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Vitamin B12 deficiency resulting from decreased production and availability of intrinsic factor secondary to autoimmune-induced gastric mucosa atrophy.

Biermer-Erhlich Anemia; Hunter-Addison Anemia; Lederer Anemia; Macrocytic Achylic Anemia; Biermer Anemia; Addison-Biermer Anemia.

It affects males and females equally. The most common form, Adult Onset Pernicious Anemia, affects people after the age of 35 years. Studies suggest that about 1% of the elderly population is affected. Congenital Pernicious Anemia is very rare and has an onset of age between 4 and 28 months. Juvenile Pernicious Anemia has symptoms similar to the adult-onset type, seems to occur between the ages of 4 and 20 years. North America and in Europe among people of Scandinavian, English, or Irish descent has the higher prevalence. It is extremely rare among Asians. Approximately 1.9% of cases may go undiagnosed. Pernicious anemia shows a 10-fold increase in patients with multiple myeloma and a 250-fold increase in adults with immunoglobulin deficiency.

Autosomal dominant inheritance with incomplete penetrance.

Autoantibodies against gastric parietal cells account for the defect in intrinsic factor production and availability. The resultant vitamin B12 deficiency produces megaloblastic changes in red cells and neuropathies. The latter result from demyelination with the accumulation of odd-chain fatty acids secondary to impaired cobalamin-dependent degradation of methylmalonyl coenzyme A to succinyl-CoA.

Decreased oral absorption of cobalt-60-labeled vitamin B12.

Usual symptoms of anemia. Sore tongue. Patients may present with symptoms and signs of lateral and posterior spinal column involvement with progression to paraplegia and bowel/bladder dysfunction if left untreated.

Patients with anemia should have the red cell indices examined to exclude megaloblastic changes. Document preexisting neurologic deficits. Investigations: CBC, red cell indices.

Avoid nitrous oxide administration in patients with increased mean corpuscular volume or in patients with documented vitamin B12 deficiency. Regional anesthesia may be relatively contraindicated in patients with preexisting neurologic deficits.

Irreversible oxidation of coenzyme B12 and methionine synthase by N2O. It has been shown that patients with preexisting B12 deficiencies can develop megaloblastic anemia and neurologic deficits after 2 hours or less of nitrous oxide exposure. The neurologic deficits developed 2 to 6 weeks postoperatively and improved with B12 therapy.

Congenital Transcobalamin II Deficiency (Transcobalamine II Deficiency): Retinal degeneration and megaloblastic anemia in early infancy that is caused by impairment of cobalamin utilization.

Acquired Vitamin B12 Deficiency: This can occur in infants breast-fed by a vegetarian mother, in vegetarian children, and in children who have undergone large resection of the small bowel (ileum) and who do not receive supplemental vitamin B12. Infection with the fish tapeworm Diphyllobothrium latum is nowadays a rare cause of pernicious anemia.

Marie RM, Le Biez E, Bisson P, et al: Nitrous oxide anesthesia-associated myelopathy. Arch Neurol 57:380, 2000.  ...

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