Triamterene NSAIDs

Lithium intoxication can be precipitated by the use of diuretics, particularly thiazides and metola-zone, and ACE inhibitors. NSAIDs can also precipitate lithium toxicity, mainly due to NSAID inhibition of prostaglandin-dependent renal excretion mechanisms. NSAIDs also impair renal function and cause sodium and water retention, effects which can predispose to interactions. Many case reports describe the antagonistic effects of NSAIDs on diuretics and antihypertensive drugs. The combination of triamterene and indomethacin appears particularly hazardous as it may result in acute renal failure. NSAIDs may also interfere with the beneficial effects of diuretics and ACE inhibitors in heart failure. It is not unusual to see patients whose heart failure has deteriorated in spite of increased doses of frusemide who are also concurrently taking an NSAID. 

Drugs that can precipitate lactic acidosis in patients taking metformin include ACE inhibitors, thiazide diuretics, NSAIDs, and drugs such as furosemide, nifedipine, cimetidine, amiloride, triamterene, trimethoprim, and digoxin, which are all secreted in the renal tubules, compete with metformin, and can contribute to increased plasma metformin concentrations (76). 

The actions of triamterene and spironolactone depend on renal prostaglandin production. As described above for loop diuretics and thiazides, the actions of triamterene and spironolactone can also be inhibited by NSAIDs under certain conditions. 

Diclofenac Diclofenac should not be administered intravenously to patients already receiving NSAIDs or anticoagulants, including low-dose heparin. Concomitant use of diclofenac with triamterene or cyclosporin affects kidney function.50... 

Triamterene (Dytac) is a potassium-sparing diuretic which has an action and use similar to that of amiloride. The diuretic effect extends over 10 h. Gastrointestinal upsets occur. Reversible, nonoliguric renal failure may occur when triamterene is used with indomethacin (and presumably other NSAIDs). 

Thiazide diuretics do not stimulate or require prostaglandins to produce their desired effect and they do not directly interact with NSAIDs. The magnitude of increased risk of NSAID-induced AKI with concomitant triamterene cannot be estimated based on sporadic case reports [44]. 

Clinically important, potentially hazardous interactions with amiloride, aminoglycosides, amphotericin B, ampicillin, anisindione, anticoagulants, armodafinil, atorvastatin, azathioprine, azithromycin, bacampicillin, basiliximab, bezafibrate, bosentan, bupropion, carbenicillin, caspofungin, cholestyramine, clarithromycin, cloxacillin, co-trimoxazole, corticosteroids, cyclophosphamide, daclizumab, danazol, dicloxacillin, dicumarol, digoxin, diltiazem, disulfiram, echinacea, erythromycin, ethotoin, etoposide, ezetimibe, flunisolide, fluoxymesterone, fluvastatin, foscarnet, fosphenytoin, gemfibrozil, hemophilus B vaccine, HMG-CoA reductase inhibitors, imatinib, imipenem/cilastatin, influenza vaccines, ketoconazole, lanreotide, lopinavir, lovastatin, mephenytoin, methicillin, methoxsalen, methylphenidate, methylprednisolone, methyltestosterone, mezlocillin, mizolastine, mycophenolate, nafcillin, nisoldipine, NSAIDs, orlistat, oxacillin, penicillins, phellodendron, phenytoin, pravastatin, prednisolone, prednisone, pristinamycin, ranolazine, red rice yeast, rifabutin, rifampin, rifapentine, ritonavir, rosuvastatin, simvastatin, sirolimus, spironolactone, St John s wort, sulfacetamide, sulfadiazine, sulfamethoxazole, sulfisoxazole, sulfonamides, tacrolimus, telithromycin, tenoxicam, testosterone, ticarcillin, tolvaptan, trabectedin, triamterene, troleandomycin, ursodeoxycholic acid, vaccines, vecuronium, warfarin, zofenopril... 

Clinically important, potentially hazardous interactions with aldesleukin, aspirin, diflunisal, diuretics, methotrexate, NSAIDs, prednisolone, prednisone, sermorelin, tiludronate, torsemide, triamterene, urokinase... 

Clinically important, potentially hazardous interactions with ACE inhibitors, alcohol, amiloride, barbiturates, benazepril, captopril, cyclosporine, enalapril, fosinopril, juniper, lisinopril, mitotane, moexipril, narcotics, NSAIDs, potassium chloride, potassium iodide, quinapril, ramipril, trandolapril, triamterene, zofenopril... 

Drugs with nephrotoxic potential include ACE inhibitors, acetazolamide. aminoglycosides, aspirin, amphotericin B, cyclosporine, furosemide, gold salts, lithium, methicillin, methoxyflurane, NSAIDs, pentamidine, sulfonamides, tetracyclines (degraded), thiazides, and triamterene. 

A 39-ycar-old woman taking acenocoumarol, celiprolol, triamterene, cyclothiazide, pravastatin and diosmin had a rise in her prothrombin levels from 0.3 to 1 within 8 days of starting to take diclofenac and misoprostol 400 micrograms daily. A day after these two drugs had been withdrawn her prothrombin level had fallen to 0.67, and after another 3 days to 0.32. The reasons for this reaction are not known, but suspicion falls on the misoprostol beeause diclofenac, if and when it interacts with anticoagulants, increases rather than reduces their effects (see Coumarins -i- NSAIDs Diclofenac , p.429). But just why misoprostol should cause these changes is not clear. 

A 57 year-old woman who had been treated for several years with daily doses of dielofenae 150 mg, atenolol 50 mg and triamterene with hydrochlorothiazide 50/25 mg, for rheumatoid arthritis and hypertension, additionally started treatment with methotrexate 5 mg weekly. After 2 months she was admitted to hospital with pancytopenia, extensive mu-eosal uleeration and renal impairment. The authors point out that triamterene is structurally similar to folate and has anti-folate activity, which may therefore have been additive with the effects of methotrexate, but the diclofenac may also have contributed (see Methotrexate + NSAIDs , p.649). In 1998, the manufacturer noted there were two other reports of pancytopenia in patients taking methotrexate and triamterene, but again the patients were also taking NSAIDs. ... 

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