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  1. Loo CY, Tan HJ, Teh HS, Raymond AA
    Singapore Med J, 2007 Sep;48(9):834-9.
    PMID: 17728965
    INTRODUCTION: Migraine is a common disabling condition that results in considerable socioeconomic loss. The role of non-steroidal anti-inflammatory drugs (NSAIDs) in acute migraine has been well-established. We compared the efficacy of the cyclooxygenase-2 inhibitor celecoxib with the NSAID, naproxen sodium, in the treatment of acute migraine.
    METHODS: This was a randomised, open label, controlled trial. We selected patients with a diagnosis of migraine, based on the International Headache Society revised criteria. 60 patients were randomised to either celecoxib 400 mg (30 patients) or naproxen sodium 550 mg (30 patients). Patients took the study medicine for the first acute migraine episode that occurred during the study period and reported the headache reduction based on a visual analogue score (VAS). Patients were reviewed after a month to check on VAS at one and two hours, compared to the baseline. Any side effects of the medication were also recorded.
    RESULTS: Of the 52 patients who completed the study, eight did not experience any headaches. The mean VAS in the celecoxib group improved significantly from baseline (6.48 +/- 1.53) to one hour (4.28 +/- 2.11) and two hours (2.24 +/- 2.57) (p-value is less than 0.0005). The mean VAS in the naproxen sodium group also improved significantly from baseline (7.30 +/- 1.66) to one hour (4.81 +/- 2.50) and two hours (2.63 +/- 2.65) (p-value is less than 0.0005). However, there was no significant difference between the magnitudes of improvement between the treatment groups. The incidence of gastric pain was significantly higher in the naproxen sodium group (p-value is equal to 0.029).
    CONCLUSION: In comparison with naproxen sodium, celecoxib was equally effective in relieving pain in acute migraine and caused significantly less gastric pain.

    Study site: neurology outpatient clinic in Pusat Perubatan
    Universiti Kebangsaan Malaysia (PPUKM)
    Matched MeSH terms: Cyclooxygenase 2 Inhibitors/therapeutic use*
  2. Yeap SS, Goh EM, Gun SC
    Int J Rheum Dis, 2009 Dec;12(4):329-35.
    PMID: 20374371 DOI: 10.1111/j.1756-185X.2009.01431.x
    AIM: The aim of this study was to ascertain the management of gout by doctors in Malaysia.
    METHODS: A cross-sectional questionnaire survey was carried out among doctors attending rheumatology post-graduate courses, where gout was not a lecture topic.
    RESULTS: A total of 128 questionnaires were analyzed, of which the majority (67: 52.3%) were general practitioners. In the treatment of acute gout, 68.0% use non-selective non-steroidal anti-inflammatory drugs (NSAIDs), 53.9% use selective COX-2 inhibitors (coxibs), 66.4% use colchicine and 10.2% use allopurinol (ALLO). In the treatment of chronic gout, 36.7% use NSAIDs, 44.5% use coxibs, 19.5% use colchicine and 93% use ALLO. In both acute and chronic gout, corticosteroids (CS) are not used by over 90% of respondents. Fifty percent would stop ALLO during an acute attack. 95.3% do not start ALLO during an acute attack; 87.5% would start ALLO after the attack, with a median of 14 days afterwards. Once ALLO was started, 54.7% would continue indefinitely. Regarding target urate levels while on treatment, 10.9% would be satisfied with a high normal range, 21.9% middle of the range, 18.0% low normal range and 45.3% anywhere within the normal range. Fifteen percent would treat asymptomatic hyperuricemia.
    CONCLUSIONS: In Malaysia, anti-inflammatory agents are most commonly used for the treatment of acute and chronic gout, with corticosteroid usage at a low level. However, there are areas of concern regarding the diagnosis of gout and the usage of ALLO which are not consistent with current guidelines
    Matched MeSH terms: Cyclooxygenase 2 Inhibitors/therapeutic use
  3. Abdelwahab SI, Hassan LE, Sirat HM, Yagi SM, Koko WS, Mohan S, et al.
    Fitoterapia, 2011 Dec;82(8):1190-7.
    PMID: 21871542 DOI: 10.1016/j.fitote.2011.08.002
    The in vivo and in vitro mechanistic anti-inflammatory actions of cucurbitacin E (CE) (Citrullus lanatus var. citroides) were examined. The results showed that LPS/INF-γ increased NO production in RAW264.7 macrophages, whereas L-NAME and CE curtailed it. CE did not reveal any cytotoxicity on RAW264.7 and WRL-68 cells. CE inhibited both COX enzymes with more selectivity toward COX-2. Intraperitoneal injection of CE significantly suppressed carrageenan-induced rat's paw edema. ORAC and FRAP assays showed that CE is not a potent ROS scavenger. It could be concluded that CE is potentially useful in treating inflammation through the inhibition of COX and RNS but not ROS.
    Matched MeSH terms: Cyclooxygenase 2 Inhibitors/therapeutic use
  4. Lee HL, Chua SS, Mahadeva S
    J Dig Dis, 2018 Jun;19(6):342-349.
    PMID: 29732728 DOI: 10.1111/1751-2980.12607
    OBJECTIVE: To evaluate regular non-steroidal anti-inflammatory drug (NSAID) users for dyspepsia, as well as to assess the effect of preventive measures, and the reasons for non-adherence to gastroprotective agents (GPA) from a real-world perspective.
    METHODS: A prospective longitudinal study was conducted among outpatients with regular NSAID usage. The presence of dyspepsia was assessed by locally validated versions of the Leeds dyspepsia questionnaire (LDQ), GPA and the participants' adherence to the drugs were assessed at recruitment and 2 weeks later. GPA was defined as the use of antisecretory medications or cyclooxygenase-2 inhibitors.
    RESULTS: Initially, 409 participants (mean age 52.3 ± 14.6 years, 60.6% females, 48.4% treated for musculoskeletal pain) were recruited. At recruitment, 50.9% of the participants had at least one upper gastrointestinal symptom. Complete data for follow-up analysis were collected from 158 participants who were naive NSAID users, had no prior gastrointestinal medication and who could be contacted. At 2-week follow-up there was no significant difference in the LDQ score change between NSAID users treated with GPA and those did not. However, there was a greater reduction in abdominal pain/discomfort (8.8% vs 5.0%, P 
    Matched MeSH terms: Cyclooxygenase 2 Inhibitors/therapeutic use
  5. Nadarajah A, Abrahan L, Lau FL, Hwang LJ, Fakir-Bolte C
    Singapore Med J, 2006 Jun;47(6):534-42.
    PMID: 16752024
    INTRODUCTION: Cyclooxygenase (COX)-2 selective inhibitors are attractive candidates for treatment of ankle sprain because of their efficacy as anti-inflammatory and analgesic agents and their overall safety, including lack of effect on platelet aggregation. The objective of this study was to assess the efficacy and tolerability of celecoxib compared with diclofenac slow release (SR) in the treatment of acute ankle sprain in an Asian population.
    METHODS: In this seven-day, multicentre, double-blind, randomised, parallel-group trial, 370 patients with first- or second-degree ankle sprain occurring at or less than 48 hours prior to the first dose of study medication were randomised to receive celecoxib 200 mg bid (189 patients) after a 400 mg loading dose or diclofenac SR 75 mg bid (181 patients). Patients were required to demonstrate moderate to severe ankle pain on weight bearing (45 mm or greater on a 100 mm visual analogue scale [VAS]) at baseline. The primary efficacy end point was the patient's assessment of ankle pain (VAS on full weight bearing) on day 4.
    RESULTS: Celecoxib was as effective as diclofenac SR in improving the signs and symptoms of ankle sprain. At day 4, mean VAS scores for celecoxib and diclofenac SR had decreased to 28 mm and 30 mm, respectively. Treatment differences were not statistically significant. Incidence of upper gastrointestinal adverse events was low in both treatment groups (0.5 percent versus 2.2 percent for celecoxib and diclofenac SR, respectively).
    CONCLUSION: Celecoxib, a COX-2 selective inhibitor, is as effective as diclofenac SR in treating ankle sprains. With its platelet-sparing properties, celecoxib may offer an advantage over diclofenac SR in managing musculoskeletal injuries.
    Matched MeSH terms: Cyclooxygenase 2 Inhibitors/therapeutic use*
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