Sparfloxacin

Oral
Community-acquired pneumonia, Acute bacterial exacerbation of chronic bronchitis

Dosage adjustment may be necessary in severe impairment.

May be taken with or without food.

Hypersensitivity; pregnancy and lactation; children <18 yr.

History of CNS disorders, pseudomembranous colitis, superinfection, severe renal dysfunction, epilepsy, G6PD deficiency, myasthenia gravis, patients with QT prolongation, uncorrected electrolyte disturbances, bradycardia, or pre-existing cardiac disease. Avoid exposure to strong sunlight or sunlamps during treatment. Discontinue treatment if patients experience tendon pain, inflammation or rupture; subsequent use of fluoroquinolones in these patients is not recommended. Avoid in MRSA infections due to high risk of resistance. Ensure adequate fluid intake to reduce risk of crystalluria.

Diarrhoea, abdominal pain, nausea, vomiting; jaundice, renal failure, elevation of liver enzymes, BUN and creatinine; anaphylactoid reaction, headache, dizziness, convulsions; tremors, myalgia; rhabdomyolysis, thrombocytopenia and eosinophilia.
Potentially Fatal: AV block; anaphylaxis.

PO: C

Cations such as aluminum, magnesium, zinc and iron may reduce the bioavailability of sparfloxacin. May increase the plasma concentrations of theophylline and tizanidine. May enhance the effect of warfarin and glibenclamide. May decrease the renal clearance of methotrexate. Excretion may be reduced by probenecid. May alter serum levels of phenytoin.
Potentially Fatal: Corticosteroids may increase risk of tendon rupture. Increased risk of seizures with NSAIDs. Risk of additive QT prolongation effect when used with class Ia or III antiarrhythmic drugs, astemizole, terfenadine, cisapride, erythromycin, pentamidine, phenothiazines or TCAs.

Description: Sparfloxacin inhibits the supercoiling activity of DNA gyrase which is an enzyme essential for DNA replication thus promoting the breakage of DNA structures. It has activity against S. pneumoniae, S. aureus, H. influenzae, K. pneumoniae, M. catarrhalis and Mycobacterium spp.
Pharmacokinetics:
Absorption: Well absorbed from the GI tract (oral); peak plasma concentrations after 3-6 hr.
Distribution: Widely distributed into tissues including respiratory tissues. Protein-binding: 45%.
Metabolism: Hepatic (by glucuronidation).
Excretion: Excreted in equal amounts in the urine and faeces as unchanged drug and glucuronide metabolites; elimination half-life: 20 hr.

Quinolones