Vitamin B12 deficiency is a commonly underestimated medical condition, but one that can have serious consequences if left untreated. It’s not just a temporary issue; it’s a nutritional deficiency that affects several vital functions in the body. Vitamin B12, also known as cobalamin, is essential for red blood cell formation, proper nervous system function, and DNA synthesis.
Contrary to popular belief, vitamin B12 deficiency is rarely caused solely by a poor diet. While people following strict vegan or vegetarian diets are at risk, the most frequent causes are medical in nature. One of the main culprits is atrophic gastritis, a chronic condition that reduces the production of intrinsic factor—a glycoprotein essential for B12 absorption in the intestine.
Another significant cause is pernicious anemia, an autoimmune disease that destroys the stomach cells responsible for producing intrinsic factor. Intestinal diseases like Crohn’s disease, undiagnosed celiac disease, or previous surgeries involving the ileum (the portion of the intestine where B12 is absorbed) can also impair absorption. Moreover, the chronic use of medications such as proton pump inhibitors (PPIs) and metformin can interfere with cobalamin uptake, making regular monitoring necessary for patients on long-term therapy.
Diagnosing vitamin B12 deficiency requires an integrated clinical approach that combines standard blood tests with specific biochemical markers. The first step is usually measuring serum B12 levels, but this value can sometimes be misleading. That’s why it’s essential to also assess homocysteine and methylmalonic acid (MMA) levels—two biochemical markers that tend to rise in cases of real intracellular deficiency.
In suspected cases of megaloblastic anemia, a complete blood count (CBC) will show enlarged red blood cells (elevated MCV), while pancytopenia may indicate a more advanced condition. For patients suspected of having pernicious anemia, testing for anti-parietal cell antibodies and intrinsic factor antibodies is recommended to confirm the autoimmune nature of the condition.
In select cases—especially in patients who do not respond to oral therapy or when gastrointestinal disorders are suspected—further investigations such as gastroscopy with biopsy or intestinal imaging may be required.
The treatment of vitamin B12 deficiency depends on the severity of the deficiency and the underlying cause. In milder cases, and in individuals without absorption issues, oral supplementation with cyanocobalamin or methylcobalamin (typically 1000 to 2000 mcg daily) may be sufficient. However, in cases of confirmed malabsorption or pernicious anemia, intramuscular injection of B12 is necessary.
The injectable treatment usually starts with an intensive phase (weekly injections for 4–6 weeks), followed by a maintenance phase with monthly doses. In chronic conditions, lifelong supplementation may be required. It’s crucial to monitor blood levels regularly to assess treatment response and adjust dosage accordingly.
For at-risk individuals—such as the elderly, vegans, or patients on long-term medications affecting absorption—preventive supplementation is a valid strategy to avoid future complications.
Ignoring a vitamin B12 deficiency can lead to severe neurological and systemic complications. One of the most feared outcomes is subacute combined degeneration of the spinal cord, a condition that may cause sensory loss, gait disturbances, and irreversible nerve damage if not treated promptly. In children and adolescents, prolonged deficiency can affect neurological and cognitive development.
In adults, chronic deficiency has been linked to an increased risk of early cognitive decline and mood disorders, including depression and irritability. In cases of untreated megaloblastic anemia, symptoms can worsen to include severe fatigue, shortness of breath, and even heart failure due to anemia.
Early diagnosis and timely treatment are key—not only to relieve symptoms but to prevent irreversible damage. Awareness and proper medical follow-up are crucial tools in managing this important nutritional deficiency.
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