5
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      A Nationwide, Population-based Cohort Study on Potential Autoimmune Association of Ménière Disease to Atopy and Vitiligo

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Ménière disease (MD), an idiopathic disorder of sensorineural hearing loss and vertigo, shares many similarities with two common skin conditions, atopic dermatitis (AD) and vitiligo. Recent studies have suggested that MD may be related to or triggered by autoimmune conditions, notably Hashimoto thyroiditis and alopecia areata. These evidences led to the authors contemplating the possibility of immunological bridge between MD and the two skin conditions. The authors have tested this hypothesis with population-based cohort from the National Health Insurance Service Database of Korea. A cohort of 1.1 million patients was extracted from the database. Using χ 2 tests, prevalence of the two skin disorders in relation to MD status was analysed. In MD patients, the odds ratios for having concurrent AD and vitiligo were 0.717 (95% CI, 0.535–0.962, p = 0.026) and 2.149 (95% CI, 1.396–3.308, p = 0.001), respectively. Females and older patients were more than twice likely to be affected by the two skin conditions. The relationship between vitiligo and MD was significant in younger subgroup only. Socio-economic subgroup analysis revealed the observed patterns are primarily a middle-upper class phenomenon. Uncertainty regarding temporal sequence of onset, and lack of detail on disease severity and subtype kept the study from more refined conclusion. In concluding, AD and vitiligo might be linked to MD through T reg -driven action of cellular immunity, but further big data-based investigations must follow.

          Related collections

          Most cited references27

          • Record: found
          • Abstract: found
          • Article: not found

          Regulatory T cells and the immune aging process: a mini-review.

          Constant exposure to new and persisting antigens and the need to replace cellular attrition with newly built cells lead to profound remodeling of the immune system after the age of 50 years. The impact of the immunosenescence process varies amongst the different cellular subsets represented within the immune system. Emerging data suggest that progressive aging significantly affects frequencies, subset distribution and functional competence of regulatory T cells (Tregs). Given the central role of Tregs in immune homeostasis, age-related loss of Treg function would be predicted to cause excessive immunity, encountered in elderly humans as a syndrome of chronic, smoldering inflammation as well as the age-related increase in the risk for autoimmunity. Conversely, age-dependent gain of Treg activity would result in failing immunity, such as the rising risk of malignancies and infections amongst the elderly. Emerging data suggest that some Treg populations, specifically naturally occurring Tregs, seem to accumulate with advancing age, whereas inducible Tregs appear to be less available in the older host. More studies are necessary to elucidate functional competence of old Tregs, with an emphasis on comparing the efficacy of young and old Tregs for defined functional domains. Mechanisms of declining Treg inducibility are not understood, but may provide an opportunity for targeted immunomodulation in the elderly. On the horizon is the potential to develop novel therapeutic interventions that target Tregs to make the elderly more efficient in fighting cancers and infections and dampen the risk for senescence-associated inflammation.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Vitiligo.

            Vitiligo is an acquired depigmenting disorder that affects 0.5% to 2% of the world population. Three different forms are classified according to the distribution of lesions; namely non-segmental, segmental and mixed vitiligo. Vitiligo is associated with polymorphisms in genes involved in the immune response and in melanogenesis. However, environmental factors are required for the development of manifest disease. In general, the diagnosis is clinical and no laboratory tests or biopsies are required. Metabolic alterations are central to current concepts in pathophysiology. They induce an increased generation of reactive oxygen species and susceptibility to mild exogenous stimuli in the epidermis. This produces a senescent phenotype of skin cells, leads to the release of innate immune molecules, which trigger autoimmunity, and ultimately causes dysfunction and death of melanocytes. Clinical management aims to halt depigmentation, and to either repigment or depigment the skin, depending on the extent of disease. New therapeutic approaches include stimulation of melanocyte differentiation and proliferation through α-melanocyte-stimulating hormone analogues and through epidermal stem cell engineering. Several questions remain unsolved, including the connection between melanocyte depletion and stem cell exhaustion, the underlying degenerative mechanisms and the biological mediators of cell death. Overall, vitiligo is an excellent model for studying degenerative and autoimmune processes and for testing novel approaches in regenerative medicine. For an illustrated summary of this Primer, visit: http://go.nature.com/vIhFSC.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Pathophysiology of Meniere's syndrome: are symptoms caused by endolymphatic hydrops?

              The association of Meniere's syndrome with endolymphatic hydrops has led to the formation of a central hypothesis: many possible etiologic factors lead to hydrops, and hydrops in turn generates the symptoms. However, this hypothesis of hydrops as being the final common pathway has not been proven conclusively. To examine human temporal bones with respect to the role of hydrops in causing symptoms in Meniere's syndrome. If the central hypothesis were true, every case of Meniere's syndrome should have hydrops and every case of hydrops should show the typical symptoms. Review of archival temporal bone cases with a clinical diagnosis of Meniere's syndrome (28 cases) or a histopathologic diagnosis of hydrops (79 cases). All 28 cases with classical symptoms of Meniere's syndrome showed hydrops in at least one ear. However, the reverse was not true. There were 9 cases with idiopathic hydrops and 10 cases with secondary hydrops, but the patients did not exhibit the classic symptoms of Meniere's syndrome. A review of the literature revealed cases with asymptomatic hydrops (similar to the current study), as well as cases where symptoms of Meniere's syndrome existed during life but no hydrops was observed on histology. We also review recent experimental data where obstruction of the endolymphatic duct in guinea pigs resulted in cytochemical abnormalities within fibrocytes of the spiral ligament before development of hydrops. This result is consistent with the hypothesis that hydrops resulted from disordered fluid homeostasis caused by disruption of regulatory elements within the spiral ligament. Endolymphatic hydrops should be considered as a histologic marker for Meniere's syndrome rather than being directly responsible for its symptoms.
                Bookmark

                Author and article information

                Contributors
                doctordk@naver.com
                k@kyuh.ac.kr
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                13 March 2019
                13 March 2019
                2019
                : 9
                : 4406
                Affiliations
                [1 ]ISNI 0000 0000 8674 9741, GRID grid.411143.2, Department of Dermatology, College of Medicine, , Konyang University, ; Daejeon, Republic of Korea
                [2 ]ISNI 0000 0000 9370 7312, GRID grid.253755.3, School of Medicine, Department of Medical Statistics, , Catholic University of Daegu, ; Gyeongsan, South Korea
                [3 ]ISNI 0000 0004 0470 5964, GRID grid.256753.0, Department of Otorhinolaryngology-Head and Neck Surgery, Chuncheon Sacred Heart Hospital, , Hallym University College of Medicine, ; Chuncheon, Republic of Korea
                [4 ]ISNI 0000 0004 0470 5964, GRID grid.256753.0, Institute of New Frontier Research, , Hallym University College of Medicine, ; Chuncheon, Republic of Korea
                [5 ]ISNI 0000 0000 8674 9741, GRID grid.411143.2, Department of Otorhinolaryngology–Head and Neck Surgery, , College of Medicine, Konyang University, ; Daejeon, Republic of Korea
                [6 ]ISNI 0000 0000 8674 9741, GRID grid.411143.2, Department of Biomedical Informatics, College of Medicine, , Konyang University, ; Daejeon, Republic of Korea
                [7 ]ISNI 0000 0000 8674 9741, GRID grid.411143.2, Myunggok Medical Research Institute, College of Medicine, , Konyang University, ; Daejeon, Republic of Korea
                Author information
                http://orcid.org/0000-0003-4917-0177
                http://orcid.org/0000-0003-1230-9307
                Article
                40658
                10.1038/s41598-019-40658-8
                6416401
                30867466
                0cd7c39f-b51d-4c19-b705-5a54d1e7f247
                © The Author(s) 2019

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 28 August 2018
                : 21 February 2019
                Categories
                Article
                Custom metadata
                © The Author(s) 2019

                Uncategorized
                Uncategorized

                Comments

                Comment on this article