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Thromb Res. 2014 Jun;133(6):1130-4. doi: 10.1016/j.thromres.2014.03.031. Epub 2014 Mar 21.

Thrombin generation in patients with idiopathic sudden sensorineural hearing loss.

Author information

1
Angelo Bianchi Bonomi, Hemophilia and Thrombosis Center, Department of Clinical Sciences and Community Health, Università degli Studi di Milano and IRCCS Cà Granda Maggiore Hospital Foundation, Milano, Italy. Electronic address: armando.tripodi@unimi.it.
2
Department of Biomedical, Surgical and Dental Sciences, University of Milan, Università degli Studi di Milano and IRCCS Cà Granda Maggiore Hospital Foundation, Milano, Italy.
3
Department of Clinical Sciences and Community Health, Università degli Studi di Milano and IRCCS Cà Granda Maggiore Hospital Foundation, Milano, Italy.
4
Angelo Bianchi Bonomi, Hemophilia and Thrombosis Center, Department of Clinical Sciences and Community Health, Università degli Studi di Milano and IRCCS Cà Granda Maggiore Hospital Foundation, Milano, Italy.
5
Angelo Bianchi Bonomi Hemophilia and Thrombosis Center, Department of Pathophysiology and Transplantation, Università degli Studi di Milano and IRCCS Ca' Granda Maggiore Hospital Foundation, Milano, Italy.
6
Department of Biomedical, Surgical and Dental Sciences, Università degli Studi di Milano, Department of Hematology-Oncology and BMT Unit, IRCCS Cà Granda Maggiore Hospital Foundation, Milan, Italy.

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.

KEYWORDS:

Hypercoagulability; Prothrombotic genotypes; Thrombin generation

PMID:
24690481
DOI:
10.1016/j.thromres.2014.03.031
[Indexed for MEDLINE]
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