A common cause of cobalamin malabsorption is pernicious anemia, an autoimmune disease in which the fundamental defect is atrophy of the gastric (parietal cell) oxyntic mucosa that eventually leads to the complete absence of IF and hydrochloric acid secretion (Fig. 1). The autoimmune gastritis (leading to chronic atrophic gastritis) associated with pernicious anemia involves the fundus and body of the stomach, and the histologic appearance of the gastric mucosa (infiltration with plasma cells and lymphocytes) is strongly reminiscent of autoimmune lesions. Because cobalamin is absorbed only by binding to IF and uptake by ileal IF-cobalamin receptors, the net consequence is severe cobalamin malabsorption leading to cobalamin deficiency.

Fig1. HISTOLOGIC FEATURES OF STOMACH IN PERNICIOUS ANEMIA COMPARED TO NORMAL. The normal gastric mucosa (A) is contrasted to that seen in pernicious anemia (B), in which there is atrophy of gastric glands, intestinal metaplasia with goblet cells, and loss of parietal cells (not visible at this magnification).

The annual incidence of pernicious anemia is approximately 25 new cases per 100,000 persons older than 40 years. Although the average age of onset is about 60 years, pernicious anemia is no respecter of age, race, or ethnic origin. The predisposition to devel oping pernicious anemia may have a genetic basis, but neither the mode of inheritance nor the initiating events or primary mechanism is precisely understood. There is a positive family history for about 30% of patients, among whom the risk for familial pernicious anemia is 20 times as high as in the general population; about 20% of siblings of patients are projected to develop pernicious anemia by the age of 90 years, and pernicious anemia has developed con cordantly in identical twins. There is a significant association of pernicious anemia with other autoimmune diseases, including Graves disease (30%), Hashimoto thyroiditis (11%), vitiligo (8%), Addison disease, idiopathic hypoparathyroidism, primary ovarian failure, myasthenia gravis, type 1 diabetes mellitus, and adult hypogammaglobulinemia.

Autoimmune gastritis progresses over decades to atrophic body gastritis and pernicious anemia. Serum anti-IF antibodies are highly specific (100%) for pernicious anemia, but the sensitivity is only about 50%. Earlier, the clinical use of anti-parietal cell antibodies was limited because of low specificity. This necessitated use of additional surrogate markers (high serum gastrin and low pepsinogen I levels) that reflected loss of acid- and IF-secreting parietal (oxyntic) cells. However, newer enzyme-linked immunosorbent assays (ELISA) for anti-parietal cell antibodies, which are directed against gastric H+/K+ ATPase, are 30% more sensitive than previous (immunofluorescence) assays. A reanalysis of the clinical utility of combining anti-IF and newer anti-parietal cell antibody tests to noninvasively diagnose pernicious anemia points to this approach as very promising. Thus among 81 patients with biopsy-proven atrophic body gastritis and pernicious anemia, combining anti-IF antibodies (37% sensitivity; 100% specificity) with newer anti-parietal cell antibodies (sensitivity 91%; specificity 90%) significantly increased their diagnostic performance for pernicious anemia, yielding overall 73% sensitivity while maintaining 100% specificity.

Juvenile pernicious anemia can manifest in the second decade with severe cobalamin deficiency in conjunction with many of the associated endocrinopathies and autoantibodies observed in adults.

Undiagnosed pernicious anemia is common among free-living elderly persons (over 60 years of age) who have only minimal clinical manifestations of cobalamin deficiency (i.e., 1.9% of a Southern California survey population had unrecognized and untreated pernicious anemia). The prevalence was 2.7% in women and 1.4% in men, but 4.3% of the African American women and 4.0% of the women of European descent had pernicious anemia.

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مواضيع ذات صلة

Subclinical Hyperthyroidism

Thyrotoxic Periodic Paralysis: Clinical Features

Nutritional Causes of Folate Deficiency

Neurologic Dysfunction with Cobalamin Deficiency

Sclerosing Thyroiditis (Riedel’s Thyroiditis) : Clinical Features

Infectious Thyroiditis

Leukopenia

Morphologic Expression of Megaloblastosis

Presentations Associated with Sideroblastic Anemia or Porphyrinuria

Sideroblastic Anemia and Porphyrinuria Caused by Drugs

Addison’s Disease

Cushing’s Disease