Both corticosteroids and nonsteroidal antiinflammatory drugs (NSAIDs) are known to cause adverse effects in dogs and cats. The theoretical risk for toxicity is increased when these drugs are used concurrently and this practice is generally contraindicated.
However, corticosteroids and NSAID combinations may have additive therapeutic benefits when treating some disease conditions because they sequentially block the arachidonic acid cascade production of prostaglandins (PGs).
This effect may be adverse, though, as PGs also benefit and protect the gastrointestinal (GI) tract, hemostasis, and renal function.
COX-derived PGs are very important in modulating GI mucosa defense and repair, with COX–1-derived PGs supporting mucosal blood flow, mucus and bicarbonate secretion, and normal platelet aggregation, while COX–2-derived PGs modulate the inflammatory response so that normal healing can occur.
PATHOPHYSIOLOGY
The mucosa of the GI tract is regularly exposed to a wide range of potentially damaging substances, including those that are ingested (bones, drugs, etc) and endogenous secretions (gastric acid, bile salts). The GI mucosa is not only able to resist damage by these substances for the most part, but it has tremendous reparative capacity when damage does occur.
Systemically, cyclooxygenase (COX)-derived PGs are very important in modulating GI mucosa defense and repair, with COX–1-derived PGs supporting mucosal blood flow, mucus and bicarbonate secretion, and normal platelet aggregation, while COX–2-derived PGs modulate the inflammatory response so that normal healing can occur. Hemostasis is highly influenced by PGs, with platelet aggregation and vasoconstriction promoted by platelet-derived thromboxane A2 and inhibition of platelet aggregation and vasodilation promoted by endothelium-derived prostacyclin. Renal PGs help maintain normal blood flow and glomerular filtration rate (GFR).