Thrombin generation in patients with idiopathic sudden sensorineural hearing loss

• Published in: Thrombosis research Vol. 133; no. 6; pp. 1130 - 1134
• Main Authors: Tripodi, Armando, Capaccio, Pasquale, Pignataro, Lorenzo, Chantarangkul, Veena, Menegatti, Marzia, Bamonti, Fabrizia, Clerici, Marigrazia, De Giuseppe, Rachele, Peyvandi, Flora
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 01.06.2014
• Subjects: Adult; Aged; Aged, 80 and over; Blood Coagulation Disorders - blood; Blood Platelets - cytology; Blood Platelets - metabolism; Case-Control Studies; Female; Hearing Loss, Sensorineural - blood; Hearing Loss, Sensorineural - genetics; Hearing Loss, Sudden - blood; Hearing Loss, Sudden - genetics; Hematology, Oncology and Palliative Medicine; Humans; Hypercoagulability; Male; Middle Aged; Platelet-Rich Plasma - metabolism; Prothrombotic genotypes; Thrombin - biosynthesis; Thrombin generation; Thrombomodulin - blood; Young Adult; Hypercoagulability; Thrombin generation; Prothrombotic genotypes
• ISSN: 0049-3848; 1879-2472; 1879-2472
• DOI: 10.1016/j.thromres.2014.03.031

The pathogenesis of idiopathic sudden sensorineural hearing loss (ISSNHL) is still unknown. Systemic hemostasis derangement causing local vascular occlusion might be one of the pathogenetic mechanisms. Forty-one patients with ISSNHL and 48 healthy subjects were investigated. We measured thrombin generation in the presence or absence of thrombomodulin in platelet-poor or platelet-rich plasma by means of a home-made method based on calibrated automated thrombin generation, which should mimic much more closely than any other conventional coagulation test the balance of coagulation operating in vivo. DNA analyses for the most common prothrombotic genotypes such as factor V Leiden, prothrombin G20210A, MTHFR or platelet GPIIIa A1/A2 were also carried out in patients and controls. Patients generated as much thrombin as controls both in platelet-rich and platelet-poor plasma and the frequency of the most common prothrombotic genotypes were similar in patients and controls. The results suggest that the pathogenesis of ISSNHL is not due to systemic blood hypercoagulability. Other culprits such as local vascular abnormalities, viral infections, immune-mediated mechanisms or abnormalities of inner ear and central nervous system should be advocated to explain ISSNHL.