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Not to be confused with quinoline.
Essential structure of all quinolone antibiotics: the blue drawn remainder of R is usually piperazine; if the connection contains fluorine (red), it is a fluoroquinolone.
Nalidixic acid
Ciprofloxacin
Levofloxacin
Trovafloxacin
See also: 2- and 4-Quinolones
The quinolones are a family of synthetic broad-spectrum antibacterial drugs.[1][2][3] The first generation of quinolones began with the introduction of nalidixic acid in 1962 for treatment of urinary tract infections in humans.[4] Nalidixic acid was discovered by George Lesher and coworkers in a distillate during an attempt at chloroquine synthesis.[5] Quinolones exert their antibacterial effect by preventing bacterial DNA from unwinding and duplicating (please see the Mechanism of Action section for details).[6] The majority of quinolones in clinical use belong to the subset fluoroquinolones, which have a fluorine atom attached to the central ring system, typically at the 6-position or C-7 position.
Contents
- 1 Medical uses
- 2 Adverse effects
- 3 Contraindications
- 4 Pharmacology
- 5 Mechanism of action
- 5.1 Mechanism of toxicity
- 6 Interactions
- 7 Antibiotic misuse and bacterial resistances
- 8 History
- 9 Legal status
- 9.1 Current litigation
- 9.2 Boxed warnings
- 10 Generations
- 10.1 First-generation
- 10.2 Second-generation
- 10.3 Third-generation
- 10.4 Fourth-generation
- 10.5 In development
- 11 Veterinary use
- 12 References
- 13 External links
Medical uses[edit]
Fluoroquinolones are broad-spectrum antibiotics (effective for both gram negative and gram positive bacteria) that play an important role in treatment of serious bacterial infections, especially hospital-acquired infections and others in which resistance to older antibacterial classes is suspected. Because the use of broad-spectrum antibiotics encourages the spread of multidrug resistant strains and the development of Clostridium difficile infections, treatment guidelines from the Infectious Disease Society of America, the American Thoracic Society, and other professional organizations recommend minimizing the use of fluoroquinolones and other broad-spectrum antibiotics in less severe infections and in those in which risk factors for multidrug resistance are not present.
Fluoroquinolones are featured prominently in the The American Thoracic Society guidelines for the treatment of hospital-acquired pneumonia.[7] The Society recommends fluoroquinolones not be used as a first-line agent for community-acquired pneumonia,[8] instead recommending macrolide or doxycycline as first-line agents. The Drug-Resistant Streptococcus pneumoniae Working Group recommends fluoroquinolones be used for the ambulatory treatment of community-acquired pneumonia only after other antibiotic classes have been tried and failed, or in those with demonstrated drug-resistant Streptococcus pneumoniae.[9]
Fluoroquinolones are often used for genitourinary infections, and are widely used in the treatment of hospital-acquired infections associated with urinary catheters. In community-acquired infections, they are recommended only when risk factors for multidrug resistance are present or after other antibiotic regimens have failed. However, for serious acute cases of pyelonephritis or bacterial prostatitis where the patient may need to be hospitalised, fluoroquinolones are recommended as first-line therapy.[10]
Due to sickle-cell disease patients being at increased risk for developing osteomyelitis from the Salmonella genus, fluoroquinolones are the "drugs of choice" due to their ability to enter bone tissue without chelating it as tetracyclines are known to do.
Adverse effects[edit]
See also: Adverse effects of fluoroquinolones
In general, fluoroquinolones are well tolerated, with most side effects being mild to moderate. On occasion, serious adverse effects occur.[11][12] In August 2013, the U.S. Food and Drug Administration issued a Safety Alert requiring drug labels and for all fluoroquinolone antibacterial drugs "be updated to better describe the serious side effect of peripheral neuropathy. This serious nerve damage potentially caused by fluoroquinolones may occur soon after these drugs are taken and may be permanent." Only those taken by mouth or injection were covered by the alert, while those used topically on the eyes and ears were not.
Some of the serious adverse effects that occur more commonly with fluoroquinolones than with other antibiotic drug classes include central nervous system (CNS) and tendon toxicity.[13][14] The currently marketed quinolones have safety profiles similar to those of other antimicrobial classes.[13] Fluoroquinolones are sometimes associated with an QTc interval prolongation and cardiac arrhythmias,[15] convulsions, tendon rupture, torsade de pointes and hypoglycemia.[16]
These adverse reactions are a class effect of all quinolones; however, certain quinolones are more strongly associated with increased toxicity to certain organs. For example, moxifloxacin carries a higher risk of QTc prolongation,[17] and gatifloxacin has been most frequently linked to disturbed blood sugar levels, although all quinolones carry these risks.[18][19] Some quinolones were withdrawn from the market because of these adverse events (for example, sparfloxacin was associated with phototoxicity and QTc prolongation; thrombocytopenia and nephritis were seen with tosufloxacin; and hepatotoxicity with trovafloxacin).[20] Simultaneous use of corticosteroids is present in almost one-third of quinolone-associated tendon rupture.[21] The risk of adverse events is further increased if the dosage is not properly adjusted, for example if there is renal insufficiency.[18]
The serious events may occur during therapeutic use at therapeutic dose levels or with acute overdose. At therapeutic doses, they include: CNS toxicity, cardiovascular toxicity, tendon / articular toxicity, and, rarely, hepatic toxicity.[22] Caution is required in patients with liver disease.[23] Events that may occur in acute overdose are rare, and include renal failure and seizure.[22] Susceptible groups of patients, such as children and the elderly, are at greater risk of adverse reactions during therapeutic use.[13][14] Tendon damage may manifest during, as well as after fluoroquinolone therapy has been completed.[24]
Fluoroquinolones, clindamycin, and fourth generation cephalosporins are considered high-risk antibiotics for the development of Clostridium difficile and MRSA infections.[25][26] Quinolones, in comparison to other antibiotic classes, have among the highest risk of causing colonization with MRSA and Clostridium difficile.[25][27][28] A previously rare strain of C. difficile that produces a more severe disease with increased levels of toxins is becoming epidemic, and may be connected to the use of fluoroquinolones.[29] The European Center for Disease Prevention and Control recommends fluoroquinolones and the antibiotic clindamycin should be minimized in clinical practice due to their high association with C. difficile, a potentially life-threatening super-infection.[27]
The CNS is an important target for fluoroquinolone-mediated neurotoxicity. Spontaneous adverse event reporting in Italy by doctors showed fluoroquinolones among the top three prescribed drugs reported for causing adverse neurological and psychiatric effects. These neuropsychiatric effects included tremor, confusion, anxiety, insomnia, agitation, and, in severe cases, psychosis. Moxifloxacin came out worst among the quinolones for causing CNS toxicity.[30] Some support and patient advocacy groups refer to these adverse events as "fluoroquinolone toxicity". Some people from these groups claim to have suffered serious long-term harm to their health from using fluoroquinolones. A class-action lawsuit was filed on behalf of individuals alleging harm by the use of fluoroquinolones, as well as action by the consumer advocate group, Public Citizen.[31][32] Partly as a result of the efforts of Public Citizen, the FDA ordered boxed warnings on all fluoroquinolones, advising consumers of an enhanced risk of tendon damage.[33]
The risk of fluoroquinolone-induced tendon injury is elevated in juveniles, and thus the approved uses of fluoroquinolones in persons less that 18 years of age are limited to the use of ciprofloxacin to treat certain types of complicated urinary tract infections and inhalation anthrax. The increased risk of adverse events in juveniles conferred by ciprofloxacin compared to non-fluoroquinolone antibiotics has been demonstrated in controlled clinical trials, and is supported by an internal FDA review of spontaneous adverse event reports.[34][35]
In the field of veterinary medicine, flouroquinolones such as enrofloxacin and ciprofloxacin can cause retinopathies in cats because their ABCG2 transporter has several amino acid differences that are detrimental to their function.[citation needed]
Contraindications[edit]
Quinolones are contraindicated if a patient has epilepsy, QT prolongation, pre-existing CNS lesions, CNS inflammation or suffered a stroke.[11] There are safety concerns of fluoroquinolone use during pregnancy and, as a result, are contraindicated except for when no other safe alternative antibiotic exists.[36] However, one meta-analysis looking at the outcome of pregnancies involving Quinolone use in the first trimester found no increased risk of malformations.[37] They are also contraindicated in children due to the risks of damage to the musculoskeletal system.[38] Their use in children is not absolutely contraindicated, however. For certain severe infections where other antibiotics are not an option, their use can be justified.[39] Quinolones should also not be given to people with a known hypersensitivity to the drug.[40][41] Quinolone antibiotics should not be administered to patients who are dependent on benzodiazepines, since they compete directly with benzodiazepines at the GABA-A receptor, acting as a competitive antagonist and thus possibly precipitating a severe acute and potentially fatal withdrawal effect.[42][43][44]
Pharmacology[edit]
The basic pharmacophore, or active structure, of the fluoroquinolone class is based upon the quinoline ring system.[45] The addition of the fluorine atom at C6 distinguishes the successive-generation fluoroquinolones from the first-generation quinolones. The addition of the C6 fluorine atom has since been demonstrated to not be required for the antibacterial activity of this class (circa 1997).[46]
Various substitutions made to the quinoline ring resulted in the development of numerous fluoroquinolone drugs available today. Each substitution is associated with a number of specific adverse reactions, as well as increased activity against bacterial infections, whereas the quinoline ring, in and of itself, has been associated with severe and even fatal adverse reactions.[47]
Mechanism of action[edit]
Structure of bacterial DNA gyrase complexed with DNA and two ciprofloxacin molecules (green)
Fluoroquinolones inhibit the topoisomerase II ligase domain, leaving the two nuclease domains intact. This modification, coupled with the constant action of the topoisomerase II in the bacterial cell, leads to DNA fragmentation via the nucleasic activity of the intact enzyme domains. Recent evidence has shown eukaryotic topoisomerase II is also a target for a variety of quinolone-based drugs. Thus far, most of the compounds that show high activity against the eukaryotic type II enzyme contain aromatic substituents at their C-7 positions.[48]
Fluoroquinolones can enter cells easily via porins and, therefore, are often used to treat intracellular pathogens such as Legionella pneumophila and Mycoplasma pneumoniae. For many Gram-negative bacteria, DNA gyrase is the target, whereas topoisomerase IV is the target for many Gram-positive bacteria. Some compounds in this class have been shown to inhibit the synthesis of mitochondrial DNA.[49][50][51][52][53][54][55]
Mechanism of toxicity[edit]
The mechanisms of the toxicity of fluoroquinolones has been attributed to their interactions with different receptor complexes, such as blockade of the GABAa receptor complex within the central nervous system, leading to excitotoxic type effects[11] and oxidative stress.[56]
Interactions[edit]
Theophylline, nonsteroidal anti-inflammatory drugs and corticosteroids enhance the toxicity of fluoroquinolones.[57][58][59]
Products containing multivalent cations, such as aluminium- or magnesium-containing antacids and products containing calcium, iron, or zinc, invariably result in marked reduction of oral absorption of fluoroquinolones.[60] Taking colloidal silver along with several versions of quinolones might decrease how much antibiotic the body absorbs.[61]
Other drugs that interact with fluoroquinolones include antacids, sucralfate, probenecid, cimetidine, warfarin, antiviral agents, phenytoin, cyclosporine, rifampin, pyrazinamide, and cycloserine.[59]
Many fluoroquinolones, especially ciprofloxacin, inhibit the cytochrome P450 isoform CYP1A2.[62] This inhibition causes an increased level of drugs that are metabolized by this enzyme. This includes antidepressants such as amitriptyline and imipramine, clozapine (an atypical antipsychotic), caffeine, olanzapine (an atypical antipsychotic), ropivacaine (a local anaesthetic), theophylline (a xanthine), and zolmitriptan (a serotonin receptor agonist).[62]
Antibiotic misuse and bacterial resistances[edit]
See also: Antibiotic misuse and Antibiotic resistance
Resistance to quinolones can evolve rapidly, even during a course of treatment. Numerous pathogens, including Staphylococcus aureus, enterococci, and Streptococcus pyogenes now exhibit resistance worldwide.[63] Widespread veterinary usage of quinolones, in particular in Europe, has been implicated.[64]
Fluoroquinolones have been recommended to be reserved for the use in patients who are seriously ill and may soon require immediate hospitalization.[65] Though considered to be very important and necessary drugs required to treat severe and life-threatening bacterial infections, the associated antibiotic misuse remains unchecked, which has contributed to the problem of bacterial resistance. The overuse of antibiotics such as happens with children suffering from otitis media (ear infections) has given rise to a breed of super bacteria that are resistant to antibiotics entirely.[66]
For example, the use of the fluoroquinolones had increased threefold in an emergency room environment in the United States between 1995 and 2002, while the use of safer alternatives, such as macrolides, declined significantly.[67][68] Fluoroquinolones had become the most commonly prescribed class of antibiotics to adults in 2002. Nearly half (42%) of these prescriptions were for conditions not approved by the FDA, such as acute bronchitis, otitis media, and acute upper respiratory tract infection, according to a study supported in part by the Agency for Healthcare Research and Quality.[68][69] In addition, they are commonly prescribed for medical conditions, such as acute respiratory illness, that are usually caused by viral infections.[70]
Within a recent study concerning the proper use of this class in the emergency rooms of two academic hospitals, 99% of these prescriptions were revealed to be in error. Out of the 100 total patients studied, 81 received a fluoroquinolone for an inappropriate indication. Out of these cases, 43 (53%) were judged to be inappropriate because another agent was considered first line, 27 (33%) because there was no evidence of a bacterial infection to begin with (based on the documented evaluation), and 11 (14%) because of the need for such therapy was questionable. Of the 19 patients who received a fluoroquinolone for an appropriate indication, only one patient of 100 received both the correct dose and duration of therapy.[71]
Three mechanisms of resistance are known.[72] Some types of efflux pumps can act to decrease intracellular quinolone concentration.[73] In Gram-negative bacteria, plasmid-mediated resistance genes produce proteins that can bind to DNA gyrase, protecting it from the action of quinolones. Finally, mutations at key sites in DNA gyrase or topoisomerase IV can decrease their binding affinity to quinolones, decreasing the drugs' effectiveness.
History[edit]
Nalidixic acid is considered to be the predecessor of all members of the quinolone family, including the second, third and fourth generations commonly known as fluoroquinolones. This first generation also included other quinolone drugs, such as pipemidic acid, oxolinic acid, and cinoxacin, which were introduced in the 1970s. They proved to be only marginal improvements over nalidixic acid.[74] Though it is generally accepted nalidixic acid is to be considered the first quinolone drug, this has been disputed over the years by a few researchers who believe chloroquine, from which nalidixic acid is derived, is to be considered the first quinolone drug, rather than nalidixic acid.
Since the introduction of nalidixic acid in 1962, more than 10,000 analogs have been synthesized, but only a handful have found their way into clinical practice.
- Advocacy Groups and Regulation:
Several advocacy groups have petitioned the FDA to increase the prominence of adverse effect warnings on the labels of fluroquinolone antibacterials, and to withdraw others from the market.[75][76][77][78][79][80][81]
Legal status[edit]
Current litigation[edit]
A significant number of cases are pending before the United States District Court, District of Minnesota, involving the drug Levaquin. On 13 June 2008, a Judicial Panel On Multidistrict Litigation (MDL) granted the Plaintiffs’ motion to centralize individual and class-action lawsuits involving Levaquin in the District of Minnesota over objection of Defendants, Johnson and Johnson / Ortho McNeil.[32]
On 6 July 2009, the New Jersey Supreme Court had also designated litigation over Levaquin as a mass tort and has assigned it to an Atlantic County, N.J., judge. The suits charge the drug has caused Achilles tendon ruptures and other permanent damage.[82] Of a total of about 3400 cases, 845 were recently settled out of court after Johnson and Johnson prevailed in three of the first four cases to go to trial[83][84]
Several class action lawsuits had been filed in regards to the adverse reactions allegedly suffered by those exposed to ciprofloxacin during the anthrax scare of 2001.
Boxed warnings[edit]
In the US, the package insert for fluoroquinolone antibiotics includes a boxed warning of increased risk of developing tendonitis and tendon rupture in patients of all ages taking fluoroquinolones for systemic use. This risk is further increased in individuals over 60 years of age, taking corticosteroid drugs, and have received kidney, heart, or lung transplants. Another boxed warning says fluoroquinolones, due to their neuromuscular blocking activity, may exacerbate muscle weakness in persons with myasthenia gravis. Serious adverse events, including deaths and requirement for ventilatory support, have been reported in this group of patients. Avoidance of fluoroquinolones in patients with known history of myasthenia gravis is advised.[85]
Generations[edit]
Researchers divide the quinolones into generations based on their antibacterial spectrum.[86][87] The earlier-generation agents are, in general, more narrow-spectrum than the later ones, but no standard is employed to determine which drug belongs to which generation. The only universal standard applied is the grouping of the nonfluorinated drugs found within this class (quinolones) within the 'first-generation' heading. As such, a wide variation exists within the literature dependent upon the methods employed by the authors.
- Some researchers group these drugs by patent dates[citation needed]
- Some by a specific decade (i.e., '60s, '70s, '80s, etc.)[citation needed]
- Others by the various structural changes[citation needed]
The first generation is rarely used today. Nalidixic acid was added to the OEHHA Prop 65 list as a carcinogen on 15 May 1998.[88] A number of the second-, third-, and fourth-generation drugs have been removed from clinical practice due to severe toxicity issues or discontinued by their manufacturers. The drugs most frequently prescribed today consist of Avelox (moxifloxacin), Cipro (ciprofloxacin), Levaquin (levofloxacin), and, to some extent, their generic equivalents.
First-generation[edit]
- cinoxacin (Cinobac) (discontinued by manufacturer)[89]
- nalidixic acid (NegGram, Wintomylon)[89]
- oxolinic acid (Uroxin)
- piromidic acid (Panacid)
- pipemidic acid (Dolcol)
- rosoxacin (Eradacil)
Second-generation[edit]
The second-generation class is sometimes subdivided into "Class 1" and "Class 2".[90]
- ciprofloxacin (Alcipro,Ciprobay, Cipro, Ciproxin)[89][91]
- enoxacin (Enroxil, Penetrex)[89]
- fleroxacin (Megalone, Roquinol)
- lomefloxacin (Maxaquin)[89]
- nadifloxacin (Acuatim, Nadoxin, Nadixa)
- norfloxacin (Lexinor, Noroxin, Quinabic, Janacin)[89][92]
- ofloxacin (Floxin, Oxaldin, Tarivid)[89]
- pefloxacin (Peflacine)
- rufloxacin (Uroflox)
Third-generation[edit]
Unlike the first- and second-generations, the third-generation is active against streptococci.[90]
- balofloxacin (Baloxin)
- grepafloxacin (Raxar) (removed from clinical use)
- levofloxacin (Cravit, Levaquin)
- pazufloxacin (Pasil, Pazucross)
- sparfloxacin (Zagam)
- temafloxacin (Omniflox) (removed from clinical use)[93]
- tosufloxacin (Ozex, Tosacin)
Fourth-generation[edit]
Fourth generation fluoroquinolones act at DNA gyrase and topoisomerase IV.[94] This dual action slows development of resistance.
- clinafloxacin[91]
- gatifloxacin (Zigat, Tequin) (Zymar -opth.) (Tequin removed from clinical use)[95]
- gemifloxacin (Factive)
- moxifloxacin (Avelox,Vigamox)[89]
- sitafloxacin (Gracevit)
- trovafloxacin (Trovan) (removed from clinical use)[89][91]
- prulifloxacin (Quisnon)
In development[edit]
- delafloxacin — an anionic fluoroquinoline in clinical trials
- JNJ-Q2 — completed Phase II for MRSA
- nemonoxacin
Veterinary use[edit]
The quinolones have been widely used in agriculture, and several agents have veterinary, but not human, applications.
- danofloxacin (Advocin, Advocid) (for veterinary use)
- difloxacin (Dicural, Vetequinon) (for veterinary use)
- enrofloxacin (Baytril) (for veterinary use)
- ibafloxacin (Ibaflin) (for veterinary use)
- marbofloxacin (Marbocyl, Zenequin) (for veterinary use)
- orbifloxacin (Orbax, Victas) (for veterinary use)
- sarafloxacin (Floxasol, Saraflox, Sarafin) (for veterinary use)
However, the agricultural use of fluoroquinolones in the U.S. has been restricted since 1997, due to concerns over the development of antibiotic resistance.[96]
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- ^ Scherer, K.; Bircher, AJ. (January 2005). "Hypersensitivity reactions to fluoroquinolones". Curr Allergy Asthma Rep 5 (1): 15–21. doi:10.1007/s11882-005-0049-1. PMID 15659258.
- ^ Unseld E, Ziegler G, Gemeinhardt A et al. (1990). "Possible interaction of fluoroquinolones with the benzodiazepine-GABAA-receptor complex". Br J Clin Pharmacol 30: 63–70.
- ^ John Girvan McConnell. Benzodiazepine tolerance, dependency, and withdrawal syndromes and interactions with fluoroquinolone antimicrobials. Br J Gen Pract. 2008 May 1; 58(550): 365–366.
- ^ Halliwell RF, Davey PG, Lambert JJ. Antagonism of GABAA receptors by 4-quinolones. J Antimicrob Chemother. 1993;31:457–462.
- ^ Schaumann, R.; Rodloff, A. C. (January 2007). "Activities of Quinolones Against Obligately Anaerobic Bacteria" (PDF). Anti-Infective Agents in Medicinal Chemistry (Formerly Current Medicinal Chemistry - Anti-Infective Agents) (Bentham Science Publishers) 6 (1): 49–56.
- ^ Chang Y.H.; Se H.K.; Young K.K (22 July 1997). "Novel 5-amino-6-methylquinolone antibacterials: A new class of non-6-fluoroquinolones". Bioorganic & Medicinal Chemistry Letters (Elsevier) 7 (14): 1875–1878. doi:10.1016/S0960-894X(97)00324-7.
- ^ CANN HM, VERHULST HL (January 1961). "Fatal acute chloroquine poisoning in children". Pediatrics 27 (1): 95–102. PMID 13690445.
- ^ Elsea, SH.; Osheroff, N.; Nitiss, JL. (July 1992). "Cytotoxicity of quinolones toward eukaryotic cells. Identification of topoisomerase II as the primary cellular target for the quinolone CP-115,953 in yeast" (pdf). J Biol Chem 267 (19): 13150–3. PMID 1320012.
- ^ Bergan T.; Bayer (1988). "Pharmacokinetics of fluorinated quinolones". Academic Press: 119–154.
- ^ Bergan T; Dalhoff A, Thorsteinsson SB (1985). A review of the pharmacokinetics and tissue penetration of ciprofloxacin. pp. 23–36.
- ^ Castora, FJ.; Vissering, FF.; Simpson, MV. (September 1983). "The effect of bacterial DNA gyrase inhibitors on DNA synthesis in mammalian mitochondria". Biochim Biophys Acta 740 (4): 417–27. PMID 6309236.
- ^ Kaplowitz, Neil (2005). "Hepatology highlights". Hepatology 41 (2): 227. doi:10.1002/hep.20596.
- ^ Enzmann, H.; Wiemann, C.; Ahr, HJ.; Schlüter, G. (April 1999). "Damage to mitochondrial DNA induced by the quinolone Bay y 3118 in embryonic turkey liver". Mutat Res 425 (2): 213–24. doi:10.1016/S0027-5107(99)00044-5. PMID 10216214.
- ^ Holden, HE.; Barett, JF.; Huntington, CM.; Muehlbauer, PA.; Wahrenburg, MG. (1989). "Genetic profile of a nalidixic acid analog: a model for the mechanism of sister chromatid exchange induction". Environ Mol Mutagen 13 (3): 238–52. doi:10.1002/em.2850130308. PMID 2539998.
- ^ Suto, MJ.; Domagala, JM.; Roland, GE.; Mailloux, GB.; Cohen, MA. (December 1992). "Fluoroquinolones: relationships between structural variations, mammalian cell cytotoxicity, and antimicrobial activity". J Med Chem 35 (25): 4745–50. doi:10.1021/jm00103a013. PMID 1469702.
- ^ Saint F, Salomon L, Cicco A, de la Taille A, Chopin D, Abbou CC (December 2001). "[Tendinopathy associated with fluoroquinolones: individuals at risk, incriminated physiopathologic mechanisms, therapeutic management]". Prog. Urol. (in French) 11 (6): 1331–4. PMID 11859676.
- ^ "Moderate Interaction: Quinolones/Corticosteroids". Medscape. Retrieved 2 September 2008.
- ^ Cohen JS (December 2001). "Peripheral Neuropathy Associated with Fluoroquinolones" (PDF). Ann Pharmacother 35 (12): 1540–7. doi:10.1345/aph.1Z429. PMID 11793615.
- ^ a b "Fluoroquinolone Adverse Effects and Drug Interactions". Medscape. Retrieved 2 September 2008.
- ^ Fluoroquinolone Adverse Effects and Drug Interactions: Drug-Drug Interactions Author from: the Department of Pharmacy Practice, School of Pharmacy, University of Colorado Health Sciences Center, Denver, Colorado. Retrieved on 17 December 2009
- ^ Cupp, Melanie Johns; Timothy S. Tracy (2003). "Colloidal Silver". Forensic Science and Medicine: 87–90. doi:10.1007/978-1-59259-303-3_6. Retrieved 30 June 2013.
- ^ a b Swedish environmental classification of pharmaceuticals Facts for prescribers (Fakta för förskrivare)
- ^ M Jacobs, Worldwide Overview of Antimicrobial Resistance. International Symposium on Antimicrobial Agents and Resistance 2005.
- ^ Nelson, JM.; Chiller, TM.; Powers, JH.; Angulo, FJ. (April 2007). "Fluoroquinolone-resistant Campylobacter species and the withdrawal of fluoroquinolones from use in poultry: a public health success story" (PDF). Clin Infect Dis 44 (7): 977–80. doi:10.1086/512369. PMID 17342653.
- ^ Jim Hoover, for Bayer Corporation, Alaska Pharmacy and Therapeutics Committee 19 March 2004
- ^ Froom J, Culpepper L, Jacobs M, et al. (July 1997). "Antimicrobials for acute otitis media? A review from the International Primary Care Network". BMJ 315 (7100): 98–102. doi:10.1136/bmj.315.7100.98. PMC 2127061. PMID 9240050.
- ^ MacDougall C, Guglielmo BJ, Maselli J, Gonzales R (March 2005). "Antimicrobial drug prescribing for pneumonia in ambulatory care". Emerging Infect. Dis. 11 (3): 380–4. doi:10.3201/eid1103.040819. PMC 3298265. PMID 15757551.
- ^ a b Linder JA, Huang ES, Steinman MA, Gonzales R, Stafford RS (March 2005). "Fluoroquinolone prescribing in the United States: 1995 to 2002". The American Journal of Medicine 118 (3): 259–68. doi:10.1016/j.amjmed.2004.09.015. PMID 15745724.
- ^ K08 HS14563 and HS11313
- ^ Neuhauser, MM; Weinstein, RA; Rydman, R; Danziger, LH; Karam, G; Quinn, JP (2003). "Antibiotic resistance among gram-negative bacilli in US intensive care units: implications for fluoroquinolone use". JAMA: the Journal of the American Medical Association 289 (7): 885–8. doi:10.1001/jama.289.7.885. PMID 12588273. "From 1995 to 2002, inappropriate antibiotic prescribing for acute respiratory infections, which are usually caused by viruses and thus are not responsive to antibiotics, declined from 61 to 49 percent. However, the use of broad-spectrum antibiotics such as the fluoroquinolones, jumped from 41 to 77 percent from 1995 to 2001. Overuse of these antibiotics will eventually render them useless for treating antibiotic-resistant infections, for which broad-spectrum antibiotics are supposed to be reserved."
- ^ Lautenbach E, Larosa LA, Kasbekar N, Peng HP, Maniglia RJ, Fishman NO (March 2003). "Fluoroquinolone utilization in the emergency departments of academic medical centers: prevalence of, and risk factors for, inappropriate use". Arch. Intern. Med. 163 (5): 601–5. doi:10.1001/archinte.163.5.601. PMID 12622607.
- ^ Robicsek A, Jacoby GA, Hooper DC (October 2006). "The worldwide emergence of plasmid-mediated quinolone resistance". Lancet Infect Dis 6 (10): 629–40. doi:10.1016/S1473-3099(06)70599-0. PMID 17008172.
- ^ Morita Y, Kodama K, Shiota S, Mine T, Kataoka A, Mizushima T, Tsuchiya T (July 1998). "NorM, a Putative Multidrug Efflux Protein, of Vibrio parahaemolyticus and Its Homolog in Escherichia coli". Antimicrob. Agents Chemother. 42 (7): 1778–82. PMC 105682. PMID 9661020.
- ^ Norris, S; Mandell, GL (1988). "The quinolones: history and overview". The quinolones: history and overview. San Diego: Academic Press Inc. pp. 1–22.
- ^ "Petition to Require a Warning on All Fluoroquinolone Antibiotics (HRG Publication #1399)". Public Citizen. 1 August 1996. Retrieved 27 December 2008.
- ^ "Public Citizen Petitions the FDA to Include a Black Box Warning on Fluoroquinolone Antibiotics (HRG Publication #1781)". Public Citizen. 29 August 2006. Retrieved 27 December 2008.
- ^ Public Citizen; Michael T. Kickpatrick (3 January 2008). "In The United States District Court For The District Of Columbia" (PDF). USA: Carey & Danis, LLC.
- ^ Lisa Madigan (18 May 2005). "Office Of The Attorney General State Of Illinois, CITIZEN PETITION" (PDF). USA: FDA.
- ^ Joseph Baker; Sidney Wolfe, Peter Lurie (1 May 2006). "Petition to the FDA to Immediately Ban the Antibiotic Gatifloxacin (Tequin) (HRG Publication #1768)". USA: Public Citizen.
- ^ "Letter to the Food and Drug Administration to immediately ban the antibiotic trovafloxacin (Trovan) (HRG Publication #1485)". USA: Public Citizen. 3 June 1999.
- ^ Larry D. Sasich,; Sidney M. Wolfe, Allison Zieve, Patricia Christen, Ben Christen (9 June 1998). "Petition to the Food and Drug Administration to immediately stop the distribution of dangerous, misleading prescription drug information to the public. (HRG Publication #1442)". USA: Public Citizen.
- ^ Charles Toutant (6 July 2009). "Litigation Over Johnson & Johnson Antibiotic Levaquin Designated N.J. Mass Tort". New Jersey Law Journal.
- ^ "Levaquin MDL | United States District Court - District of Minnesota, United States District Court - District of Minnesota".
- ^ "Johnson & Johnson Settles 845 Levaquin Lawsuits - Businessweek".
- ^ Risk of fluoroquinolone-associated Myasthenia Gravis Exacerbation February 2011 Label Changes for Fluoroquinolones FDA, online access 16 March 2011
- ^ Ball P (2000). "Quinolone generations: natural history or natural selection?". J. Antimicrob. Chemother. 46 Suppl T1 (Supplement 3): 17–24. PMID 10997595.
- ^ "New Classification and Update on the Quinolone Antibiotics - May 1, 2000 - American Academy of Family Physicians". Retrieved 18 March 2008.
- ^ [Nalidixic Acid, case number 389-08-02, listing mechanism AB, NTP (1989b)]
- ^ a b c d e f g h i "Quinolones: A Comprehensive Review - February 1, 2002 - American Family Physician".
- ^ a b Oliphant CM, Green GM (February 2002). "Quinolones: a comprehensive review". Am Fam Physician 65 (3): 455–64. PMID 11858629.
- ^ a b c Paul G. Ambrose; Robert C. Owens, Jr (1 March 2000). "Clinical Usefulness Of Quinolones". Seminars in Respiratory and Critical Care Medicine (Medscape).
- ^ The European Medicines Agency (24 July 2008). "EMEA Restricts Use of Oral Norfloxacin Drugs in UTIs". Doctor's Guide.
- ^ Paul G. Ambrose; Robert C. Owens, Jr (1 March 2000). "New Antibiotics in Pulmonary and Critical Care Medicine: Classification Of Quinolones By Generation". USA: Medscape.
- ^ Gupta (2009). Clinical Ophthalmology: Contemporary Perspectives, 9/e. Elsevier India. pp. 112–. ISBN 978-81-312-1680-4. Retrieved 20 September 2010.
- ^ Schmid, Randolph E. (1 May 2006). "Drug Company Taking Tequin Off Market". Associated Press. Archived from the original on 25 Nov 2007. Retrieved 1 May 2006. [dead link]
- ^ "FDA Order Prohibits Extralabel Use Of Fluoroquinolones And Glycopeptides". U.S. Food and Drug Administration. 2 June 1997. Retrieved 16 April 2013.
External links[edit]
- Quinolone at the Open Directory Project
- Fact Sheet: Quinolones
- Information to healthcare professionals on fluoroquinolone safety from the U.S. Food and Drug Administration
- Fluoroquinolones "Family Practice Notebook" entry page for Fluoroquinolones
- Structure Activity Relationships "Antibacterial Agents; Structure Activity Relationships," André Bryskier MD
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UpToDate Contents
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- 1. フルオロキノロン類fluoroquinolones [show details]… resistant to ofloxacin in animal models, and no other quinolone has been shown to have activity against this spirochete. The newer fluoroquinolones have retained much of the activity of ciprofloxacin and ofloxacin …
- 2. フルオロキノロン類、ドキシサイクリン、およびトリメトプリムスルファメトキサゾールに対する肺炎レンサ球菌の耐性resistance of streptococcus pneumoniae to the fluoroquinolones doxycycline and trimethoprim sulfamethoxazole [show details]… resistant to ciprofloxacin but not to the other quinolones, whereas isolates with mutations in gyrA only and isolates with mutations in both parC and gyrA tend to be resistant to all fluoroquinolones . Isolates …
- 3. 嚢胞性線維腺症：呼吸器症状が急性増悪した場合の治療cystic fibrosis treatment of acute pulmonary exacerbations [show details]…CF, we use oral ciprofloxacin at a dose of 40 mg/kg/day (up to 2 grams daily) divided every 12 hours, instead of standard doses of ciprofloxacin . The intravenous dose of ciprofloxacin is 30 mg/kg per …
- 4. フルオロキノロン類に対する過敏反応hypersensitivity reactions to fluoroquinolones [show details]… history of drug allergy . Moxifloxacin – The best concentration of moxifloxacin for use in skin testing is not entirely clear. In 16 patients without a history of quinolone allergy, prick testing with …
- 5. 成人の骨髄炎：治療osteomyelitis in adults treatment [show details]…conditions . We do not favor use of trimethoprim-sulfamethoxazole, linezolid, tedizolid, clindamycin, fluoroquinolones, quinupristin-dalfopristin, or tigecycline for definitive therapy of osteomyelitis due to S …
English Journal
- Carbonic anhydrase I, II, IV and IX inhibition with a series of 7-amino-3,4-dihydroquinolin-2(1H)-one derivatives.
- Bozdag M1, Bua S1, Osman SM2, AlOthman Z2, Supuran CT1.
- Journal of enzyme inhibition and medicinal chemistry.J Enzyme Inhib Med Chem.2017 Dec;32(1):885-892. doi: 10.1080/14756366.2017.1337759.
- PMID 28644059
- Effect of thermal treatments on the degradation of antibiotic residues in food.
- Tian L1, Khalil S1, Bayen S1.
- Critical reviews in food science and nutrition.Crit Rev Food Sci Nutr.2017 Nov 22;57(17):3760-3770. doi: 10.1080/10408398.2016.1164119.
- PMID 27052471
- Investigational drugs in phase I and phase II clinical trials for the treatment of community-acquired pneumonia.
- Liapikou A1, Cillóniz C2, Torres A2.
- Expert opinion on investigational drugs.Expert Opin Investig Drugs.2017 Nov;26(11):1239-1248. doi: 10.1080/13543784.2017.1385761. Epub 2017 Oct 3.
- PMID 28952384
Japanese Journal
- SYNTHESIS, BIOLOGICAL ACTIVITIES, AND TAUTOMERISM OF 4-QUINOLONES AND RELATED COMPOUNDS
- Heterocycles : an international journal for reviews and communications in heterocyclic chemistry 91(1), 1-39, 2015-01-01
- NAID 40020363620
- Bacteriological Profile and Antibiotic Susceptibility Pattern of Neonatal Sepsis at a Teaching Hospital in Bayelsa State, Nigeria
- Tropical Medicine and Health 43(3), 183-190, 2015
- NAID 130005102110
- 日米の有害事象自発報告データベースを用いた解析の比較と活用展望:―ニューキノロン系抗菌薬による有害事象の安全性シグナルを用いて―
- 医薬品情報学 17(1), 15-20, 2015
- NAID 130005084058
Related Links
- The quinolones are a family of synthetic broad-spectrum antibacterial drugs The first generation of the quinolones began with the introduction of nalidixic acid in 1962 for treatment of urinary tract infections in humans. Nalidixic acid was ...
- Compare quinolones. Includes user reviews and ratings for individual medications. Find related monographs and prescribing information.
Related Pictures
★リンクテーブル★
| リンク元 | 「抗菌薬」「急性尿細管間質性腎炎」 |
「抗菌薬」
- first aid step 1 2006 p.165
定義
作用機序による分類
- 細胞壁合成阻害：βラクタム系抗菌薬(ペニシリン系抗菌薬、セフェム系抗菌薬、モノバクタム系抗菌薬、カルバペネム系抗菌薬)
- 核酸合成阻害 ：ニューキノロン系抗菌薬、メトロニダゾール
- タンパク質合成阻害
- 30S：アミノグリコシド系抗菌薬、テトラサイクリン系抗菌薬
- 50S：マクロライド系抗菌薬、クリンダマイシン、クロラムフェニコール、ストレプトグラミン系抗菌薬、オキソゾリニドン系抗菌薬(リゾネリド)
- first aid step 1 2006 p.165
| Mechanism of action | Drugs | |
| 1 | Block cell wall synthesis by inhibition of peptidoglycan cross-linking | penicillin, ampicillin, ticarcillin, piperacillin, imipenem, aztreonam, cephalosporins |
| 2 | Block peptidoglycan synthesis | bacitracin, vancomycin, cycloserine |
| 3 | Disrupt bacterial/fungal cell membranes | polymyxins |
| 4 | Disrupt fungal cell membranes | amphotericin B, nystatin, fluconazole/azoles |
| 5 | Block nucleotide synthesis | sulfonamides, trimethoprim |
| 6 | Block DNA topoisomerases | quinolones |
| 7 | Block mRNA synthesis | rifampin |
| 8 | Block protein synthesis at 50S ribosomal subunit | chloramphenicol, erythromycin/macrolides, lincomycin, clindamycin, streptogramins (quinupristin, dalfopristin), linezolid |
| 9 | Block protein synthesis at 30S ribosomal subunit | aminoglycosides, tetracyclines, spectinomycin ATuSi → あつし |
薬物動態
- 濃度依存性：アミノグリコシド系抗菌薬、ニューロキノロン系抗菌薬
- 時間依存性：βラクタム系抗菌薬
治療期間
小児
- 尾内一信 ; 第 39 回日本小児感染症学会教育講演 2 小児感染症の抗菌薬療法 -耐性菌時代の適正使用-
| 感染臓器・臨床診断 | 原因菌 | 投与期間（抗菌薬） |
| 髄膜炎 | インフルエンザ菌 | 7-10日 |
| 肺炎球菌 | 10-14日 | |
| 髄膜炎菌 | 7-10日 | |
| GBS，腸内細菌，リステリア | 21日 | |
| 中耳炎 | ＜2 歳 | 10日 |
| 2 歳≦ | 5-7日 | |
| 咽頭炎 | A 群連鎖球菌 | 10日(ペニシリン系薬) |
| 5日(セフェム系薬) | ||
| 肺炎 | 肺炎球菌，インフルエンザ菌 | 解熱後3-4日 |
| 黄色ブドウ球菌 | 3-4週間 | |
| マイコプラズマ，クラミジア | 10-21日 | |
| 腎臓、膀胱炎、腎盂腎炎 | 大腸菌，プロテウス，腸球菌 | 3日 |
| 14日 | ||
| 骨髄炎 | 黄色ブドウ球菌 | 21日 |
| 連鎖球菌，インフルエンザ菌 | 14日 |
主要な感染症の抗菌薬投与期間
- 感染レジマニュ p.27
| 骨 | 骨髄炎 | 4-6週 | |
| 耳鼻咽喉 | 中耳炎 | 5-7日 | |
| 副鼻腔炎 | 5-14日 | ||
| A群溶連菌咽頭炎 | 10日 | ||
| 肺 | 肺炎 | 肺炎球菌 | 7-10日 or 解熱後3日間 |
| インフルエンザ菌 | 10-14日 | ||
| マイコプラズマ | 14日(7-10日) | ||
| レジオネラ | 21日 | ||
| 肺化膿症 | 28-42日 | ||
| 心臓 | 感染性心内膜炎 | α連鎖球菌 | 2-4週 |
| 黄色ブドウ球菌 | 4-6週 | ||
| 消化管 | 腸炎 | 赤痢菌 | 3日 |
| チフス | 14日(5-7日) | ||
| パラチフス | |||
| 腹膜炎 | 特発性 | 5日 | |
| 二次性 | 10-14日 | ||
| 胆肝膵 | 肝膿瘍 | 細菌性 | 4-8週 |
| アメーバ性 | 10日 | ||
| 尿路 | 膀胱炎 | 3日 | |
| 急性腎盂腎炎 | 14日(7-10日) | ||
| 急性腎盂腎炎・再発 | 6週 | ||
| 慢性前立腺炎 | 1-3ヶ月 | ||
| 髄腔 | 髄膜炎 | インフルエンザ菌 | 7-10日 |
| 髄膜炎菌 | |||
| 肺炎球菌 | 10-14日 | ||
| リステリア | 21日 | ||
| 敗血症 | 敗血症 | コアグラーゼ陰性ブドウ球菌 | 5-7日 |
| 黄色ブドウ球菌 | 28日(14日) | ||
| グラム陰性桿菌 | 14日(7-14日) | ||
| カンジダ | 血液培養陰性化後, 14日 | ||
ソース不明
妊婦に避けるべき抗菌薬
- Antibiotics to avoid in pregnancy
- Sulfonamides––kernicterus.
- Aminoglycosides––ototoxicity.
- Fluoroquinolones––cartilage damage.
- Erythromycin––acute cholestatic hepatitis in mom
- (and clarithromycin––embryotoxic).
- Metronidazole––mutagenesis.
- Tetracyclines––discolored teeth, inhibition of bone growth.
- Ribavirin (antiviral)––teratogenic.
- Griseofulvin (antifungal)––teratogenic.
- Chloramphenicol––“gray baby.”
- SAFE Moms Take Really Good Care.
使っても良い
- YN.H-24
- βラクタム系
- エリスロマイシン、アジスロマイシン
参考
- 抗菌薬インターネットブック
- まとまっていてよい
- http://www.antibiotic-books.jp
抗菌薬一覧
「急性尿細管間質性腎炎」
原因
- 薬剤性
- antibiotics (lactams, sulfonamides, quinolones, vancomycin, erythromycin, minocycline, rifampin, ethambutol, acyclovir)
- NSAIDs,COX-2阻害薬
- 利尿薬(thiazides, furosemide, triamterene)
- 抗てんかん薬(フェニトイン、フェノバルビタール、カルバマゼピン、バルプロ酸)
- その他(カプトプリル、H2受容体阻害薬、プロトンポンプ阻害薬、mesalazine、indinavir、アロプリノール)
- 感染症
- 細菌(Streptococcus、Staphylococcus、Legionella、Salmonella、Brucella、Yersinia、Corynebacterium diphtheriae)
- ウイルス(Epstein-Barr virus、cytomegalovirus、Hantavirus、polyomavirus、HIV)
- その他(レプトスピラ、リケッチア、マイコプラズマ)
- 特発性