QT time prolongation
Adverse drug events
|Elevated alkaline phosphatase|
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Explanations of the substances for patients
We have no additional warnings for the combination of norfloxacin and abarelix. Please also consult the relevant specialist information.
The reported changes in exposure correspond to the changes in the plasma concentration-time curve [ AUC ]. We do not expect any change in exposure for norfloxacin, when combined with abarelix (100%). We do not expect any change in exposure for abarelix, when combined with norfloxacin (100%).
The pharmacokinetic parameters of the average population are used as the starting point for calculating the individual changes in exposure due to the interactions.
Norfloxacin has a low oral bioavailability [ F ] of 35%, which is why the maximum plasma level [Cmax] tends to change strongly with an interaction. The terminal half-life [ t12 ] is rather short at 3.5 hours and constant plasma levels [ Css ] are reached quickly. The protein binding [ Pb ] is very weak at 12.5%. The metabolism does not take place via the common cytochromes and the active transport takes place partly via BCRP, MRP4 and OATP1A2.
The bioavailability of abarelix is unknown. The terminal half-life [ t12 ] is rather long at 316.8 hours and constant plasma levels [ Css ] are only reached after more than 1267.2 hours. The protein binding [ Pb ] is 97.5% strong. The metabolism via cytochromes is currently still being worked on.
|Serotonergic Effects a||0||Ø||Ø|
Rating: According to our knowledge, neither norfloxacin nor abarelix increase serotonergic activity.
|Kiesel & Durán b||0||Ø||Ø|
Rating: According to our knowledge, neither norfloxacin nor abarelix increase anticholinergic activity.
QT time prolongation
Rating: In combination, norfloxacin and abarelix can potentially trigger ventricular arrhythmias of the torsades de pointes type.
General adverse effects
|Side effects||∑ frequency||nor||aba|
|Elevated alkaline phosphatase||1.0 %||+||n.a.|
|Elevated transaminases||1.0 %||+||n.a.|
|Elevated serum creatinine||1.0 %||+||n.a.|
|Stevens johnson syndrome||0.0 %||0.01||n.a.|
|Toxic epidermal necrolysis||0.0 %||0.01||n.a.|
|Clostridium difficile diarrhea||0.0 %||0.01||n.a.|
Hemolytic anemia: norfloxacin
Allergic skin reactions like pruritus and rash: norfloxacin
Anaphylactic reaction: norfloxacin
DRESS syndrome: norfloxacin
Myasthenia gravis: norfloxacin
Rupture of tendon: norfloxacin
Peripheral neuropathy: norfloxacin
Feeling nervous: norfloxacin
Tubulointerstitial nephritis: norfloxacin
Aortic aneurysm: norfloxacin
Based on your answers and scientific information, we assess the individual risk of undesirable side effects. These recommendations are intended to advise professionals and are not a substitute for consultation with a doctor. In the restricted test version (alpha), the risk of all substances has not yet been conclusively assessed.
Abstract: The authors report on a case of tamoxifen/norfloxacin interaction leading to QT interval prolongation in an 83-year-old female patient with extracranial meningioma treated with radiation and hormonal therapy (with Tamoxifen). This case report highlights the potential risk of tamoxifen causing depression of electrical impulse in sinoatrial node, leading to symptomatic sinus bradycardia with prolonged QT interval. At the same time it indicates the need to be on the look out for drug interactions (in our case between tamoxifen and norfloxacin), as well as to be aware of other drugs possibly inducing QT interval prolongation (Fig. 2, Ref. 7).
Abstract: Transporters in proximal renal tubules contribute to the disposition of numerous drugs. Furthermore, the molecular mechanisms of tubular secretion have been progressively elucidated during the past decades. Organic anions tend to be secreted by the transport proteins OAT1, OAT3 and OATP4C1 on the basolateral side of tubular cells, and multidrug resistance protein (MRP) 2, MRP4, OATP1A2 and breast cancer resistance protein (BCRP) on the apical side. Organic cations are secreted by organic cation transporter (OCT) 2 on the basolateral side, and multidrug and toxic compound extrusion (MATE) proteins MATE1, MATE2/2-K, P-glycoprotein, organic cation and carnitine transporter (OCTN) 1 and OCTN2 on the apical side. Significant drug-drug interactions (DDIs) may affect any of these transporters, altering the clearance and, consequently, the efficacy and/or toxicity of substrate drugs. Interactions at the level of basolateral transporters typically decrease the clearance of the victim drug, causing higher systemic exposure. Interactions at the apical level can also lower drug clearance, but may be associated with higher renal toxicity, due to intracellular accumulation. Whereas the importance of glomerular filtration in drug disposition is largely appreciated among clinicians, DDIs involving renal transporters are less well recognized. This review summarizes current knowledge on the roles, quantitative importance and clinical relevance of these transporters in drug therapy. It proposes an approach based on substrate-inhibitor associations for predicting potential tubular-based DDIs and preventing their adverse consequences. We provide a comprehensive list of known drug interactions with renally-expressed transporters. While many of these interactions have limited clinical consequences, some involving high-risk drugs (e.g. methotrexate) definitely deserve the attention of prescribers.