Studies on Vitamin B₁₂ Status in the Elderly – Prophylactic and Therapeutic Consequences

Abstract

Because of the large liver stores (about 5 mg), low turnover rate (0.143%) and small daily requirement (3 micrograms), vitamin B12 deficiency does not occur under normal circumstances. This is not the case in individuals with chronic inflammatory or trophic changes at vitamin B12 absorption sites. Without supplementation, vitamin B12 deficiency can be expected within 5 years of gastrectomy. Characteristic features of type A gastritis are hyposecretion and mucosal atrophy in the fundus and body of the stomach, with absent intrinsic factor. In the small intestine, active and/or passive absorption is impaired by extensive ileal resection, exocrine pancreatic insufficiency and chronic inflammatory disorders such as Crohn's disease. Definitive plasma concentrations cannot be quoted for vitamin B12 deficiency. Dietary habits, subjective symptoms, hematological laboratory results, function tests and gastrointestinal endoscopic and histological findings must all be taken into account in the diagnosis. Modern diagnostic parameters, such as methylmalonic acid and homocysteine serum assays, are useful for achieving early diagnosis and hence optimal treatment. With their assured availability, parenteral vitamin B12 preparations remain the treatment of choice. Results from vitamin B12 bioavailability studies in healthy subjects suggest that > 300 micrograms probably suffices as an oral maintenance dose after parenteral loading. Further well-documented cases are needed in order to establish whether these doses are adequate in malabsorption syndromes and gastrointestinal diseases. Various case reports indicate the value of prophylactic and therapeutic oral vitamin B12 administration, especially in disorders of homocysteine metabolism, a substance postulated as a further important risk factor for atherosclerosis.

Prevalence of and risk factors for vitamin B12 deficiency in patients with Crohnʼs disease

“…Patients were initially identified by ICD-9 codes (555.x) and the diagnosis of CD was confirmed by review of their clinical, laboratory, endoscopic, histologic, and radiographic information. Patients were excluded from participation if they were previously diagnosed with B 12 deficiency or were receiving supplemental B 12 at the time of initial visit (n ϭ 7). Patients were also excluded if they had a known cause of B 12 deficiency other than inflammatory bowel disease (n ϭ 1).…”

“…B 12 deficiency typically results in ineffective erythropoiesis and megaloblastic anemia as well as sometimes irreversible neurologic and psychiatric abnormalities including personality changes, neuropsychiatric deficits, parasthesias, ataxia, and a shuffling gait. Animal products are the principal source of B 12 for humans and gastrointestinal absorption occurs via a well-described mechanism. 1 Dietary cobalamin is cleaved from its binding protein by acid and pepsin in the stomach and binds to R factor, which is produced in the saliva and stomach.…”

“…The IF-cobalamin compound then travels to the ileum where it binds to a specific receptor, cobalamin, and then is absorbed through the ileal mucosa. 2 Any abnormality along the pathway can result in B 12 malabsorption, which in turn can lead to B 12 deficiency. B 12 deficiency is uncommon in younger individuals but increases with age, and the prevalence in the elderly may be as great as 12%.…”

“…Fifteen percent of patients with CD have isolated ileal inflammation and an additional 30% of patients have ileocolonic disease. 4 Long-term inflammation of the mucosa can lead to impaired absorption and can also lead to fibrosis and strictures that necessitate surgical resection of segments of bowel including the ileum, and thus patients with CD may be at particular risk for B 12 deficiency. Conversely, ulcerative colitis (UC) is an inflammatory disease limited to the colon, with little or no ileal involvement, and it appears that the prevalence of B 12 deficiency in UC patients is similar to the general population.…”

“…A recent study suggested that in patients with CD, having a history of ileal resection regardless of the length of resection were not at risk for B 12 deficiency. 9 We hypothesized that the prevalence of B 12 deficiency among CD patients remains high despite the use of newer medical therapies and might justify routine screening for B 12 deficiency, at least in a subset of patients with CD. The aims of the current study were to assess the prevalence of B 12 abnormalities in a population with CD and to identify risk factors associated with an abnormal B 12 concentration.…”