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Pernicious anemia; Other names: Vitamin B 12 deficiency anemia, Biermer's anemia, [1] Addison's anemia, [2] Addison–Biermer anemia [3] Micrograph showing nodular enterochromaffin-like cell hyperplasia, as demonstrated with chromogranin A immunostaining, in the body of the stomach. Parietal cells are not readily apparent.
In researching pernicious anemia, Addison in 1849 came across the changed "bronzed" appearance of the adrenal glands. [10] What is now called Addison's disease, sometimes called bronze skin disease, is the progressive destruction of the glands, resulting in adrenocortical hormone deficiency.
Skin coloration was of particular importance, as it was the only clinical feature distinguishing Addison's disease of the adrenals from another "Addison's disease" (described by the same author six years earlier, in 1849), [10] which corresponded to a hematological condition better known today as pernicious anemia and by its other eponymous ...
Pernicious anemia is the most common cause of vitamin B 12 deficiency anemia in adults, which results from malabsorption of vitamin B 12 due to a lack or loss of intrinsic factor. [2] [8] There are relatively few studies which have assessed the impact of haematological measures in response to B 12 supplementation.
The frequency rate of Addison's disease in the human population is sometimes estimated at one in 100,000. [39] Some put the number closer to 40–144 cases per million population (1/25,000–1/7,000). [1] [40] [41] Addison's can affect persons of any age, sex, or ethnicity, but it typically presents in adults between 30 and 50 years of age.
Autoimmune hemolytic anemia: Anti-red blood cell antibodies Confirmed 1-3 per 100,000 [89] Immune thrombocytopenia: Anti-platelet antibodies Confirmed 3.3 per 100,000 (adults), 50 per 100,000 (children) [90] Thrombotic thrombocytopenic purpura: ADAMTS13 autoantibodies Confirmed 1-2 per million [91] Antiphospholipid syndrome: Antiphospholipid ...
He called it "pernicious anemia" because of the disease's insidious course, and because it was deemed to be untreatable at the time. In 1849, Thomas Addison described the same disease, however Biermer's description was much more comprehensive. Historically, pernicious anemia has also been called "Addison-Biermer disease".
Megaloblastic anemia (MA) is associated with GSE and is believed to be the result of B 12 and folate deficiency. [23] In GSE, it appears to be associated with the IgA-less phenotype. [24] Unlike other forms of megaloblastic anemia, GSEA MA is not a form of autoimmune gastritis. [25] Pernicious anemia (PA).