From the Guidelines
Vitamin B12 deficiency should be treated immediately with hydroxocobalamin 1 mg intramuscularly to prevent permanent neurological damage and other disabilities, as recommended by the most recent guidelines 1. The disabilities from B12 deficiency occur because this vitamin is essential for nerve function, DNA synthesis, and red blood cell formation. Without adequate B12, myelin sheaths around nerves deteriorate, causing neurological symptoms, while impaired DNA synthesis affects red blood cell production. Some of the key disabilities associated with vitamin B12 deficiency include:
- Neurological problems such as numbness and tingling in the hands and feet
- Difficulty walking
- Memory loss
- Cognitive impairment
- Megaloblastic anemia causing fatigue, weakness, and shortness of breath For people with neurological involvement, hydroxocobalamin 1 mg intramuscularly should be administered on alternate days until there is no further improvement, then hydroxocobalamin 1 mg intramuscularly every 2 months, as recommended by NICE guidelines 1. In cases without neurological involvement, hydroxocobalamin 1 mg intramuscularly should be administered three times a week for 2 weeks, followed by maintenance treatment with 1 mg intramuscularly every 2–3 months for life, as recommended by the British Obesity and Metabolic Surgery Society guidelines 1. Early treatment is crucial as some neurological damage may become permanent if the deficiency persists for too long. It is also important to identify and address the underlying cause of the deficiency, such as a diet low in vitamin B12 or certain health conditions, to prevent future deficiencies. Some common risk factors for vitamin B12 deficiency include a diet low in animal source foods, certain health conditions such as atrophic gastritis or coeliac disease, and the use of certain medications such as metformin or H2 receptor antagonists, as outlined in the NICE guideline summary 1.
From the FDA Drug Label
PRECAUTIONS General Vitamin B12 deficiency that is allowed to progress for longer than 3 months may produce permanent degenerative lesions of the spinal cord. Neurologic manifestations will not be prevented with folic acid, and if not treated with vitamin B12, irreversible damage will result. Failure to do so will result in return of the anemia and in development of incapacitating and irreversible damage to the nerves of the spinal cord Also, patients should be warned about the danger of taking folic acid in place of vitamin B12, because the former may prevent anemia but allow progression of subacute combined degeneration.
Vitamin B12 deficiency disabilities include:
- Permanent degenerative lesions of the spinal cord
- Irreversible damage to the nerves of the spinal cord
- Incapacitating and irreversible damage
- Subacute combined degeneration These disabilities can occur if the deficiency is allowed to progress for longer than 3 months or if not treated with vitamin B12 2.
From the Research
Vitamin B12 Deficiency Disabilities
- Vitamin B12 deficiency can affect individuals at all ages, but most particularly elderly individuals, and can cause various disabilities, including hematological and neurological manifestations 3.
- The consequences and severity of B12 deficiency are variable depending on the degree of deficiency and its duration, and major organ systems affected include the blood, bone marrow, and nervous system 4.
- Nervous system involvement can result in cognitive impairment, psychosis, and defective myelin synthesis and repair, leading to disabilities such as megaloblastic anemia and neurological impairments 4, 5.
- Vitamin B12 deficiency can masquerade as a multitude of illnesses, presenting different perspectives from the point of view of the hematologist, neurologist, gastroenterologist, general physician, or dietician, making diagnosis and treatment challenging 6.
- Supplementation with high doses of oral cobalamin can be effective in correcting plasma markers of vitamin B12 deficiency, but the effects of lower oral doses are uncertain, and daily doses of 647 to 1032 mug of cyanocobalamin were associated with 80% to 90% of the estimated maximum reduction in the plasma methylmalonic acid concentration 7.
Risk Factors for Vitamin B12 Deficiency Disabilities
- Groups at higher risk of vitamin B12 deficiency include vegans, vegetarians, older adults, individuals with limited diets, breastfed and preterm infants, and those who primarily consume foods prepared or cooked in ways that reduce vitamin B12 content 5.
- Iatrogenic factors linked to medication use or surgical procedures can also increase the risk of vitamin B12 deficiency, and recognizing these diverse risk factors can help develop strategies for prevention and intervention 5.
- Increased physician vigilance and heightened patient awareness are crucial for early presentation and testing of vitamin B12 deficiency, and testing sometimes occurs during a phase of vitamin B12 insufficiency before the main onset of the disease 6.
Diagnosis and Treatment of Vitamin B12 Deficiency Disabilities
- Diagnostic biomarkers for B12 status include decreased levels of circulating total B12 and transcobalamin-bound B12, and abnormally increased levels of homocysteine and methylmalonic acid, but the exact cut-offs to classify clinical and subclinical deficiency remain debated 3, 4.
- Management depends on B12 supplementation, either via high-dose oral routes or via parenteral administration, and the chosen test often depends on its availability rather than on the diagnostic performance and sensitivity to irrelevant factors interfering with vitamin B12 markers 3, 6.
- Future directions for diagnostics of B12 status and health interventions are also discussed, including the use of holotranscobalamin, serum methylmalonic acid, and plasma homocysteine measurements in routine practice 6.