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2. Áߵ ¶Ç´Â ÁßÁõ °íÇ÷¾Ð(stage 2) ȯÀÚ¿Í °°ÀÌ Ä¡·á ¸ñÇ¥ Ç÷¾Ð¿¡ µµ´ÞÇϱâ À§ÇØ º¹ÇÕÁ¦ Åõ¿©°¡ ÇÊ¿äÇÑ °æ¿ìÀÇ Ãʱâ¿ä¹ý
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- À̸£º£»ç¸£Åº 150 mg ¶Ç´Â È÷µå·ÎŬ·Î·ÎƼ¾ÆÁöµå¸¸À¸·Î Ç÷¾ÐÀÌ ÀûÀýÇÏ°Ô Á¶ÀýµÇÁö ¾ÊÀº ȯÀÚ¿¡°Ô À̸£º£»ç¸£Åº 150 mg/È÷µå·ÎŬ·Î·ÎƼ¾ÆÁöµå 12.5 mg 1ÀÏ 1ȸ 1Á¤À» Åõ¿©ÇÑ´Ù.
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2. Áߵ ¶Ç´Â ÁßÁõ °íÇ÷¾Ð(stage 2) ȯÀÚ¿¡ Ãʱâ¿ä¹ýÀ¸·Î Åõ¿©ÇϰíÀÚ ÇÏ´Â °æ¿ì ±âÀúÄ¡Ç÷¾Ð, Ä¡·á ¸ñÇ¥ Ç÷¾Ð, ´ÜÀÏÁ¦¿Í ºñ±³ÇÏ¿© Ä¡·á¸ñÇ¥ µµ´ÞÀÌ Áõ°¡ÇÒ °ÍÀ̶ó°í ¿¹»óµÇ´Â Á¤µµ µîÀ» °í·ÁÇÏ¿© °³º°ÈÇØ¾ß ÇÑ´Ù. Åë»ó À̸£º£»ç¸£Åº 150 mg/È÷µå·ÎŬ·Î·ÎƼ¾ÆÁöµå 12.5 mg 1ÀÏ 1ȸ 1Á¤ ¿ä¹ýÀ¸·Î ½ÃÀÛÇϸç, Ç÷¾ÐÁ¶ÀýÀÌ ÇÊ¿äÇÑ °æ¿ì 1 ¢¦ 2ÁÖ ÈÄ ÃÖ´ë À̸£º£»ç¸£Åº 300 mg/È÷µå·ÎŬ·Î·ÎƼ¾ÆÁöµå 25 mg±îÁö Áõ·®ÇÒ ¼ö ÀÖ´Ù. Ç÷·ù·® ¼Õ½Ç(intravascular volume depletion)ÀÌ Àִ ȯÀÚ¿¡ ÀÌ ¾àÀ» Ãʱ⠿ä¹ýÀ¸·Î Åõ¿©ÇÏ´Â °ÍÀº ±ÇÀåµÇÁö ¾Ê´Â´Ù.
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| Related FDA Approved Drug |
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Irbesartan and diuretics / C09DA04
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| Mechanism of Action |
Hydrochlorothiazide¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ As a diuretic, hydrochlorothiazide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like hydrochlorothiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of hydrochlorothiazide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.
Irbesartan¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Irbesartan is a nonpeptide angiotensin II antagonist that selectively blocks the binding of angiotensin II to the AT1 receptor. In the renin-angiotensin system, angiotensin I is converted by angiotensin-converting enzyme (ACE) to form angiotensin II. Angiotensin II stimulates the adrenal cortex to synthesize and secrete aldosterone, which decreases the excretion of sodium and increases the excretion of potassium. Angiotensin II also acts as a vasoconstrictor in vascular smooth muscle. Irbesartan, by blocking the binding of angiotensin II to the AT1 receptor, promotes vasodilation and decreases the effects of aldosterone. The negative feedback regulation of angiotensin II on renin secretion also is inhibited, but the resulting rise in plasma renin concentrations and consequent rise in angiotensin II plasma concentrations do not counteract the blood pressure–lowering effect that occurs.
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| Pharmacology |
Hydrochlorothiazide¿¡ ´ëÇÑ Pharmacology Á¤º¸ Thiazides such as hydrochlorothiazide promote water loss from the body (diuretics). They inhibit Na+/Cl- reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue.
Irbesartan¿¡ ´ëÇÑ Pharmacology Á¤º¸ Irbesartan is a specific competitive antagonist of AT1 receptors with a much greater affinity (more than 8500-fold) for the AT1 receptor than for the AT2 receptor and no agonist activity.
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| Metabolism |
Hydrochlorothiazide¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Not Available
Irbesartan¿¡ ´ëÇÑ Metabolism Á¤º¸ # Phase_1_Metabolizing_Enzyme:Cytochrome P450 2C9 (CYP2C9)
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| Protein Binding |
Hydrochlorothiazide¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 67.9%
Irbesartan¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ 90% bound to serum proteins (primarily albumin and a1-acid glycoprotein) with negligible binding to cellular components of blood.
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| Half-life |
Hydrochlorothiazide¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 5.6 and 14.8 hours
Irbesartan¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 11-15 hours
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| Absorption |
Hydrochlorothiazide¿¡ ´ëÇÑ Absorption Á¤º¸ 50-60%
Irbesartan¿¡ ´ëÇÑ Absorption Á¤º¸ Rapid and complete with an average absolute bioavailability of 60-80%. Food has no affect on bioavailability.
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| Pharmacokinetics |
HydrochlorothiazideÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- ÀÌ´¢È¿°ú ¹ßÇö½Ã°£ : °æ±¸ : 2½Ã°£ À̳»
- ÃÖ´ëÈ¿°ú ¹ßÇö½Ã°£ : 4½Ã°£
- ÀÛ¿ëÁö¼Ó½Ã°£ : 6-12½Ã°£
- Èí¼ö : °æ±¸ : 60-80%
- ¼Ò½Ç : ¹Ìº¯Èü·Î ½Å¹è¼³µÈ´Ù.
IrbesartanÀÇ ¾à¹°µ¿·ÂÇÐÀÚ·á
- ÃÖ°íÇ÷Áß³óµµ µµ´Þ½Ã°£ : 1.5 -2 ½Ã°£
- Ç×°íÇ÷¾Ð È¿°ú ¹ßÇö - Åõ¿© ½ÃÀÛ ÈÄ 2ÁÖ À̳»
- Ç×°íÇ÷¾Ð ÃÖ´ë È¿°ú - Åõ¿© ½ÃÀÛ ÈÄ 2-6ÁÖ »çÀÌ
- »ýü³»ÀÌ¿ë·ü : 60-80%
- ºÐÆ÷¿ëÀû : 53-93 L
- ¹Ý°¨±â : 11-15 ½Ã°£
- ´ë»ç : CYP2C9¿¡ ÀÇÇØ ´ë»çµÊ
- ¼Ò½Ç : 78% ´ëº¯, 22% ´¢¹è¼³
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| Biotransformation |
Hydrochlorothiazide¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hydrochlorothiazide is not metabolized.
Irbesartan¿¡ ´ëÇÑ Biotransformation Á¤º¸ Hepatic. Irbesartan is metabolized via glucuronide conjugation and oxidation. In vitro studies of irbesartan oxidation by cytochrome P450 isoenzymes indicated irbesartan was oxidized primarily by 2C9; metabolism by 3A4 was negligible.
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| Toxicity |
Hydrochlorothiazide¿¡ ´ëÇÑ Toxicity Á¤º¸ The most common signs and symptoms observed are those caused by electrolyte depletion (hypokalemia, hypochloremia, hyponatremia) and dehydration resulting from excessive diuresis. If digitalis has also been administered, hypokalemia may accentuate cardiac arrhythmias. The oral LD50 of hydrochlorothiazide is greater than 10 g/kg in the mouse and rat.
Irbesartan¿¡ ´ëÇÑ Toxicity Á¤º¸ Hypotension and tachycardia; bradycardia might also occur from overdose, LD50=mg/kg(orally in rat)
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| Drug Interactions |
Hydrochlorothiazide¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Amantadine The diuretic increases the adverse effect of amantadineDeslanoside Possible electrolyte variations and arrhythmiasDigitoxin Possible electrolyte variations and arrhythmiasDigoxin Possible electrolyte variations and arrhythmiasLithium The thiazide diuretic increases serum levels of lithiumDofetilide Increased risk of cardiotoxicity and arrhythmiasDiazoxide Significant hyperglycemic effect
Irbesartan¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Amiloride Increased risk of hyperkaliemiaDrospirenone Increased risk of hyperkaliemiaSpironolactone Increased risk of hyperkaliemiaPotassium Increased risk of hyperkaliemiaLithium The ARB increases serum levels of lithiumTriamterene Increased risk of hyperkaliemia
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CYP450 Drug Interaction |
[CYP450 TableÁ÷Á¢Á¶È¸] Irbesartan¿¡ ´ëÇÑ P450 table
SUBSTRATES
CYP 2C9
NSAIDs:
diclofenac
ibuprofen
piroxicam
Oral Hypoglycemic Agents:
tolbutamide
glipizide
Angiotensin II Blockers:
NOT candesartan
**irbesartan**
losartan
NOT valsartan
celecoxib
fluvastatin naproxen
phenytoin
sulfamethoxazole
tamoxifen
tolbutamide
torsemide
warfarin
INHIBITORS
CYP 2C9
amiodarone
fluconazole
isoniazid
INDUCERS
CYP 2C9
rifampin
secobarbital
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| Food Interaction |
Hydrochlorothiazide¿¡ ´ëÇÑ Food Interaction Á¤º¸ Avoid alcohol.Avoid excess salt/sodium unless otherwise instructed by your physician.Take with food.Increase potassium intake; add a banana or orange juice; unless instructed otherwise.Avoid natural licorice.Do not take calcium, aluminum, magnesium or Iron supplements within 2 hours of taking this medication.
Irbesartan¿¡ ´ëÇÑ Food Interaction Á¤º¸ Take without regard to meals.
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| Drug Target |
[Drug Target]
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| Description |
Hydrochlorothiazide¿¡ ´ëÇÑ Description Á¤º¸ A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It has been used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism. [PubChem]
Irbesartan¿¡ ´ëÇÑ Description Á¤º¸ Irbesartan is an angiotensin II receptor antagonist used mainly for the treatment of hypertension.
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| Dosage Form |
Irbesartan¿¡ ´ëÇÑ Dosage_Form Á¤º¸ Tablet Oral
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| Drug Category |
Hydrochlorothiazide¿¡ ´ëÇÑ Drug_Category Á¤º¸ Antihypertensive AgentsDiureticsSodium Chloride Symporter Inhibitors
Irbesartan¿¡ ´ëÇÑ Drug_Category Á¤º¸ Angiotensin II Receptor AntagonistsAngiotensin II Type 1 Receptor BlockersAntihypertensive Agents
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| Smiles String Canonical |
Hydrochlorothiazide¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ NS(=O)(=O)C1=C(Cl)C=C2NCNS(=O)(=O)C2=C1
Irbesartan¿¡ ´ëÇÑ Smiles_String_canonical Á¤º¸ CCCCC1=NC2(CCCC2)C(=O)N1CC1=CC=C(C=C1)C1=CC=CC=C1C1=NNN=N1
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| Smiles String Isomeric |
Hydrochlorothiazide¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ NS(=O)(=O)C1=C(Cl)C=C2NCNS(=O)(=O)C2=C1
Irbesartan¿¡ ´ëÇÑ Smiles_String_isomeric Á¤º¸ CCCCC1=NC2(CCCC2)C(=O)N1CC1=CC=C(C=C1)C1=CC=CC=C1C1=NNN=N1
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| InChI Identifier |
Hydrochlorothiazide¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C7H8ClN3O4S2/c8-4-1-5-7(2-6(4)16(9,12)13)17(14,15)11-3-10-5/h1-2,10-11H,3H2,(H2,9,12,13)/f/h9H2
Irbesartan¿¡ ´ëÇÑ InChI_Identifier Á¤º¸ InChI=1/C25H28N6O/c1-2-3-10-22-26-25(15-6-7-16-25)24(32)31(22)17-18-11-13-19(14-12-18)20-8-4-5-9-21(20)23-27-29-30-28-23/h4-5,8-9,11-14H,2-3,6-7,10,15-17H2,1H3,(H,27,28,29,30)/f/h29H
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| Chemical IUPAC Name |
Hydrochlorothiazide¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 6-chloro-1,1-dioxo-3,4-dihydro-2H-benzo[e][1,2,4]thiadiazine-7-sulfonamide
Irbesartan¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 2-butyl-3-[[4-[2-(2H-tetrazol-5-yl)phenyl]phenyl]methyl]-1,3-diazaspiro[4.4]non-1-en-4-one
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µå·°ÀÎÆ÷ ÀǾàÇмúÁ¤º¸´Â ½ÄǰÀǾàǰ¾ÈÀüóÀÇ Á¦Ç°Çã°¡»çÇ×, Çмú¹®Çå, Á¦¾àȸ»ç Á¦°øÁ¤º¸ µîÀ» ±Ù°Å·Î ÀÛ¼ºµÈ Âü°í Á¤º¸ÀÔ´Ï´Ù.
Á¤º¸ÀÇ Á¤È®¼ºÀ» À§ÇØ ³ë·ÂÇϰí ÀÖÀ¸³ª ÆíÁý»óÀÇ ¿À·ù, Çã°¡»çÇ× º¯°æ, Ãß°¡ÀûÀÎ Çмú¿¬±¸ ¶Ç´Â Àӻ󿬱¸ ¹ßÇ¥ µîÀ¸·Î ÀÎÇØ ¹ß»ýÇÏ´Â ¹®Á¦¿¡ ´ëÇØ µå·°ÀÎÆ÷´Â
Ã¥ÀÓÀ» ÁöÁö ¾Ê½À´Ï´Ù. ÀÚ¼¼ÇÑ ³»¿ëÀº ¡°Ã¥ÀÓÀÇ ÇÑ°è ¹× ¹ýÀû°íÁö¡±¸¦ ÂüÁ¶ÇØ ÁֽʽÿÀ.
¹Ýµå½Ã Á¦Á¶¡¤¼öÀÔ»ç, ÆÇ¸Å»ç, ÀÇ»ç, ¾à»ç¿¡°Ô ÃÖÁ¾ÀûÀ¸·Î È®ÀÎÇϽñ⠹ٶø´Ï´Ù.
ÀüÈ: 02-3486-1061 ¤Ó À̸ÞÀÏ: webmaster@druginfo.co.kr
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