胺基配糖體 Aminoglycosides

胺基配糖體 Aminoglycosides 通論

Gentamicin injection 2ml/amp. (Gentamicin 80mg/amp.)

Savox injection 125mg/ml  10ml/vial (Amikacin 125mg/ml)
Neomycin Sulfate Capsule /Ointment (250mg/cap. 5mg/gm)


Mechanisms of action

Aminoglycosides have several potential antibiotic mechanisms, some as protein synthesis inhibitors, although their exact mechanism of action is not fully known:

  • They interfere with the proofreading process, causing increased rate of error in synthesis with premature termination.[9]
  • Also, there is evidence of inhibition of ribosomal translocation where the peptidyl-tRNA moves from the A-site to the P-site.[9]
  • They can also disrupt the integrity of bacterial cell membrane.[10]

They bind to the bacterial 30S ribosomal subunit[11][12] (some work by binding to the 50S subunit[13])

There is a significant variability in the relationship between the dose administered and the resultant plasma level in blood. Therapeutic drug monitoring (TDM) is necessary to obtain the correct dose. These agents exhibit a post-antibiotic effect in which there is no or very little drug level detectable in blood, but there still seems to be inhibition of bacterial re-growth. This is due to strong, irreversible binding to the ribosome, and remains intracellular long after plasma levels drop. This allows a prolonged dosage interval. Depending on their concentration, they act as bacteriostatic or bactericidal agents.[citation needed]

The protein synthesis inhibition of aminoglycosides does not usually produce a bactericidal effect, let alone a rapid one as is frequently observed on susceptible Gram-negative bacilli. Aminoglycosides competitively displace cell biofilm-associated Mg2+ and Ca2+ that link the polysaccharides of adjacent lipopolysaccharide molecules. "The result is shedding of cell membrane blebs, with formation of transient holes in the cell wall and disruption of the normal permeability of the cell wall. This action alone may be sufficient to kill most susceptible Gram-negative bacteria before the aminoglycoside has a chance to reach the 30S ribosome."[14]

The antibacterial properties of aminoglycosides were believed to result from inhibition of bacterial protein synthesis through irreversible binding to the 30S bacterial ribosome. This explanation, however, does not account for the potent bactericidal properties of these agents, since other antibiotics that inhibit the synthesis of proteins (such as tetracycline) are not bactericidal. Recent experimental studies show that the initial site of action is the outer bacterial membrane. The cationic antibiotic molecules create fissures in the outer cell membrane, resulting in leakage of intracellular contents and enhanced antibiotic uptake. This rapid action at the outer membrane, it is presumed, accounts for most of the bactericidal activity. Energy is needed for aminoglycoside uptake into the bacterial cell. Anaerobes have less energy available for this uptake, so aminoglycosides are less active against anaerobes.[citation needed]

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. The most frequent use of aminoglycosides is empiric therapy for serious infections such as septicemia, complicated intraabdominal infections, complicated urinary tract infections, and nosocomial respiratory tract infections. Usually, once cultures of the causal organism are grown and their susceptibilities tested, aminoglycosides are discontinued in favor of less toxic antibiotics.[citation needed]

Streptomycin was the first effective drug in the treatment of tuberculosis, though the role of aminoglycosides such as streptomycin and amikacin has been eclipsed (because of their toxicity and inconvenient route of administration) except for multiple-drug-resistant strains.[citation needed]

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 beta-lactam antibiotics in streptococcal infections for their synergistic effects, in particular in endocarditis. One of the most frequent combinations is ampicillin (a beta-lactam, or penicillin-related antibiotic) and gentamicin. Often, hospital staff refer to this combination as "amp and gent" or more recently called "pen and gent" for penicillin and gentamicin.[citation needed]

Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi, and viruses.[citation needed]

Nonsense suppression

The interference with DNA proofreading has been exploited to treat genetic diseases that result from premature stop codes (leading to early termination of protein synthesis and truncated proteins). Aminoglycosides can cause the cell to overcome the stop code, insert a random amino acid, and express a full-length protein.[15]

The aminoglycoside gentamicin has been used to treat cystic fibrosis (CF) cells in the laboratory to induce them to grow full-length proteins. CF is caused by a mutation in the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. In approximately 10% of CF cases, the mutation in this gene causes its early termination during translation, leading to the formation of is truncated and non-functional CFTR protein. It is believed that gentamicin distorts the structure of the ribosome-RNA complex, leading to a mis-reading of the termination codon, causing the ribosome to "skip" over the stop sequence and to continue with the normal elongation and production of the CFTR protein.[16]

Routes of administration

Since they are not absorbed from the gut, they are administered intravenously and intramuscularly. Some are used in topical preparations for wounds. Oral administration can be used for gut decontamination (e.g., in hepatic encephalopathy). Tobramycin may be administered in a nebulized form.[citation needed]

Clinical use

The recent emergence of infections due to Gram-negative bacterial strains with advanced patterns of antimicrobial resistance has prompted physicians to reevaluate the use of these antibacterial agents.[17] This revived interest in the use of aminoglycosides has brought back to light the debate on the two major issues related to these compounds, namely the spectrum of antimicrobial susceptibility and toxicity. Current evidence shows that aminoglycosides do retain activity against the majority of Gram-negative clinical bacterial isolates in many parts of the world. Still, the relatively frequent occurrence of nephrotoxicity and ototoxicity during aminoglycoside treatment makes physicians reluctant to use these compounds in everyday practice. Recent advances in the understanding of the effect of various dosage schedules of aminoglycosides on toxicity have provided a partial solution to this problem, although more research still needs to be done in order to overcome this problem entirely.[18]

Aminoglycosides are in pregnancy category D,[19] that is, there is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience or studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.


  1. ^ MeSH Aminoglycosides
  2. ^ "Bacterial 'battle for survival' leads to new antibiotic" (Press release). Massachusetts Institute of Technology. February 26, 2008. http://web.mit.edu/newsoffice/2008/antibiotics-0226.html. Retrieved December 1, 2010. 
  3. ^ Ryden, R; Moore (1977). "BJ". J Antimicrob Chemother 3 (6): 609–613. 
  4. ^ Kroppenstedt RM, Mayilraj S, Wink JM (Jun 2005). "Eight new species of the genus Micromonospora, Micromonospora citrea sp. nov., Micromonospora echinaurantiaca sp. nov., Micromonospora echinofusca sp. nov. Micromonospora fulviviridis sp. nov., Micromonospora inyonensis sp. nov., Micromonospora peucetia sp. nov., Micromonospora sagamiensis sp. nov., and Micromonospora viridifaciens sp. nov". Syst Appl Microbiol. 28 (4): 328–39. PMID 15997706. 
  5. ^ Paul M. Dewick (2009). Medicinal Natural Products: A Biosynthetic Approach (3rd ed ed.). Wiley. ISBN 0470741678. 
  6. ^ Walter P. Hammes1 and Francis C. Neuhaus (1974). On the Mechanism of Action of Vancomycin: Inhibition of Peptidoglycan Synthesis in Gaffkya homari. 6. pp. 722–728. PMC 444726. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=444726. 
  7. ^ Protein synthesis inhibitors: macrolides mechanism of action animation. Classification of agents Pharmamotion. Author: Gary Kaiser. The Community College of Baltimore County. Retrieved on July 31, 2009
  8. ^ The Mechanism of Action of Macrolides, Lincosamides and Streptogramin B Reveals the Nascent Peptide Exit Path in the Ribosome Martin Lovmar and Måns Ehrenberg
  9. ^ a b Pharmamotion --> Protein synthesis inhibitors: aminoglycosides mechanism of action animation. Classification of agents Posted by Flavio Guzmán on 12/08/08[self-published source?]
  10. ^ Shakil, Shazi; Khan, Rosina; Zarrilli, Raffaele; Khan, Asad U. (2007). "Aminoglycosides versus bacteria – a description of the action, resistance mechanism, and nosocomial battleground". Journal of Biomedical Science 15 (1): 5–14. doi:10.1007/s11373-007-9194-y. PMID 17657587. 
  11. ^ Levison, Matthew E. (July 2009). "Aminoglycosides: Bacteria and Antibacterial Drugs". Merck Manual Professional. http://www.merck.com/mmpe/sec14/ch170/ch170b.html. 
  12. ^ "Aminoglycosides". http://www.aic.cuhk.edu.hk/web8/aminoglycosides.htm. 
  13. ^ Champney, W. S. (2001). "Bacterial Ribosomal Subunit Synthesis A Novel Antibiotic Target". Current Drug Targets - Infectious Disorders 1 (1): 19–36. doi:10.2174/1568005013343281. PMID 12455231. 
  14. ^ Lorian, Victor (1996). Antibiotics in Laboratory Medicine. Williams & Wilkins Press. pp. 589–90. ISBN 0-683-05169-5. 
  15. ^ Feero, W. Gregory; Guttmacher, Alan E.; Dietz, Harry C. (2010). "New Therapeutic Approaches to Mendelian Disorders". New England Journal of Medicine 363 (9): 852–63. doi:10.1056/NEJMra0907180. PMID 20818846. 
  16. ^ Wilschanski, Michael; Yahav, Yaacov; Yaacov, Yasmin; Blau, Hannah; Bentur, Lea; Rivlin, Joseph; Aviram, Micha; Bdolah-Abram, Tali et al. (2003). "Gentamicin-Induced Correction of CFTR Function in Patients with Cystic Fibrosis andCFTRStop Mutations". New England Journal of Medicine 349 (15): 1433–41. doi:10.1056/NEJMoa022170. PMID 14534336. 
  17. ^ Falagas, Matthew E; Grammatikos, Alexandros P; Michalopoulos, Argyris (2008). "Potential of old-generation antibiotics to address current need for new antibiotics". Expert Review of Anti-infective Therapy 6 (5): 593–600. doi:10.1586/14787210.6.5.593. PMID 18847400. 
  18. ^ Durante-Mangoni, Emanuele; Grammatikos, Alexandros; Utili, Riccardo; Falagas, Matthew E. (2009). "Do we still need the aminoglycosides?". International Journal of Antimicrobial Agents 33 (3): 201–5. doi:10.1016/j.ijantimicag.2008.09.001. PMID 18976888. 
  19. ^ Merck Manual > Bacteria and Antibacterial Drugs Last full review/revision July 2009 by Matthew E. Levison, MD


Gentamicin injection 2ml/amp. (Gentamicin 80mg/amp.)

品名規格 Gentamicin injection 80mg/amp.  2ml/amp.
廠        商 SIU GUAN-TAIWAN
代        號 IGEN
成  份  名 Gentamicin 80mg/amp.
中文名稱 健達黴素注射液40公絲/公撮(紫菌素)
藥理分類 Antibiotic agents/ Aminoglycoside/gentamicin
外        觀




Gentamicin 是一個殺菌性抗生素,能與細菌 30S ribosome 結合,抑制蛋白質合 成,並造成基因密碼判讀錯誤。Ribosome 隨後與 mRNA 分離,細菌細胞因而死 亡。


•吸收/分佈:肌肉注射吸收迅速,於注射 1 小時後可達最高血中濃度。Gentamicin 在 血中與蛋白質結合率很低,它可廣泛的分佈於細胞外液體中,故具有較大體積 細胞外液體的病人 (如有水腫及腹水的病人、新生兒及產後婦女)會有較低的血 中濃度。肥胖的病人因脂肪多,故比同體重之正常人具較小的分佈體積。 Gentamicin 亦可穿過胎盤,在膽汁、滑液 (synovial fluid)、腎臟的淋巴 (renal lymph)、痰、支氣管分泌物及肋膜液中皆可測得藥品濃度。在腦脊髓液中無法 達到有意義的濃度。 •代謝/排泄:Gentamicin 主要經由腎絲球過濾,大部份以原型排出,故尿中可達到高 濃度。腎功能正常之成人血中半衰期約為 2-3 小時,腎衰竭病人約為 24-60 小 時,新生兒及老年人血中半衰期可能較長,燙傷病人血中半衰期會明顯縮短, 故血中濃度會比預期低。血液透析 4-6 小時可清除約 50% 的藥品,8 小時的腹 膜透析所能清除的藥品少於 23%。


•治療以下病菌之嚴重感染:Pseudomonas aeruginosa, Proteus sp., Escherichia coli, Klebsiella-Enterobacter-Serratia sp., Citrobacter sp. 及 Staphylococcus sp.。 •新生兒敗血症,中樞神經系統的嚴重感染 (腦膜炎),敗血症,尿路感染,呼吸道感 染,腸胃道感染,腹膜炎或骨盆腔感染,皮膚、骨、軟組織感染,燙傷感染。 •不明病原之感染:嚴重感染且細菌培養尚無結果時,gentamicin 可與 penicillins 或 cephalosporins 併用作為初期治療。 •與 carbenicillin 併用可治療嚴重的 Pseudomonas aeruginosa 感染,與 penicillin 併用 可治療由 group D streptococci 引起的心內膜炎或新生兒的敗血症及 staphylococci 引起的肺炎。 •椎管內注射可輔助治療由 Pseudomonas 引起的嚴重中樞神經感染 (如腦膜炎及腦室 炎)。 •其他用途:Gentamicin 先以 2mg/kg 靜脈注射之後,再以 1.5mg/kg tid 與靜脈注射 clindamycin 600mg qid 併用,可治療骨盆腔發炎 (PID)。


對 gentamicin 過敏或曾對其他 aminoglycosides 產生過敏及嚴重毒性反應者。


•Gentamicin 具有潛在之腎毒性,尤其是腎功能不全或長期高劑量使用者,應特別注 意。治療前及治療中應監測腎功能。 •Gentamicin 具有耳毒性 (傷害聽神經及前庭),但多見於腎功能不全及長期高劑量使 用者。耳毒性一般為不可逆。其他可能出現的神經性症狀包括麻木、皮膚麻刺 感、肌肉抽搐及痙攣等。 •Gentamicin 血中濃度需作定期監測以確保療效及避免毒性,它的血中谷峰濃度 (peak) 不可長期持續在 12mg/ml 以上,谷底濃度 (trough) 也不可超過 2mg/ml。谷峰及 谷底濃度過高,皆會產生毒性。如發生毒性反應,血液及腹膜透析可幫助 gentamicin 由血中排出。新生兒可能需要輸血。 •懷孕期:安全性尚未確立。 •同時使用其他具神經毒性、耳毒性或腎毒性麻醉劑及利尿劑可能會加強副作用。參 閱【藥品交互作用】。 •追加感染 (superinfection):長期或重複使用抗生素可能因黴菌或不具感受性病菌的過 度生長而導致追加感染。 •治療中給予充足的水份,可減少副作用的發生。


藥品 作用
Aminoglycosides, amphotericin-B, cisplatin, bacitracin, cephalothin, vancomycin 及利尿劑 (如 ethacrynic acid, furosemide 及 mannitol) 避免同時或連續使用其他具神經毒性、耳毒性或腎毒性藥物,可能會加強副作用。某些利尿劑本身即具耳毒性,且靜脈注射利尿劑可能因改變 gentamicin 血中及組織中濃度而增強其副作用。
Carbenicillin, ticarcillin 與 gentamicin 併用可能對 pseudomonas 感染具加乘抗菌效果
Penicillins, cephalosporins 體外測試顯示 gentamicin 與 penicillins 或cephalosporins 併用對某些革蘭氏陰性菌及 enterococci 感染具加乘抗菌效果。
Penicllin 及 cephalosporins 與 gentamicin 混合於同一容器中可能會使gentamicin 失去活性。
麻醉劑(anesthetics)、非去極化性神經肌肉阻斷劑 (如 tubocuarine, gallamine, metocurine iodide 或 pancuronium)及 succinylcholine 可能會加強神經肌肉阻斷或呼吸抑制作用,給予鈣鹽或 neostigmine 可逆轉此反應。


•腎毒性:蛋白尿、血尿及尿中出現圓柱物、氮血症、寡尿、BUN 值升高、血中肌酸 酐 (creatinine) 升高。此類反應多發生於曾有腎功能不全及治療期間過長或超過 一般建議劑量者。 •神經毒性:Gentamicin 曾有引起前庭及聽神經損傷之報告,主要發生於腎功能不全 和使用高劑量或長期治療的病人。症狀多為暫時性,包括暈眩、耳鳴及聽力喪 失。聽力喪失一般會先失去高頻率之聽覺。其他因素也可能增加毒性,如脫水 或曾經使用其他具耳毒性藥物。 •周邊神經及腦病變,包括麻木、麻刺感、痙攣及類似重症肌無力症狀等曾被報告。 •其它副作用包括呼吸抑制、嗜睡、精神紊亂、沮喪、視力干擾、厭食、體重減輕、 低血壓、高血壓、紅疹、癢、蕁麻疹、灼熱感、喉頭水腫、嚴重過敏反應、發 燒、頭疼、噁心、嘔吐、唾液增多、口腔炎、紫斑症、假性腦瘤、肺纖維病 變、禿髮、關節疼、暫時性肝腫大及脾腫大等。 •檢驗值:與 gentamicin 可能有關之檢驗數值異常包括:血清中 AST, ALT, LDH 及 bilirubin 升高,鈣、鎂、鈉和鉀降低;貧血、白血球過低、顆粒性白血球過低、 暫時性顆粒性白血球缺乏症,嗜伊紅血球增多,網狀血球數增加或減少,血小 板過低症。 •注射部位疼痛,罕有皮下萎縮或脂肪壞死之報告。


•靜脈注射或肌肉注射,嚴重感染應給予每日 3mg/kg,分 3 次給藥 (q8h)。有致命性 之感染可增至每日 5 mg/kg,病情改善後應立刻減至 3mg/kg。一般療程為 7-10 天,較複雜之感染則需更長時間的治療。 •兒童:2-2.5mg/kg q8h. •嬰兒及新生兒 (一週以上):2.5mg/kg q8h。 •早產及新生兒 (小於一週):2.5mg/kg q12h。 •預防心內膜炎 (做牙齒或呼吸道處置):處置前半小時給予 ampicillin 1-2g 及 gentamicin 1.5mg/kg (不超過 80mg)靜脈或肌肉注射,8 小時後可給予第 2 次劑 量,或 6 小時後給予 penicillin V 1g q6h。 •預防心內膜炎(腸胃道或生殖泌尿道手術):處置前 0.5-1 小時給予 ampicillin 2g 及 gentamicin 1.5mg/kg (不超過 80mg)靜脈或肌肉注射,8 小時內再給第 2 次劑 量。 *兒童劑量:30,000 units/kg aqueous penicillin G (或 50 mg/kg ampicillin)加上 2mg/kg gentamicin。 •腎功能不全的病人,可依下列方法調整劑量或增長投藥間隔,如有可能,仍應監測 血中濃度: *增長投藥間隔:將血中肌酸酐值乘以 8 小時,如血中肌酸酐為 2mg/dl 時,投藥 間隔可增長為 16 (即 2x8)小時。 * 調整劑量:正常劑量除以血中肌酸酐值,如 60kg 的病人,正常劑量為60mg q8h,血中肌酸酐為 2mg/dl 時,可給予 30mg (60mg÷2) q8h。 •靜脈注射:成人可用 50-200ml 0.9% sodium chloride 或 5% dextrose in water 稀釋, 嬰兒及兒童則用較少之稀釋液,靜脈輸注 0.5-2 小時或直接靜脈注射 2-3 分 鐘。 •脊椎內注射:應使用不含保藏劑之製劑。成人 4-8mg qd;兒童及嬰兒 (> 3 個月), 1-2mg qd。

Savox injection 125mg/ml  10ml/vial (Amikacin 125mg/ml)

品名規格 Savox injection 125mg/ml   10ml/vial
廠        商 信東生技
代        號 IAMIK
成  份  名 Amikacin 125mg/ml
中文名稱 沙偉注射液125公絲?公撮(艾米克信)
藥理分類 Antibiotic agents/Aminoglycoside/Amikacin
外        觀






IMIV infusion


IV infusion之稀釋劑:

5% Dextrose 5% Dextrose With 0.2% NaCl,5% Dextrose With 0.45% NaCl,0.9% NaCl,Lactated Ringer's Injection,Lactated Ringer's Injection With 5% Dextrose。



宜調製成 0.25mg/mL ~ 5mg/mL之濃度。( 每 1mL Amikacin + 稀釋液 500 ~ 25mL)




本劑主成分Amikacin Sulfate是屬於一種半合成胺基醣H(Aminoglycosides)類抗生素,抗菌範圍廣泛,對革蘭氏陽性菌及陰性菌均有感受性,甚至對 Gentamicin、Tobramycin及 Kanamycin產生抵抗性之病菌亦為有效。





Amikacin Sulfate抗菌範圍廣泛,對於下列病原菌皆具有感受性,包括




綠膿菌屬(Pseudomonas Species),變形菌屬(Proteus Species)( 口引 咪陽性菌及口引 咪陰性菌)沙雷氏菌屬(Serratia),大腸桿菌(Escherichia Coli),克雷白氏菌屬(Klebsiolla),大腸菌屬(Enterobacter) ,Providencia菌,Acinetobacter菌,Mima-Herellea之前期菌及Citrobacter菌。



革蘭氏陽性菌:對會產生Penicillin 分解酶及非Penicillin分解酶之葡萄球菌屬(Staphylococcus)(包括對methicillin產生抗性之感受菌),對部分鏈球菌屬,如:化膿性鏈球菌(Streptococcus Pyogenes),腸球菌(Enterococci)及肺炎鏈球菌(Streptococcus Pneumoniace)(即Diplococcus Pneumoniae之前)。



或者以上之感受菌產生對抗胺基醣H(Amino- glycosides)類之抗生素時,如Gentamicin,Tobramycin及Kanamycin採用Amikacin (即本劑)亦仍有效,實驗證實使用Amikacin不易引起抗藥性。



1. 本劑經肌肉注射後吸收極為迅速,以250mg (3.7 mg/kg),375mg(5mg/kg)和500mg (7.5mg/kg)分別肌肉注射1小時後即達12mcg/ml,16 mcg/ ml和21mcg/ml之最高血中濃度,且10小時後尚保持0.3mcg/ml,1.2mcg/ml和2.1mcg/ml之有效濃度。  
2. 於30分鐘內緩慢點滴靜注本劑500mg(7.5mg/kg)立即可達38mcg/ml之最高血中濃度,且30分鐘,1小時和10小時尚保持24mcg/ml,18mcg/ml和0.75 mcg/ml之有效濃度。  
3. 本劑可輕易滲入全身各處細胞外液,並以原型排泄入尿中,主要經由腎絲球體過濾。對於腎功能正常的人,肌肉注射本劑後,8小時內之排泄率為91.9%,24小時內之排泄率則高達98.2%。
4. 本劑以注射方式投與,經證實可滲入腦脊髓液,胸膜液,羊水及腹膜腔。
5. 重覆投與本劑亦無造成藥物積蓄之慮。


副 作 用









病人對Amikacin有過敏前歷,或曾因Amikacin或其他具有聽神經毒性或腎毒性的藥物,如:Streptomycin,Vancomycin,Gentamicin, Kanamycin,Tobramycin,Neomycin,Polymyxin B,Colistin或Viomycin等而導致第八腦神經障害者,最好在醫師的建議下認為治療的優點重於藥物所可能導致的危害時才宜使用本劑。


本劑與Ethacrynic acid或Furosemide和其他作用快的利尿劑接連使用,有增加聽神經毒性的危險,可能造成不可恢復的耳聾。



禁  忌


其  它


成人及兒童之使用劑量:7.5~15mg/kg/day平分二次投與(成人之對應劑量為每次 250~500mg,每天兩次)。


新生兒及早產兒之使用劑量:初劑量為10mg /kg,然後15mg/kg/day平分二次投與。










靜脈注射使用:下列注射劑適用於靜脈注射液之稀釋劑:5% Dextrose Injection,5% Dextrose With 0.2% Sodium Chloride Injection,5% Dextrose With 0.45% Sodium Chloride Injection,Normal Saline,Lactated Ringer's Injection,Lactated Ringer's Injection With 5% Dextrose,這些溶液宜調製成0.25mg/ml~5 mg/ml濃度之注射液,在室溫(25℃)下,可保存24小時。靜脈注射的調製液必須足夠滴注30~60分鐘。

Neomycin Sulfate Capsule /Ointment (250mg/cap. 5mg/gm)

品名規格 Neomycin sulfate capsule Neomycin ointment
廠        商 西德有機化學 人人化學製藥
代        號 ONEO RNEO
成  份  名 Neomycin 250mg/cap. Neomycin 5mg/gm
中文名稱 新黴素 膠囊 新黴素軟膏

Antibiotic agents/Aminoglycoside/Amikacin

外        觀




Neomycin 口服只有極微量吸收,因此可用於抑制腸胃道細菌的生長。其抗菌範 圍包括 Enterobacter aerogenes, E. coli, Klebsiella sp., Proteus sp., 及 Pseudomonas aeruginosa 等。很快由腎臟排出,未吸收的部份則由糞便中以原型排出。


•手術前用於腸道作為局部殺菌之準備工作。 •用於肝昏迷病人以清除腸道中產生氨的細菌。 •其他用途:單獨使用 neomycin 或與 niacin 併用可降低 LDL 膽固醇。 【禁忌】腸阻塞及對 aminoglycosides 敏感。


•雖然 neomycin 幾乎不由腸胃黏膜吸收,但若有潰瘍時吸收可能增加。腎功能不全的 病人可能因此在體內蓄積過量藥品而產生毒性。 •服藥期間,宜對腎功能及聽力做定期性測試,尤其是患有肝病或腎病之病人。若導 致腎功能減退,應減量或停藥。 •懷孕期:安全性尚未確立。 •追加感染 (superinfection):長期或重複使用抗生素可能因黴菌或不具感受性病菌的 過度生長而導致追加感染。 •不宜用於嬰兒及兒童。


藥品 作用
Digitalis 可能使 digitalis 吸收減少而使療效降低,分開服用仍無法避免此交互作用。有少數病人 ( < 10%) 在腸胃道內即代謝 digoxin,neomycin 可能提高這些病人 digoxin 的血中濃度。
Methotrexate Neomycin 可能減少 methotrexate 的吸收。
Penicillin V potassium Neomycin 曾引起 penicillin V potassium 吸收不良,避免同時服藥。
口服抗凝血劑 Neomycin 可能使 vitamin K 吸收不良而間接增強了抗凝血劑的效果。
利尿劑 同時使用利尿劑如 ethacrynic acid, furosemide, bumetanide, urea 及mannitol (尤其是以靜脈給藥),可能引起腎及聽覺副作用。



噁心、嘔吐及腹瀉為較常見之副作用。長期使用曾有吸收不良症候群 (malabsorption syndrome),主要症狀為糞便中脂質增加、血中 carotene 減少及 xylose 吸收減少。Clostridium difficile 引起的偽膜性結腸炎亦曾被報告過。肝昏迷 病人長期及高劑量使用曾引起腎毒性及耳毒性。


•完成全程治療,勿任意停藥。 •可能引起噁心、嘔吐或腹瀉。 •若有耳鳴、聽覺障礙或暈眩感時應立即告知醫師。


•直腸肛門手術預防感染:手術前 3 天開始給予口服 bisacodyl,前 2 天給予 magnesium sulfate。再於手術前 1 天給予 3 次的 1g neomycin 及含有 1g erythromycin 基的腸衣錠,分別於下午 1 時、2 時及晚上 11 時給藥。 •肝昏迷病人輔助治療:每日 4-12g,分次服用。兒童劑量為每日 50-100mg/kg,分次 服用。持續治療 5-6 天。慢性肝衰竭病人可能需要每日 4g,且需較長的治療 期。