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Pathology -Pernicious Anemia (Vitamin B12 Deficiency)
Pernicious anemia is the most prevalent form of vitamin B12 (cobalamin) deficient anemia. The fundamental problem is decreased secretion of intrinsic factor (IF) from the stomach mucosa due to autoimmune atrophic gastritis, where autoantibodies result in the death of IF and hydrochloric acid-secreting parietal cells. After cleavage of R-factor, IF binds to vitamin B12 to facilitate absorption of the vitamin in the terminal ileum. Vitamin B12 deficiency is slow to develop as the liver can store several years supply of cobalamin; however, other causes can include decreased gastric acid secretion (prevents pancreatic enzyme cleavage of Rfactor), other absorptive disorder (Celiac’s disease, Crohn’s disease, bacterial overgrowth), and a pure vegan (not vegetarian) diet. In dietary deficiency, administration of radiolabeled cobalamin will result in increased urinary excretion of the radiolabeled vitamin, as it is absorbed normally. In pernicious anemia, increased urine excretion will only be noticed after the administration of exogenous IF (a positive Schilling test). As in this case, it is more likely in people with a personal history (Hashimoto’s thyroiditis) or a familial history (RA) of autoimmune illnesses. Vitamin B12 deficiency can be distinguished from folate-deficiency anemia by the presence of neurologic symptoms, including peripheral neuropathy with sensorimotor changes, decreased vibratory sense and proprioception (indicated here with balance changes and a positive Romberg’s sign), hyperspasticity, and mild cognitive impairment.
Pernicious anemia is the most prevalent form of vitamin B12 (cobalamin) deficient anemia. The fundamental problem is decreased secretion of intrinsic factor (IF) from the stomach mucosa due to autoimmune atrophic gastritis, where autoantibodies result in the death of IF and hydrochloric acid-secreting parietal cells. After cleavage of R-factor, IF binds to vitamin B12 to facilitate absorption of the vitamin in the terminal ileum. Vitamin B12 deficiency is slow to develop as the liver can store several years supply of cobalamin; however, other causes can include decreased gastric acid secretion (prevents pancreatic enzyme cleavage of Rfactor), other absorptive disorder (Celiac’s disease, Crohn’s disease, bacterial overgrowth), and a pure vegan (not vegetarian) diet. In dietary deficiency, administration of radiolabeled cobalamin will result in increased urinary excretion of the radiolabeled vitamin, as it is absorbed normally. In pernicious anemia, increased urine excretion will only be noticed after the administration of exogenous IF (a positive Schilling test). As in this case, it is more likely in people with a personal history (Hashimoto’s thyroiditis) or a familial history (RA) of autoimmune illnesses. Vitamin B12 deficiency can be distinguished from folate-deficiency anemia by the presence of neurologic symptoms, including peripheral neuropathy with sensorimotor changes, decreased vibratory sense and proprioception (indicated here with balance changes and a positive Romberg’s sign), hyperspasticity, and mild cognitive impairment.
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