Coxpar

For the short-term treatment of postoperative pain in adults. The decision to prescribe a selective cyclooxygenase-2 (COX-2) inhibitor should be based on an assessment of the individual patient's overall risks.

Commonside effects are-
Change in your blood pressure (up or down)
You may get back pain
Ankles, legs and feet may swell (fluid retention)
You may feel numb- your skin may lose sensitivity to pain and touch
You may get vomiting, stomach ache, indigestion, constipation, bloating and wind
Tests may show abnormal kidney function
You may feel agitated or find it hard to sleep
Dizziness
There is a risk of anaemia- changes in red blood cells after an operation that may cause fatigue and breathlessness
You may get a sore throat or difficulty breathing (shortness of breath)
Your skin may be itchy
You may pass less urine than usual.
Dry socket (inflammation and pain after a tooth extraction)
Increased sweating
Low levels of potassium in blood test results.

Coxpar has been studied in dental, orthopaedic, gynaecologic (principally hysterectomy) and coronary artery bypass graft surgery. There is limited experience in other types of surgery, for example gastrointestinal or urological surgery. Modes of administration other than IV or IM (e.g. intra-articular, intrathecal) have not been studied and should not be used. Because of the possibility for increaed adverse reactions at higher doses of Coxpar, other COX-2 inhibitors and NSAIDs, patients treated with Coxpar should be reviewed following dose increase and, in the absence of an increase in efficacy, other therapeutic options should be considered. There is limited clinical experience with Coxpar treatment beyond three days. If, during treatment, patients deteriorate in any of the organ system functions described below, appropriate measures should be taken and discontinuation of Coxpar therapy should be considered.

Parecoxib is a prodrug of valdecoxib. Valdecoxib is a selective COX-2 inhibitor within the clinical dose range. Cyclooxygenase is responsible for generation of prostaglandins. Two isoforms, COX-1 and COX-2, have been identified. COX-2 is the isoform of the enzyme that has been shown to be induced by pro-inflammatory stimuli and has been postulated to be primarily responsible for the synthesis of prostanoid mediators of pain, inflammation, and fever. COX-2 is also involved in ovulation, implantation and closure of the ductus arteriosus, regulation of renal function, and central nervous system functions (fever induction, pain perception and cognitive function). It may also play a role in ulcer healing. COX-2 has been identified in tissue around gastric ulcers in man but its relevance to ulcer healing has not been established.
The difference in antiplatelet activity between some COX-1 inhibiting NSAIDs and COX-2 selective inhibitors may be of clinical significance in patients at risk of thrombo-embolic reactions. COX-2 selective inhibitors reduce the formation of systemic (and therefore possibly endothelial) prostacyclin without affecting platelet thromboxane. The clinical relevance of these observations has not been established.