A recent gastric biopsy study showed that Helicobacter pylori infected cells expressed COX-2. This raises the question whether inhibitors of COX-2 will affect host reaction to the agent. This issue needs to be examined. Renal effects are not clear. COX-2 is expressed in the normal human kidney.
Increased expression is reported during salt restriction and in glomerulonephritis.
This has, however, been reversible and has not caused many withdrawals in the trials as far as I am aware. Structurally, it was observed that a sulfonamide group promoted COX-2 selectivity, which could be a problem with regard to creating potential for adverse reactions. However, this has been checked by sulfonyl or sulfone substitution. Nevertheless, risk groups for adverse drug reactions, such as patients with SLE, need to be watched carefully. Unchecked thromboxane formation and diminished prostacyclin production could, in theory, be causing vascular occlusion.