| ¿µ¹® | hemolytic anemia | ÇÑ±Û | ¿ëÇ÷ºóÇ÷ |
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| ¼³¸í | ¿ëÇ÷ºóÇ÷À̶õ ÀûÇ÷±¸ÀÇ °úµµÇÑ ÆÄ±«¿¡ ÀÇÇÑ ºóÇ÷ÀÌ´Ù. ¿ø·¡ 120ÀÏ Á¤µµÀÇ ¼ö¸íÀ» °¡Áö´Â ÀûÇ÷±¸ÀÇ ¼ö¸íÀÌ Âª¾ÆÁö´Â °ÍÀÌ´Ù. ¿©±â¿¡´Â ¿©·¯ °¡Áö ¿øÀÎÀÌ ÀÖÀ» ¼ö°¡ Àִµ¥ ´ëÇ¥ÀûÀÎ ¿øÀÎÀ¸·Î´Â ÀûÇ÷±¸¿¡ ´ëÇÑ Ç×ü°¡ »ý±â´Â °Í(¹ßÀÛ¼º¾ß°£Ç÷»ö¼Ò´¢Áõ)°ú ÀûÇ÷±¸ÀÚüÀÇ ÀÌ»ó(À¯Àü¼ºµÕ±ÙÀûÇ÷±¸Áõ), ±×¸®°í ´Ù¸¥ Áúº´¿¡ ÀÇÇØ¼ 2Â÷ÀûÀ¸·Î »ý±â´Â °ÍÀÌ ÀÖ´Ù. |
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| ¿µ¹® | hemolytic disease of newborn | ÇÑ±Û | ½Å»ý¾Æ¿ëÇ÷º´ |
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| ¼³¸í | ½Å»ý¾Æ¿¡¼ ÀûÇ÷±¸°¡ ºñÁ¤»óÀûÀ¸·Î ¸¹ÀÌ ÆÄ±«µÇ´Â º´À¸·Î žÆÀû¸ð±¸Áõ(erythroblastosis fetalis)¿Í °°Àº ¶æÀ¸·Î ¾²ÀδÙ. À̰ÍÀº ¾î¸Ó´Ï¿¡°Ô¼ »ý»êµÈ ½Å»ý¾Æ³ª žÆÀÇ ÀûÇ÷±¸¿¡ ´ëÇÑ Ç×ü°¡ ŹÝÀ» °Ç³Ê¿Í¼ žÆÀÇ ÀûÇ÷±¸¿Í °áÇÕÇÏ¿©¼ »ý±â´Â ¿ëÇ÷¼ººóÇ÷À» À̸£´Â ¸». Áï ½Å»ý¾Æ³ª žÆÀÇ ÀûÇ÷±¸ÀÇ Ç×ü°¡ ¾î¸Ó´ÏÀÇ ¸ö¿¡¼ »ý»êÀÌ µÇ°í À̰ÍÀÌ Å¹ÝÀ» ÅëÇØ¼ žƿ¡°Ô ³Ñ¾î°¡¼ žÆÀÇ ÀûÇ÷±¸¿Í °áÇÕÀ» Çϰí ÀÌ Ç×ü¿Í °áÇÕÇÑ ÀûÇ÷±¸´Â ÆÄ±«°¡ µÇ¾î¼ ºóÇ÷ÀÌ »ý±ä °ÍÀ» žÆÀû¸ð±¸ÁõÀ̶ó°í ÇÑ´Ù. À̰ÍÀº Rh Àû¸ð±¸Áõ(Rh erythroblastosis)¿Í ABO Àû¸ð±¸Áõ(ABO erythroblastosis)·Î ³ª´ ¼ö°¡ ÀÖ´Ù. |
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| ¿µ¹® | anemia | ÇÑ±Û | ºóÇ÷ |
|---|---|---|---|
| ¼³¸í | Ç÷¾×ÀÌ ¼øÈ¯ÇÏ´Â ¸ñÀû Áß¿¡¼ °¡Àå Áß¿äÇÑ °ÍÀº ¿©·¯ °¡Áö ¿µ¾ç¼Ò¸¦ ¸»ÃÊÀÇ Àå±â·Î º¸±ÞÇÏ°í ¸»ÃÊÀÇ Àå±â¿¡¼ ³ª¿À´Â ¿©·¯ ³ëÆó¹°À» ÄáÆÏÀ̳ª Æó·Î º¸³» ¹è¼³¹°À» ó¸®ÇÏ´Â µ¥ ÀÖ´Ù. ±× Áß¿¡¼ »ê¼ÒÀÇ ¿î¹ÝÀº °¡Àå Áß¿äÇѵ¥ ¹Ù·Î ÀÌ »ê¼ÒÀÇ ¿î¹ÝÀ» ´ã´çÇÏ´Â °ÍÀÌ ÀûÇ÷±¸ÀÌ´Ù. ÀûÇ÷±¸¿¡´Â Ç÷»ö¼Ò¶ó´Â ¹°ÁúÀÌ ÀÖ¾î À̰ÍÀÌ »ê¼Ò¿Í °áÇÕÇÏ¿© »ê¼Ò¸¦ ¸»ÃÊÀÇ Àå±â·Î ¿î¹ÝÇÒ ¼ö°¡ ÀÖ´Ù. ºóÇ÷À̶õ ´ÜÀ§ºÎÇÇÀÇ Ç÷¾×¼Ó¿¡ ÀûÇ÷±¸ÀÇ ¾çÀÌ ÀûÀº °æ¿ì¸¦ ¸»ÇÑ´Ù. ÀûÇ÷±¸ÀÇ ¾çÀ» ³ªÅ¸³»´Â °ÍÀ¸·Î´Â 3°¡Áö ¹æ¹ýÀÌ ÀÖ´Ù. ÀûÇ÷±¸ÀÇ ¼ýÀÚ¸¦ Á÷Á¢ Ç¥ÇöÇÏ´Â ¹æ¹ý°ú, Ç÷»ö¼ÒÀÇ ¾çÀ» Á¤·®ÇÏ¿© ±× ¾çÀ» Ç¥½ÃÇÏ´Â ¹æ¹ý°ú, Ç÷¾×¼Ó¿¡¼ ÀûÇ÷±¸°¡ Â÷ÁöÇÏ´Â ¾ç(ÀûÇ÷±¸µîÀûÀ²)À» ³ªÅ¸³»´Â ¹æ¹ýÀÌ ±×°ÍÀÌ´Ù. ´ë°³ ºóÇ÷À̶ó ÇÔÀº ³²¼º¿¡¼ Ç÷»ö¼Ò < 14g/dl, Ç÷»ö¼Ò < 42%, ÀûÇ÷±¸ÀÇ ¼ö < 4,000,000/mm3ÀÏ °æ¿ìÀ̰í, ¿©¼º¿¡¼± Ç÷»ö¼Ò < 12g/dl, Ç÷»ö¼Ò < 36%, ÀûÇ÷±¸ÀÇ ¼ö < 3,300,000/mm3ÀÏ °æ¿ì¸¦ ÁöĪÇÑ´Ù. |
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| ¿µ¹® | pernicious anemia | ÇÑ±Û | ¾Ç¼ººóÇ÷ |
|---|---|---|---|
| ¼³¸í | ¾Ç¼º(»ý¸íÀ» À§ÇùÇϸç, Ä¡·á¿¡ ÀúÇ×ÇÏ´Â °æ¿ì¿¡ ´ë°³ ¾Ç¼ºÀ̶ó ºÎ¸§. ¿¹¸¦ µé¾î ÁøÇàµÈ ¾ÏÀÇ °æ¿ì)À̶ó À̸§ºÙ¾î ÀÖÁö¸¸, ½ÇÁ¦ÀûÀ¸·Î´Â ¾Ç¼ºÀÌ ¾Æ´Ï´Ù. ºóÇ÷ÀÇ ÀÏÁ¾ÀÌ´Ù. Á¤»óÀûÀ¸·Î ÀûÇ÷±¸´Â ¹ß´Þ°ú ¼º¼÷°úÁ¤¿¡¼ ºñŸ¹Î B12°¡ ÇʼöÀûÀÌ´Ù. ÀÌ ºñŸ¹Î B12ÀÇ Ç÷Áß³óµµ°¨¼Ò¿¡ ÀÇÇØ ÀûÇ÷±¸»ý¼º¿¡ ÁöÀåÀ» °¡Á®¿À°Ô µÇ°í, Ç÷¾×³»¿¡ Ư¡ÀûÀÎ °Å´ëÀû¸ð±¸(megaloblast)ÀÇ Çü¼ºÀÌ ³ªÅ¸³ª´Â Áúº´À» ¸»ÇÑ´Ù. |
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| ¿µ¹® | aplastic anemia | ÇÑ±Û | Àç»ýºÒ·®ºóÇ÷ |
|---|---|---|---|
| ¼³¸í | Àç»ýºÒ·®¼º ºóÇ÷À̶õ °ñ¼öÀÇ ÀÌ»óÀ¸·Î »ý±â´Â ºóÇ÷ÀÌ´Ù. °ñ¼ö¶õ »À¼Ó¿¡ Á¸ÀçÇÏ´Â °ÍÀ¸·Î Ç÷±¸¸¦ »ý¼ºÇÏ´Â ¼¼Æ÷µé°ú ¹Ì¼º¼÷ÇÑ Ç÷±¸µé·Î ÀÌ·ç¾îÁ® ÀÖ´Ù. À̰͵éÀÌ ¿©·¯ °¡Áö ¿øÀο¡ ÀÇÇØ¼ ÆÄ±«µÇ¾úÀ» ¶§ »ý±â´Â ºóÇ÷À» Àç»ýºÒ·®ºóÇ÷À̶ó°í ÇÑ´Ù. ±×·¯¹Ç·Î ÀûÇ÷±¸¸¸ÀÇ °¨¼Ò°¡ ¾Æ´Ï¶ó ¸ðµç Ç÷±¸ ¼¼Æ÷ÀÇ °¨¼Ò¸¦ º¼ ¼ö ÀÖ´Ù. Ä¡·á·Î´Â Ç÷±¸ »ý¼ºÀ» ÀÚ±ØÇϴ ȣ¸£¸óÀ» Åõ¿©ÇÏ´Â °ÍÀÌ ÀÖÁö¸¸ À̰ÍÀ¸·Î´Â ÆÄ±«µÈ Ç÷±¸¸¦ »ý¼ºÇÏ´Â ¼¼Æ÷ÀÇ Àç»ýÀÌ ÀϾÁö ¸øÇϹǷΠ¿ÏÀüÇÑ Ä¡·á¶ó°í´Â º¼ ¼ö°¡ ¾ø´Ù. ¿ÏÀüÇÑ Ä¡·á·Î´Â ³²ÀÇ °ñ¼ö¸¦ äÃëÇØ¼ À̰Ϳ¡¼ºÎÅÍ Ç÷±¸¸¦ »ý¼ºÇÏ´Â ¼¼Æ÷¸¦ ºÐ¸®, ȯÀÚ¿¡°Ô À̽ÄÇÏ´Â °ñ¼öÀ̽ÄÀÌ ÀÖ´Ù. |
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| AHA | acetohydroxamic acid; acquired hemolytic anemia; acute hemolytic anemia; American Heart Association;... |
|---|---|
| HNSHA | hereditary nonspherocytic hemolytic anemia |
| CNSHA | congenital nonspherocytic hemolytic anemia |
| MHD | maintenance hemodialysis; mean hemolytic dose; mental health department; minimum hemolytic dilution;... |
| CNHD | congenital nonspherocytic hemolytic disease |
| MAHA | Microangiopathic hemolytic anemia |
|---|---|
| BHS | Beta-hemolytic streptococci |
| CH 50 | Complement hemolytic activity |
| DHTR | Delayed hemolytic transfusion reaction |
| GABHS | Group A beta hemolytic streptococcal |
| anaemia, haemolytic, congenital nonspherocytic | Any one of a group of congenital haemolytic anaemias in which there is no abnormal haemoglobin or spherocytosis and in which there is a defect of glycolysis in the erythrocyte. In some cases, pyruvate kinase deficiency has been demonstrated; in other cases, glucose-6-phosphate dehydrogenase deficiency has been demonstrated. (12 Dec 1998) |
|---|---|
| anemia | <haematology> Too few red blood cells in the bloodstream, resulting in insufficient oxygen to tissues and organs. Origin: Gr. Haima = blood (16 Dec 1997) |
| hemolytic anaemia | <disease, haematology> Anaemia resulting from reduced red cell survival time and haemolysis, either due to an intrinsic defect in the erythrocyte (hereditary spherocytosis or ellipsocytosis, enzyme defects, haemoglobinopathy) or an extrinsic damaging agent. For example autoantibody (autoimmune haemolytic anaemia), iso antibody, parasitic invasion of the cells (malaria), bacterial or chemical haemolysins, mechanical damage to erythrocytes. Origin: Gr. Haima = blood (18 Nov 1997) |
| Albright's hereditary osteodystrophy | An inherited form of hyperparathyroidism associated with ectopic calcification and ossification and skeletal defects, notably the small fourth metacarpals, but intelligence is normal. There are dominant, recessive and X-linked forms. See: pseudohypoparathyroidism. Synonym: Albright's syndrome. (05 Mar 2000) |
| angioedema, hereditary | A genetic form of angioedema. (Angioedema is also referred to as Quinke's disease.) Persons with it are born lacking an inhibitor protein (called C1 esterase inhibitor) that normally prevents activation of a cascade of proteins leading to the swelling of angioedema. Patients can develop recurrent attacks of swollen tissues, pain in the abdomen, and swelling of the voice box (larynx) which can compromise breathing. The diagnosis is suspected with a history of recurrent angioedema. It is confirmed by finding abnormally low levels of C1 esterase inhibitor in the blood. Treatment options include antihistamines and male steroids (androgens) that can also prevent the recurrent attacks. Also called hereditary angioneurotic oedema. (12 Dec 1998) |
| angioneurotic oedema, hereditary | A genetic form of angioedema. (Angioedema is also referred to as Quinke's disease.) Persons with it are born lacking an inhibitor protein (called C1 esterase inhibitor) that normally prevents activation of a cascade of proteins leading to the swelling of angioedema. Patients can develop recurrent attacks of swollen tissues, pain in the abdomen, and swelling of the voice box (larynx) which can compromise breathing. The diagnosis is suspected with a history of recurrent angioedema. It is confirmed by finding abnormally low levels of C1 esterase inhibitor in the blood. Treatment options include antihistamines and male steroids (androgens) that can also prevent the recurrent attacks. Also called hereditary angioedema. (12 Dec 1998) |
| canine hereditary blindness | An autosomal dominant condition seen in dogs of the collie and several other breeds. (05 Mar 2000) |
| colourectal neoplasms, hereditary nonpolyposis | A syndrome characterised by autosomal dominant inheritance, a low mean age (41 years) for occurrence of colon cancer, and a marked increase in the proportion of tumours in the proximal colon. (12 Dec 1998) |
| corneal dystrophies, hereditary | Bilateral hereditary disorders of the cornea, usually autosomal dominant, which may be present at birth but more frequently develop during adolescence and progress slowly throughout life. Central macular dystrophy is transmitted as an autosomal recessive defect. (12 Dec 1998) |
| hereditary | <genetics> Transferred via genes from parent to child. (16 Dec 1997) |
| hereditary amyloidosis | <neurology> A disorder in which various peripheral nerves are infiltrated with amyloid and their functions disturbed, an abnormal prealbumin is also formed and is present in the blood; characteristically, it begins during mid-life and is found largely in persons of Portuguese descent. Other rare clinical types occur. Inheritance: autosomal dominant. Synonym: familial amyloidosis, hereditary amyloidosis. (05 Mar 2000) |
| hereditary angioedema | A genetic form of angioedema. (angioedema is also referred to as quinke's disease.) persons with it are born lacking an inhibitor protein (called c1 esterase inhibitor) that normally prevents activation of a cascade of proteins leading to the swelling of angioedema. Patients can develop recurrent attacks of swollen tissues, pain in the abdomen, and swelling of the voice box (larynx) which can compromise breathing. The diagnosis is suspected with a history of recurrent angioedema. It is confirmed by finding abnormally low levels of c1 esterase inhibitor in the blood. Treatment options include antihistamines and male steroids (androgens) that can also prevent the recurrent attacks. Also called hereditary angioneurotic oedema. (12 Dec 1998) |
| hereditary angioneurotic oedema | A genetic form of angioedema. (angioedema is also referred to as quinke's disease.) persons with it are born lacking an inhibitor protein (called c1 esterase inhibitor) that normally prevents activation of a cascade of proteins leading to the swelling of angioedema. Patients can develop recurrent attacks of swollen tissues, pain in the abdomen, and swelling of the voice box (larynx) which can compromise breathing. The diagnosis is suspected with a history of recurrent angioedema. It is confirmed by finding abnormally low levels of c1 esterase inhibitor in the blood. Treatment options include antihistamines and male steroids (androgens) that can also prevent the recurrent attacks. Also called hereditary angioedema. (12 Dec 1998) |
| hereditary angio oedema | <biochemistry> Condition in which there seems to be uncontrolled production of C2 kinin because of a deficiency in C1 inhibitor levels. (18 Nov 1997) |
| hereditary areflexic dystasia | A rare autosomal dominant neurological disorder with many of the clinical features of hereditary hypertrophic sensorimotor polyneuropathy combined with an essential tremor. Synonym: hereditary areflexic dystasia. (05 Mar 2000) |
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