Nutrition and Oral Medicine (Nutrition and Health)

246 Part IV / Select Diseases and ConditionsIntrinsic factor (IF) produced in gastric parietal cells binds to cobalamine and protects itfrom degradation until it can be absorbed in the ileum. Anti-IF antibodies and antibodiesdirected against gastric parietal cells result in a lack of IF and subsequent poor absorptionof cobalamine and megaloblastic anemia. Correct identification of the underlying cause(i.e., folate vs cobalamine deficiency) is important, rather than empirical folate therapy,which will improve only the anemia and not the neurological symptoms of a cobalaminedeficiency (paresthesia, impaired neurocognitve function).3.1.2. CLINICAL FEATURES3.1.2.1. General FeaturesSymptoms of anemia may include weakness, light-headedness, shortness of breath,palpitations, and angina. Physical findings in the patient with florid cobalamin deficiencyinclude pale skin, with slightly icteric skin and eyes, and rapid pulse. There may beanorexia with varying degrees of weight loss. Megaloblastosis of the small intestineepithelium may result in diarrhea, resulting in malabsorption and contributing to weightloss. A hallmark feature of PA is the neurological symptoms of peripheral paresthesia,weakness, ataxia, and even dementia. Early demyelination can progress to axonal degenerationand neuronal death. These neurological symptoms are a direct result of the cobalaminedeficiency (not the anemia) and can be permanent even after correction of both thecobalamine deficiency and the related anemia. Empirical treatment of undiagnosed PAusing folate can correct the anemia but mask the underlying cobalamine deficiency, thusplacing the patient at risk for worsening neurological symptoms.3.1.2.2. Oral FeaturesOral findings can occur quite early in PA and include atrophic glossitis (red andsmooth tongue), burning mouth, and aphthous stomatitis. Any patient over age 40 withunexplained weakness and these oral findings should have a complete blood count withRBC indices and a B 12 and folate level. A thorough diet, nutrition, and health history isalso important to detect other contributing factors.3.1.3. DIAGNOSISDiagnostic tests for pernicious anemia include the Shilling Test, which uses radiolabeledB 12 to demonstrate inadequate absorption and urinary excretion of cobalamine,and anti-IF (60% of patients) or antiparietal cell (90% of patients) antibodies.3.1.4. TREATMENTThere is no treatment directed at reducing the auto-antibody production. Once thediagnosis of PA is established, replacement therapy with monthly parenteral B 12 or oraldaily doses of B 12 leads to rapid correction of symptoms (2,5,6). Prognosis is excellent,although established neurological symptoms may remain. Continuous evaluation andmonitoring are necessary because of the increased prevalence of gastric polyps andpossibility of gastric carcinoma in later years (7).3.1.5. ORAL HEALTH AND NUTRITION COMPLICATIONS AND MANAGEMENT3.1.5.1. Oral Complications and ManagementThe oral complications of PA (glossitis, burning mouth, aphthous stomatitis) generallyimprove with adequate cobalamine replacement. If burning persists and significantly