| ¿µ¹® | rachitis(=rickets) | ÇÑ±Û | ±¸·çº´ |
|---|---|---|---|
| ¼³¸í | ºñŸ¹ÎDÀÇ ºÎÁ·À¸·Î ¹ß»ýÇÑ´Ù. ÁÖ·Î ºûÀ» ¸¹ÀÌ ÂÉÀÌÁö ¸øÇÑ ¾î¸°¾ÆÀÌ¿¡°Ô¼ ¹ß»ýÇÑ´Ù. ºñŸ¹ÎD´Â À§Ã¢ÀÚ°ü¿¡¼ Ä®½·ÀÇ Èí¼ö¸¦ ÃËÁøÇϰí, ¿ÀÁÜÀ¸·Î Ä®½·ÀÇ ºÐºñ¸¦ °¨¼Ò½ÃÄÑ, Ç÷ÁßÄ®½·³óµµ¿Í Àλ꿰ÀÇ ³óµµ¸¦ Áõ°¡½ÃŰ´Â °ÍÀ¸·Î ¾Ë·ÁÁ® ÀÖ´Ù. µû¶ó¼ À̰ÍÀÌ ºÎÁ·ÇÒ °æ¿ì Àü¹ÝÀûÀÎ »ÀÀÇ ¼ºÀåÀå¾Ö·Î ۰¡ Å©Áö ¾Ê°í, ±¸ºÎ·¯Áø °ñ°Ý°ú ½±°Ô ºÎ¼Áö´Â °ñ°ÝÀ» °¡Áö°Ô µÈ´Ù. Ä¡·á´Â ºñŸ¹ÎDÀÇ °ø±ÞÀÌ´Ù. |
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| ¿µ¹® | vitamin | ÇÑ±Û | ºñŸ¹Î |
|---|---|---|---|
| ¼³¸í | »ýü¿¡ ²À ÇÊ¿äÇÑ ¿µ¾çºÐÀÌÁö¸¸, ³»ºÎ¿¡¼ ÇÕ¼ºµÇÁö ¾ÊÀ¸¹Ç·Î ¹Ýµå½Ã ¿ÜºÎ¿¡¼ º¸ÃæÇؾ߸¸ µÇ´Â °ÍÀ» ¸»ÇÑ´Ù. ºÎÁ·½Ã »ý¸íÀ¯Áö°¡ ¾î·Á¿ì¸ç, ƯÈ÷ ÀϺΠºñŸ¹ÎÀº °ú´Ù½Ã¿¡µµ ÀÌ»óÀ» À¯¹ßÇϹǷΠÇ×»ó ÀûÁ¤¼öÁØÀ» À¯ÁöÇØ¾ß ÇÑ´Ù. ºñŸ¹Î A, D, E, K´Â Áö¿ë¼º ºñŸ¹ÎÀ¸·Î ÃàÀûÀÌ °¡´ÉÇϳª, ³ª¸ÓÁö´Â ¼ö¿ë¼ºÀ¸·Î ¸ÅÀÏ ¼·ÃëÇØ¾ß ÇÑ´Ù. ºñŸ¹Î B2(vitamin B2) RiboflavinÀ̶ó°íµµ ÇÔ. ÁÖ·Î ¿ìÀ¯, Ä¡Áî, °è¶õ, °£, µî¿¡ ¸¹´Ù. ºÎÁ·½Ã ÀÔ¼úÁÖÀ§°¡ °¥¶óÁö´Â ÀÔ¼ú¿°, ÀÔ¼ú¾È¿¡ ¿°ÁõÀÌ »ý±â´Â ÀԾȿ°, ±×¸®°í °¢Á¾ ÇǺκ´ µîÀÌ ¹ß»ýÇÑ´Ù. ÁÖ·Î °¡³ÇÑ ÈÄÁø±¹¿¡ ¸¹ÀÌ ¹ß»ýÇϸç, ÀϺΠ¿©¼º¿¡¼ Áö³ªÄ£ ´ÙÀÌ¾îÆ®·Î ÀÎÇØ ¹ß»ýÇϱ⵵ ÇÑ´Ù. ºñŸ¹Î B6(vitamin B6) À̰ÍÀº pyridoxineÀ̶ó°íµµ ºÎ¸£¸ç pyridoxine, pyridoxal ¹× pyridoxamine ¼¼ °¡ÁöÀÇ ÈÇÕ¹°ÀÌ ÀÖ´Ù. À̵éÀº ¸ðµÎ ü³»¿¡¼ pyridoxal phosphate·Î Ȱ¼ºÈµÇ¾î Á¶È¿¼Ò·Î ÀÛ¿ëÇÑ´Ù. À̴ ü³» ¾Æ¹Ì³ë»ê ´ë»ç¿¡ Áß¿äÇÑ ¿ªÇÒÀ» ÇÏ´Â Á¶È¿¼ÒÀÌ´Ù. ÀÌ ºñŸ¹ÎÀÌ °áÇÌµÇ¸é ´Ù¹ß¼º ¸»ÃʽŰ濰, ºóÇ÷ ¹× ÇǺκ´ÀÌ »ý±ä´Ù. ºñŸ¹Î B12(vitamin B12) ÀûÇ÷±¸ÀÇ »ý¼º¿¡ ÇʼöºÒ°¡°áÇÑ ºñŸ¹ÎÀÌ´Ù. ºÎÁ·½Ã Ư¡ÀûÀÎ ´ëÀûÇ÷¸ð±¸)°¡ Ç÷¾×³»¿¡¼ °üÂûµÈ´Ù. ´ëºÎºÐÀÇ ½Ä»çÇÏ´Â ¹°Áú¿¡ µé¾îÀÖÀ¸¹Ç·Î ÀÎüÀÇ ³»ÀûÀÌ»óÀÌ ÀÖÁö ¾Ê°í´Â Àß ¹ß»ýÇÏÁö ¾Ê´Â´Ù. ´ëÇ¥ÀûÀÎ °æ¿ì°¡ ¾Ç¼ººóÇ÷·Î½á, ÀÌ ºñŸ¹ÎÀº À§¿¡¼ ºÐºñµÇ´Â ³»ÀÎÀÚ(intrinsic factor)¿Í ÀÌÀÚÈ¿¼ÒÀÇ ÀÛ¿ëÀÌ ÀÖ¾î¾ß¸¸ Èí¼ö°¡ µÇ´Â µ¥, ¸¸¾à ¿©±â¿¡ ÀÌ»óÀÌ ÀÖÀ¸¸é Á¦´ë·Î Èí¼ö°¡ µÇÁö ¾ÊÀ¸¹Ç·Î Ç÷¾×³»¿¡ Á¤»óÀûÇ÷±¸ÀÇ °¨¼Ò¿Í °Å´ëÀûÇ÷±¸ÀÇ Áõ°¡°¡ ³ªÅ¸³ª, ºóÇ÷ÀÌ ¹ß»ýÇÑ´Ù. ÀÌ ºóÇ÷¿¡ ´ëÇÑ Áø´ÜÀº ½¯¸µ°Ë»ç(Schilling test)·Î½á °¡´ÉÇϸç, Ä¡·á´Â ºñŸ¹ÎÀÇ Åõ¿©ÀÌ´Ù. ºñŸ¹Î C(vitamin C) ÁַΠǪ¸¥ ä¼Ò¿¡ ¸¹´Ù. ¿¾³¯¿¡ ¼¾ç¿¡¼ ¹è¸¦ Ÿ°í Ç×ÇØÇÏ´ø »ç¶÷µé¿¡°Ô¼ ÀÌÀ¯¸¦ ¾Ë ¼ö ¾ø´Â ÀæÀº ÃâÇ÷°ú ¸ÛÀ¸·Î ÀÚÁÖ »ç¸ÁÇÏ´Â °æ¿ì°¡ »ý°Ü ±«Ç÷º´(scurvy)À̶ó°í ºÒ¸®¿ü´Ù. ³ªÁß¿¡ ±× ÀÌÀ¯°¡ Ǫ¸¥ ä¼ÒÀÇ ¼·ÃëºÎÁ·À¸·Î ÀÎÇÑ ºñŸ¹ÎC °áÇÌÀÎ °ÍÀ» ¾Ë¾Ò´Ù. ÀÌ ºñŸ¹ÎÀº °áÇÕÁ¶Á÷ÀÇ Çü¼º¿¡ Áß¿äÇÑ ÀÛ¿ëÀ» ÇϹǷΠ¸¸¾à ºÎÁ·½Ã °áüÁ¶Á÷ÀÇ Çü¼ºÀÌ Á¦´ë·Î ÀϾÁö ¾Ê¾Æ Ç÷°üÀÌ ¼Õ»óµÇ¾î ÀæÀº ÃâÇ÷°ú ¸ÛÀÌ µé¸é Àß ³´Áö ¾Ê´Â Áõ»ó, ±×¸®°í °áÇÕÁ¶Á÷ÀÌ ÀÖ´Â »À¿¡µµ ÀÌ»óÀÌ ¹ß»ýÇÑ´Ù. Ä¡·á´Â ºñŸ¹ÎÀÇ ¼·ÃëÀÌ´Ù. ºñŸ¹Î D(vitamin D) Ç÷ÁßÄ®½·³óµµÀÇ Á¶Àý¿¡ Áß¿äÇÑ ÀÛ¿ëÀ» ÇÑ´Ù. ÀÌ ºñŸ¹ÎÀº À§Ã¢ÀÚ°ü¿¡¼ÀÇ Ä®½·Èí¼ö¸¦ ÃËÁøÇϰí, ¼Òº¯À¸·ÎÀÇ ¹è¼³À» °¨¼Ò½ÃÄÑ, Ç÷ÁßÄ®½·³óµµ¿Í Àλ꿰³óµµÀÇ Áõ°¡¸¦ °¡Á®¿Â´Ù. µû¶ó¼ ¼Ò¾Æ±â¿¡¼ °¨¼Ò½Ã »ÀÀÇ ¼ºÀåÀÌ ¾î·Æ°í, ½±°Ô ºÎ·¯Áö´Â °æÇâÀ» °¡Áö°í, ½ÉÇÏ¸é °öÃß°¡ µÇ´Â ±¸·çº´(rickets)ÀÌ ¹ß»ýÇÑ´Ù. ¼ºÀο¡¼ °¨¼Ò½Ã¿¡´Â »ÀÀÇ Ä®½·³óµµ°¡ °¨¼ÒÇÏ¿© »ý±â´Â °ñ¿¬ÈÁõ(osteomalacia)ÀÌ ¹ß»ýÇÑ´Ù. Ä¡·á´Â ºñŸ¹ÎÀÇ Åõ¿©ÀÌ´Ù. ºñŸ¹Î E(vitamin E) ÁַΠǪ¸¥ ÀÙÀ» °¡Áø ä¼Ò¿Í ±Í¸®(wheat germ)¿¡ ¸¹´Ù. »ê¼Ò¿¡ ´ëÇÑ µ¶¼ºÀ» °¨¼Ò½ÃŰ´Â °ÍÀ¸·Î ¾Ë·ÁÁ® ÀÖ¾î, »ê¼Òµ¶¼ºÀ¸·Î ¹ß»ýµÇ´Â °ÍÀ¸·Î ÃßÁ¤µÇ´Â ¹Ì¼÷¾Æ¸Á¸·ÁõÀÇ ¿¹¹æ¿¡ »ç¿ëµÈ´Ù. ¶ÇÇÑ ºÎÁ·½Ã ¿ëÇ÷ÀÌ ÀϾÙ. ºñŸ¹Î K(vitamin K) °£¿¡¼ ¸¸µé¾îÁö´Â Ç÷¾×ÀÀ°í¹°ÁúÀÇ »ý¼º¿¡ ÇʼöÀûÀÌ´Ù. µû¶ó¼ ºÎÁ·½Ã Ç÷¾×ÀÀ°í°¡ ÀÌ·ç¾îÁöÁö ¾Ê¾Æ Á¶±×¸¸ »óó¿¡µµ ÃâÇ÷°æÇâÀ» º¸ÀδÙ. ÁÖ·Î °£, ä¼Ò±â¸§, ÀÙÀ» °¡Áø ä¼Ò µî¿¡ ¸¹´Ù. ´ë°³ ºÎÁ·Àº ½Å»ý¾Æ¿¡°Ô¼ ¸¹ÀÌ °üÂûµÈ´Ù. |
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| ¿µ¹® | IDDM(Insulin-Dependent Diabetes Mellitus) | ÇÑ±Û | Àν¶¸°ÀÇÁ¸´ç´¢º´ |
|---|---|---|---|
| ¼³¸í | IDDMÀº ´ç´¢º´ÀÇ Ä¡·á¿¡ ¹Ýµå½Ã Àν¶¸°ÀÌ ÇÊ¿äÇÑ °æ¿ì¸¦ ¸»ÇÑ´Ù. ÁÖ·Î ¿øÀÎÀÌ ÀÌÀÚ¿¡ ÀÖ´Â Àν¶¸°À» ºÐºñÇÏ´Â ¼¼Æ÷ÀÇ ÆÄ±«À̸ç ÀÌ·Î ÀÎÇØ¼ ´ç´¢º´ÀÇ Ä¡·áÁ¦·Î ¾²ÀÌ´Â Àν¶¸°ÀÇ ºÐºñ¸¦ ÃËÁøÇÏ´Â ¾à¹°ÀÌ ÀÌ IDDM¿¡¼´Â ¾²ÀÏ ¼ö°¡ ¾ø°í ¿ÀÁ÷ Àν¶¸°¸¸ÀÌ Ä¡·áÁ¦·Î ¾µ ¼ö°¡ ÀÖ´Ù. ÀüÇüÀûÀÎ Àν¶¸° ÀÇÁ¸Çü ´ç´¢º´Àº ¼Ò¾Æ¿¡¼ ÈçÈ÷ ¹ß»ýÇϰí Àν¶¸° ºÐºñ¼¼Æ÷ÀÇ ÆÄ±«¿¡ ÀÇÇØ¼ Àν¶¸° ºÐºñ´ÉÀº °ÅÀÇ ¾ø´Ù. |
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| VDDR | vitamin D-dependent rickets |
|---|---|
| HVDRR | hypocalcemic vitamin D-resistant rickets |
| VDRR | vitamin D-resistant rickets |
| PDDR | pseudovitamin D-dependent rickets |
| VDD | atrial synchronous ventricular inhibited [pacemaker]; vitamin D-dependent |
| VDRR | Vitamin D resistant rickets |
|---|---|
| XLH | X-Linked hypophosphataemic rickets |
| HYP | hypophosphataemic rickets |
| 1,25(OH)(2)D(3) | 1, 25(OH)(2) Vitamin D(3 |
| 1,25-D | 1, 25-dihydroxy vitamin D |
familial leiomyomatosis cutis et uteri (°¡Á·¼º ÇǺΠÀڱà ±ÙÁ¾Áõ
| vitamin d-resistant rickets | <radiology> X-linked recessive, defect in renal tubular resorption of phosphate, presents at 1 yr, progressive limb deformities X-ray: less severe changes than other rickets, presents later Differential diagnosis features: family hx, normal serum calcium, marked hypophosphataemia (decreased PO4), no secondary hyperparathyroidism (12 Dec 1998) |
|---|---|
| acute rickets | Bone changes seen in infantile scurvy, consisting of subperiosteal haemorrhage and deficient osteoid tissue formation; often used to indicate simultaneous occurrence of rickets and scurvy. Synonym: acute rickets. Hereditary hypophosphatemic rickets, with hypercalciuria, an inherited disorder in which there is a defect in renal tubular reabsorption. (05 Mar 2000) |
| adult rickets | <pathology> A condition marked by softening of the bones (due to impaired mineralisation, with excess accumulation of osteoid), with pain, tenderness, muscular weakness, anorexia and loss of weight, resulting from deficiency of vitamin D and calcium. Origin: Gr. Malakia = softness (18 Nov 1997) |
| refractory rickets | Rickets that does not respond to treatment with usual doses of vitamin D and adequate dietary calcium and phosphorus. Most often due to inherited renal tubular disorder e.g., Fanconi syndrome. Renal rickets, a form of rickets occurring in children in association with and apparently caused by renal disease with hyperphosphatemia. Synonym: pseudorickets, renal fibrocystic osteosis, renal infantilism, renal osteitis fibrosa. (05 Mar 2000) |
| rickets | <rheumatology, orthopaedics> A condition caused by deficiency of vitamin D, especially in infancy and childhood, with disturbance of normal ossification. The disease is marked by bending and distortion of the bones under muscular action, by the formation of nodular enlargements on the ends and sides of the bones, by delayed closure of the fontanelles, pain in the muscles and sweating of the head. Vitamin D and sunlight together with an adequate diet are curative, provided that the parathyroid glands are functioning properly. Origin: Gr. Rhachitis = a spinal complaint (18 Nov 1997) |
| coeliac rickets | Arrested growth, and osseous deformities associated with defective absorption of fat and calcium in coeliac disease. (05 Mar 2000) |
| haemorrhagic rickets | Bone changes seen in infantile scurvy, consisting of subperiosteal haemorrhage and deficient osteoid tissue formation; often used to indicate simultaneous occurrence of rickets and scurvy. Synonym: acute rickets. Hereditary hypophosphatemic rickets, with hypercalciuria, an inherited disorder in which there is a defect in renal tubular reabsorption. (05 Mar 2000) |
| scurvy rickets | infantile scurvy |
| familial hypophosphatemic rickets | <radiology> X-linked recessive, defect in renal tubular resorption of phosphate, presents at 1 yr, progressive limb deformities X-ray: less severe changes than other rickets, presents later Differential diagnosis features: family hx, normal serum calcium, marked hypophosphataemia (decreased PO4), no secondary hyperparathyroidism (12 Dec 1998) |
| late rickets | <pathology> A condition marked by softening of the bones (due to impaired mineralisation, with excess accumulation of osteoid), with pain, tenderness, muscular weakness, anorexia and loss of weight, resulting from deficiency of vitamin D and calcium. Origin: Gr. Malakia = softness (18 Nov 1997) |
| aid to families with dependent children | Financial assistance provided by the government to indigent families with dependent children who meet certain requirements as defined by the social security act, title IV, in the u.s. (12 Dec 1998) |
| androgen-dependent secretory protease | <enzyme> Glycoprotein from dog prostate; hydrolyzes arginine and lysine-containing amide and ester protease substrates Registry number: EC 3.4.99.- Synonym: ads-protease (26 Jun 1999) |
| antibody-dependent cell cytotoxicity | The phenomenon of antibody-mediated target cell destruction by non-sensitised effector cells. The identity of the target cell varies, but it must possess surface IgG whose fc portion is intact. The effector cell is a "killer" cell possessing fc receptors. It may be a lymphocyte lacking conventional b- or T-cell markers, or a monocyte, macrophage, or polynuclear leukocyte, depending on the identity of the target cell. The reaction is complement-independent. (12 Dec 1998) |
| antibody-dependent enhancement | Enhancement of viral infectivity caused by non-neutralizing antibodies. There are at least two mechanisms known to account for this: mediation by fc receptors (receptors, fc) or by complement receptors (receptors, complement). Either the virus is complexed with antiviral IgG and binds to fc receptors, or virus is coated with antiviral IgM and binds to complement receptors. (12 Dec 1998) |
| aromatic NADH-dependent nitroreductase | <enzyme> See also record for 1-nitroreductase; type I nitroreductase is not inhibited by oxygen Registry number: EC 1.- Synonym: nitrofuran reductase, nitrofurazone reductase, type I nitroreductases, NADH-dependent nitro reductase, nitrofurantoin reductase, p-dinitrobenzene reductase, benznidazole nitroreductase, nifurtimox nitroreductase, oxygen-insensitive NADPH nitroreductase, nitrobenzene nitroreductase (26 Jun 1999) |
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