Reports suggest that NSAIDs may diminish the antihypertensive effect of angiotensin-converting enzyme (ACE)
inhibitors. This interaction should be given consideration in patients taking NSAIDs concomitantly with ACE
Concomitant administration of aspirin (1000 mg TID) to healthy volunteers tended to increase the AUC (10%) and
Cmax (24%) of meloxicam. The clinical significance of this interaction is not known; however, as with
other NSAIDs, concomitant administration of meloxicam and aspirin is not generally recommended because of the
potential for increased adverse effects. Concomitant administration of low-dose aspirin with MOBIC may result in an
increased rate of GI ulceration or other complications, compared to use of MOBIC alone. MOBIC is not a substitute for
aspirin for cardiovascular prophylaxis.
Pretreatment for four days with cholestyramine significantly increased the clearance of meloxicam by 50%. This
resulted in a decrease in t1/2, from 19.2 hours to 12.5 hours, and a 35% reduction in AUC. This suggests
the existence of a recirculation pathway for meloxicam in the gastrointestinal tract. The clinical relevance of this
interaction has not been established.
Concomitant administration of 200 mg cimetidine QID did not alter the single-dose pharmacokinetics of 30 mg
Movalis 15 mg once daily for 7 days did not alter the plasma concentration profile of digoxin after b-acetyldigoxin administration for 7 days at clinical doses. In vitro testing found no protein
binding drug interaction between digoxin and meloxicam.
Clinical studies, as well as post-marketing observations, have shown that NSAIDs can reduce the natriuretic effect
of furosemide and thiazide diuretics in some patients. This effect has been attributed to inhibition of renal
prostaglandin synthesis. Studies with furosemide agents and meloxicam have not demonstrated a reduction in
natriuretic effect. Furosemide single and multiple dose pharmacodynamics and pharmacokinetics are not affected by
multiple doses of meloxicam. Nevertheless, during concomitant therapy with furosemide and MOBIC, patients should be
observed closely for signs of declining renal function, as well as to assure diuretic efficacy.
In clinical trials, NSAIDs have produced an elevation of plasma lithium levels and a reduction in renal lithium
clearance. In a study conducted in healthy subjects, mean pre-dose lithium concentration and AUC were increased by
21% in subjects receiving lithium doses ranging from 804 to 1072 mg BID with meloxicam 15 mg QD as compared to
subjects receiving lithium alone. These effects have been attributed to inhibition of renal prostaglandin synthesis
by MOBIC. Patients on lithium treatment should be closely monitored when MOBIC is introduced or withdrawn.
A study in 13 rheumatoid arthritis (RA) patients evaluated the effects of multiple doses of meloxicam on the
pharmacokinetics of methotrexate taken once weekly. Movalis did not have a significant effect on the
pharmacokinetics of single doses of methotrexate. In vitro, methotrexate did not displace meloxicam from its
human serum binding sites.
Anticoagulant activity should be monitored, particularly in the first few days after initiating or changing MOBIC
therapy in patients receiving warfarin or similar agents, since these patients are at an increased risk of bleeding.
The effect of meloxicam on the anticoagulant effect of warfarin was studied in a group of healthy subjects receiving
daily doses of warfarin that produced an INR (International Normalized Ratio) between 1.2 and 1.8. In these subjects,
meloxicam did not alter warfarin pharmacokinetics and the average anticoagulant effect of warfarin as determined by
prothrombin time. However, one subject showed an increase in INR from 1.5 to 2.1. Caution should be used when
administering MOBIC with warfarin since patients on warfarin may experience changes in INR and an increased risk of
bleeding complications when a new medication is introduced.