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• W2059988266 abstract "To the Editor: Cobalamin deficiency in older people may cause diffuse neuropsychiatric disorders that are often difficult to recognize in the initial stages and, therefore, difficult to associate with cobalamin deficiency.1 Thus, screening in older people might be justified.2 Evaluation of suspected cobalamin deficiency in the individual with low or low-normal serum cobalamin concentration may be done in two very different ways: (1) by measurement of indicators of intracellular deficiency, primarily methylmalonic acid in serum or urine as reviewed recently in this journal,2 or (2) by diagnosing conditions that may lead to or may be associated with cobalamin deficiency, primarily severe gastric or duodenal mucosal atrophy. We have found a 90% sensitivity and 100% specificity for severe atrophic gastritis by measuring serum pepsinogen-I (in press). Measurement of serum gastrin further increases the diagnostic sensitivity for type-A gastritis,3 and a concentration exceeding 200 pmol/L in the fasting individual is strongly suggestive of severe atrophic gastritis.4 Ingestion of food may increase concentrations of both gastrin (up to 100% increase) and pepsinogen-I (10% increase). We studied 368 individuals (168 men, 200 women) of a total of 530 individuals aged 75 years or older in the predominantly rural community of Mölnlycke, Sweden who were invited by personal letter to participate in a health survey. The participants attended non-fasting the Primary Care Centre during the day. Serum was stored at -20°C or below before assay of cobalamins, gastrin, and pepsinogen-I. All individuals with a cobalamin concentration < 150 pmol/L (lower limit of normal reference interval = 130 pmol/L) were recalled for follow-up within 3 weeks, and those with serum gastrin ≤ 50 pmol/L and serum pepsinogen-I ≥ 30 μg/L (lower reference limits for fasting individuals), i.e., not indicative of atrophic gastritis, were offered endoscopy,5 as was a subsample of others with low cobalamin concentration. Serum methylmalonic acid (by isotope-dilution using gas chromatography-mass spectrometry with upper normal reference limit of 0.4 μmol/L) was determined in 14 randomly selected individuals before and 6 months after cobalamin treatment. Serum cobalamin concentration < 150 pmol/L was found in 41 patients (11% of those screened). In addition, 17 individuals received substitution therapy. Sixteen subjects consented to be examined by upper gastrointestinal endoscopy (Table 1). Three randomly selected individuals with serum gastrin ≥ 50 pmol/L and pepsinogen-I < 30 μg/L (supporting the diagnosis of atrophic antrum-saving gastritis, Group A) had this diagnosis verified, as did two individuals with biochemical findings indicative of total atrophic gastritis, Group B. Of 10 individuals with laboratory test results not supporting a diagnosis of atrophic gastritis (Group D), two were found to have celiac disease, and atrophic gastritis was found in one individual. No cause could be established for the others (n = 7). Methylmalonic acid concentration in serum was high in 13 of 14 randomly selected patients. It decreased to normal in all 13 individuals after 6 months of cobalamin therapy or, in one case, borderline-normal. Our findings of a high prevalence (11% < 150 pmol/L) of low serum cobalamin concentration in persons aged more than 75 years is in agreement with results from other studies.1,2 The finding of an increased serum concentration of methylmalonic acid in 13 out of 14 in a random sample of our individuals indicates that about 10% of our population suffers from cobalamin deficiency. The finding of two individuals (of 41 with serum cobalamins < 150 pmol/L) with previously unrecognized celiac disease in the group of individuals with gastrin and pepsinogen-I concentrations not indicative of atrophic gastritis (Table 2) shows the importance of awareness of this condition in older people. For instance, in a study of cases diagnosed at the age of 60 years of more, the average diagnostic delay was 28 years!6 Both patients in this study had typical light-microscopical signs of celiac disease with villous atrophy of the duodenal mucosa, but only one had gastrointestinal symptoms that disappeared with gluten-free diet. This patient also had signs of malabsorption when further tested. Thus, endoscopic evaluation might be indicated in cases with cobalamin deficiency if other laboratory tests such as gastrin and pepsinogen-I in serum do not support the diagnosis of atrophic gastritis. In conclusion, our results support the views in the recent timely review by Stabler2 that cobalamin deficiency is found frequently enough in older people to justify screening. In addition, we consider etiological evaluation of cobalamin deficiency to be indicated in selected cases." @default.
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• W2059988266 date "1996-10-01" @default.
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• W2059988266 title "PREVALENCE AND DIAGNOSIS OF COBALAMIN DEFICIENCY IN OLDER PEOPLE" @default.
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• W2059988266 doi "https://doi.org/10.1111/j.1532-5415.1996.tb01388.x" @default.
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