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BackgroundSudden sensorineural hearing loss (SSNHL) is defined as a rapid onset sensorineural hearing loss occurring over a 72-hour period with a decrease in hearing ofa€‰>a€‰30 decibels (dB) affecting at least 3 consecutive frequencies [1]. Gel patterns demonstrating the 4a€‰G and 5a€‰G alleles in the promoter region of the PAI-1 gene. SSNHL sudden sensorineural hearing loss; Odds ratios (OR) with 95a€‰% confidence intervals (CI) and results (p values) of I‡2 analysis (chi-square test) were calculated for genotype frequencies compared with control.
We further examined to see if the polymorphism of PAI-1 gene is associated with clinical outcome in patients with SSNHL (Tablea€‰2).
DiscussionOne of most probable mechanisms of SSNHL appears to be impaired cochlear blood circulation involving the pathogenic micro-thrombotic mechanism [20].
Competing interestsAuthors declare that there is no financial or non-financial competing interests in relation to this manuscript.Authorsa€™ contributionsSC, SP, MB, AM and TY conceived of the study, and participated in its design and coordination and helped to draft the manuscript.
According to the National Institutes of Health (NIH), approximately 4000 new cases of SSHL occur each year in the United States. While SSHL characterizations remain varied, the NIH defines the condition as an idiopathic hearing loss of sensorineural origin, greater than 30 dB in three contiguous frequencies that occurs in less than three days.
In the idiopathic camp, there are a number of possible causal ideologies at work-vascular, viral, genetic, lifestyle, and disease-related causes, Dr. There is a strong link to the genetic and lifestyle ideologies and a much weaker one to viral and vascular, Dr. With regard to incidence and prevalence of direct effect SSHL, he said both were hard to quantify because the data are such that a reliable denominator is not available. 103 patients with SSNHL and 113 age and sex-matched controls were enrolled at University of Ferrara, Italy and hearing loss outcome was measured at least 3a€‰months after the onset of hearing loss.
The majority of patients with SSNHL have no identifiable causes and are thus classified as a€?idiopathica€? [2].
This result may be of clinical significance in diagnosis, treatment, and prognosis for SSNHL patients and may provide a new therapeutic strategy for SSNHL. HC, CY, DC and JK involved in drafting the manuscript or revising it critically for important intellectual content and performed the statistical analysis. Despite much attention, even a definitive definition of the malady escapes researchers, making successful therapies even harder to uncover. It can affect anyone, but for unknown reasons it happens most often to people between the ages of 30 and 60.
SSHL occurs most often in people between ages 30 and 60; a number of causal ideologies have been proposed.
Direct effect deals with things we know caused the hearing loss-largely loud noise, trauma, or toxins. SSNHL affects 5 to 20 persons for each 100,000 individuals annually and can be devastating because they can lose their hearing permanently. All the patients underwent audiological examinations including pure tone audiometry, speech recognition threshold, immittance measurements such as tympanogram and acoustic reflex; other audiometric tests for the differential diagnosis of cochlear vs retrocochlear pathologies were performed in selected cases. It has been known that elevated plasma levels of PAI-1 are associated with SSNHL [6], but the role of the PAI-1 is controversial [6, 11].


IK and CC carried out the molecular genetic studies, participated in drafted the manuscript.
In an effort to spur discussion and a possible movement toward consensus, an international panel gathered to examine the epidemiology of SSHL and discuss traditional treatment modalities at the recent American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) annual meeting here.The experts also wheeled out some of the more promising research and cutting-edge treatment modalities available. Hoffer, MD, of the Naval Medical Center in San Diego, said that, in addition, the root causes of SSHL could be broken into two separate types-idiopathic and direct effect. Basically, someone gets blown up, they get a hearing loss and we know it was direct effect. The vascular hypothesis comes from a Japanese study showing subjects had an increased incidence of SSHL when switching from a traditionally Japanese diet to an American diet.This showed promise at the time, Dr. Genotype distribution was tested in patients and compared to controls by chi-square and odd-ratio analysis. The etiology of SSNHL is still unclear although the most recent studies suggest viral infection, vascular impairment, intracochlear membrane rupture, and autoimmune process as possible causes [3, 4].
Auditory brainstem response (ABR) was always performed except when hearing loss exceeded 80a€‰dB in the acute frequencies. Among the unilateral cases, the degree of SSNHL was mild in 6 patients, moderate in 15, severe in 8, and profound in 4; one bilateral case was moderate degree in both side. Hoffer said, but when combined with other, similar research, it became clear that genetic causes were at play. The codominant and recessive models were used for the multiple logistic regression analyses of the PAI-1 gene allele. Several studies have been reported on the association between cardiovascular risk factors and SSNHL, showing that high concentrations of cholesterol, fibrinogen, and homocysteine were risk factors [5a€“9].
Audiometric inclusion criterion was a decrease in hearing of at least 30a€‰dB in 3 contiguous frequencies. He also said viral ideology research is conflicting and cannot be reproduced, but that he is still convinced there has to be some kind of infectious variable at work.
Patients did not receive vestibular evaluation because exclusion criteria were the presence of vertigo or suspected Menierea€™s disease. Elevation in plasma levels of PAI-1 has been reported to be associated with many diseases, such as cardiovascular diseases [14], stroke [15] and asthma [16a€“18]. Any participant with a history of head trauma was also excluded from the study.All the subjects provided their informed consent for the study and blood was taken as usual for routine laboratory exams, in the morning before starting the pharmacological therapy. One of most probable causes of SSNHL appears to be impaired cochlear blood circulation involving the pathogenic micro-thrombotic mechanism [19, 20]. Cochlear function is very sensitive to changes in blood supply which is mainly derived from the labyrinthine artery.
Vascular compromise of the cochlea caused by reduced blood flow, vasospasm, thrombosis or embolus, may result in SSNHL [13, 21]. Additionally, their study elected only severe SSNHL patients with a loss of 60a€‰dB or more. Our previous case report demonstrated the effectiveness of fibrinolytic therapy for sudden hearing loss with an improvement of 50a€‰dB using a recombinant tPA, which appeared to improve the microcirculation of the inner ear [20].


We examined follow-up audiometry at least 6a€‰months after the initial episode of hearing loss and considered a hearing improvement more than 20a€‰dB as a significant recovery. These findings suggest that PAI-1 is a possible risk factor and a potential therapeutic target for SSNHL.The PAI-1 gene has variation in the promoter region on the basis of a single guanosine insertion-deletion (5a€‰G or 4a€‰G) [16]. It is not clear whether the discrepancy between these two studies is due to different population (Italian vs German) or different severity of the disease.It has been known that there is no effective treatment of SSNHL other than systemic corticosteroids which is generally used but has limitation to some patients [2]. Therefore we chose 20a€‰dB as a clear cut-off for significant improvement, which would include partial and complete recovery. Our study suggests that lowering plasma levels of PAI-1 may be a strategy to prevent SSNHL, especially in people who are likely to have high plasma levels of PAI-1, such as subjects who are obese, diabetic, or smokers [16, 18]. The age and sex-matched healthy Italian subjects (na€‰=a€‰113) were enrolled in the same geographical area. Increased PAI-1 levels facilitate the inhibition of the fibrinolytic system [16], which may impair cochlear blood circulation and thus predispose the development of SSNHL [6, 20].
Control subjects had no history of hearing loss, circulatory or metabolic diseases, or autoimmune disorders. They were healthy clinic staffs and clinic patients with other otolaryngology disorders, such as allergic rhinitis, who gave their consent for the study.
We had a limited number of long-term follow-up audiometry results, which resulted in a lack of power in our analysis. We previously reported a case which showed significant improvement of hearing (> 50a€‰dB) with recombinant tPA treatment two years after the development of SSNHL [20]. This case is an interesting observation that may suggest a link between fibrinolytic treatment and clinical outcome in patients with SSNHL. We also used chi-square test (I‡2) and odd-ratio analysis for the association between genotype distribution and hearing outcome. In the multiple logistic regression analyses for each PAI-1 gene allele, we used multiple inheritance models, including codominant model (the relative hazard differed between subjects with one minor allele and those with two minor alleles) and recessive model (only subjects with two minor alleles were at increased risk of the disease). Prognosis of sudden deafness with special reference to risk factors of microvascular pathology.
Usefulness of high doses of glucocorticoids and hyperbaric oxygen therapy in sudden sensorineural hearing loss treatment. Antiviral treatment of idiopathic sudden sensorineural hearing loss: A prospective, randomized, double-blind clinical trial. Prognostic indicators of management of sudden sensorineural hearing loss in an Asian hospital.



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