Type II collagen antibodies in patients with sensorineural hearing loss

Sutjita, Made; Peter, JamesB.; Baloh, RobertW.; Oas, JohnG.; Laurent, Claude; Nordang, Leif

doi:10.1016/0140-6736(92)90386-h

Cited by 13 publications

(6 citation statements)

References 6 publications

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“…The high incidence of ACOII described in Meniere's disease, otosclerosis, and sensorineural deafness (4)(5)(6)(7)(8) contrasts with the findings in our patients. In fact, raised ACOII values were found in only in 1 of 49 otosclerosis, 1 of 45 sensorineural hearing loss and in none of 9 Meniere's cases.…”

Section: Discussioncontrasting

confidence: 99%

“…Autoimmunity processes trigger different diseases of the inner ear (12) related to the presence of ACOII (4)(5)(6)(7)(8). Raised values of ACOII were found in 52-75% of patients with otosclerosis (5,8), in 42-75% of patients with Meniere's disease (5,8) and 25 -44% of patients with sensorineural deafness (6 -8), although this has been questioned by others (9,10).…”

Section: Discussionmentioning

confidence: 99%

“…Clinical and experimental approaches contributed to the understanding of the relationship between autoimmune disease and inner ear pathologies. Beside, the presence of anti-type II collagen antibodies (ACOII) (4)(5)(6)(7)(8) has been related to otosclerosis, Meniere's disease and other sensorineural hearing losses, although the involvement of these autoantibodies has been also questioned (9,10).…”

Section: Introductionmentioning

confidence: 99%

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Autoimmune Deafness is not Related to Hyperreactivity to Type II Collagen

López-González

Lucas²,

Sánchez³

et al. 1999

Acta Oto-Laryngologica

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The pathogenic role of anti-type II collagen was analysed in a variety of hearing losses, in age-matched controls and in different autoimmune diseases. The immune reactivity of peripheral blood lymphocytes to type II collagen was studied by the degree of proliferation measured as the incorporation of bromodeoxyuridine in cultured lymphocytes. The anti-type II collagen antibodies showed a very low incidence in the hearing loss group. Lymphocytes of otosclerosis, Meniere's disease and other sensorineural deafness patients proliferated in response to concanavalin A and to type II collagen to a lower extent than peripheral blood lymphocytes from healthy controls. Nonetheless, these differences were not statistically significant. The immune hyperreactivity to type II collagen cannot explain the autoimmune mechanism of hearing losses. Humoral and cellular hyperreactivities to inner ear proteins different from type II collagen, could explain the autoimmune mechanism of deafness.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Autoimmune Deafness is not Related to Hyperreactivity to Type II Collagen

López-González

Lucas²,

Sánchez³

et al. 1999

Acta Oto-Laryngologica

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“…Antibodies against type II collagen have been demonstrated in patients with a variety of inner ear diseases and also to predict steroid responsiveness to autoimmune SNHL 89,99,100 . However, a recent study was unable to confirm this finding as only one of eight patients who had steroid responsive disease had demonstrable antibodies to type II collagen 101 …”

Section: Diagnosismentioning

confidence: 99%

Autoimmune sensorineural hearing loss

Mathews

Kumar

2003

Clin Otolaryngol

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Autoimmune sensorineural hearing loss has been increasingly recognized as a clinical entity since its description by McCabe in 1979. Recognition and proper management of this condition is important, as it is one of the very few forms of sensorineural hearing loss that can be successfully treated by medical therapy. Recent studies have provided experimental evidence to suggest that immune processes can cause sensorineural hearing loss in animals and humans. However, antigenic targets within the inner ear are diverse and as a result conclusive evidence for specific autoimmune damage to the inner ear has been elusive. This review focuses on the recent progress in understanding of the aetio-pathogenesis of autoimmune hearing loss along with a description of the various clinical conditions in which they occur. Recent advances in the laboratory diagnosis and management of this interesting condition are also described.

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“…According to the inflammation hypothesis, VN may be caused by acute infection with different viruses [7] or by reactivation of latent Herpes virus in the vestibular ganglia [8,9]. Bilateral VN may be caused by autoimmune processes [10]. New reports even suspect vascular risk factors for VN [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Vestibular Nerve Atrophy After Vestibular Neuritis – Results from a Prospective High-Resolution MRI Study

Freund

Weber²,

Schneider

et al. 2020

Rofo

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Purpose Sudden unilateral peripheral vestibular deficit is mostly termed vestibular neuritis (VN), even if its cause or the exact location of the lesion remains unclear. Thus, therapy is mostly symptomatic. We aimed to prove if there is peripheral atrophy after VN with persistent canal paresis. Methods After approval by the ethics committee and according to the declaration of Helsinki and with informed consent, ten patients with persistent canal paresis after VN and ten age-matched healthy controls were included. High-resolution measurement (in-plane resolution 0.2 mm) of the internal auditory canal (IAC) using a 3 D CISS sequence at 3 Tesla was performed. The course of the pertaining nerves was reconstructed in the 3 D dataset and the measurement was performed at 60 % of the length of the IAC. The cross-sectional areas of the superior (SVN) and inferior vestibular nerve (IVN) were taken independently by two blinded readers. Results The interrater difference regarding the area was 22 %. We found significant atrophy of the SVN with a 24 % smaller area (p = 0.026) and found a smaller ratio of SVN/IVN on the symptomatic side (p = 0.017). Concerning single subject data, only 5 patients showed extensive atrophy of the NVS, while 5 patients did not. The time since symptom onset did not significantly influence the atrophy. Conclusion MRI measuring of the area of the NVS after VN could detect atrophy after VN. However, only 5 patients exhibited marked atrophy, while the other 5 patients did not. With the background of stringent inclusion criteria (more than 6 months of symptom duration and proven persistent canal paresis), one has to wonder if there might be different etiologies behind the apparently identical symptoms. Key Points: Citation Format

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Type II collagen antibodies in patients with sensorineural hearing loss

Cited by 13 publications

References 6 publications

Autoimmune Deafness is not Related to Hyperreactivity to Type II Collagen

Autoimmune Deafness is not Related to Hyperreactivity to Type II Collagen

Autoimmune sensorineural hearing loss

Vestibular Nerve Atrophy After Vestibular Neuritis – Results from a Prospective High-Resolution MRI Study

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