How I treat cobalamin (vitamin B12) deficiency

Abstract

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)

Laboratory Evaluation for Vitamin B12 Deficiency: The Case for Cascade Testing

“…Some might argue that a low threshold for B 12 therapy is reasonable as a preventative measure, rather than waiting for symptomatic deficiency to develop. 1 This issue deserves further study, particularly with the recent increase in gastric procedures for morbid obesity.…”

Challenges in Diagnosing Pernicious Anemia: A Case Series

“…The treatment of vitamin B12 deficiency due to malabasorption/PA is parenteral hydroxocobalamin and is life long, with recurrence of symptoms on discontinuation [13,14]. Our patients both presented with longstanding symptoms of both anemia and neurological symptoms.…”

“…The samples obtained endoscopically confirmed chronic atrophic gastritis affecting the gastric body and antrum. Methylmalonic acid levels in urine were requested; the results were 271 mg/g/creat [4][5][6][7][8][9][10][11][12][13][14][15]. With the information gathered so far from the clinical aspects and the focused investigations, a diagnosis of megaloblastic anemia due to pernicious anemia was made and therapy instituted with daily hydroxocobalamin injections (1000 µg) for 1 week, weekly injections for one month, and monthly injections thereafter.…”

Consumo De Alimentos Fortificados en Estudiantes Secundarios De La Región Metropolitana De Chile

“…Esta vitamina es un micronutriente esencial tanto para la maduración de los glóbulos rojos como en las múltiples funciones en diversas rutas metabólicas necesarias para la función del sistema nervioso central y periférico. La B12 juega un rol central en el metabolismo de un carbono, su déficit se ve a menudo en personas mayores, su deficiencia clínica se presenta con signos neurológicos anormales, pérdida de conocimiento, neuropatía perifé-rica y trastornos psiquiátricos (22).…”