Furosemide and Tenoxicam

A study in 12 patients showed that 20-40 mg tenoxicam daily had no significant effect on the urinary excretion of sodium or chloride due to 40 mg Furosemide, and blood pressure, heart rate and body weight also were not affected.

Mechanism
Uncertain and complex. It seems almost certain that a number of different mechanisms come into play. One possible mechanism is concerned with the synthesis of renal pro-staglandins which occurs when the loop diuretics cause sodium excretion If this synthesis is blocked by drugs such as the NSAID’s, then both natriuresis and renal blood flow will be altered. Indomethacm is a non-specific inhibitor of cyclo-oxygenase, whereas suhndac selectively inhibits cyclo-oxygenase outside the kidney which might explain why it interacts to a lesser extent.

Importance and management
The furosemide-indomethacm interaction is very well documented and of clinical importance, whereas far less is known about the interactions with other NSAID’s. Concurrent use often need not be avoided but the effects should be checked. Patients at greatest risk are likely to be the elderly with cardiac failure and/or renal insufficiency. Some of the data comes from studies in normal subjects rather than patients so that the total picture is still far from clear Diclofenac, diflurusal, flurbiprofen, naproxen, piroxicam and tolfenamic acid are known to interact m some individuals, but not necessarily to the same extent as indomethacm. If raising the diuretic dosage is ineffective, another NSAID such as azapropazone, lbuprofen, pirprofen, suhndac or tenoxicam may prove not to interact significantly (this is not necessarily true for patients with cirrhosis and ascites. Not every NSAID seems to have been investigated but be alert for this interaction with any of them. Phenylbutazone and oxy-phenbutazone would be expected to interact because they cause sodium retention and oedoma.