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 FDA : Cµî±Þ
(dexamethasone; )
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»ó±â ÀÓºÎÅõ¿©¿¡ ´ëÇÑ Á¤º¸´Â Àü»êó¸® µÇ¸é¼ ÀÔ·Â ¿À·ù °¡´É¼ºÀÌ Á¸ÀçÇÕ´Ï´Ù. ¿À·ù °¡´É¼ºÀ» ÃÖ¼ÒÈÇϱâ À§ÇÏ¿© ¸¹Àº ³ë·ÂÀ» ±â¿ïÀ̰í ÀÖÀ¸³ª, ±× Á¤È®¼º¿¡ ´ëÇÏ¿© È®½ÅÀ» µå¸± ¼ö ¾ø½À´Ï´Ù. ÀÌ¿¡ ´ëÇØ ȸ»ç´Â Ã¥ÀÓÀ» ÁöÁö ¾Ê½À´Ï´Ù.
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¹Ýµå½Ã °ø½Å·Â ÀÖ´Â ¹®ÇåÀ» ´Ù½Ã Çѹø Âü°í ÇϽñ⠹ٶó¸ç ÀÇ»ç ¶Ç´Â ¾à»çÀÇ ÆÇ´Ü¿¡ µû¶ó Åõ¿©¿©ºÎ°¡ °áÁ¤µÇ¾î¾ß ÇÕ´Ï´Ù.
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½ÅÀå¾Ö, °£Àå¾Ö½Ã ¿ë·®Á¶Àý |
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| DUR (ÀǾàǰ»ç¿ëÆò°¡) |
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°í½ÃµÈ º´¿ë±Ý±â ³»¿ëÀº ¾ø½À´Ï´Ù.
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| µ¶¼ºÁ¤º¸ |
Dexamethasone¿¡ ´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 |
Dexamethasone¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Dexamethasone is a glucocorticoid agonist. Unbound dexamethasone crosses cell membranes and binds with high affinity to specific cytoplasmic receptors. This results in a modification of transcription and, hence, protein synthesis in order to achieve inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, suppression of humoral immune responses, and reduction in edema or scar tissue. The antiinflammatory actions of dexamethasone are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.
Neomycin¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Aminoglycosides like neomycin "irreversibly" bind to specific 30S-subunit proteins and 16S rRNA. Specifically neomycin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes.
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| Pharmacology |
Dexamethasone¿¡ ´ëÇÑ Pharmacology Á¤º¸ Dexamethasone and its derivatives, dexamethasone sodium phosphate and dexamethasone acetate, are synthetic glucocorticoids. Used for its antiinflammatory or immunosuppressive properties and ability to penetrate the CNS, dexamethasone is used alone to manage cerebral edema and with tobramycin to treat corticosteroid-responsive inflammatory ocular conditions.
Neomycin¿¡ ´ëÇÑ Pharmacology Á¤º¸ Neomycin is an aminoglycoside antibiotic. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with penicillin-related antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses.
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| Metabolism |
Dexamethasone¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 3A4 (CYP3A4)
Neomycin¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Not Available
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| Protein Binding |
Dexamethasone¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 70%
Neomycin¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ Protein binding studies have shown that the degree of aminoglycoside protein binding is low and, depending upon the methods used for testing, may be between 0% and 30%.
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| Half-life |
Dexamethasone¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 36-54 hours
Neomycin¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 2 to 3 hours
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| Absorption |
Dexamethasone¿¡ ´ëÇÑ Absorption Á¤º¸ 80-90%
Neomycin¿¡ ´ëÇÑ Absorption Á¤º¸ Poorly absorbed from the normal gastrointestinal tract. Although only approximately 3% of neomycin is absorbed through intact intestinal mucosa, significant amounts may be absorbed through ulcerated or denuded mucosa or if inflammation is present.
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| Pharmacokinetics |
DexamethasoneÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- ´ë»çÈ¿°ú Áö¼Ó½Ã°£ : 72½Ã°£±îÁö Áö¼ÓµÉ ¼ö ÀÖ´Ù. Acetate´Â ÀÛ¿ë ¹ßÇö ½Ã°£À» ÃËÁø½ÃŲ Àå½Ã°£ Áö¼ÓÇü repository Á¦Á¦ÀÌ´Ù.
- ´ë»ç : °£¿¡¼ ´ë»ç
- ¹Ý°¨±â
- Á¤»ó ½Å±â´É : 1.8¡3.5½Ã°£
- »ý¸®Àû ¹Ý°¨±â : 36¡54½Ã°£
- ÃÖ´ëÈ¿°ú ¹ßÇö½Ã°£
- °æ±¸ : 1¡2½Ã°£ À̳»
- ±ÙÀ°ÁÖ»ç : 8½Ã°£ À̳»
- ¼Ò½Ç : ´¢³ª º¯À¸·Î ¹è¼³
Neomycin SulfateÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- Èí¼ö : °æ±¸, °æÇÇ : Èí¼öµÇ´Â ¾çÀÌ ¹Ì¹ÌÇÏ´Ù. (3%)
- ºÐÆ÷ : ºÐÆ÷¿ëÀû : 0.36 L/kg
- ´ë»ç : ¼Ò·®ÀÌ °£¿¡¼ ´ë»çµÈ´Ù.
- ¹Ý°¨±â : 3 ½Ã°£ (³ªÀÌ¿Í ½Å±â´É¿¡ ÀÇÁ¸)
- Ç÷ÁßÃÖ°í³óµµ µµ´Þ½Ã°£ :
- °æ±¸ : 1-4 ½Ã°£
- ±ÙÀ°ÁÖ»ç : 2 ½Ã°£ À̳»
- ¼Ò½Ç :
- ÁÖ»çÁ¦ : ½Å¹è¼³ (30-50%°¡ ¹Ìº¯Èü·Î ¹è¼³)
- °æ±¸ : 97%°¡ ¹Ìº¯Èü·Î º¯¹è¼³
Polymyxin B SulfateÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- Èí¼ö :
- º¹¸·¿¡¼ Àß Èí¼öµÈ´Ù.
- À§Àå°ü(½Å»ý¾Æ Á¦¿Ü), Á¡¸·, ÇǺο¡¼´Â Àß Èí¼öµÇÁö ¾Ê´Â´Ù.
- ºÐÆ÷ :
- ³úô¼ö¾×À¸·ÎÀÇ ºÐÆ÷´Â ¹Ì¹ÌÇÏ´Ù.
- ŹÝÅë°ú
- ¹Ý°¨±â : 4.5-6 ½Ã°£, ½Å±â´É ÀúÇϽà ¿¬ÀåµÈ´Ù.
- Ç÷ÁßÃÖ°í³óµµ µµ´Þ½Ã°£ : IM : 2½Ã°£ À̳»
- ¼Ò½Ç : »ç±¸Ã¼ ¿©°ú¸¦ ÅëÇØ 60% ÀÌ»óÀÌ ¹Ìº¯Èü·Î ½Å¹è¼³µÈ´Ù.
|
| Biotransformation |
Dexamethasone¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic.
Neomycin¿¡ ´ëÇÑ Biotransformation Á¤º¸ Neomycin undergoes negligible biotransformation after parenteral administration.
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| Toxicity |
Dexamethasone¿¡ ´ëÇÑ Toxicity Á¤º¸ Oral, rat LD50: >3 gm/kg. Signs of overdose include retinal toxicity, glaucoma, subcapsular cataract, gastrointestinal bleeding, pancreatitis, aseptic bone necrosis, osteoporosis, myopathies, obesity, edemas, hypertension, proteinuria, diabetes, sleep disturbances, psychiatric syndromes, delayed wound healing, atrophy and fragility of the skin, ecchymosis, and pseudotumor cerebri.
Neomycin¿¡ ´ëÇÑ Toxicity Á¤º¸ LD50 = 200 mg/kg (rat). Because of low absorption, it is unlikely that acute overdosage would occur with oral neomycin. However, prolonged administration could result in sufficient systemic drug levels to produce neurotoxicity, ototoxicity and/or nephrotoxicity.
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| Drug Interactions |
Dexamethasone¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Ambenonium The corticosteroid decreases the effect of anticholinesterasesAminoglutethimide Aminogluthetimide decreases the effect of dexamethasoneAmobarbital The barbiturate decreases the effect of the corticosteroidAnisindione The corticosteroid alters the anticoagulant effectAprepitant Aprepitant increases the effect and toxicity of dexamethasoneAprobarbital The barbiturate decreases the effect of the corticosteroidAspirin The corticosteroid decreases the effect of salicylatesButabarbital The barbiturate decreases the effect of the corticosteroidButalbital The barbiturate decreases the effect of the corticosteroidButethal The barbiturate decreases the effect of the corticosteroidDicumarol The corticosteroid alters the anticoagulant effectDihydroquinidine barbiturate The barbiturate decreases the effect of the corticosteroidEdrophonium The corticosteroid decreases the effect of anticholinesterasesEthotoin The enzyme inducer decreases the effect of the corticosteroidFosphenytoin The enzyme inducer decreases the effect of the corticosteroidHeptabarbital The barbiturate decreases the effect of the corticosteroidHexobarbital The barbiturate decreases the effect of the corticosteroidImatinib Decreases levels of imatinibMephenytoin The enzyme inducer decreases the effect of the corticosteroidMethohexital The barbiturate decreases the effect of the corticosteroidMethylphenobarbital The barbiturate decreases the effect of the corticosteroidMidodrine Increased arterial pressureNeostigmine The corticosteroid decreases the effect of anticholinesterasesPentobarbital The barbiturate decreases the effect of the corticosteroidPhenobarbital The barbiturate decreases the effect of the corticosteroidPhenytoin The enzyme inducer decreases the effect of the corticosteroidPrimidone The barbiturate decreases the effect of the corticosteroidPyridostigmine The corticosteroid decreases the effect of anticholinesterasesQuinidine barbiturate The barbiturate decreases the effect of the corticosteroidRifampin The enzyme inducer decreases the effect of the corticosteroidSecobarbital The barbiturate decreases the effect of the corticosteroidSunitinib Possible decrease in sunitinib levelsTalbutal The barbiturate decreases the effect of the corticosteroidWarfarin The corticosteroid alters the anticoagulant effectBismuth The corticosteroid decreases the effect of salicylatesAcenocoumarol The corticosteroid alters the anticoagulant effectSalicylate-magnesium The corticosteroid decreases the effect of salicylatesSalsalate The corticosteroid decreases the effect of salicylates
Neomycin¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Not Available
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸]
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| Food Interaction |
Dexamethasone¿¡ ´ëÇÑ Food Interaction Á¤º¸ Avoid alcohol.Take with food to reduce irritation.Avoid taking with grapefruit juice.
Neomycin¿¡ ´ëÇÑ Food Interaction Á¤º¸ Not Available
|
| Drug Target |
[Drug Target]
|
| Description |
Dexamethasone¿¡ ´ëÇÑ Description Á¤º¸ An anti-inflammatory 9-fluoro-glucocorticoid. [PubChem]
Neomycin¿¡ ´ëÇÑ Description Á¤º¸ A component of neomycin that is produced by Streptomyces fradiae. On hydrolysis it yields neamine and neobiosamine B. (From Merck Index, 11th ed)
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| Drug Category |
Dexamethasone¿¡ ´ëÇÑ Drug_Category Á¤º¸ Adrenergic AgentsAnti-inflammatory AgentsAntiemeticsAntineoplastic Agents, HormonalGlucocorticoids
Neomycin¿¡ ´ëÇÑ Drug_Category Á¤º¸ Anti-Bacterial AgentsAntibiotics
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| Smiles String Canonical |
Dexamethasone¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CC1CC2C3CCC4=CC(=O)C=CC4(C)C3(F)C(O)CC2(C)C1(O)C(=O)CO
Neomycin¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ NCC1OC(OC2C(N)CC(N)C(O)C2OC2OC(CO)C(OC3OC(CN)C(O)C(O)C3N)C2O)C(N)C(O)C1O
|
| Smiles String Isomeric |
Dexamethasone¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ C[C@@H]1C[C@H]2[C@@H]3CCC4=CC(=O)C=C[C@]4(C)[C@@]3(F)[C@@H](O)C[C@]2(C)[C@@]1(O)C(=O)CO
Neomycin¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ NC[C@H]1O[C@H](O[C@@H]2[C@@H](N)C[C@@H](N)[C@H](O)[C@H]2O[C@@H]2O[C@H](CO)[C@@H](O[C@H]3O[C@@H](CN)[C@@H](O)[C@H](O)[C@H]3N)[C@H]2O)[C@H](N)[C@@H](O)[C@@H]1O
|
| InChI Identifier |
Dexamethasone¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C22H29FO5/c1-12-8-16-15-5-4-13-9-14(25)6-7-19(13,2)21(15,23)17(26)10-20(16,3)22(12,28)18(27)11-24/h6-7,9,12,15-17,24,26,28H,4-5,8,10-11H2,1-3H3/t12-,15+,16+,17+,19+,20+,21+,22+/m1/s1
Neomycin¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C23H46N6O13/c24-2-7-13(32)15(34)10(28)21(37-7)40-18-6(27)1-5(26)12(31)20(18)42-23-17(36)19(9(4-30)39-23)41-22-11(29)16(35)14(33)8(3-25)38-22/h5-23,30-36H,1-4,24-29H2/t5-,6+,7-,8+,9-,10-,11-,12+,13-,14-,15-,16-,17-,18-,19-,20-,21-,22-,23+/m1/s1
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| Chemical IUPAC Name |
Dexamethasone¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ (8S,9R,10S,11S,13S,14S,16R,17R)-9-fluoro-11,17-dihydroxy-17-(2-hydroxyacetyl)-10,13,16-trimethyl-6,7,8,11,12,14,15,16-octahydrocyclopenta[a]phenanthren-3-one
Neomycin¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ (2R,3S,4R,5R,6R)-5-amino-2-(aminomethyl)-6-[(1R,2R,3S,4R,6S)-4,6-diamino-2-[(2S,3R,4S,5R)-4-[(2R,3R,4R,5S,6S)-3-amino-6-(aminomethyl)-4,5-dihydroxyoxan-2-yl]oxy-3-hydroxy-5-(hydroxymethyl)oxolan-2-yl]oxy-3-hydroxycyclohexyl]oxyoxane-3,4-diol
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| Drug-Induced Toxicity Related Proteins |
DEXAMETHASONE ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Brain-cadherin (BR-cadherin) Drug:dexamethasone Toxicity:osteoblast differentiation. [¹Ù·Î°¡±â] Replated Protein:Glucocorticoid-induced leucine zipper (GILZ) Drug:dexamethasone Toxicity:apoptosis. [¹Ù·Î°¡±â] Replated Protein:Signal transducer and activator of transcription 3 Drug:dexamethasone Toxicity:apoptosis. [¹Ù·Î°¡±â] Replated Protein:Heme oxygenase 1 Drug:dexamethasone Toxicity:oxidative injury. [¹Ù·Î°¡±â] Replated Protein:Alkaline phosphatase Drug:dexamethasone Toxicity:osteoblast differentiation. [¹Ù·Î°¡±â] Replated Protein:Interleukin-6 Drug:dexamethasone Toxicity:apoptosis. [¹Ù·Î°¡±â] Replated Protein:Ornithine decarboxylase Drug:dexamethasone Toxicity:pathogenesis of peptic ulcers. [¹Ù·Î°¡±â] Replated Protein:Aromatic-L-amino-acid decarboxylase Drug:dexamethasone Toxicity:pathogenesis of peptic ulcers. [¹Ù·Î°¡±â] Replated Protein:Interleukin-4 Drug:dexamethasone Toxicity:dexamethasone-induced differentiation of mouse myeloid leukemia cells. [¹Ù·Î°¡±â] Replated Protein:Gastrin Drug:dexamethasone Toxicity:pathogenesis of peptic ulcers. [¹Ù·Î°¡±â] Replated Protein:Interleukin-4 Drug:dexamethasone Toxicity:dexamethasone-induced differentiation of mouse myeloid leukemia cells. [¹Ù·Î°¡±â] Replated Protein:Cadherin-11 Drug:dexamethasone Toxicity:osteoblast differentiation. [¹Ù·Î°¡±â] Replated Protein:Haptoglobin Drug:dexamethasone Toxicity:hepatic lipidosis(fatty liver). [¹Ù·Î°¡±â] Replated Protein:Interferon alpha-7 Drug:dexamethasone Toxicity:apoptosis. [¹Ù·Î°¡±â] Replated Protein:C-jun-amino-terminal kinase-interacting protein Drug:dexamethasone Toxicity:apoptosis of multiple myeloma cells. [¹Ù·Î°¡±â] Replated Protein:Mitogen-activated protein kinase Drug:dexamethasone Toxicity:Dex-induced apoptosis. [¹Ù·Î°¡±â] Replated Protein:Cadherin-4 Drug:dexamethasone Toxicity:osteoblast differentiation. [¹Ù·Î°¡±â] Replated Protein:Glucose transporter 4 Drug:dexamethasone Toxicity:cushing's syndrome. [¹Ù·Î°¡±â] Replated Protein:Nuclear factor NF-kappa-B Drug:dexamethasone Toxicity:pulmonary inflammation. [¹Ù·Î°¡±â] Replated Protein:Signal transducer and activator of transcription 3 Drug:dexamethasone Toxicity:oxidative injury such as endotoxins and heme. [¹Ù·Î°¡±â] Replated Protein:Thrombomodulin Drug:dexamethasone Toxicity:deep venous thrombosis (DVT). [¹Ù·Î°¡±â] Replated Protein:Islet amyloid polypeptide Drug:dexamethasone Toxicity:marked stimulatory effect. [¹Ù·Î°¡±â] NEOMYCIN ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:NMDA receptor-regulated protein Drug:neomycin Toxicity:excitotoxic activation. [¹Ù·Î°¡±â]
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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. DEXAMETHASONE[GGT Increase][Composite Activity](Score) NA(Marginal) 0(Active) 0[Alkaline Phosphatase Increase](Activity Score) NA(Number of Rpts) NA(Index value) NA[SGOT Increase](Activity Score) NA(Number of Rpts) NA(Index value) NA[SGPT Increase](Activity Score) NA(Number of Rpts) NA(Index value) NA[LDH Increase](Activity Score) NA(Number of Rpts) NA(Index value) NA[GGT Increase](Activity Score) NA(Number of Rpts) NA(Index value) NA
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