NSAIDs Vancomycin

WARNING Renal impair is the major tox foUow administration instructions Uses CMV retinitis w/ HIV Action Selective inhibition of viral DNA synth Dose Rx 5 mg/kg IV over 1 h once/wk for 2 wk w/ probenecid Maint 5 mg/kg IV once/2 wk w/ probenecid (2 g PO 3 h prior to cidofovir, then 1 g PO at 2 h 8 h after cidofovir) X in renal impair Caution [C, -] Contra Probenecid or sulfa allergy Disp Inj SE Renal tox, chills, fever, HA, NA /D, thrombocytopenia, neutropenia Interactions t Nephrotox W/ aminoglycosides, amphot icin B, foscar-net, IV pentamidine, NSAIDs, vancomycin t effects W/zidovudine EMS Monitor ECG for hypocalcemia (t QT int val) and hypokalemia (flattened T waves) OD May cause renal failure hydration may be effective in reducing drug levels/effects Cilostazol (Pletal) TAntiplatelet, Arterial Vasodilator/ Phosphodiesterase Inhibitor] Uses Reduce Sxs of intermittent claudication Action Phosphodiesterase in inhibitor t s cAMP in pits blood vessels, vasodilation inhibit pit aggregation Dose 100 mg PO bid, 1/2 h before or 2 h after breakfast dinner Caution [C, +/-] Contra CHE, hemostatic disorders. 

Albumin, aminophylline, aspirin, heparin, insulin, metoclopramide, NSAIDs, muromonab-CD3 (OKT3), opiates, penicillins, propafenone, quinidine, senna, sulfonamide antimicrobials, and vancomycin... 

P-lactam antimicrobials, erythromycin, nitrofurantoin, rifampin, sulfonamide antimicrobials, and vancomycin 0 Diuretics (all classes), NSAIDs... 

Nephrotoxins (N) orototoxins (0) (eg., amphotericin B (N), cisplatin (N/0), cyclosporine (N), furosemide (0), NSAIDs (N), radio contrast (N), vancomycin (N) Additive adverse effects Monitor aminoglycoside SDC and renal function... 

INDOMETACIN AMINOGLYCOSIDES T amikacin, gentamicin, and vancomycin levels in neonates Uncertain indometacin possibly 1 renal clearance of these aminoglycosides Halve the dose of antibiotic. Uncertain whether this applies to adults but suggest check levels. Otherwise use an alternative NSAID... 

The following are the most common causes of drug-induced urticaria antibiotics, notably penicillin (more following parenteral administration than by ingestion), barbiturates, captopril, levamisole, NSAIDs, quinine, rifampin, sulfonamides, thiopental, and vancomycin. 

An elderly woman who had been treated with low-dose methotrexate 5 mg weekly and loxoprofen for one month developed acute pyelonephritis. Intravenous eefotiam was started, and on day 7 she developed severe watery diarrhoea. Analysis showed pancytopenia and Clostridium difficile infection. Methotrexate and cefotiam were stopped, and vancomycin started, and the patient reeovered. It was suggested that the combination of the antineoplastic drug and antibacterial increased the risk of Clostridium difficile diarrhoea. In addition, the NSAID (see Methotrexate + NSAIDs , p.649) and renal impairment from the pyelonephritis could have eontrib-uted to the methotrexate toxicity. This appears to be an isolated ease, and any interaetion with cefotiam is not established. 

Other predicted interactions of tacrolimus include additive neuro- or nephrotoxicity with aciclovir, aminoglycosides, co-trimoxazole, ganciclovir, gyrase inhibitors, NSAIDs (see NSAIDs , (p.1081)) or vancomycin (nephrotoxicity has been seen with amphotericin B and tacrolimus). ... 

Urticaria is the second most common cutaneous reaction induced by drugs, often in association with angioedema and anaphylaxis. Many drugs are implicated including p-lactams, NSAIDs, sulfonamides, vancomycin, and contrast media. ACE inhibitors are responsible for approximately one in six patients admitted to hospital with angioedema. 

Macrocyclic antibiotics, for example, erythromycin and vancomycin, have also been used as impregnating agents for TLC resolution of enantiomers of dansyl amino acids by Bhushan and Parshad [6] and Bhushan and Thiong o [7]. Separation in this case is due to chirality of macrocyclic antibiotic molecule, which is ionizable and contains hydrophobic and hydrophilic moieties as well providing enantioseparation via n-n complexation, H-bonding, inclusion in a hydrophobic pocket, dipole stacking, steric interactions, or combination thereof. In view of the scope of the chapter and nonavailability of reports related to NSAIDs, these are not being discussed here. 

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