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  • Title: A case report of pernicious anemia and recurrent aphthous stomatitis.
    Author: Garcia BG, Cardoso MF, de Faria O, Gomez RS, Mesquita RA.
    Journal: J Contemp Dent Pract; 2009 Mar 01; 10(2):83-9. PubMed ID: 19279976.
    Abstract:
    AIM: The aim of this report is to present the management of a patient with pernicious anemia afflicted with recurrent aphthous stomatitis (RAS). BACKGROUND: RAS is one of the most common lesions of the oral mucosa. Although the exact etiology of RAS is still unknown different hematinic deficiencies have been proposed. CASE REPORT: Painful recurrent ulcers covered with a grayish pseudomembrane surrounded by an erythematous margin were identified on the tongue and in the buccal mucosa of a 71-year-old woman. The patient also presented with depapilation of the tongue. The clinical diagnosis was RAS. Laboratory tests including a hemogram were ordered to determine existing levels of folic acid, iron, ferritin, and vitamins B2, B6, and B12. Levels of serum vitamin B12 and serum hemoglobin were low. The laboratory investigation also showed a medium corpuscular volume of 104.1 fl. A gastroduodenoscopy revealed no macroscopic abnormality. A gastric biopsy showed mucosal atrophy in the gastric corpus with evidence of intestinal metaplasia. Antibodies against an intrinsic factor were negative. The diagnosis pernicious anemia was made, with RAS caused by vitamin B12 malabsorption. Treatment consisted of the administration of 1.0 ml of hydroxocolabamin intramuscularly twice weekly over four weeks followed by 1.0 ml once weekly for four weeks. Clinical resolution was observed after two months. SUMMARY: The association of RAS with vitamin B12 malabsorption is a rare event. However, along with conventional RAS clinical management, iron, folic acid, vitamin B deficiencies, and nutritional intolerance must be considered. Evaluation of the predisposing factors is imperative in treating patients with RAS including vitamin B12 malabsorption. CLINICAL SIGNIFICANCE: Determination of the levels of vitamin B12 should be the basis for replacement therapy. Such therapy can be considered a benefit to the patients with RAS as its etiology remains unclear. Clinicians must be alert to the possibility this lesion could be a signal of systemic disease.
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