AGE-RELATED-CHANGES IN COBALAMIN (VITAMIN-B-12) HANDLING - IMPLICATIONS FOR THERAPY

Authors
Citation
H. Nilssonehle, AGE-RELATED-CHANGES IN COBALAMIN (VITAMIN-B-12) HANDLING - IMPLICATIONS FOR THERAPY, Drugs & aging, 12(4), 1998, pp. 277-292
Citations number
165
Categorie Soggetti
Pharmacology & Pharmacy","Geiatric & Gerontology
Journal title
ISSN journal
1170229X
Volume
12
Issue
4
Year of publication
1998
Pages
277 - 292
Database
ISI
SICI code
1170-229X(1998)12:4<277:AIC(H->2.0.ZU;2-L
Abstract
Cobalamin (vitamin B-12) deficiency is more common in the elderly than in younger patients. This is because of the increased prevalence of c obalamin malabsorption in this age group, which is mainly caused by (a utoimmune) atrophic body gastritis. Cobalamin supplementation is affor dable and nontoxic, and it may prevent irreversible neurological damag e if started early. Elderly individuals with cobalamin deficiency may present with neuropsychiatric or metabolic deficiencies, without frank macrocytic anaemia. An investigation of symptoms and/or signs include s the diagnosis of deficiency as well as any underlying cause. Deficie ncy states can still exist even when serum cobalamin levels are higher than the traditional lower reference limit. Cobalamin-responsive elev ations of serum methylmalonic acid (MMA) and homocysteine are helpful laboratory tools for the diagnosis. The health-related reference range s for homocysteine and MMA appear to vary with age and gender. Atrophi c body gastritis is indirectly diagnosed by measuring serum levels of gastrin and pepsinogens, and it may cause dietary cobalamin malabsorpt ion despite a normal traditional Schilling's test. The use of gastrosc opy may also be considered to diagnose dysplasia; bacterial overgrowth and intestinal villous atrophy in healthy patients with atrophic body gastritis or concomitant iron or folic acid deficiency. Elderly patie nts respond to cobalamin treatment as fully as younger patients, with complete haematological recovery and complete or good partial resoluti on of neurological deficits. Chronic dementia responds poorly but shou ld, nevertheless, be treated if there is a metabolic deficiency las in dicated by elevated homocysteine and/or MMA levels). Patients who are at risk from cobalamin deficiency include these with a gastrointestina l predisposition (e.g. atrophic body gastritis or previous partial gas trectomy), autoimmune disorders [type 1 (insulin-dependent) diabetes m ellitus and thyroid disorders], those receiving long term therapy with gastric acid inhibitors or biguanides, and these undergoing nitrous o xide anaesthesia. To date, inadequate cobalamin intake has not proven to be a major risk factor. Intervention trials of cobalamin, folic aci d and pyridoxine (vitamin B-6) in unselected elderly populations are c urrently under way.