Tongue diseases could be reflections of altered systemic conditions or, also, initial forms of local and often severe pathologies (for example, carcinomas) [1, 2]. The most commonly encountered tongue diseases resulting from systemic conditions are median rhomboid glossitis, atrophic glossitis, fissured tongue, and geographic tongue, while among local conditions, there are papilloma, hairy tongue and leukoplakia with their possible malignant evolution [2, 3].
Atrophic glossitis (AG) is an inflammatory disorder of the tongue mucosa that shows a smooth, glossy appearance with a red or pink background . The smooth appearance is linked to the atrophy of filiform papillae that causes the development of circinate erythematous ulcer-like lesions of the dorsum and the lateral border of the tongue [2, 4]. This disease is primarily related to various conditions such as amyloidosis, chemical irritations, drug reactions, local infections such as candidiasis, nutritional deficiencies, pernicious anemia, malnutrition, sarcoidosis, Sjögren’s syndrome, systemic infections, psoriasis, vasculoerosive diseases or celiac disease [1, 2, 4, 5]. Since there are so many different possible causes, etiological identification of AG can be extremely difficult, so that various analyses and investigations are needed before diagnosis . For the same reason, the etiology sometimes remains unknown until symptoms other than tongue inflammation are identified .
Celiac disease (CD) is a disorder linked to an autoimmune intolerance to gliadin, a protein contained in gluten. The main target of this intolerance is the mucosa of the small intestine with development of histological lesions characterized by various degrees of villous atrophy, crypt hyperplasia, damage to the surface epithelium, and an increased number of activated lymphocytes and other inflammatory cells infiltrating the lamina propria.
CD diagnosis is based on observation of systemic clinical signs followed by blood analysis and is finally determined by a histopathological examination of the small intestine. Today, the greatest difficulty in obtaining this diagnosis is the identification of clinical signs that are not ‘typical’ for CD so that many patients never arrive at the gastroenterological examination stage. CD can be divided into different clinical forms known as classical, atypical, subclinical and latent. The classical form is characterized by intestinal symptoms such as chronic diarrhea, weight loss, growth deficit and vomiting; all other symptoms from other sites determine the atypical, subclinical and latent forms . Clinical signs could also be divided into two groups of direct or indirect symptoms . Direct symptoms are directly linked to the immune disorder, while indirect symptoms are the consequence of the intestinal damage that causes poor absorption of nutrients in the cells of the basal layer.
Once the disease is suspected through the identification of these clinical signs, serological analysis is necessary to confirm this diagnosis. Principal serological markers used for CD diagnosis are the tissue transglutaminase (tTG) antibody test and the IgA-endomysial antibody (EmA) test, while other tests such as antigliadin (AGA) or antireticulum (ARA) are no longer routinely performed . Another serological test often performed when CD is suspected is the HLA-DQB1 haplotype. HLA typing is an important marker for demonstrating the possibility that a patient is affected by CD. Interest is increasing in the link between the development of the different clinical forms of CD and the different HLA-DQB1 genotypes [9, 10]. Recently more and more importance has been given to the link between this gene expression and the development of atypical and latent forms .
Early CD diagnosis is indispensable for avoiding long term effects linked to untreated pathology. Various reports in the literature describe how patients with a never-identified CD showed an increasing incidence of small bowel malignancies, adenocarcinoma and enteropathy-associated T-cell lymphoma .
The aim of this case presentation is to highlight how AG could be the only previous sign that can be used to suspect a gluten intolerance and how it is always necessary to identify tongue inflammation etiology.