hydroxocobalamin and Dementia

The purpose of this narrative review is to highlight insights into the importance and frequency of metabolic vitamin B12 (B12) deficiency, reasons why it is commonly missed, and reasons for the widespread but mistaken belief that treatment of B12 deficiency does not prevent stroke or improve cognitive function. Metabolic B12 deficiency is common, being present in 10%-40% of the population; is frequently missed; is easily treated; and contributes importantly to cognitive decline and stroke in older people. Measuring serum B12 alone is not sufficient for diagnosis; it is necessary to measure holotranscobalamin or functional markers of B12 adequacy such as methylmalonic acid or plasma total homocysteine. B-vitamin therapy with cyanocobalamin reduces the risk of stroke in patients with normal renal function but is harmful (perhaps because of thiocyanate accumulation from cyanide in cyanocobalamin) in patients with renal impairment. Methylcobalamin may be preferable in renal impairment. B12 therapy slowed gray matter atrophy and cognitive decline in the Homocysteine and B Vitamins in Cognitive Impairment Trial. Undiagnosed metabolic B12 deficiency may be an important missed opportunity for prevention of dementia and stroke; in patients with metabolic B12 deficiency, it would be prudent to offer inexpensive and nontoxic supplements of oral B12, preferably methylcobalamin or hydroxycobalamin. Future research is needed to distinguish the effects of thiocyanate from cyanocobalamin on hydrogen sulfide, and effects of treatment with methylcobalamin on cognitive function and stroke, particularly in patients with renal failure.

Topics: Animals; Biomarkers; Delayed Diagnosis; Dementia; Dietary Supplements; Humans; Hydroxocobalamin; Prevalence; Risk; Stroke; Vitamin B 12; Vitamin B 12 Deficiency; Vitamin B Complex

Cobalamin deficiency is associated with a wide spectrum of hematologic, neurologic, gastroenterologic and psychiatric disorders or symptoms. We report a case of a 50-year-old man with complex partial seizures with secondary generalization, mood oscillations and psychotic symptoms alternating with confusion and reversible dementia secondary to cobalamin deficiency in the absence of typical neurologic and/or hematologic symptoms and signs. Exclusion of epilepsy, acute, atrophic or expansive lesion of central nervous system and usual etiology associated with reversible dementia (infectious diseases, an endocrine etiology and deficiency of vitamins other than cobalamin); finding of cobalamin deficiency only and complete neuropsychiatric recovery after substitution, confirmed etiology. Typical and atypical psychiatric manifestations due to cobalamin deficiency that precede neurologic and/or hematologic signs and symptoms can recover completely after adequate replacement therapy.

Topics: Carbamazepine; Dementia; Diazepam; Electroencephalography; Haloperidol; Hematology; Humans; Hydroxocobalamin; Male; Middle Aged; Mood Disorders; Neurology; Psychotic Disorders; Seizures; Vitamin B 12 Deficiency

Topics: Aged; Anemia, Pernicious; Cognition; Dementia; Hematinics; Humans; Hydroxocobalamin; Male; Psychometrics; Treatment Outcome; Vitamin B 12 Deficiency

Topics: Aging; Child; Dementia; Electroencephalography; Female; Homocystinuria; Humans; Hydroxocobalamin; Leucovorin; Magnetic Resonance Imaging; Metabolism, Inborn Errors; Methylmalonic Acid; Vitamin B 12

Topics: Age of Onset; Anemia, Hemolytic; Anemia, Megaloblastic; Blood Transfusion; Child; Child, Preschool; Dementia; Demyelinating Diseases; Diagnostic Errors; Family Health; Female; Gas Chromatography-Mass Spectrometry; Humans; Hydroxocobalamin; Metabolism, Inborn Errors; Methylation; Nuclear Family; Paralysis; Vitamin B 12 Deficiency