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Folic acid trimethoprim-sulfamethoxazole

The answer is c. (Hardman, pp 1058-1059. Katzung, pp 793-795.) Trimethoprim inhibits dihydro folic acid reductase. Sulfamethoxazole inhibits p-aminobenzoic acid (PABA) from being incorporated into folic acid by competitive inhibition of dihydropteroate synthase. Either action inhibits the synthesis of tetrahydrofolic acid. [Pg.80]

Because trimethoprim and sulfamethoxazole have their effects at different points in the folic acid synthetic pathway, a synergistic effect results when the two are administered together. The incidence of bacterial resistance to the combination is less than that observed when the drugs are used individually. Resistance is an increasing problem in a number of bacteria, but is especially problematic in the Enterobacteriaceae, against which the combination is used in AIDS patients for Pneumocystis carinii pneumonia prophylaxis. [Pg.518]

As indicated earher, sulfonamides are effective in both gram-positive and gramnegative bacteria. Mostly prescribed for humans in the United States, in this class is sulfamethoxazole, mostly in combination with trimethoprim (SMZ-TMP) in a 5 1 ratio. Trimethoprim inhibits dihydropholic acid reductase and this, just like sulfonamides, also interferes with the synthesis of folic acid (Fig. 1.8). As a matter of fact, use of the combined SMZ-TMP has been steadily increasing recently as is displayed by the number of prescriptions (Fig. 1.7). Oral doses of sulfonamides are absorbed well and eliminated by the liver and kidney with 20-60% excreted as the parent compound (Queener and Gutierrez, 2003). [Pg.55]

Blockade of sequential steps in a metabolic sequence Trimethoprim-sulfamethoxazole is the best-known example of this mechanism of synergy (see Chapter 46). Blockade of the two sequential steps in the folic acid pathway by trimethoprim-sulfamethoxazole results in a much more complete inhibition of growth than achieved by... [Pg.1110]

In acute and chronic urinary tract infection, the combination of trimethoprim and sulfamethoxazole (Bactrim, Septra) exerts a truly synergistic effect on bacteria. The sulfonamide inhibits the utilization of p-amino-benzoic acid in the synthesis of folic acid (Figure 2.3), whereas trimethoprim, by inhibiting dihydrofolic acid reductase, blocks the conversion of dihydrofolic acid to tetrahydrofolic acid, which is essential to bacteria in the denovo synthesis of purines, pyrimidines, and certain amino acids. Because mammalian organisms do not synthesize folic acid and therefore need it as a vitamin in their daily diets, trimethoprim-sulfamethoxazole does not interfere with the metabolism of mammalian cells. [Pg.27]

The synergistic antimicrobial activity of co-trimoxazole results from its inhibition of two sequential steps in the synthesis of tetrahydro-folic acid sulfamethoxazole inhibits the incorporation of PABA into folic acid, and trimethoprim prevents reduction of dihydrofolate to tetrahydrofolate (see Figure 29.5). Co-trimoxazole exhibits more potent antimicrobial activity than sulfamethoxazole or trimethoprim alone (seed Figure 29.6). [Pg.305]

The synergistic combination of trimethoprim (TMP), and sulfamethoxazole (SMZ), both folic acid antagonist antibacterial agents, was introduced over 30 years ago for its effect against a variety of infective organisms, including Pneumocystis carinii (PC). Prior to the AIDS era, TMP-SMZ, also referred as cotrimoxazole, was used predominantly for the... [Pg.356]

The sulfonamides and pyrimethamine (e.g. for equine protozoal myeloencephalitis (EPM) can cause abortion in mares and abnormalities in newborn foals (see Chs 2 and 3) even when the mares received folic acid supplementation. Trimethoprim-sulfamethoxazole given to mares for up to 1 week prior to and after breeding does not appear to potentiate early embryonic death and has not been associated with an increase in birth defects in foals (J. Brendemuehl, personal communication, 2001). Birth defects have not been identified in foals born to mares undergoing... [Pg.183]

Clinically important, potentially hazardous interactions with acitretin, aldesleukin, aminoglycosides, amiodarone, amoxicillin, ampicillin, aspirin, bacampicillin, bismuth, carbenicillin, chloroquine, cisplatin, cloxacillin, co-trimoxazole, dapsone, demeclocycline, dexamethasone, diclofenac, dicloxacillin, etodolac, etoricoxib, etretinate, fenoprofen, flurbiprofen, folic acid antagonists, haloperidol, hydrocortisone, ibuprofen, indomethacin, influenza vaccines, ketoprofen, ketorolac, lithium, magnesium trisalicylate, meclofenamate, mefenamic acid, methicillin, mezlocillin, minocycline, nabumetone, nafcillin, naproxen, NSAIDs, omeprazole, oxacillin, oxaprozin, oxytetracycline, paromomycin, penicillin G, penicillin V, penicillins, phenylbutazone, piperacillin, piroxicam, polypeptide antibiotics, prednisolone, prednisone, probenecid, procarbazine, rofecoxib, salicylates, salsalate, sapropterin, sulfadiazine, sulfamethoxazole, sulfapyridine, sulfasalazine, sulfisoxazole, sulindac, tazobactum, tenoxicam, tetracycline, ticarcillin, tolmetin, trimethoprim, vaccines... [Pg.369]

Trimethoprim is often given in conjunction with the sulfonamide sulfamethoxazole (Fig. 10.17). The latter inhibits the incorporation of PABA into folic acid, while the former inhibits dihydrofolate reductase. Therefore, two enzymes in the one biosynthetic route are inhibited. This is a very effective method of inhibiting a biosynthetic route and has the advantage that the doses of both drugs can be kept down to safe levels. To get the same level of inhibition using a single drug, the dose level of that... [Pg.165]

Inhibition of folic acid pathway Trimethoprim- sulfamethoxazole... [Pg.324]

D. Bacteria must synthesize the folate that is required for their biosynthetic processes they do not have a transporter to bring folate into the cell. Trimethoprim inhibits prokaryotic DHFR (eukaryotic is not affected) and sulfamethoxazole is an analog of p-aminobenzoic acid (PABA), a precursor to folic acid. Bacteria will use this analog instead of PABA and produce a nonfunctional folate. [Pg.33]

Co-trimoxazole (Septrin) is a well-known combination of a sulfonamide (sulfamethoxazole) with trimethoprim. This combination inhibits enzymes at two points of folic acid (32.2) utilisation - the sulfonamide inhibits incorporation of p-aminobenzoic acid during bacterial folic acid synthesis, and trimethoprim inhibits its conversion into tetrahydrofolate. The overall result is synergistic, i.e. there is a greater activity than the sum of the two components. [Pg.660]

The combination of trimethoprim and sulfamethoxazole (usually five parts sulfamethoxazole to one part trimethoprim) interferes with the synthesis of active folic acid by means of two separate reactions. In the first, sulfonamides compete with PABA and prevent its conversion to dihydro-folic acid. In the second, trimethoprim, by inhibiting the activity of dihydrofolic acid reductase, prevents the conversion of dihydrofolic acid into tetrahydrofolic acid, which is necessary for the synthesis of DNA. These reactions are summarized in Figure 90. [Pg.662]

The combination of trimethoprim and snlfamethoxazole (nsnally five parts sulfamethoxazole to one part trimethoprim) interferes with the synthesis of active folic acid by means of two separate reactions. In the first, snlfonamides... [Pg.709]

Both of these drugs interfere with bacterial synthesis of folic acid and the production of nucleotides. Sulfamethoxazole decreases the enzymatic conversion of PABA, and trimethoprim decreases the activity of dihydrofolate reductase. Thus, the actions are synergistic (see Figure p 2621. [Pg.272]

Trimethoprim is the only weak base listed (fluoroquinolones and sulfonamides are acidic compounds), and its high lipid solubility at blood pH allows penetration of the drug into prostatic and vaginal fluid to reach levels similar to those in plasma. Leukopenia and thrombocytopenia may occur in folate deficiency when the drug is used alone or in combination with sulfamethoxazole. Fluoroquinolones do not exacerbate symptoms of folic acid deficiency. The answer is (D). [Pg.410]

Simultaneous didanosine, folic acid, ganciclovir, lamivudine, nevirapine, pyrazinamide, ranitidine, rifampin, stavudine, sulfamethoxazole, trimethoprim, zidovudine Noninterfering adefovir, amprenavir, delavirdine, efavirenz, fluconazole, indinavir, itraconazole, methadone, nelfinavir, oxazepam, pyrimethamine, rifampin, ritonavir, saquinavir, zalcitabine... [Pg.2]


See other pages where Folic acid trimethoprim-sulfamethoxazole is mentioned: [Pg.203]    [Pg.203]    [Pg.313]    [Pg.27]    [Pg.300]    [Pg.349]    [Pg.3216]    [Pg.2269]    [Pg.200]    [Pg.497]    [Pg.18]    [Pg.329]    [Pg.203]    [Pg.1668]    [Pg.64]   


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Folic

Folic acid

Trimethoprim

Trimethoprim-sulfamethoxazol

Trimethoprim/sulfamethoxazole

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