Trimethoprim drug interactions

Several drug interactions involving amantadine and rimantadine are clinically significant. Anticholinergic drugs can potentiate the toxicity of amantadine. Thiazide-triamterene, trimethoprim-sulfamethoxazole, quinine, and quinidine increase plasma amantadine levels. Cimetidine decreases rimantadine clearance, and aspirin and acetaminophen decrease rimantadine plasma levels. 

A 59-year-old woman presents to an urgent care clinic with a 4-day history of frequent and painful urination. She has had fevers, chills, and flank pain for the last 2 days. Her physician advised her to immediately come to the clinic for evaluation. In the clinic she is febrile (38.5°C [101.3°F]) but otherwise stable and states she is not experiencing any nausea or vomiting. Her urine dipstick test is positive for leukocyte esterase. Urinalysis and urine culture are also ordered. Her past medical history is significant for three urinary tract infections in the past year. Each of these episodes was uncomplicated, treated with trimethoprim-sulfamethoxazole, and promptly resolved. She also has osteoporosis for which she takes a daily calcium supplement. The decision is made to treat her with oral antibiotics for a complicated urinary tract infection with close follow-up. Given her history what would be a reasonable empiric antibiotic choice Depending on the antibiotic choice are there potential drug interactions she should be counseled on ... 

W discuss three examples of "drug target" interactions (l)biotin-avidin (2) dihydrofolate reductase-trimethoprim, and (3)DNA-in-tercalator. The first is the strongest characterized protein-ligand association, the second a prototype enzyme-inhibitor interaction, and the third describes drugs interacting with nucleic acids. 

Lee BL, Medina 1, Benowitz NL, Jacob P, 3rd, Wofsy CB, Mills Jt. Dapsone, trimethoprim, and sulfamethoxazole plasma levels during treatment of Pneumocystis pneumonia in patients with the acquired immunodeficiency syndrome (AIDS). Evidence of drug interactions. Annals of internal medicine. 1989 Apr 15 110(8) 606-n. 

Fleischman SH, Brooks CL. Protein-drug interactions Characterization of inhibitor binding in complexes of DHFR with trimethoprim and related derivatives. Proteins 1990 7 52-61. 

Emtricitabine is not metabolized to a significant extent by CYPs, and it is not susceptible to any known metabolic drug interactions. The possibility of a pharmacokinetic interaction involving renal tubular secretion, such as that between trimethoprim and lamivudine, has not been investigated for emtricitabine, although the drug does not alter the pharmacokinetics of tenofovir. 

Because of indinavir s metabolism, a number of drug interactions are possible. Indinavir interacts with rifabutin or ketoconazole, leading to increased or decreased indinavir concentration, respectively, in the blood plasma. Administration of drug combinations of indinavir with antiviral nucleoside analogues, cimetidine, quinidine, trimethoprim/sulfamethoxazole, fluconazole, or isoniazid resulted in an increased activity of indinavir. Indinavir is ... 

Johnson JF, Dobmeier ME. Symptomatic hypoglycemia secondary to a glipizide-trimethoprim/sulfamethoxazole drug interaction. DICP Ann Pharmacother (1990) 24, 250-1. 

S. H. Fleishman and C. L. Brooks III, Proteins, 7, 52 (1990). Protein-Drug Interactions Characterization of Inhibitor Binding in Complexes of DHFR with Trimethoprim and Related Derivatives. 

Drugs that may interact with folic acid include aminosalicylic acid, oral contraceptives, dihydrofolate reductase inhibitors (eg, methotrexate, trimethoprim), sulfasalazine, hydantoins. 

Drugs that may interact with lamivudine include zalcitabine and trimethoprim/sulfamethoxazole. 

Antibiotics can be classified according to their effects on the biochemistry or molecular biology of pathogens. There are ribosomal inhibitors (macrolides), cell wall disrupters 0-lactams), DNA disturbers (fluoroquinolones), and metabolic poisons (trimethoprim-sulfamethoxazole). Antibiotics also can be classified according to whether they are static (inhibitory) or cidal (lethal). The classification of drugs as either static or cidal is based on laboratory assessment of the interaction of pathogen and antibiotic drug. 

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