Introduction 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. Material and Methods 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. Results 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. Conclusions 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. © 2014 Elsevier Ltd. All rights reserved.
Thrombin generation in patients with idiopathic sudden sensorineural hearing loss
De Giuseppe R.;
2014-01-01
Abstract
Introduction 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. Material and Methods 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. Results 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. Conclusions 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. © 2014 Elsevier Ltd. All rights reserved.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
