Pharmacodynamics
Like other NSAIDS, the anti-inflammatory and analgesic effects of lornoxicam are due to its inhibitory action on prostaglandin and thromboxane synthesis by inhibiting both COX-1 and COX-2. This results in the reduction of inflammation, pain, fever and swelling mediated by prostaglandins.
Pharmacokinetics
Lornoxicam is rapidly and almost completely absorbed from the GI tract (90-100%). It is 99% bound to plasma proteins (almost exclusively to serum albumin). Lornoxicam is completely metabolized by CYP2C9, so only negligible amounts of intact lornoxicam are excreted unchanged in the urine. Approximately 2/3 of the drug is excreted by the liver and 1/3 by the kidneys in the active form. The half-life is 3-5 hours.
Drug Interactions
Drug interactions are typical with NSAIDs. Combination with vitamin K antagonists such as warfarin increases the risk of bleeding. Combination with ciclosporin may result in decreased renal function and, in rare cases, acute kidney injury. Lornoxicam may also increase the adverse effects of lithium, methotrexate and digoxin and its derivatives. The effect of diuretics, ACE inhibitors and angiotensin II receptor antagonists may be reduced, but this is only relevant in patients with special risks such as heart failure.