F. L. Alovero, X. S. Pan, J. E. Morris, R. H. Manzo and L. M. Fisher, “Engineering the Specificity of Antibacterial Fluoroquinolones, Benzene Sulfonamide Modifications at C-7 of Ciprofloxacin Change Its Primary Target in Streptococcus Pneumoniae from Topoisomerase IV to Gyrase,” Antimicrobial Agents and Chemotherapy, Vol. 44, No. 2, 2000, pp. 320-325. doi:10.1128/AAC.44.2.320-325.2000

has been cited by the following article:

• TITLE: Ciprofloxacin Cardiotoxicity and Hepatotoxicity in Humans and Animals

  AUTHORS: Elias Adikwu, Nelson Brambaifa

  KEYWORDS: Ciprofloxacin; Cardiotoxicity; Hepatotoxicity; Humans; Animals

  JOURNAL NAME: Pharmacology & Pharmacy, Vol.3 No.2, April 25, 2012

  ABSTRACT: Ciprofloxacin is generally well tolerated; the most common adverse effects include gastro intestinal tract, central nervous system and hematological system effects. Recently rising cases of Ciprofloxacin associated toxicity have been reported. Experiment using animal models and clinical experience showed that Ciprofloxacin induced cardiotoxicity is marked by increase QT and QTC interval and prolonged action potential duration. This increases the risk of arrhythmia (tosarde de pointes). Ciprofloxacin induced cardiotoxic effect could be associated with blocking cardiac voltage—gated potassium channels particularly the rapid component (IKr) of the delayed rectifier potassium current. Drug interaction with inhibitors of Cytochrome P450 (CYP) mediated metabolism could be one of the underlying mechanisms. Several cases of Ciprofloxacin induced hepatoxicity have been also reported. These were characterized by extensive hepatocellular necrosis, mixed inflammatory infiltrate and abundant esinophils in the liver. Elevated liver enzymes which include serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and gramma-glutamyltranferase and prolong prothrobin time were reported. The hepatotoxic effect of Ciprofloxacin as reported could be due to oxidative stress induced in the liver by Ciprofloxacin through the generation of oxidative radicals leading to depletion of protein content in hepatocytes as a consequence of nucleic acids diminution and DNA damage. This may lead to significant decrease in the number and degeneration in mitochondria which is responsible for energy supply. Conclusion: Ciprofloxacin induced cardiotoxicity and hepatotoxicity is relatively low in humans but patients’ liver and cardiac function may be considered before Ciprofloxacin use.