| 영문 | iron deficiency anemia | 한글 | 철결핍빈혈 |
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| 설명 | 적혈구의 기능은 산소를 운반하는데 있다. 적혈구 속에 산소와 결합을 하여 산소를 운반하는 혈색소라는 물질이 있다. 철은 이 혈색소의 중요한 부분을 이루는 것으로 철이 없으면 혈색소가 만들어질 수가 없다. 혈색소가 없으면 역시 적혈구도 만들어지지 않으므로 체내에 철이 부족하면 빈혈이 생긴다. 이 철결핍성 빈혈은 빈혈의 원인 중에서 가장 흔한 것이다(약 25%를 차지한다). 철저장량의 저하-결핍, 혈청철농도의 저하, 트란스페린량 상승, 트란스페린포화도의 저하, 혈색소농도 또는 헤마토크리트의 저하, 저색소성대적혈구를 특징으로 하는 빈혈로서, 생체 내에서 철이 장기에 걸쳐 결핍되며 그 때문에 혈색소 생산 감소에 의해 일어난다. 창자에서의 철흡수량 부족, 철의 수요 증대(유아기, 사춘기, 임신), 철소실과잉(출혈)에 의해 일어나며, 특히 사춘기에서 폐경기까지의 여성에게 많다. 증상으로서는 얼굴창백, 피로감, 피부창백, 손톱 변화(스푼 모양) 등을 나타낸다. 구강 영역에서는 혀의 접촉통, 발적, 건조감, 삼킴곤란을 수반하면 플러머-빈슨(Plummer-Vinson)증후군이라고 한다. 혈액 소견은 혈청철은 저하하며, 철결합능력의 상승, 저색소성 작은적혈구성을 나타낸다. |
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| MD | Doctor of Medicine [Lat. Medicinae Doctor]; magnesium deficiency; main duct; maintenance dose; major... |
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| GDH | glucose dehydrogenase; glutamate dehydrogenase; glycerophosphate dehydrogenase; glycol dehydrogenase... |
| LAD | lactic acid dehydrogenase; left anterior descending [artery]; left axis deviation; leukocyte adhesio... |
| IGD | idiopathic growth hormone deficiency; interglobal distance; isolated gonadotropin deficiency |
| MCD | magnetic circular dichroism; mast-cell degranulation; mean cell diameter; mean of consecutive differ... |
| G6PD | Glucose-6-Phosphate dehydrogenase deficiency |
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| ATD | 1-antitrypsin deficiency |
| AMD | Acid maltase deficiency |
| AIDS | Acquire Immune Deficiency Syndrome |
| AIDS | Acquired Immune Deficiency Disease Syndrome |
| glucose-6-phosphate dehydrogenase deficiency | A deficiency of glucose-6-phosphate dehydrogenase, an enzyme important for maintaining cellular concentrations of reduced nucleotides. Deficiency of this enzyme is the commonest disease-causing enzyme defect in humans affecting an estimated 400 million people. The gene for this enzyme is on the X chromosome and there are various polymorphic forms. Males with the enzyme deficiency develop haemolytic anaemia when red blood cells are exposed to oxidant drugs such as the antimalarial primaquine, the sulfonamide antibiotics or sulfones, naphthalene moth balls, or fava beans. It can also cause anaemia of the newborn, and chronic nonspherocytic haemolytic anaemia. Inheritance: X-linked. (12 Sep 2002) |
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| glucose-6-dehydrogenase deficiency | <biochemistry> An inherited condition that results in a deficiency in glucose-6-phosphate dehydrogenase. Particular drugs (sulphonamides) can exacerbate this problem. The result is haemolytic anaemia. (27 Sep 1997) |
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| glucosephosphate dehydrogenase deficiency | A disease-producing enzyme deficiency subject to many variants, some of which cause a deficiency of enzyme activity in erythrocytes, leading to haemolytic anaemia. (12 Dec 1998) |
| pyruvate dehydrogenase complex deficiency | An autosomal recessive pyruvate metabolism disorder resulting from deficient enzyme activity in one of several proteins of pyruvate dehydrogenase complex, resulting in deficiency of acetyl CoA. Deficiency in acetyl CoA product reduces the synthesis of acetylcholine, thereby causing neurological abnormalities. Clinical presentations include lactic acidosis, mental retardation, and ataxia. (12 Dec 1998) |
| deficiency, glucose-6-phosphate dehydrogenase | Deficiency of G6PD is the commonest disease-causing enzyme defect in humans affecting an estimated 400 million people. The G6PD gene is on the X chromosome. Males with the enzyme deficiency develop anaemia due to breakup of their red blood cells when they are exposed to oxidant drugs such as the antimalarial primaquine, the sulfonamide antibiotics or sulfones, naphthalene moth balls, or fava beans. (12 Dec 1998) |
| abdominal muscle deficiency syndrome | <syndrome> Congenital absence (partial or complete) of abdominal muscles, in which the outline of the intestines is visible through the protruding abdominal wall; in males, genitourinary anomalies (urinary tract dilation and cryptorchidism) are also found; genetics unclear. (05 Mar 2000) |
| adult lactase deficiency | Onset of lactase deficiency, with resulting milk intolerance and malabsorption, in adulthood. Inherited forms may not be manifested until adulthood; any process that damages the intestinal lining cells can cause lactase deficiency in adults. (05 Mar 2000) |
| alpha-1 antitrypsin deficiency | <chest medicine> Deficiency of the protease inhibitor alpha-1 antitrypsin, leads primarily to degradation of elastin of the alveolar walls, as well as other structural proteins of a variety of tissues. The lack of this protein leads to damage of various organs, but mainly to the lung and liver. symptoms may become apparent at a very early age or in adulthood, manifesting either as shortness of breath or liver related symptoms (jaundice, fatigue, fluid in the abdomen, mental changes, or gastrointestinal bleeding). There are several options for treatment of the lung disease, including replacement of the missing protein. Treatment of the liver disease is a well-timed liver transplant (12 Dec 1998) |
| alpha-1-proteinase deficiency | Absence of a serum proteinase inhibitor that may cause nodular non-suppurative panniculitis. (05 Mar 2000) |
| alpha-antitrypsin deficiency | <enzyme> A specific enzyme (alpha 1 antitrypsinase) that when absent genetically can result in panacinar emphysema (lung disease) and liver disease. There is no specific treatment for this condition other than supportive care for the liver and lung complications. Medications such as alpha-1proteinase inhibitor is given regularly to these patients. Incidence: approximately 1 in 10,000. (02 Jan 1998) |
| anaemia, iron deficiency | Deficiency of iron results in anaemia because iron is necessary to make haemoglobin, the key molecule in red blood cells responsible for the transport of oxygen. In iron deficiency anaemia, the red cells are unusally small (microcytic) and pale (hypochromic). Characteristic features of iron deficiency anaemia in children include failure to thrive (grow) and increased infections. The treatment of iron deficiency anaemia, whether it be in children or adults, is with iron and iron-containing foods. Food sources of iron include meat, poultry, eggs, vegetables and cereals (especially those fortified with iron). According to the National Academy of Sciences, the Recommended Dietary Allowances of iron are 15 milligrams per day for women and 10 milligrams per day for men. Anaemia characterised by low or absent iron stores, low serum iron concentration, elevated free erythrocyte porphorin, low transferrin saturation, elevated transferrin, low serum ferritin, low haemoglobin concentration or haematocrit, and hypochromic microcytic red blood cells. Symptoms may include pallor, angular stomatitis and other oral lesions, gastrointestinal complaints, retinal haemorrhages and exudates, and thinning and brittleness of the nails. Among the causes of iron-deficiency anaemia are inadequate iron intake, impaired iron absorption, increased blood loss and increased requirements such as infancy, pregnancy, and lactation. (12 Dec 1998) |
| antibody deficiency disease | <syndrome> Any of a group of disorders associated with a defective antibody production due to defects in the B-type lymphocyte system or in T-type lymphocytes; chief manifestation is an increased susceptibility to infection by various microorganisms. See: agammaglobulinaemia, hypogammaglobulinaemia, immunodeficiency. Synonym: antibody deficiency disease. (05 Mar 2000) |
| antibody deficiency syndrome | <syndrome> Any of a group of disorders associated with a defective antibody production due to defects in the B-type lymphocyte system or in T-type lymphocytes; chief manifestation is an increased susceptibility to infection by various microorganisms. See: agammaglobulinaemia, hypogammaglobulinaemia, immunodeficiency. Synonym: antibody deficiency disease. (05 Mar 2000) |
| antitrypsin deficiency | Deficiency of a1-antitrypsin, a glycoprotein of the postalbumin region of human serum. Many forms are known which may be moderate (40 to 60% of normal activity) or severe (less than 10% of normal), all autosomal dominant; the severe form is often associated with familial emphysema or hepatic cirrhosis. (05 Mar 2000) |
| arch length deficiency | The difference between the available circumference of the dental arch and that required to accommodate the succedaneous teeth in proper alignment. (05 Mar 2000) |
| arginase deficiency | <biochemistry> Arginase is the fifth enzyme of the urea cycle and catalyses the hydrolysis of arginine to ornithine and urea as the final step in the detoxification of ammonia. Deficiency of the enzyme results in hyperargininaemia and episodic hyperammonaemia, leading to moderate to severe mental retardation and spasticity. at least two isozymes of arginase exist in man. AI (the enzyme deficient in the disorder) is cytosolic and found primarily in liver and red blood cells, whereas AII is mitochondrial and found predominantly in kidney but also to a lesser extent in liver, brain, and other tissues. While AII activity appears to be induced in AI deficiency, it is only partially effective in maintaining urea cycle function. The normal in vivo function of AII is unclear. Arginase deficiency is diagnosed by observing high arginine concentrations on either qualitative or quantitative plasma or urine amino acid analysis. The diagnosis is confirmed by finding markedly decreased or absent arginase activity in an isotopic red blood cell enzymatic assay. The AI gene has been cloned, sequenced, and localised to human chromosome band 6q23. (17 Dec 1997) |
| glucose-6-phosphate dehydrogenase deficiency |
a deficiency of an enzyme - G6PD - in red blood cells, causing hemolytic anemia.
출처: www.uchospitals.edu/online-library/content=P00090
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제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
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제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
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