Vitamin B12 Deficiency: Chemistry of Vitamin B12 and its Potential Effects | ||
| Egyptian Journal of Chemistry | ||
| Volume 68, Issue 13, December 2025, Pages 597-605 PDF (290.57 K) | ||
| Document Type: Review Articles | ||
| DOI: 10.21608/ejchem.2025.396874.11949 | ||
| Authors | ||
| Khaulah Abdulaziz Alswaied* ; Arwa Mohammad Emam; Arwa Abdullah Alhamed; Turki Ali Aljabaan; Mohammed Abdullah Alzaher; Khloud Awadh Alhizan; Zainab Ali Alqarni; Khlood Khaldan Alharbi; Ebtesam Owaid Alshammari; Afnan Mohammed Al Dosari; Hala Halal Al Mutairi; Wasan Mohammed Alshikhi; Seham Ahmed Alanazi; Fahad Husayyan Al Enazi; Suhoud Saud Alotaibi | ||
| Ministry of National Guard, Saudi Arabia | ||
| Abstract | ||
| Background: Vitamin B12 (cobalamin) is an essential water-soluble vitamin crucial for DNA synthesis, fatty acid metabolism, and myelin sheath maintenance. Deficiency arises from dietary insufficiency, malabsorption (e.g., pernicious anemia, Crohn’s disease), or toxin exposure (e.g., nitrous oxide). Long-term deficiency leads to megaloblastic anemia and irreversible neurological damage, including subacute combined degeneration of the spinal cord (SCDSC). Aim: This review examines the biochemistry, pathophysiology, clinical manifestations, and management of vitamin B12 deficiency, emphasizing diagnostic challenges and therapeutic strategies. Methods: A comprehensive analysis of B12 absorption, metabolic roles, and deficiency etiologies was conducted. Diagnostic approaches (serum B12, methylmalonic acid [MMA], homocysteine levels) and treatment modalities (parenteral/oral supplementation) were evaluated. Results: Deficiency manifests as macrocytic anemia (elevated MCV, hypersegmented neutrophils) and neurological symptoms (neuropathy, ataxia, cognitive decline). Elevated MMA and homocysteine confirm diagnosis, particularly in borderline serum B12 cases. Treatment involves intramuscular B12 (1000 mcg/month) or high-dose oral therapy (1000–2000 mcg/day) for malabsorption. Early intervention improves hematologic recovery, but neurological damage may persist if treatment is delayed. Conclusion: Vitamin B12 deficiency requires prompt recognition and lifelong management in malabsorptive etiologies. Interprofessional collaboration (clinicians, dietitians, pharmacists) optimizes outcomes, particularly in high-risk groups (vegans, post-gastrectomy patients, elderly). Proactive screening and patient education are critical to preventing irreversible complications. | ||
| Keywords | ||
| Vitamin B12 deficiency; cobalamin; megaloblastic anemia; subacute combined degeneration; methylmalonic acid; pernicious anemia | ||
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