Discussion
Melanocytes in the depigmented skin and autofluorescent parietal cells ( PC) in the gastric mucosa were partially or totally missing. In normal conditions, melanocytes within epidermis , PC within gastric mucosa and thyrocytes in thyroid gland are hold in place through the intervention of adhesion molecules such as E- Cadherin,or integrins. In vitiligo a defect of E- Cadherin was reported to induce an impairment of cell adhesivity leading to a melanocyte detachment (4,5 ).So, in both diseases the autoimmune process could be preceeded by a cell adhesivity impairment leading to a detachment of either melanocytes in vitiligo or PC in AAG. Generalized vitiligo involves genetic susceptibility loci shared with other auto-immune diseases. AAG may coexist with polyglandular autoimmune (PGA), in 10% to 15% syndromes type 1 ( including hypo-parathyroidism, Addison’s disease, diabetes mellitus, and mucocutaneous candidiasis) and in 15% of PGA type 3 patients (with diabetes mellitus, and autoimmune thyroid diseases ).AAG and vitiligo have been associated with thyroiditis since the early 1960. Thyrogastric autoimmunity was described faced the presence of thyroid antibodies or autoimmune thyroid disease in patient with pernicious anemia(7). In less than 10% of the vitiligo patients, a clinical suspicion of AAG was provided by the concomitant presence of other autoimmune diseases.The prevalence of Autoimmune Atrophic Gastritis (A.A.G) in vitiligo patients, certainly underdiagnosed, was estimated about 15%.
Conclusion  : A common autoimmune mechanisms is suggested for both diseases pathogenesis. A gastroscopy check- up should be performed in vitiligo patients with a positive detection of antiparietal cell antibodies or evocative symptoms.
Conflicts of interest: The authors have no conflict of interest to disclose Contents of the manuscript have not been previously published and are not currently submitted elsewhere