indication

For the treatment of serious infections caused by susceptible anaerobic bacteria, including Bacteroides spp., Peptostreptococcus, anaerobic streptococci, Clostridium spp., and microaerophilic streptococci. May be useful in polymicrobic infections such as intra-abdominal or pelvic infections, osteomyelitis, diabetic foot ulcers, aspiration pneumonia and dental infections. May also be used to treat MSSA and respiratory infections caused by S. pneumoniae and S. pyogenes in patients who are intolerant to other indicated antibiotics or who are infected with resistant organism. May be used vaginally to treat vaginosis caused by Gardnerella vaginosa. Clindamycin reduces the toxin producing effects of S. aureus and S. pyogenes and as such, may be particularly useful for treating necrotizing fasciitis. May be used topically to treat acne.

pharmacology

Clindamycin is an antibiotic, similar to and a derivative of lincomycin. Clindamycin can be used in topical or systemic treatment. It is effective as an anti-anaerobic antibiotic and antiprotozoal.

mechanism of action

Systemic/vaginal clindamycin inhibits protein synthesis of bacteria by binding to the 50S ribosomal subunits of the bacteria. Specifically, it binds primarily to the 23s RNA subunit. Topical clindamycin reduces free fatty acid concentrations on the skin and suppresses the growth of Propionibacterium acnes (Corynebacterium acnes) , an anaerobe found in sebaceous glands and follicles.

toxicity

Adverse effects include nausea (may be dose-limiting), diarrhea, pseudomembranous colitis, allergic reactions, hepatoxicity, transient neutropenia and eosinophilia and agranulocytosis. Pseudomembranous colitis occurs in 0.01 - 10% of patients and occurs more commonly than with other antibiotics. Use of the topical formulation of clindamycin results in absorption of the antibiotic from the skin surface. Diarrhea, bloody diarrhea, and colitis (including pseudomembranous colitis) have been reported with the use of topical and systemic clindamycin.

biotransformation

Hepatic

absorption

Rapidly absorbed after oral administration with peak serum concentrations observed after about 45 minutes. Absorption of an oral dose is virtually complete (90%) and the concomitant intake of food does not appreciably modify the serum concentrations; serum levels have been uniform and predictable from person to person and dose to dose. Clindamycin does not penetrate the blood brain barrier.

half life

2.4 hours

route of elimination

Approximately 10% of the bioactivity is excreted in the urine and 3.6% in the feces; the remainder is excreted as bioinactive metabolites.

drug interactions

Aluminium: The aluminium salt decreases the absorption of lincosamides

Atracurium: The agent increases the effect of muscle relaxant

Attapulgite: The aluminium salt decreases the absorption of lincosamides

Cyclosporine: Clindamycin may decrease the therapeutic effect of cyclosporine.

Dihydroxyaluminium: The aluminium salt decreases the absorption of lincosamides

Doxacurium chloride: The agent increases the effect of muscle relaxant

Kaolin: The aluminium salt decreases the absorption of lincosamides

Metocurine: The agent increases the effect of muscle relaxant

Mivacurium: The agent increases the effect of muscle relaxant

Pancuronium: The agent increases the effect of muscle relaxant

Pipecuronium: The agent increases the effect of muscle relaxant

Rocuronium: The agent increases the effect of muscle relaxant

Succinylcholine: The agent increases the effect of muscle relaxant

Tubocurarine: The agent increases the effect of muscle relaxant

Vecuronium: The agent increases the effect of muscle relaxant