Atrophic glossitis: Etiology, serum autoantibodies, anemia, hematinic deficiencies, hyperhomocysteinemia, and management

Abstract

Atrophic glossitis (AG) is characterized by the partial or complete absence of filiform papillae on the dorsal surface of the tongue. AG may reflect the significant deficiencies of some major nutrients including riboflavin, niacin, pyridoxine, vitamin B12, folic acid, iron, zinc, and vitamin E. Moreover, protein-calorie malnutrition, candidiasis, Helicobacter pylori colonization, xerostomia, and diabetes mellitus are also the etiologies of AG. Our previous study found the serum gastric parietal cell antibody (GPCA), thyroglobulin antibody (TGA), and thyroid microsomal antibody (TMA) positivities in 26.7%, 28.4%, and 29.8% of 1064 AG patients, respectively. We also found anemia, serum iron, vitamin B12, and folic acid deficiencies, and hyperhomocysteinemia in 19.0%, 16.9%, 5.3%, 2.3%, and 11.9% of 1064 AG patients, respectively. Moreover, GPCA-positive AG patients tended to have relatively higher frequencies of hemoglobin, iron, and vitamin B12 deficiencies and hyperhomocysteinemia than GPCA-negative AG patients. Supplementations with vitamin BC capsules plus corresponding deficient hematinics for those AG patients with hematinic deficiencies can achieve complete remission of oral symptoms and AG in some AG patients. Therefore, it is very important to examine the complete blood count, serum hematinic, homocysteine, and autoantibody levels in AG patients before we start to offer treatments for AG patients.

Keywords: Anemia; Atrophic glossitis; Gastric parietal cell antibody; Hematinic deficiency; Hyperhomocysteinemia.