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THU0324 Inner Ear Dysfunction as an Expression of Atherosclerosis in Primary Antiphospholipid Syndrome

Background Microvascular oclussion may occur as part of the manifestations of the antiphospholipid syndrome (APS). One of these manifestations is Sensorineural hearing loss (SHL). Objectives To determine the prevalence of inner ear dysfunction in patients with primary APS and its association, if any, with carotid intima-media thickness (IMT). Methods From a cohort of 50 patients with primary APS we investigated the presence of inner ear dysfunction defined as SHL and/or labyrinthine affection based on the following symptoms: unilateral or bilateral sudden or progressive hearing loss, tinnitus and recurrent vertigo. Patients with the above-described symptoms underwent audiometric assessment. Those with vestibular symptoms also had balance function testing. Inner ear dysfunction was defined as hearing loss below normal values (mild hearing loss: audition loss <35dB; moderate hearing loss: audition loss ranging from 35to 60dB; and severe hearing loss >60 to 90dB) or presence of labyrinthine affection. Cardiovascular risk factors such as dyslipidemia, diabetes mellitus, arterial hypertension and carotid IMT were assessed. For the statistical analysis we employed descriptive statistics and chi square test. Results We detected 15 patients with hearing loss (30%) with a mean age of 51.6 years, mean APS disease evolution 12.7 years, treated with oral anticoagulants (INR between 2-3) and statins, 3 had arterial hypertension, 2, diabetes mellitus, 6 with dyslipidemia, and 8 had history of ischemic stroke. One patient presented sudden SHL that improved with corticosteroids, another one had left vestibular paresis as a stroke sequelae. Twelve patients were diagnosed with mild to moderate bilateral SHL and 3 with unilateral SHL. Only 2 patients had conductive hypoacusia due to otosclerosis, 5 had tinnitus and vertigo and were diagnosed as labyrinthine affection that improved with vestibular rehabilitation therapy. Three patients required hearing aid. Interestingly 12/15 patients (80%) with bilateral hearing loss presented carotid IMT with a mean of 1.2 mm ±0.2 (range from 0.8 to 2.9 mm). In contrast, 14/35 (40%) with carotid IMT did not have hearing loss (p< 0.002). Conclusions Inner ear dysfunction is present in primary APS patients and is associated with carotid IMT. SHL may be an atherosclerosis expression. Other alternative therapies, besides the strict control of risk factors for atherosclerosis are needed. Auditive assessment must be performed at least once a year in order to identify and delay the presence of disability. References Mouadeb DA, et al. Antiphospholipid inner ear syndrome. Laryngoscope 2005;115: 879-83. Yehudai D, Shoenfeld Y, Toubi E. The autoimmune characteristics of progressive or sudden sensorineural hearing loss. Autoimmunity. 2006;39(2):153-8. Disclosure of Interest None Declared