), ADP (0.2 mm), 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).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 CD42a and CD42b, whereas 9/15 samples were negative for CD61 and CD41. The other six patients had either partial or full expression of CD61/CD41. 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 μg, which may suggest ability to detect qualitative abnormality of GPIIb/IIIa).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. |
Databáze: | OpenAIRE |
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