NUCOTRIE-90 Tab

Description

Etoricoxib for pain and inflammationNUCOTRIE
Authored by Helen Allen, 02 Nov 2016
Etoricoxib is a medicine called a non-steroidal anti-inflammatory drug. It is also known as an ‘NSAID’.
Tell your doctor if you have ever had an allergic reaction to any other anti-inflammatory medicine.
Take etoricoxib once daily.
About NUCOTRIE (Etoricoxib) tablets
Type of medicine A non-steroidal anti-inflammatory drug (NSAID)
Used for Relief of pain and inflammation
Also called NUCOTRIE
Available as Tablets
Anti-inflammatory painkillers like NUCOTRIE are also called non-steroidal anti-inflammatory drugs (NSAIDs), or sometimes just ‘anti-inflammatories’. Etoricoxib eases pain and swelling (inflammation) in conditions like osteoarthritis, rheumatoid arthritis and ankylosing spondylitis, and it may also be used for short periods of time in gout.
Etoricoxib works by blocking the effect of a natural chemical called cyclo-oxygenase-2 (COX-2) enzyme. This enzyme helps to make other chemicals, called prostaglandins, in the body. Some prostaglandins are produced at sites of injury or damage, and cause pain and inflammation. By blocking the effect of COX-2 enzymes, fewer prostaglandins are produced, which means pain and inflammation are eased.

J Indian Med Assoc. 2007 May;105(5):260-2.
A study on the effects of diclofenac sodium and etoricoxib in the treatment of osteoarthritis.
Ghosh S1, Paul S, Das N, Bhattacharyya TK.
Author information
Abstract
Diclofenac sodium, a non-selective cyclo-oxygenase inhibitor and etoricoxib, a selective cyclo-oxygenase-2 inhibitor have been widely used in treatment of patients with osteo-arthritis. Five hundred and eighty-five patients with uncomplicated knee osteo-arthritis were randomly allocated into 3 equal groups and received either diclofenac sodium, etoricoxib or placebo in a double-blind manner. The response in both the drug groups was comparable and much more than placebo group. The study shows that etoricoxib provides better clinical efficacy and gastro-intestinal tolerability in osteo-arthritis in comparison to diclofenac sodium presumably due to the selective inhibition of cyclo-oxygenase-2 by etoricoxib.

A Comparison of the Therapeutic Efficacy and Tolerability of Etoricoxib and Diclofenac in Patients With Osteoarthritis
J. Zacher; D. Feldman; R. Gerli; D. Scott; S.-M. Hou; D. Uebelhart; I. W. Rodger; Z. E. Ozturk
DISCLOSURES
Curr Med Res Opin. 2003;19(8)
Summary and Introduction
Objective: To evaluate and compare the efficacy and tolerability of etoricoxib and diclofenac in patients with osteoarthritis of the knee or hip.
Methods: In this 6-week double-blind, active comparator controlled, parallel-group study eligible osteoarthritis patients were randomised to receive either etoricoxib 60 mg once daily (n = 256) or diclofenac 50 mg three times daily (n = 260). The primary study endpoint was the Western Ontario McMaster osteoarthritis index (WOMAC) pain subscale. Other endpoints included were the WOMAC stiffness and physical function subscales, and the Patient’s Global Assessment of Response to Therapy (PGART) questionnaire. Early efficacy was evaluated using WOMAC first question (pain walking on a flat surface) and PGART 4 h after the morning dose of each drug on days 1 and 2. Rescue medication (paracetamol) used was also recorded. The study was designed to show comparable efficacy between etoricoxib 60 mg once daily and diclofenac 50 mg three times daily with respect to the primary endpoint and was conducted outside the United States at 67 centres in 29 countries.
Results: Etoricoxib (60 mg once daily) was comparable in efficacy to diclofenac (150 mg daily) on all the above parameters. The one exception was in the assessment of early efficacy where etoricoxib demonstrated significantly greater benefit within 4 h of taking the first dose on the first day of therapy ( p = 0.007) as evaluated by the percentage of patients with good or excellent (PGART) responses. The treatment effects of both drugs were similar by the time day 2 was reached and were sustained throughout the 6 weeks of therapy. Both treatments were generally well tolerated.
Conclusions: Etoricoxib is clinically effective in the therapy of osteoarthritis providing a magnitude of effect comparable to that of the maximum recommended daily dose of diclofenac. The onset of clinical benefit with etoricoxib on day one is more rapid than that of diclofenac. Both drugs were generally well tolerated.
Osteoarthritis (OA) is the most common chronic degenerative joint disorder in the world. It is estimated to affect approximately 25 million people in the United States and millions more worldwide.[1] In the United States it also accounts for about 12 million doctors’ visits annually. The disease affects principally the knees, hips, spine, hands and feet and once established it progresses steadily over time, causing chronic pain, joint stiffness with loss of function and physical limitation and consequent reduction in the quality of a patient’s life.[2,3] It has been estimated that about one-third of adults over the age of 50 years has osteoarthritis of the knee.[3,4]
The treatment guidelines for osteoarthritis include both pharmacological and non-pharmacological modalities, the latter including patient education and physical exercise. Within the pharmacological category the mainstay of therapy has been the non-steroidal anti-inflammatory drugs (NSAIDs), typified by diclofenac, ibuprofen and naproxen.[4,5] Such drug therapy is aimed principally at relieving pain and stiffness and at improving joint mobility. It is now well established that these drugs act to provide symptomatic relief of the pain of osteoarthritis by inhibiting the enzyme cyclooxygenase (COX) that is responsible for manufacturing prostaglandins (PGs).[6] PGE2 is widely regarded as the key prostanoid responsible for generating the pain and inflammation associated with osteoarthritis. However, the use of these drugs, especially if high doses are required, is limited by their gastrointestinal toxicity.[7,8] Indeed, the World Health Organization has stated that NSAID-induced gastrointestinal damage is the most common serious, drug-induced, adverse event worldwide. It has long been recognised that this toxicity is manifest in the upper GI tract as perforations, ulcers and bleeding ulcers.[7,8,9] More recently, however, it has become clear that bleeding from the lower gastrointestinal tract is a very significant problem that has long been overlooked.[10] Furthermore, this toxicity does not require long-term administration for it to be manifest. NSAID-induced bleeding from the gastrointestinal tract is evident even in healthy subjects after only a few days of therapy.[9,11,12]
Today it is recognised that prostanoids are synthesised by two distinct isoforms of cyclo-oxygenase, termed COX-1 and COX-2.[6,13] COX-1 is constitutively expressed and functionally active in a wide range of tissues including the gastrointestinal tract, kidney, lungs and cardiovascular system, including the platelets. Indeed, the view has now been widely adopted that COX-1-derived prostanoids are essential for ‘housekeeping’ functions throughout the body and especially in the GI tract, kidney and platelets.[6,9]PGE2, for example, is recognised as an essential component for the maintenance of gastrointestinal mucosal integrity which it orchestrates by maintaining sub-mucosal blood flow, amongst other actions [6,14,15] In contrast, although mRNA for COX-2 is found in many tissues of the body, it is not normally present as a functionally active enzyme. To become so it requires to be induced or upregulated by certain key cytokines, growth factors and mitogens.[6,16] It is precisely this process that is present at sites of pain and inflammation where up-regulation of COX-2 generates high local concentrations of prostanoids, principally PGE2. The traditional NSAIDs are all non-selective for COX-1 and COX-2 in that at therapeutically effective doses they inhibit both enzymes to a considerable degree.[17] Thus, it is apparent that the therapeutic utility of NSAIDs is a consequence of their inhibition of COX-2 whilst their toxicity is inextricably linked to their capacity to inhibit COX-1.[18]
In the past 4 years drugs that are selective for COX-2 have become available for the treatment of patients with arthritic conditions, including osteoarthritis. These drugs, typified by rofecoxib, celecoxib and valdecoxib, have been shown to have unequivocal benefits in patients with arthritis whilst possessing a substantially improved gastrointestinal tolerability profile.[19,20,21,22,23,24,25,26] A more selective COX-2 inhibitor, etoricoxib[27,28] (> 100-fold selectivity for COX-2 over COX-1), that is structurally unrelated to either celecoxib or rofecoxib, has recently been approved in a large number of countries worldwide, for use in patients with arthritic diseases. In published reports, from the phase IIb/III clinical trials conducted for registration purposes, etoricoxib has been shown to provide clinically meaningful benefit to patients with both osteoarthritis[29] and rheumatoid arthritis.[30,31] In the studies in osteoarthritis the dose of etoricoxib that demonstrated maximal efficacy was 60 mg administered once daily.
In the present report we describe the results of a study designed to compare the clinical efficacy and tolerability of etoricoxib with that of diclofenac, the most commonly used NSAID, in patients with osteoarthritis of either the knee or the hip.