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Pharmacology: Pharmacodynamics: Lincomycin inhibits bacterial protein synthesis by binding to the 23S RNA of the 50S subunit of the bacterial ribosome.
Lincomycin is predominantly bacteriostatic in vitro.
Cross-resistance has been demonstrated between clindamycin and lincomycin. Resistance in staphylococci and streptococci is most often due to methylation of specific nucleotides in the 23S RNA of the 50S ribosomal subunit, which can determine cross resistance to macrolides and streptogramins B (MLSB phenotype). Macrolide-resistant isolates of these organisms should be tested for inducible resistance to lincomycin/clindamycin using the D-zone test.
Pharmacokinetics: Intramuscular administration of a single dose of 600mg of lincomycin produces average peak serum concentrations of 11.6mcg/ml at 60 minutes and maintains therapeutic concentrations for 17 to 20 hours for most susceptible gram-positive organisms. Urinary excretion after this dose ranges from 1.8 to 24.8% (mean: 17.3%).
A two-hour intravenous infusion of 600mg of lincomycin achieves average peak serum concentrations of 15.9mcg/ml and maintains therapeutic concentrations for 14 hours for most susceptible gram-positive organisms. Urinary excretion ranges from 4.9 to 30.3% (mean: 13.8%).
The biological half-life after intramuscular or intravenous administration is 5.4 ± 1.0 hours. The serum half-life of lincomycin may be prolonged in patients with severe renal impairment compared to patients with normal renal function.
In patients with hepatic impairment, serum half-life may be two-fold longer than in patients with normal hepatic function. Hemodialysis and peritoneal dialysis are not effective in removing lincomycin from the serum.
Tissue distribution studies indicate that bile is an important route of excretion. Significant concentrations have been demonstrated in most body tissues. Although lincomycin appears to diffuse into cerebrospinal fluid (CSF), concentrations of lincomycin in the CSF appear inadequate for the treatment of meningitis.
