- 同
- Lanoxin
- 関
- Digoxin
WordNet
- digitalis preparation (trade name Lanoxin) used to treat congestive heart failure or cardiac arrhythmia; helps the heart beat more forcefully (同)Lanoxin
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/06/06 14:54:19」(JST)
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Not to be confused with Dioxin.
| Systematic (IUPAC) name | |
|---|---|
| 4-[(3S,5R,8R,9S,10S,12R,13S,14S)-3-[(2S,4S,5R,6R)-5-[(2S,4S,5R,6R)-5-[(2S,4S,5R,6R)-4,5-dihydroxy-6-methyl-oxan-2-yl]oxy-4-hydroxy-6-methyl-oxan-2-yl]oxy-4-hydroxy-6-methyl-oxan-2-yl]oxy-12,14-dihydroxy-10,13-dimethyl-1,2,3,4,5,6,7,8,9,11,12,15,16,17-tetradecahydrocyclopenta[a]phenanthren-17-yl]-5H-furan-2-one | |
| Clinical data | |
| Trade names | Lanoxin |
| AHFS/Drugs.com | monograph |
| MedlinePlus | a682301 |
| Pregnancy cat. | A (Au), C (U.S.) |
| Legal status | S4 (Au), POM (UK), ℞-only (U.S.) |
| Routes | Oral, Intravenous |
| Pharmacokinetic data | |
| Bioavailability | 60 to 80% (Oral) |
| Protein binding | 25% |
| Metabolism | Hepatic (16%) |
| Half-life | 36 to 48 hours (patients with normal renal function) |
| Excretion | Renal |
| Identifiers | |
| CAS number | 20830-75-5 Y |
| ATC code | C01AA05 |
| PubChem | CID 2724385 |
| DrugBank | DB00390 |
| ChemSpider | 2006532 Y |
| UNII | 73K4184T59 Y |
| KEGG | D00298 Y |
| ChEBI | CHEBI:4551 Y |
| ChEMBL | CHEMBL1751 Y |
| Chemical data | |
| Formula | C41H64O14 |
| Mol. mass | 780.938 g/mol |
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SMILES
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InChI
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| Physical data | |
| Melt. point | 249.3 °C (481 °F) |
| Solubility in water | 0.0648 mg/mL (20 °C) |
| Y (what is this?) (verify) |
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Digoxin INN (/dɨˈdʒɒksɨn/[1]) is a purified cardiac glycoside extracted from the foxglove plant, Digitalis lanata.[2] Its corresponding aglycone is digoxigenin, and its acetyl derivative is acetyldigoxin. Digoxin is widely used in the treatment of various heart conditions, namely atrial fibrillation, atrial flutter and sometimes heart failure that cannot be controlled by other medication. Digoxin preparations are commonly marketed under the trade names Lanoxin, Digitek, and Lanoxicaps. It is also available as a 0.05 mg/ml oral solution and 0.25 mg/ml or 0.5 mg/ml injectable solution. It is marketed by GlaxoSmithKline and many other pharmaceutic manufacturers.
Contents
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Medical use[edit]
Today, the most common indications for digoxin are atrial fibrillation and atrial flutter with rapid ventricular response. Beta blockers and/or calcium channel blockers should be the first choice.[3][4] High ventricular rate leads to insufficient diastolic filling time. By slowing down the conduction in the AV node and increasing its refractory period, digoxin can reduce the ventricular rate. The arrhythmia itself is not affected, but the pumping function of the heart improves owing to improved filling.
The use of digoxin in heart problems during sinus rhythm was once standard, but is now controversial. In theory, the increased force of contraction should lead to improved pumping function of the heart, but its effect on prognosis is disputable, and other effective treatments are now available. Digoxin is no longer the first choice for congestive heart failure, but can still be useful in patients who remain symptomatic despite proper diuretic and ACE inhibitor treatment.
Digitalis/digoxin has recently fallen out of favor because it did not demonstrate a mortality benefit in patients with congestive heart failure; however, it did demonstrate a reduction in hospitalizations for this condition.[5] Because other therapies have shown a mortality benefit in congestive heart failure, maximizing other therapies (e.g., beta blockers) first is recommended before using digoxin.
Pharmacokinetic properties[edit]
Digoxin is usually given by mouth, but can also be given by IV injection in urgent situations (the IV injection should be slow, and heart rhythm should be monitored). While IV therapy may be better tolerated (less nausea), digoxin has a very long distribution half-life into the cardiac tissue, which will delay its onset of action by a number of hours. The half-life is about 36 hours, digoxin is given once daily, usually in 125-μg or 250-μg doses.
In patients with decreased kidney function, the half-life is considerably longer, calling for a reduction in dose or a switch to a different glycoside, such as digitoxin (not available in the United States), which has a much longer elimination half-life of around seven days, elimination is mainly by renal excretion and involves P-glycoprotein which leads to significant clinical interactions with other drugs commonly used in patients with heart problems. These include: spironolactone, verapamil and amiodarone.
Effective plasma levels vary depending on the medical indication. For congestive heart failure, levels between 0.5 and 1.0 ng/ml are recommended.[6] This recommendation is based on post hoc analysis of prospective trials, suggesting higher levels may be associated with increased mortality rates. For heart rate control (atrial fibrillation), plasma levels are less defined and are generally titrated to a goal heart rate. Typically, digoxin levels are considered therapeutic for heart rate control between 1.0 and 2.0 ng/ml. In suspected toxicity or ineffectiveness, digoxin levels should be monitored. Plasma potassium levels also need to be closely controlled (see side effects below).
Quinidine, verapamil, and amiodarone increases plasma levels of digoxin (by displacing tissue binding sites and depressing renal digoxin clearance), so plasma digoxin must be monitored carefully.
Researchers at Yale University looked at data from an earlier study to see if digoxin affected men and women differently. That study determined digoxin, which has been used for centuries and makes the heart contract more forcefully, did not reduce deaths overall, but did result in less hospitalization. Researcher Dr. Harlan Krumholz said they were surprised to find women in the study who took digoxin died "more frequently" (33%) than women who took a placebo pill (29%). They calculated digoxin increased the risk of death in women by 23%. There was no difference in the death rate for men in the study.
Digoxin is also used as a standard control substance to test for p-glycoprotein inhibition.
Adverse effects[edit]
Main article: Digoxin toxicity
The occurrence of adverse drug reactions is common, owing to its narrow therapeutic index (the margin between effectiveness and toxicity). Adverse effects are concentration-dependent, and are rare when plasma digoxin concentration is <0.8 μg/l.[7] They are also more common in patients with low potassium levels (hypokalemia), since digoxin normally competes with K+ ions for the same binding site on the Na+/K+ ATPase pump.
Common adverse effects (≥1% of patients) include loss of appetite, nausea, vomiting and diarrhea as gastrointestinal motility increases. Other common effects are blurred vision, visual disturbances (yellow-green halos and problems with color perception), confusion, drowsiness, dizziness, insomnia, nightmares, agitation, and depression, as well as a higher acute sense of sensual activities.[8] Less frequent adverse effects (0.1%–1%) include: acute psychosis, delirium, amnesia, convulsions, shortened QRS complex, atrial or ventricular extrasystoles, paroxysmal atrial tachycardia with AV block, ventricular tachycardia or fibrillation, and heart block.[7] Rarely, digoxin has been shown to cause thrombocytopenia. Gynaecomastia (enlargement of breast tissue) is mentioned in many textbooks as a side effect, thought to be due to the estrogen-like steroid moiety of the digoxin molecule,[9] but when systematically sought, the evidence for this is equivocal.[10] The pharmacological actions of digoxin usually result in electrocardiogram changes, including ST depression or T wave inversion, which do not indicate toxicity. PR interval prolongation, however, may be a sign of digoxin toxicity. Additionally, increased intracellular Ca2+ may cause a type of arrhythmia called bigeminy (coupled beats), eventually ventricular tachycardia or fibrillation. The combination of increased (atrial) arrhythmogenesis and inhibited atrioventricular conduction (for example paroxysmal atrial tachycardia with A-V block - so-called "PAT with block") is said to be pathognomonic (i.e. diagnostic) of digoxin toxicity.[11]
An often described, but rarely seen, adverse effect of digoxin is a disturbance of color vision (mostly yellow and green) called xanthopsia. Vincent van Gogh's "Yellow Period" may have somehow been influenced by concurrent digitalis therapy. Other oculotoxic effects of digoxin include generalized blurry vision, as well as seeing a "halo" around each point of light.[12] The latter effect can also be seen in van Gogh's Starry Night. Evidence of van Gogh's digoxin use is supported by multiple self portraits that include the foxglove plant, from which digoxin is obtained. (e.g. Portrait of Dr. Gachet)
Digoxin plasma concentrations may increase while on antimalarial medication hydroxychloroquine (based on two case reports from 1982).[13]
In overdose, the usual supportive measures are needed. If arrhythmias prove troublesome, or malignant hyperkalaemia occurs (inexorably rising potassium level due to paralysis of the cell membrane-bound, ATPase-dependent Na/K pumps), the specific antidote is antidigoxin (antibody fragments against digoxin, trade names Digibind and Digifab).[14] Toxicity can also be treated with higher than normal doses of potassium. Digoxin is not removed by hemodialysis or peritoneal dialysis with enough effectiveness to treat toxicity.
Digoxin has potentially dangerous interactions with verapamil,[15] amiodarone, erythromycin, and epinephrine (as would be injected with a local anesthetic).
Actions[edit]
| This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (April 2012) |
The main pharmacological effects of digoxin are on the heart. Extracardiac effects are responsible for some of the therapeutic and many of the adverse effects (see above). It has mechanical effects as it increases myocardial contractility; however, the duration of the contractile response is just slightly increased. Overall, the heart rate is decreased, while blood pressure increases as the stroke volume is increased, leading to increased tissue perfusion. Myocardial efficiency is due to improved hemodynamics, and the ventricular function curve is improved.
Other, electrical effects are an initial brief increase in action potential, followed by a decrease as the K+ conductance increases due to an increased intracellular amounts of Ca2+ ions. The refractory period of the atria and ventricles is decreased, while it increases in the sinoatrial and AV nodes. A less negative resting membrane potential is made, leading to increased excitability. Other, more indirect effects are cholinomimetic because of vagal stimulation, giving rise to AV nodal delay.
The conduction velocity increases in the atria, but decreases in the AV node. The effect upon Purkinje fibers and ventricles is negligible. Automaticity is also increased, in the atria, AV node, Purkinje fibers and ventricles.
ECG changes are increased PR interval, due to decreased AV conduction, and a decreased QT interval because of the altered duration of decreased action potential. Also, the T wave is inverted, accompanied by ST depression. It may cause AV junctional rhythm and ectopic beats (bigeminy) resulting in ventricular tachycardia and fibrillation.
Slight vasodilation is seen in heart failure. This effect is contrary to effects that should be seen as a result of increased intracellular calcium levels, but this occurs since digoxin improves hemodynamics, which leads to restored angiotensin levels and decreased sympathetic discharge, causing indirect vasodilation.
Digoxin also affects the kidney by increased renal blood flow and increased glomerular filtration rate. A mild diuretic effect is seen only in heart failure.
Mechanism of action[edit]
The mechanism of action is not completely understood; however, the current hypothesis is outlined below.
Digoxin binds to a site on the extracellular aspect of the α-subunit of the Na+/K+ ATPase pump in the membranes of heart cells (myocytes) and decreases its function. This causes an increase in the level of sodium ions in the myocytes, which leads to a rise in the level of intracellular calcium ions. This occurs because the sodium/calcium exchanger on the plasma membrane depends on a constant inward sodium gradient to pump out calcium. Digoxin decreases the sodium concentration gradient and the subsequent calcium outflow, thus raising the calcium concentration in myocardiocytes and pacemaker cells.
Increased intracellular calcium lengthens phase 4 and phase 0 of the cardiac action potential, which leads to a decrease in heart rate.[16] Increased amounts of Ca2+ also leads to increased storage of calcium in the sarcoplasmic reticulum, causing a corresponding increase in the release of calcium during each action potential. This leads to increased contractility (the force of contraction) of the heart without increasing heart energy expenditure.
There is also evidence that digoxin increases vagal activity, thereby decreasing heart rate by slowing depolarization of pacemaker cells in the AV node.[17] This negative chronotropic effect would therefore be synergistic with the direct effect on cardiac pacemaker cells. Digoxin is used widely in the treatment of various arrhythmias.
Society and culture[edit]
Charles Cullen admitted in 2003 to killing as many as 40 hospital patients with overdoses of heart medication—usually digoxin—at hospitals in New Jersey and Pennsylvania over his 16-year career as a nurse. On March 10, 2006, he was sentenced to 18 consecutive life sentences and is not eligible for parole.[18]
On April 25, 2008, the FDA issued a press release[19] alerting the public to a Class I recall of Digitek, a brand of digoxin produced by Mylan.[20] Some tablets had been released at double thickness and therefore double strength, causing some patients to experience digoxin toxicity. A class-action lawsuit against the Icelandic generic drug maker Actavis was announced two weeks later.[21]
On March 31, 2009, the FDA announced another generic digoxin pill recall by posting this company press release on the agency's web site: "Caraco Pharmaceutical Laboratories, Ltd. Announces a Nationwide Voluntary Recall of All Lots of Digoxin Tablets Due to Size Variability".
This March 31 press release from Caraco, a generic pharmaceutical company, states:
[All] tablets of Caraco brand Digoxin, USP, 0.125 mg, and Digoxin, USP, 0.25 mg, distributed prior to March 31, 2009, which are not expired and are within the expiration date of September, 2011, are being voluntarily recalled to the consumer level. The tablets are being recalled because they may differ in size and therefore could have more or less of the active ingredient, digoxin.
A 2008 study suggested digoxin has beneficial effects not only for the heart, but also in reducing the risk of certain kinds of cancer.[22] However, comments on this study suggested that digoxin is not effective at reducing cancer risk at therapeutic concentrations of the drug,[23] so the results need further investigation.[24]
References[edit]
- ^ OED
- ^ Hollman A (1996). "Digoxin comes from Digitalis lanata". British Medical Journal 312 (7035): 912.
- ^ Sticherling C, Oral H, Horrocks J et al. (November 2000). "Effects of digoxin on acute, atrial fibrillation-induced changes in atrial refractoriness" (pdf). Circulation 102 (20): 2503–2508. doi:10.1161/01.CIR.102.20.2503. PMID 11076824.
- ^ Hallberg P, Lindbäck J, Lindahl B, Stenestrand U, Melhus H (October 2007). "Digoxin and mortality in atrial fibrillation: a prospective cohort study". European Journal of Clinical Pharmacology 63 (10): 959–971. doi:10.1007/s00228-007-0346-9. PMID 17684738.
- ^ "The effect of digoxin on mortality and morbidity in patients with heart failure. The Digitalis Investigation Group". The New England Journal of Medicine 336 (8): 525–533. February 1997. doi:10.1056/NEJM199702203360801. PMID 9036306.
- ^ Hunt SA, Abraham, WT, Chin, MH et al. (September 2005). "ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society" (pdf). Circulation 112 (12): e154–e235. doi:10.1161/CIRCULATIONAHA.105.167586. PMID 16160202.
- ^ a b Rossi S, ed. (2006). Australian Medicines Handbook 2006. Adelaide. ISBN 0-9757919-2-3.
- ^ Tripathi KD (ed.). Essentials of Medical Pharmacology (6th ed.). New Delhi: Jaypee Publications. ISBN 81-8448-085-7.
- ^ Moscovitz T, Aldrighi JM, Abrahanshon PA et al. (April 2005). "Repercussions of digoxin, digitoxin and estradiol on the endometrial histomorphometry of oophorectomized mice". Gynecology and Endocrinology 20 (4): 213–220. doi:10.1080/09513590400021219. PMID 16019364.
- ^ Thompson DF, Carter JR (1993). "Drug-induced gynecomastia". Pharmacotherapy 13 (1): 37–45. PMID 8094898.
- ^ Doering W, König E, Sturm W (1977). "(title in German)" [Digitalis intoxication: specifity and significance of cardiac and extracardiac symptoms. part I: Patients with digitalis-induced arrhythmias (author's transl)]. Zeitschrift für Kardiologie (in German) 66 (3): 121–128. PMID 857452.
- ^ Goldfrank LW (2006). Goldfrank's Toxicologic Emergencies (8th ed.). New York: McGraw-Hill.
- ^ Leden I (1982). "Digoxin-hydroxychloroquine interaction?". Acta Medica Scandinavica 211 (5): 411–412. doi:10.1111/j.0954-6820.1982.tb01971.x. PMID 7113754.
- ^ Flanagan RJ, Jones AL (2004). "Fab Antibody Fragments: Some Applications in Clinical Toxicology". Drug Safety 27 (14): 1115–1133. doi:10.2165/00002018-200427140-00004. PMID 15554746.
- ^ Kaplanski J, Weinhouse E, Topaz M, Genchik G (1983). "Verapamil and digoxin: interactions in the rat". Research Communications in Chemical Pathology and Pharmacology 42 (3): 377–388. PMID 6665298.
- ^ Tripathi KD (ed.). Essentials of Medical Pharmacology (6th ed.). New Delhi: Jaypee Publications. p. 498. ISBN 81-8448-085-7.
- ^ Goodman DJ et al. (1975). "Effect of digoxin on atioventricular conduction. Studies in patients with and without cardiac autonomic innervation". Circulation 51 (2): 251–256. doi:10.1161/01.CIR.51.2.251. PMID 1089491.
- ^ "Victims' families set to confront killer". USA Today. 2006-01-01.
- ^ "Recalls, Market Withdrawals & Safety Alerts". FDA. 2008-10-15. Retrieved 2011-11-08.
- ^ "Urgent Digitek Digoxin Recall". U.S. Recall News. 2008-04-28. Retrieved 2009-07-25.
- ^ "Patients Sue Icelandic Drugmaker Over Recalled Heart Drug". Wall Street Journal. 2008-05-09. Retrieved 2009-07-25.
- ^ Zhang, H.; Qian, D. Z.; Tan, Y. S.; Lee, K.; Gao, P.; Ren, Y. R.; Rey, S.; Hammers, H.; Chang, D. (2008). "Inaugural Article: Digoxin and other cardiac glycosides inhibit HIF-1 synthesis and block tumor growth". Proceedings of the National Academy of Sciences (re: glycosides) 105 (50): 19579–19586. doi:10.1073/pnas.0809763105. PMC 2604945. PMID 19020076. edit
- ^ Lopez-Lazaro M (March 2009). "Digoxin, HIF-1, and cancer" (pdf). PNAS 106 (9): E26. Bibcode:2009PNAS..106...26L. doi:10.1073/pnas.0813047106. PMC 2651277. PMID 19240208.
- ^ Zhang, H.; Semenza, G. L. (2009). "Reply to Lopez-Lazaro: Evidence that digoxin inhibits human cancer". Proceedings of the National Academy of Sciences 106 (9): E27. doi:10.1073/pnas.0900125106. edit
Further reading[edit]
- Rang HP, Dale MM, Ritter JM, Moore PK (2003). Pharmacology (5th ed.). Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4.
- Summary of Product Characteristics, Digoxin 0,125 mg, Zentiva a.s.
- Lüllmann (2003). Pharmakologie und Toxikologie (15th ed.). Georg Thieme Verlag. ISBN 3-13-368515-5.
- Lanatoside C (isolanid, Cedilanid - four glycoside analog), Digoxigenin (aglycone analog)
External links[edit]
- U.S. National Library of Medicine: Drug Information Portal — Digoxin
- Commonly used website to calculate empiric digoxin doses for medical purposes for heart problems
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UpToDate Contents
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- 1. ジゴキシンによる治療：初回投与、モニタリング、および用量変更 treatment with digoxin initial dosing monitoring and dose modification
- 2. ジギタリス（強心配糖体）中毒 digitalis cardiac glycoside poisoning
- 3. 収縮能障害による心不全におけるジゴキシンの使用 use of digoxin in heart failure due to systolic dysfunction
- 4. ジゴキシン中毒による不整脈 cardiac arrhythmias due to digoxin toxicity
- 5. ジゴキシン中毒患者におけるジゴキシン特異的抗体（Fab）フラグメントに対する投与レジメン dosing regimen for digoxin specific antibody fab fragments in patients with digoxin toxicity
English Journal
- Should pharmacotherapy of digoxin be reviewed in male patients with heart failure in the case of association with carvedilol?
- Souza FC1, Neri JS1, Marques EB1, Barros RB1, Scaramello CB2.
- International journal of cardiology.Int J Cardiol.2015 Jul 15;191:4-6. doi: 10.1016/j.ijcard.2015.04.247. Epub 2015 May 1.
- PMID 25957928
- Development and validation of an UFLC-MS/MS assay for the absolute quantitation of nine notoginsenosides in rat plasma: Application to the pharmacokinetic study of Panax Notoginseng Extract.
- Zhou L1, Xing R2, Xie L1, Rao T1, Wang Q1, Ye W1, Fu H1, Xiao J2, Shao Y2, Kang D2, Wang G1, Liang Y3.
- Journal of chromatography. B, Analytical technologies in the biomedical and life sciences.J Chromatogr B Analyt Technol Biomed Life Sci.2015 Jul 15;995-996:46-53. doi: 10.1016/j.jchromb.2015.05.022. Epub 2015 May 19.
- Notoginsenosides, the main active gradients of Chinese traditional medicine Panax notoginseng, possesses a variety of biological activities including antioxidant property, anti-hyperglycemic, anti-obese, etc. However, pharmacokinetic evaluation for notoginsenosides is still a formidable task due to
- PMID 26021851
- Dialysate and Serum Potassium in Hemodialysis.
- Hung AM1, Hakim RM2.
- American journal of kidney diseases : the official journal of the National Kidney Foundation.Am J Kidney Dis.2015 Jul;66(1):125-32. doi: 10.1053/j.ajkd.2015.02.322. Epub 2015 Mar 28.
- Most patients with end-stage renal disease depend on intermittent hemodialysis to maintain levels of serum potassium and other electrolytes within a normal range. However, one of the challenges has been the safety of using a low-potassium dialysate to achieve that goal, given the concern about the e
- PMID 25828570
Related Links
- Lanoxin (digoxin) is used to treat congestive heart failure and atrial fibrillation. Includes Lanoxin side effects, interactions and indications. ... Keep taking Lanoxin as directed, even if you feel well. Get your prescription refilled before ...
- Lanoxin /ジゴキシンは、心不全の治療に使用される心拍リズムの異常などの慢性心房細動患者で心拍数を遅くする。一般名：ジゴキシンストリップあたり10錠
Related Pictures
★リンクテーブル★
| リンク元 | 「ジゴキシン」「digoxin」 |
「ジゴキシン」
- first aid step1 2006 p.84,241,244
- 用量を覚える：治療域血中濃度 1-2 ng/ml
薬理作用
- 心筋収縮力の増強、心拍数の抑制および刺激伝導速度の低下
- 心電図の変化
- ↑PR、↓QT、↓ST(盆状低下, scooping of ST segment)、陰性T波
動態
- 腎臓で代謝を受ける
適応
注意
- β遮断薬：房室伝導を抑制するので(陰性変伝導作用)、完全ブロックを起こす危険が高まる
- カルシウム拮抗薬：β遮断薬とカルシウム拮抗薬は、心筋の収縮力をさげ、ジギタリスの作用を増強しうる
- K+-wasting diuretics：低カリウム血症からジギタリス中毒を引き越しやすくなる
禁忌
副作用
- 消化器症状(nausea, vomiting, diarrhea)
- 循環器症状(不整脈)
- blurry yellow vision
- ゴッホの描いた「医師ガッシェの肖像 」にもジギタリスが描かれているが、晩年のゴッホは、このガッシェ博士の治療を受け、「癲癇（てんかん）」の薬として服用していて「ジギタリス中毒」で、視界が黄色がかっていたため、画風に影響を与えたとの説もある(http://blog.goo.ne.jp/yousan02/e/92dc9d78d3a967dcafa3254b81165198)
- 誘因：腎不全、低カリウム血症
- 低カリウム血症では、Na-K ATPaseがリン酸化され、ジゴキシンはリン酸化されたNa-K ATPaseと親和性が高いため(PPC.338)
「digoxin」
- 同
- Lanoxin