Pernicious anemia (also known as Biermer's anemia, Addison's anemia, or Addison–Biermer anemia) is one of many types of the larger family of megaloblastic anemias. It is caused by loss of gastric parietal cells which are responsible, in part, for the secretion of intrinsic factor, a protein essential for subsequent absorption of vitamin B12 in the ileum.
Usually seated in an atrophic gastritis, the autoimmune destruction of gastric parietal cells (and autoantibody inactivation of intrinsic factor) leads to a lack of intrinsic factor. Since the absorption from the gut of normal dietary amounts of vitamin B12 is dependent on intrinsic factor, the loss of intrinsic factor leads to vitamin B12 deficiency. While the term 'pernicious anemia' is sometimes also incorrectly used to indicate megaloblastic anemia due to 'any' cause of vitamin B12 deficiency, its proper usage refers to that caused by atrophic gastritis, parietal cell loss, and lack of intrinsic factor only.
The loss of ability to absorb vitamin B12 (B12) is the most common cause of adult B12 deficiency. Such a loss may be due to pernicious anemia (with loss of intrinsic factor) or to a number of other conditions that decrease production of gastric acid, which also plays a part in absorption of B12 from foods.
Historically, pernicious anemia (PA) was detected only after it became "clinical" (caused an overt disease state) and the anemia was well established, i.e., liver stores of B12 had been depleted. The "pernicious" aspect of the disease - prior to the discovery of treatment - was its invariably fatal prognosis, similar to leukemia at that time. However, in the time since elucidation of the cause of the disease, modern tests that specifically target B12 absorption can be used to diagnose the disease before it becomes clinically apparent. In such cases, the disease may be diagnosed and treated without the patient ever becoming ill.
Replacement of vitamin stores does not correct the defect in absorption from loss of intrinsic factor. Since the defect defines the disease, a person without the ability to absorb B12 in this way will have pernicious anemia for the remainder of his or her life. However, unless the patient has sustained permanent peripheral nerve damage before treatment, regular B12 replacement will keep PA in check, with no anemia and no further symptoms.
Although initial treatment of the disease usually involves injections of B12 to rapidly replace body stores, a number of studies have shown long-term vitamin replacement treatment may be maintained with high-dose oral B12 supplements, since sufficient B12 is absorbed from these by a normal intestine, even without any intrinsic factor. In this regard, nasal and sublingual forms of B12 have not been found to have any special value over simple swallowed tablets.
Other articles related to "pernicious anemia, anemia":
... folate deficiency symptoms, since they include all the effects of pernicious anemia and megaloblastosis, which are due to poor synthesis of DNA when the body does not have a proper supply ... The failure of blood cell production results in the once-dreaded and fatal disease, pernicious anemia ... All of the DNA synthetic effects, including the megaloblastic anemia of pernicious anemia, resolve if sufficient folate is present (since levels of 5,10-methylene-THF still remain adequate ...
... Biermer is remembered for his 1872 description of a disorder he called "progressive pernicious anemia" ... He called it "pernicious anemia" because of the disease's insidious course, and because it was deemed to be untreatable at the time ... Historically, pernicious anemia has also been called "Addison-Biermer disease" ...
... Ten Boom suffered with a special case of pernicious anemia that started in her early childhood, called congenital (or juvenile) pernicious anemia ...
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