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Pernicious anemia refers to anemia that results from lack of intrinsic factor. Lack of intrinsic factor is most commonly due to an autoimmune attack on the cells that create it in the stomach. It can also occur following the surgical removal of part of the stomach or from an inherited disorder.
From Simple English Wikipedia, the free encyclopedia Pernicious anemia is a medical problem that causes a person to have too few red blood cells (anemia) because their intestines cannot absorb vitamin B12 properly. A special protein, called intrinsic factor, helps the body get vitamin B12 from food such as meat, poultry and dairy foods.
Pernicious anemia is caused by a lack of intrinsic factor, which is required to absorb vitamin B 12 from food. A lack of intrinsic factor may arise from an autoimmune condition targeting the parietal cells (atrophic gastritis) that produce intrinsic factor or against intrinsic factor itself. These lead to poor absorption of vitamin B 12.
The page currently states Pernicious anemia is a caused by autoimmunity. I suggest this is not true. Pernicious anemia is caused by B12 deficiency, yes, but not necessarily because the immune system has attacked parietal cells or has produced anti-bodies to intrinsic factor. Mosby's Understanding Pathophysiology says:
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Vitamin B12 deficiency can lead to anemia and neurological disorders. A mild deficiency may not cause any discernible symptoms, but as the deficiency becomes more significant, symptoms of anemia may result, such as weakness, fatigue, light-headedness, rapid heartbeat, rapid breathing and pale color to the skin. It may also cause easy bruising or bleeding, including bleeding gums, gastrointestinal side effects including sore tongue, stomach upset, weight loss, and diarrhea or constipation. If the deficiency is not corrected, nerve cell damage can result. If this happens, vitamin B12 deficiency may result in tingling or numbness to the fingers and toes, difficulty walking, mood changes, depression, memory loss, disorientation and, in severe cases, dementia. Tissue deficiency resulting in negative effects in nerve cells, bone marrow, and the skin. The main type of vitamin B 12 deficiency anemia is pernicious anemia. It is characterized by a triad of symptoms: 1. Anemia with bone marrow...
Inadequate dietary intake of animal products such as eggs, meat, milk, fish, fowl (and some type of edible algae) can result in a deficiency state. Vegans, and to a lesser degree vegetarians, are at risk for B12 deficiency if they do not consume either a dietary supplement or vitamin-fortified foods. Children are at a higher risk for B12deficiency due to inadequate dietary intake, as they have fewer vitamin stores and a relatively larger vitamin need per calorie of food intake.
1. Selective impaired absorption of vitamin B12 due to intrinsic factor deficiency. This may be caused by the loss of gastric parietal cells in chronic atrophic gastritis (in which case, the resulting megaloblastic anemia takes the name of "pernicious anemia"), or may result from wide surgical resection of stomach (for any reason), or from rare hereditary causes of impaired synthesis of intrinsic factor. B12deficiency is more common in the elderly because gastric intrinsic factor, necessary f...
Increased needs by the body can occur due to AIDS and hemolysis(the breakdown of red blood cells), which stimulates increased red cell production.
The total amount of vitamin B12 stored in the body is between two and five milligrams in adults. Approximately 50% is stored in the liver, but approximately 0.1% is lost each day, due to secretions into the gut—not all of the vitamin in the gut is reabsorbed. While bile is the main vehicle for B12 excretion, most of this is recycled via enterohepatic circulation. Due to the extreme efficiency of this mechanism, the liver can store three to five years worth of vitamin B12 under normal conditio...
Vitamin B12deficiency causes particular changes to the metabolism of two clinically relevant substances in humans: 1. Homocysteine (homocysteine to methionine, catalysed by methionine synthase) leading to hyperhomocysteinemia 2. Methylmalonic acid(methylmalonyl-CoA to succinyl-CoA, of which methylmalonyl-CoA is made from methylmalonic acid in a preceding reaction) Methionine is activated to S-adenosyl methionine, which aids in purine and thymidine synthesis, myelin production, protein/neurotr...
Early changes include a spongiform state of neural tissue, along with edema of fibers and deficiency of tissue. The myelin decays, along with axial fiber. In later phases, fibric sclerosis of nervous tissues occurs. Those changes occur in dorsal parts of the spinal cord and to pyramidal tracts in lateral cords and is called subacute combined degeneration of spinal cord.Pathological changes can be noticed as well in the posterior roots of the cord and, to lesser extent, in peripheral nerves. I...
The diagnosis is frequently first suspected when a routine complete blood count shows anemia with an elevated MCV. In addition, on the peripheral blood smear, macrocytes and hypersegmented polymorphonuclear leukocytesmay be seen. Diagnosis is typically confirmed based on vitamin B12 blood levels below 120–180 pmol/L (170–250 pg/mL) in adults. Elevated serum homocysteine (over 12 μmol/L) and methylmalonic acid (over 0.4 micromol/L) levels are considered more reliable indicators of B12 deficiency than the concentration of B12 in blood. If nervous system damage is present and blood testing is inconclusive, a lumbar puncture to measure cerebrospinal fluid B-12 levels may be done. On bone marrow aspiration or biopsy, megaloblasts are seen. The Schilling test was a radio-isotope method, now outdated, of testing for low vitamin B12.
B12 can be supplemented by pill or injection and appears to be equally effective in those with low levels due to deficient absorption of B12. When large doses are given by mouth its absorption does not rely on the presence of intrinsic factor or an intact ileum. Instead, these large-dose supplements result in 1% to 5% absorption along the entire intestine by passive diffusion. Generally 1 to 2 mg daily is required as a large dose. Even pernicious anemia can be treated entirely by the oral route.
Vitamin B12deficiency is common and occurs worldwide. In the US and UK, around 6 percent of the general population have the deficiency; in those over the age of sixty, around 20 percent are deficient. In under-developed countries, the rates are even higher: across Latin America 40 percent are deficient; in some parts of Africa, 70 percent; and in some parts of India, 70 to 80 percent.
Between 1849 and 1887, Thomas Addison described a case of pernicious anemia, William Osler and William Gardner first described a case of neuropathy, Hayem described large red cells in the peripheral blood in this condition, which he called "giant blood corpuscles" (now called macrocytes), Paul Ehrlich identified megaloblasts in the bone marrow, and Ludwig Lichtheim described a case of myelopathy. During the 1920s, George Whipple discovered that ingesting large amounts of liver seemed to most rapidly cure the anemia of blood loss in dogs, and hypothesized that eating liver might treat pernicious anemia. Edwin Cohn prepared a liver extract that was 50 to 100 times more potent in treating pernicious anemia than the natural liver products. William Castle demonstrated that gastric juice contained an "intrinsic factor" which when combined with meat ingestion resulted in absorption of the vitamin in this condition. In 1934, George Whipple shared the 1934 Nobel Prize in Physiology or Medici...
Ruminants, such as cows and sheep, absorb B12 synthesized by their gut bacteria. Sufficient amounts of cobalt and copper need to be consumed for this B12synthesis to occur. In the early 20th century, during the development for farming of the North Island Volcanic Plateau of New Zealand, cattle suffered from what was termed "bush sickness". It was discovered in 1934 that the volcanic soils lacked the cobalt salts essential for synthesis of vitamin B12 by their gut bacteria. The "coast disease" of sheep in the coastal sand dunes of South Australia in the 1930s was found to originate in nutritional deficiencies of the trace elements, cobalt and copper. The cobalt deficiency was overcome by the development of "cobalt bullets", dense pellets of cobalt oxide mixed with clay given orally, which then was retained in the animal's rumen.Greer JP (2014). Wintrobe's Clinical Hematology Thirteenth Edition. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins. ISBN 978-1-4511-7268-3.Chapter 36: Megaloblastic anemias: disorde...Hunt, A.; Harrington, D.; Robinson, S. (4 September 2014). "Vitamin B12 deficiency". BMJ. 349. g5226. doi:10.1136/bmj.g5226. PMID 25189324.Pacholok SM, Stuart JJ (2011). Could It Be B12?: An Epidemic of Misdiagnoses. Fresno, CA: Linden Publishing. ISBN 978-1-61035-065-5.Hooper M (2012). Pernicious Anaemia: The Forgotten Disease – the causes and consequences of Vitamin B12 Deficiency. London: Hammersmith Press. ISBN 978-1-78161-004-6.Vitamin B12 and Folate at Lab Tests Online
維生素 B12 缺乏貧血 （英語： Vitamin B12 deficiency anemia ），是指因缺乏 維生素B 12 造成 紅血球 不足的疾病 ，惡性貧血（英語： Pernicious anemia ）是造成維生素 B 12 缺乏的原因之一 。. 最常見的發病症狀是疲倦 ，其他症狀有 呼吸困難 、皮膚蒼白、胸痛、手腳麻木 ...
Details: Pernicious anemia (per-NISH-us uh-NEE-me-uh) is a condition in which the body can't make enough healthy red blood cells because it doesn't have enough vitamin B12. Vitamin B12 is a nutrient found in some foods. The body needs this nutrient to make healthy red blood cells and to keep its nervous causes of pernicious anemia
In patients with pernicious anemia or with deficiency due to impaired absorption, less than 10% of the radiolabeled vitamin B 12 is detected. The normal test will result in a higher amount of the radiolabeled cobalamin in the urine because it would have been absorbed by the intestinal epithelium, but passed into the urine because all hepatic ...
In pernicious anemia, which is usually an autoimmune disease, autoantibodies directed against intrinsic factor or parietal cells themselves lead to an intrinsic factor deficiency, malabsorption of vitamin B 12, and subsequent megaloblastic anemia.
Definition Pernicious anemia is a disease in which the red blood cells are abnormally formed, due to an inability to absorb vitamin B 12. True pernicious anemia refers specifically to a disorder of atrophied parietal cells leading to absent intrinsic factor, resulting in an inability to absorb B 12.
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