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, meats, fish, eggs, and dairy. Cobalamin fulfills pivotal metabolic roles, supporting protein synthesis, erythropoiesis, and nervous system function.

Pernicious anemia presents with a constellation of distinctive symptoms, including an abnormal pallid-yellow discoloration of the skin, persistent fatigue, reduced appetite, headaches, and vertigo.

Additionally, neurological manifestations such as paresthesias, gait disturbances, cognitive impairments, and inflammatory alterations of the tongue may develop.

The condition arises from impaired absorption of cobalamin due to autoimmune destruction of the gastric parietal cells.

Antibodies directed against parietal cells and intrinsic factor (IF) prevent the formation of the required IF-cobalamin complex, rendering absorption in the terminal ileum impossible.

Since oral absorption of vitamin B12 fails in the absence of intrinsic factor, the primary therapeutic strategy involves parenteral (typically intramuscular or subcutaneous) administration of hydroxocobalamin or cyanocobalamin.

This lifelong substitution ensures that tissue stores remain replenished and both hematological and neurological sequelae are successfully averted.

Although Addison-Biermer anemia is primarily caused by an absorption defect rather than inadequate dietary intake, a balanced, nutrient-dense diet plays an important role in overall recovery.

Patients should focus on a wholesome diet that provides optimal amounts of all other micronutrients and holistically supports the healing process.