Clinical Trial of the Effect of Vitamin B12 in Elderly Subjects with Low Serum B12 Levels

Hughes, D.C.; Elwood, Peter Creighton; Shinton, N. K.; Wrighton, R. J.

doi:10.1136/bmj.2.5707.458

Cited by 41 publications

(21 citation statements)

References 8 publications

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“…43 However, the course of subclinical deficiency often appears stationary. [61][62][63] The biochemical abnormalities themselves frequently fluctuate 64,65 ; mildly to moderately elevated MMA levels improved spontaneously in 44% of 432 cases retested 1 to 4 years later, and only 16% worsened. 64 Those observations notwithstanding, the impulse for medical intervention is such that controlled cobalamin trials in subclinical deficiency have been called unethical by some investigators.…”

Section: Expansion and Redefinition Of Cobalamin Deficiencymentioning

confidence: 99%

How I treat cobalamin (vitamin B12) deficiency

Carmel

2008

Blood

286

233

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The challenges in medical management of cobalamin deficiency lie in attention to the unique pathophysiology that underlies cobalamin deficiency, more than in the mechanics of therapy. The central physiologic principles are that clinically important deficiency is more likely to occur (and progress) when intrinsic factor-driven absorption fails than when diet is poor and that most causes take years to produce clinically obvious deficiency. Transient defects have little clinical impact. The key management principle is the importance of follow-up, which also requires knowing how the deficiency arose. The virtues of these principles are not always fully appreciated. Recent developments have made diagnosis and management more difficult by diminishing the ability to determine cobalamin absorption status. Clinicians must also grapple with premature medicalization of isolated, mild biochemical changes that added many asymptomatic cases of still undetermined medical relevance to their caseload, often expanded by inflated cobalamin level criteria. The potential for misattribution of cobalamin-unrelated presentations to nongermane cobalamin and metabolite abnormalities has grown. Pathophysiologically based management requires systematic attention to each of its individual components: correctly diagnosing cobalamin deficiency, reversing it, defining its underlying cause, preventing relapse, managing the underlying disorder and its complications, and educating the patient. (Blood. 2008;112: 2214-2221)

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Section: Expansion and Redefinition Of Cobalamin Deficiencymentioning

confidence: 99%

How I treat cobalamin (vitamin B12) deficiency

Carmel

2008

Blood

286

233

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“…Hughes et al 23 also conducted a randomized trial of vitamin B 12 replacement in deficient subjects. They did not formally measure cognition but, based on a self‐report questionnaire and structured psychiatric interview, concluded that cobalamin was no better than placebo.…”

Section: Commentmentioning

confidence: 99%

Time Dependency of Cognitive Recovery with Cobalamin Replacement: Report or a Pilot Study

Martin¹,

Francis²,

Protetch³

et al. 1992

J American Geriatrics Society

166

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“…As detailed in the following section, other investigators have handled this problem by conducting open-label studies (Martin et al ., 1992; Carmel et al ., 1995; Cunha et al ., 1995), sometimes with comparison to historical controls (Teunisse et al ., 1996; Eastley et al ., 2000) without low B 12 levels, and only rarely with full placebo-controlled designs (de la Fournière et al ., 1997; Hvas et al ., 2004). In elderly samples with no dementia, placebo-controlled trials of B 12 have sometimes handled the ethical dilemma by excluding subjects with any evidence of anemia or neurological symptoms (Hughes et al ., 1970; Seal et al ., 2002). However, this strategy is difficult to implement in practice, since minor hematological and neurological symptoms are prevalent in the elderly, and not necessarily related to low B 12 levels.…”

Section: Discussionmentioning

confidence: 99%

Cognitive and psychiatric effects of vitamin B12 replacement in dementia with low serum B12 levels: a nursing home study

Dyck

Lyness

Rohrbaugh

et al. 2008

IPG

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Background The aim of this study is to determine whether B12 replacement would ameliorate cognitive and psychiatric symptoms in elderly subjects with dementia and low serum B12 levels. Methods A test group (n=28) of nursing home residents with low serum B12 levels (<250 pg/mL) and a matched comparison group (n=28) with normal serum B12 levels (>300 pg/mL) were evaluated by blinded raters while the test group received intramuscular (IM) B12 replacement therapy. All subjects were assessed at baseline, 8 weeks, and 16 weeks with the Dementia Rating Scale, Brief Psychiatric Rating Scale, and Geriatric Depression Scale. Results Although B12 replacement produced significant improvement in hematologic and metabolic parameters, it yielded no significant effect on cognitive or psychiatric variables. A few subjects evidenced notable individual treatment responses; however, these were not statistically more frequent than in the normal B12 group. Conclusions These results suggest that B12 replacement is unlikely to benefit cognitive or psychiatric symptoms in the vast majority of elderly dementia patients with low serum B12 levels.

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Clinical Trial of the Effect of Vitamin B12 in Elderly Subjects with Low Serum B12 Levels

Cited by 41 publications

References 8 publications

How I treat cobalamin (vitamin B12) deficiency

How I treat cobalamin (vitamin B12) deficiency

Time Dependency of Cognitive Recovery with Cobalamin Replacement: Report or a Pilot Study

Cognitive and psychiatric effects of vitamin B12 replacement in dementia with low serum B12 levels: a nursing home study

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