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Vitamin B12 is a vital chemical that is needed to maintain good nerve, red blood cell, and DNA production. A lack of this vitamin may cause a very diverse set of neurological and systemic symptoms, such as numbness and tingling in hands and feet, memory loss, walking difficulties, fatigue, anaemia, in extreme cases, with permanent nerve damage. Although dietary deficiency and absorption disorders are known to be the main causes, a contributing factor that is less mentioned and is becoming more and more relevant is the long-term use of some of the commonly prescribed drugs.
Speaking to Dr Madhukar Bhardwaj, Director & HOD - Neurology, Aakash Healthcare, "Metformin is a first-line approach to the treatment of type 2 diabetes and is one of the most common medications used in the treatment of vitamin B12 deficiency. The metformin also disrupts the calcium-dependent vitamin B12 absorption in the terminal ileum where this vitamin is absorbed."
Several studies have indicated that the risk of B12 deficiency from the use of the medication metformin is high after two to three years of continued usage. The risk is increased because of increased dosage and prolonged therapy. The neurological expression of vitamin B12 deficiency in diabetic subjects can be confused with diabetic neuropathy, which prevents effective diagnosis and treatment.
The doctor further said, "Another high-risk group that is associated with vitamin B12 deficiency is acid-suppressing drugs, especially proton pump inhibitors (PPIs) like esophrazole and pantoprazole and H2 receptor blockers, including ranitidine and famotidine. Such medications inhibit the secretion of gastric acid, that is required to liberate vitamin B12 in food proteins."
In the absence of sufficient stomach acid, the vitamin B12 is unable to bind itself to intrinsic factor, which is a protein that is necessary to absorb the vitamin. The tendency of these drugs to lower B12 levels over time, particularly in older adults who might already be at lower baseline acid production, is common in long-term usage, usually in acid reflux or gastritis.
Some anti-epileptic drugs such as phenytoin, carbamazepine have also been linked to decrease in vitamin B12 level. Such medications may disrupt the absorption of intestines and result in changes in vitamin metabolism. Long term patients under anti-seizure therapy can thus develop minor neurological changes associated with B12 deficiency which can create some confusion in the clinical presentation of the patients who already receive treatment of the neurological disorder.
Colchicine, which is used in the treatment of gout, and also some antibiotics can cause other drugs in their prolonged usage. They may compromise the work of intestinal mucosa or alter the gut flora and indirectly influence the absorption of vitamin B12. Besides this, continuous consumption of nitrous oxide, which may be experienced during a medical or dental procedure, may render vitamin B12 inactive and trigger acute neurological symptoms.
The neurological effects of vitamin B12 deficiency are especially alarming since they can develop insidiously and be irreversible in case of their early onset. Such symptoms like tingling, balance issues, cognitive slowing, mood swings, and visual disturbances will raise the concerns and need to be assessed in patients who are on long-term medication and whose level of B12 is expected to be affected.
It is recommended that high-risk populations such as diabetics who are taking metformin, chronic acid-suppressing therapy, elderly individuals, and individuals who are taking long-term anti-epileptic drugs have their vitamin B12 levels regularly checked.
Most of the symptoms can be reversed and the brain nerve damage may be prevented by early diagnosis and timely supplementation. Patient and clinical health education on medication-induced vitamin B12 deficiency is thus very important in protecting against long-term neurological well-being.