Trimthoprim

Trimethoprim a common antibacterial agent with a half life of 8-11 hours, an unknown toxic dose or serum level. A toxic level will cause bone marrow depression, methemoglobinemia, and hyperkalemia. Trimethoprim acts to block synthesis of folic acid in bacteria by blocking the activity of the bacterial dihydrofolate reductase enzyme. Humans do not make their own folic acid, accounting for the selective toxicity of this agent against bacteria.

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Trimethoprim has a bacteriostatic activity against a broad spectrum of pathogens.

Sulphonamides, the earliest class of antibacterial agents, block folic acid synthesis by acting on dihydropteroate synthase, the enzyme preceding dihydrofolate reductase in the pathway responsible for folic acid production. Trimethoprim was developed and marketed initially as a potentiator for sulphonamides. Co-trimoxazole is a combination of trimethoprim and the sulfonamide sulfamethoxazole. Since tetrahydrofolic acid synthesis is inhibited at two successive steps, the in vitro antibacterial effect of co-trimoxazole is better than that of the individual components. This synergy is more difficult to demonstrate in vivo. Pathogens resistant to both sulphonamides and trimethoprim are infrequent and a bactericidal effect may occur.^[1]

Because of increasing levels of resistance to sulphonamides and the increased risk of side-effects when used in combination, particularly Stevens-Johnson syndrome, trimethoprim is most often used as a single agent in the United Kingdom. The use of co-trimoxazole to treat bacteiral infections is no longer recommended in the UK.

References

1. ^ name=Heinz Lüllmann,272>Lüllmann, Heinz (2000). Color Atlas of Pharmacology 2nd edition,. Thieme, pp. 272. ISBN 0-86577-843-4.