Addison-Biermer Anemia: Symptoms and Treatment Methods

Addison-Biermer anemia, also referred to as pernicious or megaloblastic anemia, represents a pathological condition arising from a deficiency of vitamin B12 (cobalamin) within the human body. The primary dietary sources of this essential nutrient are animal-derived products, including offal (particularly liver), various meats such as poultry, pork, and beef, as well as fish, eggs, dairy products, and their derivatives—examples being aged cheeses, cottage cheese, plain yogurt, kefir, and buttermilk. It is critical to emphasize that vitamin B12 is entirely absent from plant-based foods, posing a significant challenge for individuals adhering to vegan or vegetarian diets without supplementation. Cobalamin fulfills pivotal metabolic roles: it is integral to protein synthesis, carbohydrate and lipid metabolism, and plays a foundational part in erythropoiesis—the process of red blood cell production within the bone marrow. Additionally, it contributes to psychological equilibrium, supports nervous system function, and participates in the repair of damaged DNA structures. The absorption of dietary vitamin B12 is contingent upon the presence of *intrinsic factor* (IF), a glycoprotein secreted by the parietal cells of the gastric mucosa. In its absence, cobalamin cannot be assimilated and is excreted from the body without metabolic benefit. Another critical site for absorption is the terminal ileum, the final segment of the small intestine, where the ultimate uptake occurs. It is essential to note that Addison-Biermer anemia is not a discrete disease entity but rather a manifestation of underlying physiological dysfunctions, frequently of autoimmune origin. The condition develops due to an autoaggressive immune response that results in the atrophy of parietal cells in the stomach, consequently leading to intrinsic factor deficiency and, by extension, impaired vitamin B12 absorption.

Pernicious anemia, clinically referred to as Addison-Biermer anemia, presents with a constellation of distinctive symptoms, including: an abnormal pallid-yellow discoloration of the skin and mucous membranes, persistent fatigue and debility even following minimal physical exertion, a marked reduction in appetite resulting in weight loss, dysfunction in taste and olfactory perception, recurrent headaches accompanied by episodes of vertigo, chronic somnolence and lethargy, peripheral edema predominantly localized to the ankles, hepatomegaly or splenomegaly, developmental and maturational delays (particularly in pediatric and adolescent populations), cognitive impairments characterized by difficulties in sustaining attention, and inflammatory alterations of the tongue—specifically glossal smoothing, erythema, and tenderness upon palpation or during mastication.

Pernicious anemia, alternatively referred to as Addison-Biermer anemia, arises from impaired absorption of cobalamin (vitamin B12), an essential cofactor in erythropoiesis—the synthesis of red blood cells. The underlying cause is a hereditary genetic mutation that disrupts the production of intrinsic factor (IF, also known as Castle’s factor) by the parietal cells lining the gastric mucosa. Under normal physiological conditions, following the ingestion of vitamin B12-rich foods, absorption depends on the presence of IF, which is secreted into the duodenal lumen. There, IF binds to cobalamin, forming a complex that facilitates transit through the small intestine to the ileum, where the vitamin is absorbed into systemic circulation via specialized protein-mediated transport mechanisms.

Pernicious anemia, clinically referred to as Addison-Biermer anemia or autoimmune-mediated megaloblastic anemia, frequently becomes apparent during childhood—most commonly around the age of 10. This timing correlates with the depletion of cobalamin (vitamin B12) stores accumulated during fetal development. The underlying pathophysiology stems from the absence of intrinsic factor (IF), a glycoprotein critical for cobalamin absorption in the distal ileum. Consequently, the cornerstone of treatment involves **parenteral administration of hydroxocobalamin**—the metabolically active form of vitamin B12—which must be maintained indefinitely to avert severe neurological and hematological sequelae.

Pernicious anemia, also referred to as Addison-Biermer anemia, is distinct from other forms of anemia in that its development is not influenced by dietary quality. The deficiency in vitamin B12 does not stem from inadequate intake through food but rather from an impairment in the body’s absorption mechanisms. Nevertheless, regardless of this specific condition, a balanced diet founded on minimally processed foods—one that is diverse in its sources of nutrients, including proteins, complex carbohydrates, healthy fats, trace minerals, vitamins, and bioactive compounds—remains a cornerstone of health maintenance and the preservation of overall physiological well-being.