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  1. Zia A, Kamaruzzaman SB, Tan MP
    Geriatr Gerontol Int, 2017 Mar;17(3):463-470.
    PMID: 26822931 DOI: 10.1111/ggi.12741
    AIM: The presemt study aimed to determine the association between the risk of recurrent and injurious falls with polypharmacy, fall risk-increasing drugs (FRID) and FRID count among community-dwelling older adults.

    METHODS: Participants (n = 202) were aged ≥65 years with two or more falls or one injurious fall in the past year, whereas controls (n = 156) included volunteers aged ≥65 years with no falls in the past year. A detailed medication history was obtained alongside demographic data. Polypharmacy was defined as "regular use of five or more prescription drugs." FRID were identified as cardiovascular agents, central nervous system drugs, analgesics and endocrine drugs; multiple FRID were defined as two or more FRID. Multiple logistic regression analyses were used to adjust for confounders.

    RESULTS: The use of non-steroidal anti-inflammatory drugs was independently associated with an increased risk of falls. Univariate analyses showed both polypharmacy (OR 2.23, 95% CI 1.39-3.56; P = 0.001) and the use of two or more FRID (OR 2.9, 95% CI 1.9-4.5; P = 0.0001) were significantly more likely amongst fallers. After adjustment for age, sex and comorbidities, blood pressure, and physical performance scores, polypharmacy was no longer associated with falls (OR 1.6, 95% CI 0.9-2.9; P = 0.102), whereas the consumption of two or more FRID remained a significant predictor for falls (OR 2.8, 95% CI 1.4-5.3; P = 0.001).

    CONCLUSIONS: Among high risk fallers, the use of two or more FRID was an independent risk factor for falls instead of polypharmacy. Our findings will inform clinical practice in terms of medication reviews among older adults at higher risk of falls. Future intervention studies will seek to confirm whether avoidance or withdrawal of multiple FRID reduces the risk of future falls. Geriatr Gerontol Int 2017; 17: 463-470.

    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  2. Yap PR, Goh KL
    Curr Pharm Des, 2015;21(35):5073-81.
    PMID: 26369685
    Non-steroidal anti-inflammatory drugs (NSAIDs) are the most prescribed group of drugs in the world. They are used primarily for pain relief in chronic inflammatory joint disease and act by inhibiting enzymes COX1 and COX2 and ultimately preventing the production of active prostanoids which are required for the innate inflammatory pathway. The use of NSAIDs have been associated with the development of gastrointestinal (GI) symptoms ranging from simple dyspepsia to life threatening GI bleeds and perforations. The definition of dyspepsia has evolved over the years and this has hampered accurate studies on the prevalence of dyspepsia as different studies used varying criteria to define dyspepsia. It is now known that NSAIDs significantly increase the risk of dyspepsia.The risk of developing peptic ulcer disease vary with specific NSAIDs and dosages but there is no correlation between the symptoms of dyspepsia and underlying peptic ulcers. The pathogenesis of dyspepsia with NSAIDs is not completely understood. Peptic ulceration alone is not able to account for the majority of dyspepsia symptoms encountered by NSAIDs users. Erosive oesophagitis secondary to NSAIDs may be contributing factor to the prevalence of dyspepsia in NSAIDs users. Altered gut permeability and changes in gastric mechanosensory function due to NSAIDs may also be a contributory factor. Management of NSAID induced dyspepsia is involves a multipronged approach. Drug avoidance if possible would be ideal. Other options include using the lowest effective dose, changing to an NSAIDs with a safer GI risk profile, avoiding concurrent use with other NSAIDs or if the patient has a previous history of peptic ulcer disease, and co-prescribing with anti-secretory medications such as proton pump inhibitors. Eradication of Helicobacter pylori has a protective role against developing peptic ulcers and may also improve symptoms of NSAIDs induced dyspepsia.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  3. Wang YH, Chen CB, Tassaneeyakul W, Saito Y, Aihara M, Choon SE, et al.
    Clin. Pharmacol. Ther., 2019 01;105(1):112-120.
    PMID: 29569740 DOI: 10.1002/cpt.1071
    Specific ethnic genetic backgrounds are associated with the risk of Stevens-Johnson syndrome / toxic epidermal necrolysis (SJS/TEN) especially in Asians. However, there have been no large cohort, multiple-country epidemiological studies of medication risk related to SJS/TEN in Asian populations. Thus, we analyzed the registration databases from multiple Asian countries who were treated during 1998-2017. A total 1,028 SJS/TEN cases were identified with the algorithm of drug causality for epidermal necrolysis. Furthermore, those medications labeled by the US Food and Drug Administration (FDA) as carrying a risk of SJS/TEN were also compared with the common causes of SJS/TEN in Asian countries. Oxcarbazepine, sulfasalazine, COX-II inhibitors, and strontium ranelate were identified as new potential causes. In addition to sulfa drugs and beta-lactam antibiotics, quinolones were also a common cause. Only one acetaminophen-induced SJS was identified, while several medications (e.g., oseltamivir, terbinafine, isotretinoin, and sorafenib) labeled as carrying a risk of SJS/TEN by the FDA were not found to have caused any of the cases in the Asian countries investigated in this study.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  4. Tan JR, Chakravarthi S, Judson JP, Haleagrahara N, Segarra I
    Naunyn Schmiedebergs Arch Pharmacol, 2013 Jul;386(7):619-33.
    PMID: 23552887 DOI: 10.1007/s00210-013-0861-4
    Sunitinib is a tyrosine kinase inhibitor for GIST and advanced renal cell carcinoma. Diclofenac is used in cancer pain management. Coadministration may mediate P450 toxicity. We evaluate their interaction, assessing biomarkers ALT, AST, BUN, creatinine, and histopathological changes in the liver, kidney, heart, brain, and spleen. ICR mice (male, n = 6 per group/dose) were administered saline (group A) or 30 mg/kg diclofenac ip (group B), or sunitinib po at 25, 50, 80, 100, 140 mg/kg (group C) or combination of diclofenac (30 mg/kg, ip) and sunitinib (25, 50, 80, 100, 140 mg/kg po). Diclofenac was administered 15 min before sunitinib, mice were euthanized 4 h post-sunitinib dose, and biomarkers and tissue histopathology were assessed. AST was 92.2 ± 8.0 U/L in group A and 159.7 ± 14.6 U/L in group B (p < 0.05); in group C, it the range was 105.1-152.6 U/L, and in group D, it was 156.0-209.5 U/L (p < 0.05). ALT was 48.9 ± 1.6 U/L (group A), 95.1 ± 4.5 U/L (p < 0.05) in group B, and 50.5-77.5 U/L in group C and 82.3-115.6 U/L after coadministration (p < 0.05). Renal function biomarker BUN was 16.3 ± 0.6 mg/dl (group A) and increased to 29.9 ± 2.6 mg/dl in group B (p < 0.05) and it the range was 19.1-33.3 mg/dl (p < 0.05) and 26.9-40.8 mg/dl in groups C and D, respectively. Creatinine was 5.9 pmol/ml in group A; 6.2 pmol/ml in group B (p < 0.01), and the range was 6.0-6.2 and 6.2-6.4 pmol/ml in groups C and D, respectively (p < 0.05 for D). Histopathological assessment (vascular and inflammation damages) showed toxicity in group B (p < 0.05) and mild toxicity in group C. Damage was significantly lesser in group D than group B (p < 0.05). Spleen only showed toxicity after coadministration. These results suggest vascular and inflammation protective effects of sunitinib, not shown after biomarker analysis.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  5. Tam LS, Wei JC, Aggarwal A, Baek HJ, Cheung PP, Chiowchanwisawakit P, et al.
    Int J Rheum Dis, 2019 Mar;22(3):340-356.
    PMID: 30816645 DOI: 10.1111/1756-185X.13510
    INTRODUCTION: Despite the availability of axial spondyloarthritis (SpA) recommendations proposed by various rheumatology societies, we considered that a region-specific guideline was of substantial added value to clinicians of the Asia-Pacific region, given the wide variations in predisposition to infections and other patient factors, local practice patterns, and access to treatment across countries.

    MATERIALS AND METHODS: Systematic reviews were undertaken of English-language articles published between 2000 and 2016, identified from MEDLINE using PubMed, EMBASE and Cochrane databases. The strength of available evidence was graded using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach. Recommendations were developed through consensus using the Delphi technique.

    RESULTS: Fourteen axial SpA treatment recommendations were developed based on evidence summaries and consensus. The first 2 recommendations cover non-pharmacological approaches to management. Recommendations 3 to 5 describe the following: the use of non-steroidal anti-inflammatory drugs as first-line symptomatic treatment; the avoidance of long-term corticosteroid use; and the utility of conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs) for peripheral or extra-articular manifestations. Recommendation 6 refers to the indications for biological DMARDs (bDMARDs). Recommendation 7 deals specifically with screening for infections endemic to Asia, prior to use of bDMARDs. Recommendations 7 to 13 cover the role of bDMARDs in the treatment of active axial SpA and include related issues such as continuing therapy and use in special populations. Recommendation 14 deals with the utility of surgical intervention in axial SpA.

    CONCLUSION: These recommendations provide up-to-date guidance for treatment of axial SpA to help meet the needs of patients and clinicians in the Asia-Pacific region.

    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  6. Somchit N, Sanat F, Gan EH, Shahrin IA, Zuraini A
    Singapore Med J, 2004 Nov;45(11):530-2.
    PMID: 15510325
    Non-steroidal anti-inflammatory drugs (NSAIDs) are used to treat musculoskeletal disorders, inflammation and to control pain. Virtually all NSAIDs are capable of producing liver injury ranging from mild reversible elevation of liver enzymes to severe hepatic necrosis.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  7. Sessler DI, Conen D, Leslie K, Yusuf S, Popova E, Graham M, et al.
    Anesthesiology, 2020 04;132(4):692-701.
    PMID: 32022771 DOI: 10.1097/ALN.0000000000003158
    BACKGROUND: The authors previously reported that perioperative aspirin and/or clonidine does not prevent a composite of death or myocardial infarction 30 days after noncardiac surgery. Moreover, aspirin increased the risk of major bleeding and clonidine caused hypotension and bradycardia. Whether these complications produce harm at 1 yr remains unknown.

    METHODS: The authors randomized 10,010 patients with or at risk of atherosclerosis and scheduled for noncardiac surgery in a 1:1:1:1 ratio to clonidine/aspirin, clonidine/aspirin placebo, clonidine placebo/aspirin, or clonidine placebo/aspirin placebo. Patients started taking aspirin or placebo just before surgery; those not previously taking aspirin continued daily for 30 days, and those taking aspirin previously continued for 7 days. Patients were also randomly assigned to receive clonidine or placebo just before surgery, with the study drug continued for 72 h.

    RESULTS: Neither aspirin nor clonidine had a significant effect on the primary 1-yr outcome, a composite of death or nonfatal myocardial infarction, with a 1-yr hazard ratio for aspirin of 1.00 (95% CI, 0.89 to 1.12; P = 0.948; 586 patients [11.8%] vs. 589 patients [11.8%]) and a hazard ratio for clonidine of 1.07 (95% CI, 0.96 to 1.20; P = 0.218; 608 patients [12.1%] vs. 567 patients [11.3%]), with effect on death or nonfatal infarction. Reduction in death and nonfatal myocardial infarction from aspirin in patients who previously had percutaneous coronary intervention at 30 days persisted at 1 yr. Specifically, the hazard ratio was 0.58 (95% CI, 0.35 to 0.95) in those with previous percutaneous coronary intervention and 1.03 (95% CI, 0.91to 1.16) in those without (interaction P = 0.033). There was no significant effect of either drug on death, cardiovascular complications, cancer, or chronic incisional pain at 1 yr (all P > 0.1).

    CONCLUSIONS: Neither perioperative aspirin nor clonidine have significant long-term effects after noncardiac surgery. Perioperative aspirin in patients with previous percutaneous coronary intervention showed persistent benefit at 1 yr, a plausible sub-group effect.

    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  8. Seong CL, Shanmuganathan M
    Indian J Pharmacol, 2016 Nov-Dec;48(6):739-740.
    PMID: 28066119 DOI: 10.4103/0253-7613.194848
    Ibuprofen is a nonsteroidal anti-inflammatory drug that is used widely in treating pain, fever, and inflammation. Its side effects are mainly due to acute renal impairment and gastric discomfort. We hereby report a rare case of Henoch-Schönlein purpura nephritis secondary to ibuprofen consumption which has not been reported in literature before.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  9. Segasothy M, Chin GL, Sia KK, Zulfiqar A, Samad SA
    Br J Rheumatol, 1995 Feb;34(2):162-5.
    PMID: 7704463
    We determined the consumption of non-steroidal anti-inflammatory drugs (NSAIDs) and the prevalence of chronic renal impairment and renal papillary necrosis (RPN) in patients with various types of arthritis. Ninety-four patients with chronic arthritis who had consumed more than 1000 capsules and/or tablets of NSAIDs were studied. Renal profiles and radiological investigations such as intravenous urogram (IVU), ultrasonography (US) and computed tomography (CT) were performed to look for evidence of RPN. Twelve patients did not complete the study. Ten of the 82 patients who had completed the study (12.2%) had radiologic evidence of RPN. Five out of 53 patients (9.4%) with rheumatoid arthritis, three out of 11 patients (27.3%) with gouty arthritis and two out of seven patients (28.6%) with osteoarthritis had RPN. Renal impairment (serum creatinine levels of 125-451 mumol/l) was found in 20 patients (24.4%). The patients had consumed 1000-26,300 capsules and/or tablets over a period ranging from 1 yr to more than 30 yr. Patients with chronic arthritis who consume excessive amount of NSAIDs are at risk of developing RPN and chronic renal impairment.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  10. Segasothy M, Samad SA, Zulfigar A, Bennett WM
    Am J Kidney Dis, 1994 Jul;24(1):17-24.
    PMID: 8023820
    The risk of renal papillary necrosis and renal dysfunction due to the chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) is unknown. In a prospective study of 259 heavy analgesic users seen in a general medical hospital over an 11-year-period beginning in January 1982, 69 new cases of analgesic nephropathy with renal papillary necrosis were confirmed by intravenous urogram (26.6%), ultrasonography (30.4%), and/or computed tomography (43%). Twenty-nine of these patients (42%) had consumed excessive quantities of NSAIDs alone; an additional nine patients (13%) had consumed NSAIDs predominantly in combinations with paracetamol, aspirin, phenacetin, caffeine, and/or traditional herbal medications. Of those patients who consumed NSAIDs alone, 17 had consumed only a single type of NSAID and the remaining 12 had consumed multiple types of NSAIDs. The amount of NSAIDs administered ranged from 1,000 to 26,600 capsules or tablets over a 2- to 25-year period. Renal impairment (serum creatinine, 126 to 778 mumol/L) was noted in 26 of these 38 patients (64.8%). The reasons given for consuming NSAIDs include gouty arthritis (18 patients), osteoarthritis (seven patients), rheumatoid arthritis (six patients), chronic headache (three patients), gouty arthritis plus chronic headache (three patients), and chronic backache (one patient). All patients were prescribed these drugs and were followed medically. The occurrence of analgesic nephropathy was predominantly in males (male to female ratio, 1.9:1). Most of the patients did not have the characteristic psychological profile attributed previously to analgesic abuse nephropathy. Associated addictive habits, such as the use of psychotropic drugs and sleeping tablets, purgative abuse, and alcoholism, were absent.(ABSTRACT TRUNCATED AT 250 WORDS)
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  11. Segasothy M, Cheong I, Kong BC, Suleiman AB, Morad Z
    Med J Malaysia, 1986 Dec;41(4):377-9.
    PMID: 3670164
    In a prospective study performed on patients admitted to the medical and renal wards of General Hospital, Kuala Lumpur, over a period of 14 months from January 1982, we documented 12 new cases of analgesic nephropathy (AN). Since then up to July 1986, we have documented a further 16 cases of AN giving a total of 28 cases over a four-and-a-half-year period.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  12. Saheb Sharif-Askari N, Syed Sulaiman SA, Saheb Sharif-Askari F, Hussain AA
    Int J Clin Pharm, 2015 Feb;37(1):105-12.
    PMID: 25488317 DOI: 10.1007/s11096-014-0046-3
    BACKGROUND: Little is known about the adverse drug reaction (ADR) related admissions among heart failure (HF) patients.

    OBJECTIVE: The aim of this study was to determine the rate, factors, and medications associated with ADR-related hospitalisations among HF patients.

    SETTING: Two government hospitals in Dubai, United Arab Emirates.

    METHODS: This was a prospective, observational study. Consecutive adult HF patients who were admitted between December 2011 and November 2012 to the cardiology units were included in this study. The circumstances of their admission were analysed.

    MAIN OUTCOME MEASURES: ADRs-related admissions of HF patients to cardiology units were identified and further assessed for their nature, causality, and preventability.

    RESULTS: Of 511 admissions, 34 were due to ADR-related hospitalisation (6.65, 95 % confidence interval 4.8-8.5 %). Number of medications taken by HF patients was the only predictors of ADR-related hospitalisations, where higher number of medications was associated with the odd ratio of 1.11 (95 % CI, 1.03-1.20, P = 0.005). More than one-third of ADR-related hospitalisations (35 %) were preventable The most frequent drugs causing ADR-related hospitalisation were diuretics (32 %), followed by non-steroidal anti-inflammatory drugs (15 %), thiazolidinediones (9 %), anticoagulants (9 %), antiplatelets (6 %), and aldosterone blockers (6 %).

    CONCLUSION: ADR-related hospitalisations account for 6.7 % of admissions of HF patients to cardiac units, one-third of which are preventable. Number of medications taken by HF patients is the only predictors of ADR-related hospitalisations. Diuretic induced volume depletion, and sodium and water retention caused by thiazolidinediones and NSAIDs medications are the major causes of ADR-related hospitalisations of HF patients.

    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  13. Rahman A, Segasothy M, Samad SA, Zulfiqar A, Rani M
    Headache, 1993 Sep;33(8):442-5.
    PMID: 8262786
    The pattern of analgesic use, abuse and incidence of analgesic-associated nephropathy in 79 patients with chronic headache was studied. Sixty-eight of these patients had migraine. Most patients had consumed a combination of analgesics (81%) while 19% had taken single analgesics for their headache. Nonsteroidal anti-inflammatory drugs were the most commonly used analgesics (96.2%) followed by paracetamol (70.9%) and aspirin, phenacetin and caffeine compounds (5.1%). Mefenamic acid was the commonest nonsteroidal anti-inflammatory drug consumed (97.4%). Analgesic abuse which was defined as a minimum total of 1 kg of analgesics such as paracetamol or aspirin, phenacetin and caffeine compounds or 400 capsules/tablets of nonsteroidal anti-inflammatory drugs was noted in 65 patients. Nonsteroidal anti-inflammatory drugs were the most commonly abused analgesics (89.2%) followed by paracetamol (38.5%). Forty-five of the 65 analgesic abusers had an intravenous urogram or ultrasound performed and renal papillary necrosis was documented in one patient. Three (4.6%) of the analgesic abusers had mildly raised serum creatinine levels. Mild proteinuria of less than 1 gm/litre was present in 27.7% of abusers. In conclusion, although analgesic use and abuse is common in patients with chronic headache, the short term incidence of analgesic-associated nephropathy (2.2%) and renal impairment (4.6%) was low. Prolonged observations will be necessary to ascertain the safety of these drugs for long term use.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  14. Pok LSL, Shabaruddin FH, Dahlui M, Sockalingam S, Mohamed Said MS, Rosman A, et al.
    Int J Rheum Dis, 2018 May;21(5):943-951.
    PMID: 29314744 DOI: 10.1111/1756-185X.13256
    AIM: To determine the incidence and direct costs of NSAID-induced upper GI adverse events in Malaysian rheumatology patients.
    METHODS: A retrospective, multi-centre, cohort study of rheumatology patients on long-term NSAIDs was conducted. Clinical data of patients treated between 2010 and 2013 were collected for a 24-month follow-up period. The costs of managing upper GI adverse events were based on patient level resource use data.
    RESULTS: Six hundred and thirty-four patients met the inclusion criteria: mean age 53.4 years, 89.9% female, diagnosis of rheumatoid arthritis (RA; 59.3%), osteoarthritis (OA; 10.3%) and both RA and OA (30.3%). Three hundred and seventy-one (58.5%) patients were prescribed non-selective NSAIDs and 263 (41.5%) had cyclo-oxygenase-2 inhibitors. Eighty-four upper GI adverse events occurred, translating into a risk of 13.2% and an incidence rate of 66.2 per 1000 person-years. GI adverse events comprised: dyspepsia n = 78 (12.3%), peptic ulcer disease (PUD) n = 5 (0.79%) and upper GI bleeding (UGIB) n = 1 (0.16%). The total direct healthcare cost of managing adverse events was Malaysian Ringgit (MR) 37 352 (US dollars [USD] 11 419) with a mean cost of MR 446.81 ± 534.56 (USD 136.60 ± 163.42) per patient, consisting mainly of GI pharmacotherapy (33.8%), oesophagoduodenoscopies (23.1%) and outpatient clinic visits (18.2%). Mean cost per patient by GI events were: dyspepsia, MR 408.98 ± 513.29 (USD125.03 ± 156.92); PUD, MR 805.93 ± 578.80 (USD 246.39 ± 176.95); UGIB, MR 1601.94 (USD 489.74, n = 1).
    CONCLUSION: The economic burden of GI adverse events due to long-term NSAIDs use in Malaysian patients with chronic rheumatic diseases is modest.
    Study site: Rheumatology clinics, Hospital Putrajaya, Hospital Selayang, Pusat Perubatan Universiti Kebangsaan Malaysia (PPUKM), University Malaya Medical Centre (UMMC), Kuala Lumpur, Malaysia
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  15. Orlikova B, Schumacher M, Juncker T, Yan CC, Inayat-Hussain SH, Hajjouli S, et al.
    Food Chem Toxicol, 2013 Sep;59:572-8.
    PMID: 23845509 DOI: 10.1016/j.fct.2013.06.051
    (R)-(+)-Goniothalamin (GTN), a styryl-lactone isolated from the medicinal plant Goniothalamus macrophyllus, exhibits pharmacological activities including cytotoxic and anti-inflammatory effects. In this study, GTN modulated TNF-α induced NF-κB activation. GTN concentrations up to 20 μM showed low cytotoxic effects in K562 chronic myelogenous leukemia and in Jurkat T cells. Importantly, at these concentrations, no cytotoxicity was observed in healthy peripheral blood mononuclear cells. Our results confirmed that GTN inhibited tumor necrosis factor-α (TNF-α)-induced NF-κB activation in Jurkat and K562 leukemia cells at concentrations as low as 5 μM as shown by reporter gene assays and western blots. Moreover, GTN down-regulated translocation of the p50/p65 heterodimer to the nucleus, prevented binding of NF-κB to its DNA response element and reduced TNF-α-activated interleukin-8 (IL-8) expression. In conclusion, GTN inhibits TNF-α-induced NF-κB activation at non-apoptogenic concentrations in different leukemia cell models without presenting toxicity towards healthy blood cells underlining the anti-leukemic potential of this natural compound.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  16. Nor Azlin MI, Maryasalwati I, Norzilawati MN, Mahdy ZA, Jamil MA, Zainul Rashid MR
    J Obstet Gynaecol, 2008 May;28(4):424-6.
    PMID: 18604680 DOI: 10.1080/01443610802150051
    Dysmenorrhoea is painful menstruation that occurs in 45-72% of all women. This was a prospective randomised study of the efficacy of etoricoxib (Arcoxia) compared with mefenamic acid (Ponstan) in treating primary dysmenorrhoea. All single, sexually inactive women with primary dysmenorrhoea were randomised into two groups (mefenamic acid and etoricoxib) of pain relief and underwent a cross-over study. The success of treatment as evidenced by pain relief, the side-effects and complications were observed and analysed. Some 80% (20 women) had significantly better pain relief with etoricoxib, compared with only 20 per cent in the mefenamic acid group (p = 0.007). Etoricoxib has significantly fewer side-effects compared with mefenamic acid (p = 0.005) with significantly reduced menstrual blood loss (p = 0.025). In conclusion, etoricoxib is a better treatment for primary dysmenorrhoea with better pain relief, less menstrual blood loss and fewer side-effects compared with mefenamic acid.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  17. Narula N, Wong ECL, Pray C, Marshall JK, Rangarajan S, Islam S, et al.
    Clin Gastroenterol Hepatol, 2023 Sep;21(10):2649-2659.e16.
    PMID: 36528284 DOI: 10.1016/j.cgh.2022.11.037
    BACKGROUND & AIMS: Several medications have been suspected to contribute to the etiology of inflammatory bowel disease (IBD). This study assessed the association between medication use and the risk of developing IBD using the Prospective Urban Rural Epidemiology cohort.

    METHODS: This was a prospective cohort study of 133,137 individuals between the ages of 20 and 80 from 24 countries. Country-specific validated questionnaires documented baseline and follow-up medication use. Participants were followed up prospectively at least every 3 years. The main outcome was the development of IBD, including Crohn's disease (CD) and ulcerative colitis (UC). Short-term (baseline but not follow-up use) and long-term use (baseline and subsequent follow-up use) were evaluated. Results are presented as adjusted odds ratios (aORs) with 95% CIs.

    RESULTS: During a median follow-up period of 11.0 years (interquartile range, 9.2-12.2 y), there were 571 incident IBD cases (143 CD and 428 UC). Incident IBD was associated significantly with baseline antibiotic (aOR, 2.81; 95% CI, 1.67-4.73; P = .0001) and hormonal medication use (aOR, 4.43; 95% CI, 1.78-11.01; P = .001). Among females, previous or current oral contraceptive use also was associated with IBD development (aOR, 2.17; 95% CI, 1.70-2.77; P < .001). Nonsteroidal anti-inflammatory drug users also were observed to have increased odds of IBD (aOR, 1.80; 95% CI, 1.23-2.64; P = .002), which was driven by long-term use (aOR, 5.58; 95% CI, 2.26-13.80; P < .001). All significant results were consistent in direction for CD and UC with low heterogeneity.

    CONCLUSIONS: Antibiotics, hormonal medications, oral contraceptives, and long-term nonsteroidal anti-inflammatory drug use were associated with increased odds of incident IBD after adjustment for covariates.

    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  18. 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: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  19. Muthu A, Qureshi A, Ismail MA
    Med J Malaysia, 1999 Sep;54(3):374-6.
    PMID: 11045068
    Non-steriodal anti-inflammatory drugs (NSAID) are not only associated with bleeding in the stomach and duodenum, but can also complicate pre-existing diverticular disease of the colon. Here, a 58 year-old male with severe per rectal bleeding is presented and the role of NSAID as a causative factor of his problem is discussed.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  20. 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 non-adherence.
    CONCLUSIONS: The use of GPA in patients on regular NSAIDs does not improve their overall dyspepsia, but it reduces abdominal pain and burping. Poor adherence to GPA may be a contributing factor.
    Study site: outpatient pharmacy, University Malaya Medical Centre (UMMC), Kuala Lumpur, Malaysia
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
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