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Pernicious anemia (PA), the commonest cause of cobalamin deficiency (CD) in the world, is an autoimmune disease of multifactorial origin and is characterized by chronic atrophic gastritis (CAG) and defective absorption of cobalamin from the terminal ileum due to interference by the intrinsic factor (IF) antibodies. PA-related CD is a lengthy process, which if untreated, can lead to irreversible hematological and neurological sequelae. Although safe and effective therapy is available and the management of PA is straightforward, the diagnosis of PA can be extremely difficult to obtain due to myriad and diverse clinical presentations, frequently coexisting diseases, and limitations of currently available diagnostic tests. Diagnostic dilemmas may occur when PA patients present with normal or spuriously high serum cobalamin levels, dysplastic features of ring sideroblasts in the bone marrow (BM), hemolysis, and concomitant diseases such as iron deficiency or thalassemia. Herein, the author discusses an overview of diagnostic difficulties, with regards to morphological mimics, coexisting diseases, limitations of currently available tests, and how to diagnose PA in the era of imperfect laboratory tests.
This article was published in the following journal.
Name: Discovery medicine
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A megaloblastic anemia occurring in children but more commonly in later life, characterized by histamine-fast achlorhydria, in which the laboratory and clinical manifestations are based on malabsorption of vitamin B 12 due to a failure of the gastric mucosa to secrete adequate and potent intrinsic factor. (Dorland, 27th ed)
Extracts of liver tissue containing uncharacterized specific factors with specific activities; a soluble thermostable fraction of mammalian liver is used in the treatment of pernicious anemia.
A glycoprotein secreted by the cells of the GASTRIC GLANDS that is required for the absorption of VITAMIN B 12 (cyanocobalamin). Deficiency of intrinsic factor leads to VITAMIN B 12 DEFICIENCY and ANEMIA, PERNICIOUS.
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Condition in which the plasma levels of homocysteine and related metabolites are elevated (>13.9 μmol/l). Hyperhomocysteinemia can be familial or acquired. Development of the acquired hyperhomocysteinemia is mostly associated with vitamins B and/or folate deficiency (e.g., PERNICIOUS ANEMIA, vitamin malabsorption). Familial hyperhomocysteinemia often results in a more severe elevation of total homocysteine and excretion into the urine, resulting in HOMOCYSTINURIA. Hyperhomocysteinemia is a risk factor for cardiovascular and neurodegenerative diseases, osteoporotic fractures and complications during pregnancy.
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