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Megaloblastic anemia : ウィキペディア英語版
Megaloblastic anemia

Megaloblastic anemia (or megaloblastic anaemia) is an anemia (of macrocytic classification) that results from inhibition of DNA synthesis during red blood cell production. When DNA synthesis is impaired, the cell cycle cannot progress from the G2 growth stage to the mitosis (M) stage. This leads to continuing cell growth without division, which presents as macrocytosis.
Megaloblastic anemia has a rather slow onset, especially when compared to that of other anemias.
The defect in red cell DNA synthesis is most often due to hypovitaminosis, specifically a deficiency of and/or folic acid. alone will not cause the syndrome in the presence of sufficient folate, as the mechanism is loss of B dependent folate recycling, followed by folate-deficiency loss of nucleic acid synthesis (specifically thymine), leading to defects in DNA synthesis. Folic acid supplementation in the absence of vitamin B prevents this type of anemia (although other vitamin B-specific pathologies may be present). Loss of micronutrients may also be a cause. Copper deficiency resulting from an excess of zinc from unusually high oral consumption of zinc-containing denture-fixation creams has been found to be a cause.
Megaloblastic anemia not due to hypovitaminosis may be caused by antimetabolites that poison DNA production directly, such as some chemotherapeutic or antimicrobial agents (for example azathioprine or trimethoprim).
The pathological state of megaloblastosis is characterized by many large immature and dysfunctional red blood cells (megaloblasts) in the bone marrow〔(【引用サイトリンク】title=Megaloblastic (Pernicious) Anemia - Lucile Packard Children's Hospital )〕 and also by hypersegmented neutrophils (those exhibiting five or more nuclear lobes ("segments"), with up to four lobes being normal). These hypersegmented neutrophils are found in the "peripheral blood" (i.e., a diagnostic smear of a blood-sample taken from the circulation).
==Causes==

* Vitamin B12 deficiency leading to folate deficiency:
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* Achlorhydria-induced malabsorption
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* Deficient intake
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* Deficient intrinsic factor, a molecule produced by cells in the stomach that is required for B12 absorption (pernicious anemia or gastrectomy)
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* Coeliac disease
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* Biological competition for vitamin B12 by diverticulosis, fistula, intestinal anastomosis, or infection by the marine parasite ''Diphyllobothrium latum (fish tapeworm)''
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* Selective vitamin B12 malabsorption (congenital—juvenile megaloblastic anemia 1—and drug-induced)
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* Chronic pancreatitis
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* Ileal resection and bypass
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* Nitrous oxide anesthesia (usually requires repeated instances).
* Folate deficiency:
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* Alcoholism
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* Deficient intake
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* Increased needs: pregnancy, infant, rapid cellular proliferation, and cirrhosis
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* Malabsorption (congenital and drug-induced)
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* Intestinal and jejunal resection
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* (indirect) Deficient thiamine and factors (e.g., enzymes) responsible for folate metabolism.
* Combined Deficiency: vitamin B12 & folate.
* Inherited Pyrimidine Synthesis Disorders: Orotic aciduria
* Inherited DNA Synthesis Disorders
* Toxins and Drugs:
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* Folic acid antagonists (methotrexate)
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* Purine synthesis antagonists (6-mercaptopurine)
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* Pyrimidine antagonists (cytosine arabinoside)
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* Phenytoin
*
* Nitrous Oxide
* Erythroleukemia

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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