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