Sulindac interaction with lithium

Unlike other NSAIDs, sulindac supposedly does not interact with lithium (SEDA-10, 82). However, there has been a report of a toxic increase in serum lithium concentration in a 23-year-old man and a 27-year-old woman (to 2.0 and 1.7 mmol/1 respectively) (690). 

The interaction of NSAIDs with lithium has been reviewed briefly (663). Most NSAIDs, although perhaps not all (for example aspirin, sulindac), if given in sufficient dosages for sufficient time, can increase the serum lithium concentration, sometimes to the point of toxicity (664,665). 

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... 

Most of the renal tubular reabsorption ofU occurs in the proximal tubule. Nevertheless, Id retention can be increased by any diuretic that leads to depletion of Na, particularly the thiazides (see Chapter 28). Renal excretion can be increased by administration of osmotic diuretics, aceta-zolamide or aminophylline, and triamterene. Spironolactone does not increase the excretion of LiL Some nonsteroidal anti-inflammatory agents can facilitate renal proximal tubular resorption of Id and thereby increase concentrations in plasma to toxic levels. This interaction appears to be particularly prominent with indomethacin, but also may occur with ibuprofen, naproxen, and COX-2 inhibitors, and possibly less so with sulindac and aspirin. A potential drug interaction can occur with angiotensin-converting enzyme inhibitors, causing lithium retention (see Chapter 29). 

NSAIDs may increase serum-lithium levels leading to toxicity, but there is great variability between different NSAIDs and also between individuals taking the same NSAID. For example, studies have found that celecoxib causes a modest 17% increase in lithium levels, yet case reports describe increases of up to 344%. Similar effects occur with other NSAIDs, and it seems likely that all NSAIDs will interact similarly. However, note that sulindac seems unique in that it is the only NSAID that has also been reported to cause a decrease in lithium levels. 

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