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5) Ç÷ûĮ·ýÀ» »ó½Â½ÃŰ´Â ¾à¹°(½ºÇǷγë¶ôÅæ, Æ®¸®¾ÏÅ×·», ¾Æ¹Ð·Î¶óÀÌµå µîÀÇ Ä®·ýÀú·ù¼º ÀÌ´¢Á¦, Ä®·ýº¸±ÞÁ¦, ÇìÆÄ¸° µî)À» º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â °íÄ®·ýÇ÷ÁõÀÌ ³ªÅ¸³¯ ¼ö ÀÖ´Ù(ƯÈ÷ ½ÅÀå¾Ö ȯÀÚ).
6) ¾Ë·ÎǪ¸®³î¿¡ ÀÇÇØ ÀÌ ¾àÀÌ ´ë»ç°¡ ÀúÇØµÉ ¼ö ÀÖÀ¸¹Ç·Î º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â Àú¿ë·®¿¡¼ Åõ¿©¸¦ ½ÃÀÛÇÏ´Â µî ½ÅÁßÈ÷ Åõ¿©ÇÑ´Ù(ƯÈ÷ ½ÅÀå¾Ö ȯÀÚ).
7) ¸®Æ¬°ú ACEÀúÇØÁ¦¸¦ º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â ¸®Æ¬µ¶¼ºÀÇ À§ÇèÀÌ ÀÖÀ¸¹Ç·Î Ç÷Áß ¸®Æ¬³óµµ¸¦ ½ÅÁßÈ÷ ¸ð´ÏÅÍÇÏ°í ¿ë·®À» Á¶ÀýÇÑ´Ù(¸®Æ¬ÀÇ ¹è¼³À» °¨¼Ò½ÃÄÑ Ç÷Áß ¸®Æ¬³óµµ°¡ Áõ°¡ÇÑ´Ù.).
8) Àεµ¸ÞŸ½Å µî ºñ½ºÅ×·ÎÀ̵强 ¼Ò¿°ÁøÅëÁ¦¿Í Ç×·ù¸¶Æ¼½º ¾à¹°°ú º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â ÀÌ ¾àÀÇ Ç÷¾Ð°ÇÏÀÛ¿ëÀÌ °¨¼ÒµÉ ¼ö ÀÖÀ¸¹Ç·Î ½ÅÁßÈ÷ Åõ¿©ÇÑ´Ù.
9) ¸é¿ª¾ïÁ¦Á¦, ¼¼Æ÷Áõ½Ä¾ïÁ¦Á¦, ÄÚ¸£Æ¼ÄÚÀ̵å¿Í º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â Ç÷±¸¼öÀÇ º¯È°¡ ³ªÅ¸³¯ ¼ö ÀÖÀ¸¹Ç·Î ÁÖÀÇÇÑ´Ù.
10) ¾ËÄڿðú º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â ¾ËÄÚ¿Ã ÀÛ¿ëÀÌ »ó½ÂÇÒ ¼ö ÀÖÀ¸¹Ç·Î ÁÖÀÇÇÑ´Ù.
11) ÇÁ·Îº£³×½Ãµå¿Í º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â ÀÌ ¾àÀÇ ½Åû¼ÒÀ²ÀÌ °¨¼ÒµÇ¹Ç·Î ÁÖÀÇÇÑ´Ù.
12) Ŭ·Î´ÏµòÀ» Åõ¿©¹Þ´ø ȯÀÚ°¡ ÀÌ ¾àÀ¸·Î ÀüȯÇÏ´Â °æ¿ì¿¡´Â Ç÷¾Ð°ÇÏÀÛ¿ëÀÌ Áö¿¬µÉ ¼ö ÀÖÀ¸¹Ç·Î ÁÖÀÇÇÑ´Ù.
13) ½Éȯ°è Ç׿ì¿ïÁ¦, Á¤½Åº´Ä¡·áÁ¦¿Í º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â ±â¸³¼º ÀúÇ÷¾ÐÀÇ À§ÇèÀÌ Áõ°¡µÉ ¼ö ÀÖ´Ù.
14) ¾Ë·ÎǪ¸®³î, ÇÁ·ÎÄ«Àξƹ̵å¿Í º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â È£Áß±¸°¨¼Ò, ÇǺÎÁ¡¸·¾È ÁõÈıº(Stevens-Johnson ÁõÈıº)ÀÌ ³ªÅ¸³µ´Ù´Â º¸°í°¡ ÀÖ´Ù.
15) ¾ÈÁö¿ÀÅٽмö¿ëü Â÷´ÜÁ¦(ARB), ¾ÈÁö¿ÀÅٽŠÀüȯ È¿¼Ò(ACE) ¾ïÁ¦Á¦ ¶Ç´Â ·¹´Ñ¾ïÁ¦Á¦(¾Ë¸®½ºÅ°·»)ÀÇ º´¿ëÅõ¿©¿¡ ÀÇÇÑ ·¹´Ñ-¾ÈÁö¿ÀÅٽŰè(RAS)ÀÇ ÀÌÁßÂ÷´ÜÀº ÀúÇ÷¾Ð, ½Ç½Å, °íÄ®·ýÇ÷Áõ ¹× ½Å±â´ÉÀÇ ÀúÇÏ(±Þ¼º½ÅºÎÀüÁõ Æ÷ÇÔ)¿Í °°Àº ÀÌ»ó»ç·ÊÀÇ ºóµµ°¡ ·¹´Ñ-¾ÈÁö¿ÀÅٽŰè(RAS)¿¡ ¿µÇâÀ» ¹ÌÄ¡´Â ¾àÁ¦ÀÇ ´Üµ¶ »ç¿ë½Ã¿¡ ºñÇØ ³ô´Ù. ÀÌ ¾à°ú ·¹´Ñ¾ïÁ¦Á¦(¾Ë¸®½ºÅ°·») ÇÔÀ¯ Á¦Á¦ÀÇ º´¿ëÀº ±ÇÀåµÇÁö ¾ÊÀ¸¸ç, ´ç´¢º´À̳ª Áߵ¡ÁßÁõÀÇ ½ÅÀå¾Ö ȯÀÚ(GFR <60 ml/min/1.73m2)´Â º´¿ëÅõ¿©Çؼ´Â ¾ÈµÈ´Ù. ÀÌ ¾à°ú ¾ÈÁö¿ÀÅٽмö¿ëü Â÷´ÜÁ¦(ARB)ÀÇ º´¿ëÀº ±ÇÀåµÇÁö ¾ÊÀ¸¸ç, ´ç´¢º´¼º ½ÅÁõ ȯÀÚ´Â º´¿ëÅõ¿©Çؼ´Â ¾ÈµÈ´Ù.
16) mTOR(mammalian target of rapamycin) ÀúÇØÁ¦¿Í º´¿ëÅõ¿©ÇÏ´Â °æ¿ì¿¡´Â Ç÷°üºÎÁ¾ À§ÇèÀÌ Áõ°¡ÇÒ ¼ö ÀÖÀ¸¹Ç·Î ÁÖÀÇÇÑ´Ù.
17) ³×ÇÁ¸±¸®½Å(Neutral endopeptidase; NEP) ÀúÇØÁ¦(¿¹, »çÄíºñÆ®¸±, ¶ó¼¼Ä«µµÆ®¸±)¿Í º´¿ëÅõ¿©Çϴ ȯÀÚ¿¡¼ Ç÷°üºÎÁ¾ÀÇ À§ÇèÀÌ Áõ°¡ÇÒ ¼ö ÀÖ´Ù. |
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°í½ÃµÈ º´¿ë±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
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[Captopril]
 [Captopril] CAS number/62571-86-2 ATC code/C09AA01 PubChem/44093 DrugBank/APRD00164 Formula/C9H15NO3S Mol. mass/217.29 Bioavailability/70–75% Metabolism/hepatic Excretion/renal Pregnancy cat./
D(AU) Legal status/
℞ Prescription only Routes/oral
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| µ¶¼ºÁ¤º¸ |
Captopril¿¡ ´ëÇÑ µ¶¼ºÁ¤º¸ : Á¤º¸º¸±â
Ãâó: ±¹¸³µ¶¼º°úÇпø µ¶¼º¹°ÁúÁ¤º¸DB : http://www.nitr.go.kr/nitr/contents/m134200/view.do |
| Mechanism of Action |
Captopril¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Captopril competes with angiotensin I for binding at the angiotensin-converting enzyme, blocking the conversion of angiotensin I to angiotensin II. As angiotensin II is a vasoconstrictor and a negative feedback mediator for renin activity, lower angiotensin II levels results in a decrease in blood pressure, an increase in renin activity, and stimulation of baroreceptor reflex mechanisms. Kininase II, an enzyme which degrades the vasodilator bradykinin, is identical to ACE and may also be inhibited.
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| Pharmacology |
Captopril¿¡ ´ëÇÑ Pharmacology Á¤º¸ Captopril, an angiotensin-converting enzyme (ACE) inhibitor, is used to treat hypertension, congestive heart failure, and renal syndromes such as diabetic nephropathy and scleroderma. The adverse effect and pharmacokinetic limitations of captopril stimulated the development enalapril and subsequent ACE inhibitors.
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| Metabolism |
Captopril¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 2D6 (CYP2D6)
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| Protein Binding |
Captopril¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ About 25-30% of the circulating drug is bound to plasma proteins
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| Half-life |
Captopril¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ Less than 3 hours
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| Absorption |
Captopril¿¡ ´ëÇÑ Absorption Á¤º¸ 75% without food (the presence of food in the gastrointestinal tract reduces absorption by about 30 to 40 percent).
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| Pharmacokinetics |
CaptoprilÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- Ç÷¾Ð°ÇÏ ÃÖ´ëÈ¿°ú ¹ßÇö½Ã°£ : 1-1.5 ½Ã°£
- ÀÛ¿ëÁö¼Ó½Ã°£ : ¿ë·®ÀÇÁ¸Àû. Àå±â°£ Ä¡·á½Ã Ç÷¾Ð°ÇÏ ÃÖ´ëÈ¿°ú°¡ ³ªÅ¸³ª´Â µ¥¿¡´Â ¼ö ÁÖ°¡ ÇÊ¿äÇÒ ¼ö ÀÖ´Ù.
- ÃÖ°íÇ÷Áß³óµµ µµ´Þ½Ã°£ : 1-2 ½Ã°£ À̳»
- Èí¼ö : 60-75%
- ´Ü¹é°áÇÕ : 25-30%
- ´ë»ç : 50%
- ¹Ý°¨±â : ½Å±â´É°ú ½É ±â´É¿¡ µû¶ó Á¿ìµÈ´Ù.
- Á¤»ó ¼ºÀÎ : 1.9 ½Ã°£
- ¿ïÇ÷¼º½ÉºÎÀü ȯÀÚ : 2.06 ½Ã°£
- ¹«´¢Áõ : 20-40 ½Ã°£
- ¼Ò½Ç : 24½Ã°£ ³»¿¡ 95%°¡ ¼Òº¯À¸·Î ¹è¼³µÈ´Ù.
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| Biotransformation |
Captopril¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic
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| Toxicity |
Captopril¿¡ ´ëÇÑ Toxicity Á¤º¸ Symptoms of overdose include coma, lethargy, low blood pressure, sluggishness, and stomach and intestinal irritation and hyperactivity.
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| Drug Interactions |
Captopril¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Amiloride Increased risk of hyperkaliemiaDrospirenone Increased risk of hyperkaliemiaLithium The ACE inhibitor increases serum levels of lithiumPotassium Increased risk of hyperkaliemiaSpironolactone Increased risk of hyperkaliemiaTizanidine Tizanidine increases the risk of hypotension with the ACE inhibitorTriamterene Increased risk of hyperkaliemia
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
Captopril¿¡ ´ëÇÑ Food Interaction Á¤º¸ Avoid alcohol.Avoid salt substitutes containing potassium.Take on empty stomach: 1 hour before or 2 hours after meals, food decreases absorption by 30 to 55%.Avoid natural licorice.Do not take calcium, aluminum, magnesium or Iron supplements within 2 hours of taking this medication.
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| Drug Target |
[Drug Target]
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| Description |
Captopril¿¡ ´ëÇÑ Description Á¤º¸ A potent and specific inhibitor of peptidyl-dipeptidase A. It blocks the conversion of angiotensin I to angiotensin II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the renin-angiotensin system and inhibits pressure responses to exogenous angiotensin. [PubChem]
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| Dosage Form |
Captopril¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Tablet Oral
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| Drug Category |
Captopril¿¡ ´ëÇÑ Drug_Category Á¤º¸ Angiotensin-converting Enzyme InhibitorsAntihypertensive Agents
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| Smiles String Canonical |
Captopril¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC(CS)C(=O)N1CCCC1C(O)=O
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| Smiles String Isomeric |
Captopril¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ C[C@H](CS)C(=O)N1CCC[C@H]1C(O)=O
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| InChI Identifier |
Captopril¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C9H15NO3S/c1-6(5-14)8(11)10-4-2-3-7(10)9(12)13/h6-7,14H,2-5H2,1H3,(H,12,13)/t6-,7+/m1/s1/f/h12H
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| Chemical IUPAC Name |
Captopril¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ (2S)-1-[(2S)-2-methyl-3-sulfanylpropanoyl]pyrrolidine-2-carboxylic acid
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| Drug-Induced Toxicity Related Proteins |
CAPTOPRIL ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Lysozyme Drug:captopril Toxicity:peripheral leukopenia. [¹Ù·Î°¡±â] Replated Protein:Angiotensin-converting enzyme Drug:captopril Toxicity:reversible proteinuria. [¹Ù·Î°¡±â] Replated Protein:Beta-glucuronidase Drug:Captopril Toxicity:peripheral leukopenia. [¹Ù·Î°¡±â] Replated Protein:Kallikrein Drug:captopril Toxicity:decreased significantly blood pressure. [¹Ù·Î°¡±â] Replated Protein:Glucose transporter II Drug:captopril Toxicity:resultant ill effects. [¹Ù·Î°¡±â] Replated Protein:B2 bradykinin receptor Drug:Captopril Toxicity:cough. [¹Ù·Î°¡±â] Replated Protein:Glucose transporter I Drug:captopril Toxicity:resultant ill effects. [¹Ù·Î°¡±â] Replated Protein:Angiotensin-converting enzyme(ACE) Drug:Captopril Toxicity:blood-pressure reduction and reduction in left ventricular mass. [¹Ù·Î°¡±â]
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| ÃֽŹ®Çå°ËÅä |
Sex Differences in Blood Pressure Response toAntihypertensive Therapy in Chinese Patients with Hypertension
BACKGROUND: Ç×°íÇ÷¾ÐÁ¦¿¡ ´ëÇÑ ¼ºº°°£ ¹ÝÀÀ¼ºÀÇ Â÷ÀÌ¿¡ ´ëÇØ¼´ÂÀß ¾Ë·ÁÁ® ÀÖÁö ¾Ê´Ù.
OBJECTIVE: Community-basedprospective clinical trial·Î Ç×°íÇ÷¾ÐÁ¦¿¡ ´ëÇÑ ¼ºº°°£ ¹ÝÀÀ¼º Â÷À̰¡ ÀÖ´ÂÁö¸¦ È®ÀÎÇϱâ À§ÇÏ¿© ÀÌ ¿¬±¸¸¦ ½ÃÇàÇÏ¿´´Ù.
METHODS: Áß±¹³»ÀÇ 7°³ÀÇ Áö¿ª¿¡¼ ÀÌÀü¿¡ °íÇ÷¾Ð Ä¡·á¸¦ ¹ÞÁö ¾Ê¾Ò´ø 4075¼¼ ȯÀÚ 3535¸í(¿©¼º:2326¸í)À» ¸ðÁýÇÏ¿´´Ù. ȯÀڵ鿡°Ô atenolol, hydrochlorothiazide (HCTZ), captopril, sustained-releasednifedipine Áß¿¡ 1°³ÀÇ ¾à¹°À» ¹«ÀÛÀ§ ¹èÁ¤ÇÏ¿©8ÁÖµ¿¾È ½ÃÇèÀ» ÁøÇàÇÏ¿´´Ù. ÀÌÈÄ ³²¼º°ú ¿©¼º »çÀÌÀÇ Æò±Õ Ç÷¾Ð °¨¼ÒÁ¤µµ, Ç÷¾ÐÀÌ Á¶ÀýµÇ´Â ºñÀ², ÀÌ»ó¹ÝÀÀÀÇ ¹ß»ý·üÀ» ºñ±³ÇÏ¿´´Ù.
RESULTS: ¿©¼ºÀÇ HCTZ¿¡ ´ëÇÑ ¹ÝÀÀ¼ºÀº À̿ϱâÇ÷¾Ð¿¡À־²¼ºº¸´Ù´õÁÁ¾Ò°í(1.8mmHg ´õ°¨¼Ò, p < 0.05) ³²¼ºº¸´Ù 57%ÀÌ»ó ´õ ¸ñÇ¥ÇÑÀ̿ϱâÇ÷¾Ð¿¡µµ´ÞÇÏ¿´´Ù(p < 0.05). Atenolol group¿¡¼´Â ¿©¼ºÀÌ ³²¼ºº¸´Ù Æò±Õ¼öÃà±â Ç÷¾ÐÀÌ 3.9 mmHgÀÌ»ó ´õ °¨¼ÒÇÏ¿´°í(p <0.05), ¿©¼ºÀÌ ³²¼ºº¸´Ù 65%ÀÌ»ó ´õ ¸ñÇ¥ÇÑ ¼öÃà±â Ç÷¾Ð¿¡ µµ´ÞÇÏ¿´À¸¸ç 57% ÀÌ»ó ´õ ¸ñÇ¥ÇÑ À̿ϱâÇ÷¾Ð¿¡µµ´ÞÇϱ⽬¿ü´Ù(p < 0.05).Nifedipine°ú captopril group¿¡¼ ¾à¹°°ú °ü·ÃµÈ ÀÌ»ó¹ÝÀÀÀÌ ¼ºº°°ú °ü·ÃÇÏ¿©À¯ÀǼº ÀÖ´Â Â÷À̸¦ º¸¿´Áö¸¸ (Nifedipine-15.8% in women vs 9.8% in men; p =0.017, captopril- 14.3% in women vs 8.4% in men; p = 0.005) HCTZ°ú atenolol group¿¡¼´Â À¯ÀǼº ÀÖ´Â Â÷À̸¦ º¸ÀÌÁö ¾Ê¾Ò´Ù.
CONCLUSIONS: ¿©¼ºÀÌ HCTZ¿Í atenolol¿¡ ´ëÇØ ´õ ÁÁÀº Ç÷¾Ð ¹ÝÀÀ¼ºÀ» ³ªÅ¸³»°í sustained-release nifedipine°ú captopril¿¡´ëÇØ ³²¼ºº¸´Ù ´õ ¸¹Àº ÀÌ»ó¹ÝÀÀÀ» ³ªÅ¸³»¾ú´Ù. À̰ÍÀº Ç×°íÇ÷¾ÐÁ¦¸¦ ¼±ÅÃÇϴµ¥ ÀÖ¾î¼ ¼ºº°À» °í·ÁÇÒ ¼öÀÖ´Ù´Â °ÍÀ» ÀǹÌÇÑ´Ù.
Ann Pharmacother2008;42:1772-81
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The database contains the following fields: The generic name of each chemical For module A10 (liver enzyme composite module): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the number of active and marginally active scores for each compound at the five individual endpoints (see research article for full description of method) Number of endpoints at which each compound is marginally active (M) Number of endpoints at which each compound is active (A) For modules A11 to A15 (alkaline phosphatase increased, SGOT increased, SGPT increased, LDH increased, and GGT increased, respectively): Overall activity category for each compound (A for active, M for marginally active, or I for inactive) based on the RI and ADR values (see the research article for full description of method) Number of ADR reports for each compound, given as <4 or ¡Ã4 Reporting Index value for each compound, except where no shipping units were available (NSU) Group 1 comprises of compounds for which ADR data were available for the first five years of marketing, so when no ADR reports were listed during this period the compounds were evaluated as inactive. Group 2 comprises of compounds for which a 'steady state' period of ADR data were available (1992-1996). In cases where no ADR reports were filed during this period, the compounds were scored as 'NA' (data not available) since they may have had one or more ADR reports during their first five years of marketing which should not be negated by a lack of ADR reports during the steady-state period. CAPTOPRIL[GGT Increase][Composite Activity](Score) I(Marginal) 0(Active) 0[Alkaline Phosphatase Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 1.1[SGOT Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 1.5[SGPT Increase](Activity Score) I(Number of Rpts) ¡Ã4(Index value) 0.7[LDH Increase](Activity Score) I(Number of Rpts) <4(Index value) 0.4[GGT Increase](Activity Score) I(Number of Rpts) <4(Index value) 0
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