Displaying publications 1 - 20 of 33 in total

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  1. 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
  2. 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
  3. 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*
  4. 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*
  5. 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*
  6. Jaarin K, Gapor MT, Nafeeza MI, Fauzee AM
    Int J Exp Pathol, 2002 Dec;83(6):295-302.
    PMID: 12657138 DOI: 10.1046/j.1365-2613.2002.00242.x
    This study examined the effects of vitamin E on the prevention of aspirin-induced gastric lesions. The study was divided into two phases. Phase 1 determined the effects of various doses of palm vitamin E on the factors affecting mucosal integrity. Thirty-two male rats of the Sprague-Dawley strain (200-250 g) were randomly divided into four groups. Group I was fed a normal diet (control), Groups II, III and IV were fed a diet supplemented with palm vitamin E in a dose of 60 mg/kg food, 100 mg/kg food and 150 mg/kg food, respectively. The rats were killed after 4 weeks of feeding for the determination of gastric malondialdehyde (MDA), acid and mucus content. There was a significant decrease in gastric MDA and gastric acid in all the palm vitamin E supplemented groups compared to control. However, these doses of palm vitamin E had no significant effect on gastric mucus. The phase 2 study determined the effect of multiple doses of palm vitamin E and tocopherol on the prevention of aspirin-induced gastric lesions. Fifty rats of the same weight and strain were randomized into seven groups. Group I was fed a normal diet; groups II to IV were fed with a palm vitamin E enriched diet in doses of 60 mg, 100 mg and 150 mg/kg food, respectively; groups V to VII were fed with a tocopherol-enriched diet in doses of 20 mg, 30 mg and 50 mg/kg food, respectively. After 4 weeks of feeding with the respective diets the rats were challenged with a single intra-gastric dose of 400 mg/kg body weight aspirin suspended in propylene glycol. The rats were killed 6 h post-aspirin exposure for the determination of gastric lesion index and gastric parameters as mentioned in the phase I study. The gastric lesions index was significantly lower in all the vitamin E groups compared to control. The lowest ulcer index was observed in the groups that received 100 mg of palm vitamin E and 30 mg tocopherol in the diet. However, there was no significant difference in ulcer indices between palm vitamin E and tocopherol-treated groups. The lower ulcer index was only accompanied by lower gastric MDA content. We conclude that both palm vitamin E in doses of 60 mg, 100 mg and 150 mg/kg food as well as tocopherol in doses of 20 mg, 30 mg and 50 mg/kg food are equally effective in preventing aspirin-induced gastric lesions. The most probable mechanism is through their ability in limiting the lipid peroxidation that is involved in aspirin-induced gastric lesions.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  7. 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*
  8. 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
  9. 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
  10. Ding WY, Lee CK, Choon SE
    Int J Dermatol, 2010 Jul;49(7):834-41.
    PMID: 20618508 DOI: 10.1111/j.1365-4632.2010.04481.x
    BACKGROUND: Adverse drug reactions are most commonly cutaneous in nature. Patterns of cutaneous adverse drug reactions (ADRs) and their causative drugs vary among the different populations previously studied.
    OBJECTIVE: Our aim is to determine the clinical pattern of drug eruptions and the common drugs implicated, particularly in severe cutaneous ADRs in our population.
    MATERIALS AND METHODS: This study was done by analyzing the database established for all adverse cutaneous drug reactions seen from January 2001 until December 2008.
    RESULTS: A total of 281 cutaneous ADRs were seen in 280 patients. The most common reaction pattern was maculopapular eruption (111 cases, 39.5%) followed by Stevens-Johnson Syndrome (SJS: 79 cases, 28.1%), drug reaction with eosinophilia and systemic symptoms (DRESS: 19 cases, 6.8%), toxic epidermal necrolysis (TEN: 16 cases, 5.7 %), urticaria/angioedema (15 cases, 5.3%) and fixed drug eruptions (15 cases, 5.3%). Antibiotics (38.8%) and anticonvulsants (23.8%) accounted for 62.6% of the 281 cutaneous ADRs seen. Allopurinol was implicated in 39 (13.9%), carbamazepine in 29 (10.3%), phenytoin in 27 (9.6%) and cotrimoxazole in 26 (9.3%) cases. Carbamazepine, allopurinol and cotrimoxazole were the three main causative drugs of SJS/TEN accounting for 24.0%, 18.8% and 12.5% respectively of the 96 cases seen whereas DRESS was mainly caused by allopurinol (10 cases, 52.6%) and phenytoin (3 cases, 15.8%).
    DISCUSSION: The reaction patterns and drugs causing cutaneous ADRs in our population are similar to those seen in other countries although we have a much higher proportion of severe cutaneous ADRs probably due to referral bias, different prescribing habit and a higher prevalence of HLA-B*1502 and HLA-B*5801 which are genetic markers for carbamazepine-induced SJS/TEN and allopurinol-induced SJS/TEN/DRESS respectively.
    CONCLUSION: The most common reaction pattern seen in our study population was maculopapular eruptions. Antibiotics, anticonvulsants and NSAIDs were the most frequently implicated drug groups. Carbamazepine and allopurinol were the two main causative drugs of severe ADRs in our population.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  11. Goh KL, Chan WK
    Aliment Pharmacol Ther, 2012 Aug;36(3):291-2; discussion 292-3.
    PMID: 22747451 DOI: 10.1111/j.1365-2036.2012.05164.x
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  12. Dhabali AA, Awang R, Hamdan Z, Zyoud SH
    Int J Clin Pharmacol Ther, 2012 Dec;50(12):851-61.
    PMID: 23006441 DOI: 10.5414/CP201689
    OBJECTIVES: The objectives of this study were 1) to obtain information regarding the prescribing pattern of nonsteroidal anti-inflammatory drugs (NSAIDs) in the primary care setting at a Malaysian university, 2) to determine the prevalence and types of potential NSAID prescription related problems (PRPs), and 3) to identify patient characteristics associated with exposure to these potential PRPs.
    METHODS: We retrospectively collected data from 1 academic year using the electronic medical records of patients in the University Sains Malaysia (USM) primary care system. The defined daily dose (DDD) methodology and the anatomical therapeutic chemical (ATC) drug classification system were used in the analysis and comparison of the data. Statements representing potential NSAID PRPs were developed from authoritative drug information sources. Then, algorithms were developed to screen the databases for these potential PRPs. Descriptive and comparative statistics were used to characterize DRPs.
    RESULTS: During the study period, 12,470 NSAID prescriptions were prescribed for 6,509 patients (mean ± SD = 1.92 ± 1.83). This represented a prevalence of 35,944 per 100,000 patients, or 36%. Based on their DDDs, mefenamic acid and diclofenac were the most prescribed NSAIDs. 573 potential NSAID-related PRPs were observed in a cohort of 432 patients, representing a prevalence of 6,640 per 100,000 NSAIDs users, or 6.6% of all NSAID users. Multivariate logistic regression analysis revealed that patients with a Malay ethnic background (p < 0.001), members of the staff (p < 0.001), having 4 or more prescribers (p < 0.001) or having 2 - 3 prescribers (p = 0.02), and representing 4 or more long-term therapeutic groups (LTTGs) (p < 0.001) or 2 - 3 LTTGs (p < 0.001) were significantly associated with an increased chance of exposure to potential NSAID related PRPs.
    CONCLUSIONS: This is the first study in Malaysia that presents data on the prescribing pattern of NSAIDs and the characteristics of potential NSAID-related PRPs. The prevalence of potential NSAID-related PRPs is frequent in the primary care setting. Exposure to these PRPs is associated with specific sociodemographic and health status factors. These results should help to raise the awareness of clinicians and patients about serious NSAID PRPs.

    Study site: University Sains Malaysia (USM) primary care system.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  13. Choon SE, Lai NM
    Indian J Dermatol Venereol Leprol, 2012 Nov-Dec;78(6):734-9.
    PMID: 23075643 DOI: 10.4103/0378-6323.102367
    BACKGROUND: The prevalence, clinical patterns, and causative drugs of cutaneous adverse drug reactions (cADR) vary among the different populations previously studied.
    AIM: To determine the prevalence, the clinical patterns of drug eruptions, and the common drugs implicated, particularly in severe cADR such as Stevens-Johnson Syndrome/Toxic epidermal necrolysis (SJS/TEN) and drug rash with eosinophilia and systemic symptoms (DRESS) in our population.
    METHODS: We analyzed the database established for all cADR seen by the department of Dermatology from January 2001 till December 2010.
    RESULTS: A total of 362 cADR were seen among 42 170 new clinic attendees, yielding an incidence rate of 0.86%. The most common reaction pattern seen was maculopapular eruption (153 cases) followed by SJS/TEN (110 cases) and DRESS (34 cases). Antibiotics was the most commonly implicated drug group (146 cases) followed by anticonvulsants (81 cases) and antigout drugs (50 cases). The most frequently implicated drug was allopurinol (50 cases). Carbamazepine, allopurinol, and cotrimoxazole were the three main causative drugs of SJS/TEN accounting for 21.8%, 20.9%, and 12.7%, respectively, of the 110 cases seen, whereas DRESS was mainly caused by allopurinol (15 cases). Mortality rates for TEN, SJS, and DRESS were 28.6%, 2.2%, and 5.9%, respectively.
    CONCLUSIONS: The low rate of cADR with a high proportion of severe reactions observed in this study was probably due to referral bias. Otherwise, the reaction patterns and drugs causing cADR in our population were similar to those seen in other countries. Carbamazepine, allopurinol, and cotrimoxazole were the three main causative drugs of SJS/TEN in our population.
    Study site: department of dermatology in Hospital Sultanah Aminah
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  14. 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*
  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. Dhiyaaldeen SM, Amin ZA, Darvish PH, Mustafa IF, Jamil MM, Rouhollahi E, et al.
    BMC Vet Res, 2014;10:961.
    PMID: 25551777 DOI: 10.1186/s12917-014-0303-7
    Non-steroidal anti-inflammatory drugs (NSAIDs) can result in peptic ulcer disease (PUD) which is a common condition worldwide. The aim of this study was to evaluate the antiulcer properties of (1-(4-hydroxy-phenyl)-3-m-tolyl-propenone) (HPTP) chalcone in rats using indomethacin as ulcerogenic agent.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects*
  17. 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
  18. 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*
  19. Gothai S, Ganesan P, Park SY, Fakurazi S, Choi DK, Arulselvan P
    Nutrients, 2016 Aug 04;8(8).
    PMID: 27527213 DOI: 10.3390/nu8080461
    Diabetes is a metabolic, endocrine disorder which is characterized by hyperglycemia and glucose intolerance due to insulin resistance. Extensive research has confirmed that inflammation is closely involved in the pathogenesis of diabetes and its complications. Patients with diabetes display typical features of an inflammatory process characterized by the presence of cytokines, immune cell infiltration, impaired function and tissue destruction. Numerous anti-diabetic drugs are often prescribed to diabetic patients, to reduce the risk of diabetes through modulation of inflammation. However, those anti-diabetic drugs are often not successful as a result of side effects; therefore, researchers are searching for efficient natural therapeutic targets with less or no side effects. Natural products' derived bioactive molecules have been proven to improve insulin resistance and associated complications through suppression of inflammatory signaling pathways. In this review article, we described the extraction, isolation and identification of bioactive compounds and its molecular mechanisms in the prevention of diabetes associated complications.
    Matched MeSH terms: Anti-Inflammatory Agents, Non-Steroidal/adverse effects
  20. 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*
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