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Clinical:Pernicious Anemia
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Important Resources for Pernicious Anemia:
Pernicious anemia (PA) is the most common cause of vitamin B12 (cobalamin) deficiency in the western hemisphere. PA most commonly occurs in persons older than 60 years and of northern European descent.[1]
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Physiology
In patients with PA, autoantibodies destroy gastric parietal cells, resulting in deficient levels of intrinsic factor, a substance that binds ingested B12 and ensures its absorption. Decreased B12 absorption results in megaloblastic anemia.
Long-term B12 deficiency can cause reversible degenerative changes in the central nervous system, predominantly in the posterior columns and corticospinal tracts, a condition known as subacute combined degeneration. Early treatment is effectively a cure, but delayed treatment can lead to permanent neurological damage.
Diagnosis
Clinical manifestations usually develop insidiously and progress as vitamin B12 stores are depleted. Patients may be asymptomatic, or may develop anorexia, glossitis (painful or burning tongue), and constipation or diarrhea. Anemia may cause fatigue, light-headedness, exertional dyspnea, or chest pain.
As the disease progresses, weakness, spasticity, and ataxia may result from demyelination of the dorsal and lateral columns of the spinal cord. Depression, dementia, memory problems, irritability or, rarely, frank psychosis may occur.
Physical examination reveals pallor with lemon-tint icterus. You may see prematurely gray hair or a beefy, red tongue. Up to 20% of patients have a palpable spleen. Weakness and absent reflexes in early stages give way to spasticity and ataxia.
Blood tests reveal macrocytic anemia, and sometimes mild leukopenia and thrombocytopenia. Elevated serum bilirubin and lactate dehydrogenase are common. A vitamin B12 level of less than 100 pg/mL is clinically significant. (The normal range is 200-900 pg/mL). Serum methylmalonic acid and homocysteine levels are elevated.
Treatment
The mainstay of treatment is lifelong vitamin B12 replacement, either parenteral or oral. Patients respond to treatment within days and the hematocrit usually returns to normal within 2 months.
Patients with PA have a 2- to 3-fold increased risk of gastric carcinoma and should be followed closely.
References
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