Elevated Antithyroid Peroxidase and Antinuclear Autoantibody Titers in Ménière’s Disease Patients: More than a Chance Association?

Nacci, Andrea; Dallan, Iacopo; Monzani, Fabio; Dardano, Angela; Migliorini, Paola; Riente, Lucrezia; Ursino, Francesco; Fattori, Bruno

doi:10.1159/000218357

Cited by 24 publications

(30 citation statements)

References 56 publications

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“…In the last years, coexisting AITD has been described in a percentage of patients with vestibular disorders, as Ménière's disease (MD) or benign paroxysmal positional vertigo (BPPV) . In the former disease, an autoimmune origin has been postulated, and we recently showed a relationship between MD and thyroid autoimmunity regardless of thyroid function .…”

Section: Introductionmentioning

confidence: 94%

Vestibular disorders in euthyroid patients with Hashimoto's thyroiditis: role of thyroid autoimmunity

Chiarella

Tognini

Nacci

et al. 2014

Clinical Endocrinology

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Section: Introductionmentioning

confidence: 94%

Vestibular disorders in euthyroid patients with Hashimoto's thyroiditis: role of thyroid autoimmunity

Chiarella

Tognini

Nacci

et al. 2014

Clinical Endocrinology

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“…In a recent report a significant association between MD and autoantibody increments, e.g. antinuclear antibodies and anti-thyroid peroxidase, was demonstrated [Nacci et al, 2010].…”

Section: Introductionmentioning

confidence: 95%

Experimental Hyperactivity of the Endolymphatic Sac

Friis

Thomsen²,

Poulsen³

et al. 2013

Audiol Neurotol

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Injury to the endolymphatic sac may play an important role in the pathogenesis of Ménière’s disease, an inner ear disorder characterized by hearing loss, tinnitus and attacks of vertigo. Isoimmunization of 16 inbred Lewis rats with a crude endolymphatic sac extract and complete Freund’s adjuvant induced hyperactivity of the endolymphatic sac. One group of rats was immunized by a single dose whereas a second group was immunized twice. Control animals were injected with Freund’s adjuvant in saline only. Serum was collected from all rats by the end of the study and harvested autoantibodies were tested by immunohistochemistry. The endolymphatic sacs were investigated by transmission electron microscopy. Endolymphatic sac stimulation was observed in all immunized rats. Based on detailed ultrastructural observations, the degree of reactivity seemed proportional to the number of injections and the extent of immunization. Moreover, the ribosome-rich cells seemed hyperactive with an extravagant content of intracellular components: numerous rough endoplasmic reticulum and free ribosomes, morphological signs of extensive endo- and exocytosis, vesicles of material with a density similar to the homogeneous substance of which many were observed to fuse with primary lysozymes. Basolateral foldings were numerous and in the subepithelial capillaries formation of multiple and apposing fenestrations were observed. No endolymphatic sac stimulation was observed in the control animals. Specific ribosome-rich cell alterations identical to those present in the endolymphatic sac of Ménière’s disease were observed 21 days after the first immunization. The observations suggest that either an autoantigen or a trophic factor, capable of inducing a hyperactivity of the ribosome-rich cells and an imbalance of the homogeneous substance metabolism, exists in the endolymphatic sac of the rat.

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“…While excess reactive oxygen species (ROS) are toxic, regulated ROS, however, play an important role in cellular signalling [9]. The ability of a cell to counteract stressful conditions, known as cellular stress response, requires the activation of pro-survival pathways and the production of molecules with anti-oxidant, anti-apoptotic or pro-apoptotic activities [6].…”

Section: Introductionmentioning

confidence: 99%

“…The ability of a cell to counteract stressful conditions, known as cellular stress response, requires the activation of pro-survival pathways and the production of molecules with anti-oxidant, anti-apoptotic or pro-apoptotic activities [6]. Among the cellular pathways conferring protection against oxidative stress, a key role is played by vitagenes, which include heat shock proteins (Hsps) heme oxygenase-1 and Hsp70, as well as the thioredoxin/thioredoxin reductase system [7][8][9][10]. Heat shock response contributes to establish a cytoprotective state in a wide variety of human diseases, including inflammation, cancer, aging and neurodegenerative disorders.…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress, Redox Homeostasis and Cellular Stress Response in Ménière’s Disease: Role of Vitagenes

et al. 2010

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Ménière's disease (MD) is characterized by the triad of fluctuating hearing loss, episodic vertigo and tinnitus, and by endolymphatic hydrops found on post-mortem examination. Increasing evidence suggests that oxidative stress is involved in the development of endolymphatic hydrops and that cellular damage and apoptotic cell death might contribute to the sensorineural hearing loss found in later stages of MD. While excess reactive oxygen species (ROS) are toxic, regulated ROS, however, play an important role in cellular signaling. The ability of a cell to counteract stressful conditions, known as cellular stress response, requires the activation of pro-survival pathways and the production of molecules with anti-oxidant, anti-apoptotic or pro-apoptotic activities. Among the cellular pathways conferring protection against oxidative stress, a key role is played by vitagenes, which include heat shock proteins (Hsps) as well as the thioredoxin/thioredoxin reductase system. In this study we tested the hypothesis that in MD patients measurable increases in markers of cellular stress response and oxidative stress in peripheral blood are present. This study also explores the hypothesis that changes in the redox status of glutathione, the major endogenous antioxidant, associated with abnormal expression and activity of carbonic anhydrase can contribute to increase oxidative stress and to disruption of systemic redox homeostasis which can be associated to possible alterations on vulnerable neurons such as spiral ganglion neurons and consequent cellular degeneration. We therefore evaluated systemic oxidative stress and cellular stress response in patients suffering from Meniere's disease (MD) and in age-matched healthy subjects. Systemic oxidative stress was estimated by measuring protein oxidation, such as protein carbonyls (PC) and 4-hydroxynonenal (HNE) in lymphocytes of MD patients, as well as ultraweak luminescence (UCL) as end-stable products of lipid oxidation in MD plasma and lymphocytes, as compared to age-matched controls, whereas heat shock proteins Hsp70 and thioredoxin (Trx) expression were measured in lymphocytes to evaluate the systemic cellular stress response. Increased levels of PC (P < 0.01) and HNE (P < 0.05) have been found in lymphocytes from MD patients with respect to control group. This was paralleled by a significant induction of Hsp70, and a decreased expression of Trx (P < 0.01), whereas a significant decrease in both plasma and lymphocyte ratio reduced glutathione GSH) vs. oxidized glutathione (GSSG) (P < 0.05) were also observed. In conclusion, patients affected by MD are under condition of systemic oxidative stress and the induction of vitagenes Hsp70 is a maintained response in counteracting the intracellular pro-oxidant status generated by decreased content of GSH as well as expression of Trx. The search for novel and more potent inducers of vitagenes will facilitate the development of pharmacological strategies to increase the intrinsic capacity of vulnerable ganglion cells to maximize antid...

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Elevated Antithyroid Peroxidase and Antinuclear Autoantibody Titers in Ménière’s Disease Patients: More than a Chance Association?

Cited by 24 publications

References 56 publications

Vestibular disorders in euthyroid patients with Hashimoto's thyroiditis: role of thyroid autoimmunity

Vestibular disorders in euthyroid patients with Hashimoto's thyroiditis: role of thyroid autoimmunity

Experimental Hyperactivity of the Endolymphatic Sac

Oxidative Stress, Redox Homeostasis and Cellular Stress Response in Ménière’s Disease: Role of Vitagenes

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