Related Experiment Video
Updated: May 8, 2026

A Method of Trigonometric Modelling of Seasonal Variation Demonstrated with Multiple Sclerosis Relapse Data
Published on: December 9, 2015
[Pathophysiology of hypervitaminosis B12: from origin to clinical event. Scoping review]
Beatriz Fernández-Téllez1, José Antonio Franco-Rico2, Edith Valdez-Martínez1
1Instituto Mexicano del Seguro Social, Centro Médico Nacional Siglo XXI, Hospital de Pediatría "Dr. Silvestre Frenk Freund", Unidad de Investigación Médica en Epidemiología Clínica. Ciudad de México, México.
Abstract:
The role that hypervitaminosis B12 may play in the clinical course of various diseases is controversial, in addition to being an overlooked laboratory finding. The objective of this review was to map the literature regarding the pathophysiological mechanisms that explain the increased serum levels of vitamin B12 (vB12) in some adult diseases. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses-Scoping Review Extension (PRISMA-ScR) checklist guided this scoping review. The search was performed in 2 electronic databases (PubMed and Google Scholar), in Spanish and English, for the years between 2000 and 2024. Twenty studies out of 568 found and screened were included. The main pathophysiological mechanisms that explained the hypervitaminosis B12 were 3: (1) oral or parenteral supplementation of vB12, which can induce the formation of autoantibodies anti-transcobalamin II; (2) serum increase of transcobalamins I, II and III by overproduction or reduction in their clearance; and (3) functional deficiency of the metabolism of transcobalamins. In sum, hypervitaminosis B12 denotes a disorder in the metabolism of vB12, and it could serve as a biomarker of a pathophysiological process with diagnostic and prognostic potential for various diseases.
Related Concept Videos
Vitamins
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Chronic Pancreatitis II: Pathophysiology