Trimthoprim

Jump to navigation Jump to search

WikiDoc Resources for Trimthoprim

Articles

Most recent articles on Trimthoprim

Most cited articles on Trimthoprim

Review articles on Trimthoprim

Articles on Trimthoprim in N Eng J Med, Lancet, BMJ

Media

Powerpoint slides on Trimthoprim

Images of Trimthoprim

Photos of Trimthoprim

Podcasts & MP3s on Trimthoprim

Videos on Trimthoprim

Evidence Based Medicine

Cochrane Collaboration on Trimthoprim

Bandolier on Trimthoprim

TRIP on Trimthoprim

Clinical Trials

Ongoing Trials on Trimthoprim at Clinical Trials.gov

Trial results on Trimthoprim

Clinical Trials on Trimthoprim at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Trimthoprim

NICE Guidance on Trimthoprim

NHS PRODIGY Guidance

FDA on Trimthoprim

CDC on Trimthoprim

Books

Books on Trimthoprim

News

Trimthoprim in the news

Be alerted to news on Trimthoprim

News trends on Trimthoprim

Commentary

Blogs on Trimthoprim

Definitions

Definitions of Trimthoprim

Patient Resources / Community

Patient resources on Trimthoprim

Discussion groups on Trimthoprim

Patient Handouts on Trimthoprim

Directions to Hospitals Treating Trimthoprim

Risk calculators and risk factors for Trimthoprim

Healthcare Provider Resources

Symptoms of Trimthoprim

Causes & Risk Factors for Trimthoprim

Diagnostic studies for Trimthoprim

Treatment of Trimthoprim

Continuing Medical Education (CME)

CME Programs on Trimthoprim

International

Trimthoprim en Espanol

Trimthoprim en Francais

Business

Trimthoprim in the Marketplace

Patents on Trimthoprim

Experimental / Informatics

List of terms related to 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.

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. pp. 272. ISBN 0-86577-843-4. Check date values in: |date= (help)


Template:WH Template:WS