It occurs as a relatively common adult form of anemia that is associated with gastric atrophy and a loss of IF production and as a rare congenital autosomal recessive form in which IF production is lacking without gastric atrophy.
By definition, pernicious anemia refers specifically to vitamin B-12 deficiency resulting from a lack of production of IF in the stomach.
Common causes of pernicious anemia include:
- Weakened stomach lining (atrophic gastritis)
- An autoimmune condition in which the body’s immune system attacks intrinsic factor protein or the cells that make it.
Very rarely, pernicious anemia is passed down through families. This is called congenital pernicious anemia. Babies with this type of anemia do not make enough intrinsic factor or cannot properly absorb vitamin 12 in the small intestine.
Vitamin B12 cannot be produced by the human body, and must be obtained from the diet. Normally, dietary B12 is absorbed by the body in the small bowel only when it is bound by the intrinsic factor (IF) produced by parietal cells of the gastric mucosa. Pernicious anemia is thought to occur when the body’s immune system mistakenly targets the IF, with a loss of parietal cells. Insufficient IF results in insufficient absorption of the vitamin. Although the normal body stores three to five years’ worth of B12 in the liver, the usually undetected autoimmune activity in one’s gut over a prolonged period of time leads to B12 depletion and the resulting anemia. Inhibition of DNA synthesis in red blood cells results in the formation of large, fragile megaloblastic erythrocytes.
The onset of pernicious anemia usually is insidious and vague. The classic triad of weakness, sore tongue, and paresthesias may be elicited but usually is not the chief symptom complex. Continue reading “Introduction to Pernicious anemia”