• Title/Summary/Keyword: NSAIDS

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DRESS syndrome with acute interstitial nephritis caused by quinolone and non-steroidal anti-inflammatory drugs (퀴놀론과 비스테로이드소염제 투여 후 발생한 급성 간질성 신염이 동반된 DRESS 증후군)

  • Kim, Soo Jin;Nam, Young-Hee;Juong, Ji Young;Kim, Eun Young;Lee, Su Mi;Son, Young Ki;Nam, Hee-Joo;Kim, Ki-Ho;Lee, Soo-Keol
    • Journal of Yeungnam Medical Science
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    • v.33 no.1
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    • pp.59-63
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    • 2016
  • Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a rare and severe drug-induced hypersensitivity syndrome characterized by hematological abnormalities and multiorgan involvement. Liver involvement is the most common visceral manifestation. However, renal failure has been rarely described. The common culprit drugs are anticonvulsants and allopurinol. We experienced a patient with DRESS syndrome with acute interstitial nephritis caused by concomitant administration of quinolone and non-steroidal anti-inflammatory drugs (NSAIDs). A 41-year-old man presented with a diffuse erythematous rash and fever which developed after administration of quinolone and NSAIDs for a month due to prostatitis. He was diagnosed with DRESS syndrome. Skin rash, fever, eosinophilia, and elevations of liver enzymes improved with conservative treatment and discontinuation of the causative drugs. However, deterioration of his renal function occurred on day 8 of admission. The levels of blood urea nitrogen and serum creatinine increased and oliguria, proteinuria and urinary eosinophils were observed. Ultrasonography showed diffuse renal enlargement. The clinical features were compatible with acute interstitial nephritis. Despite intravenous rehydration and diuretics, renal function did not improve. After hemodialysis, his renal function recovered completely within 2 weeks without administration of systemic corticosteroid.

Cadmium-induced E-cadherin Expression in Cerebrovascular Endothelial Cells (카드뮴이 뇌혈관 내피세포에서의 E-cadherin 발현에 미치는 영향)

  • Seok, Sun-Mi;Lee, Tae-Gu;Kim, Young-Chae;Moon, Chang-Hyun;Baik, Eun-Joo;Jung, Yi-Sook;Lee, Soo-Hwan
    • Environmental Analysis Health and Toxicology
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    • v.22 no.2 s.57
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    • pp.137-145
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    • 2007
  • The effect of cadmium chloride $(CdCl_2)$ on the expression of E-cadherin was examined in bEnd.3 mouse brain endothelial cells. $CdCl_2$ induced $PGE_2$ release, which were blocked by non-steroidal antinflamatory drugs (NSAIDs) such as indomethacin and NS398 indicating the expression of COX-2 might contribute to $PGE_2$ production. $CdCl_2$ decreased the expression of E-cadherin, but not VE-cadherin at levels of mRNA and protein. Reduced expression level of E-cadherin was restored by NSAIDs, which was reversed by the addition of $PGE_2$. $CdC_2$-induced decrease of E-cadherin level was also recovered by antioxidants including N-acetylcyteine (NAC) and trolox. Together with previous report which showed $CdCl_2$ induced COX-2 expression in a cellular oxidative stress dependent manner, these data suggest that $CdCl_2$ decreases E-cadherin expression through induction of cellular oxidative stress and in turn COX-2 expression in brain endothelial cells.

EFFECTS OF ISOTHIAZOLE AND ISOXAZOLE DERIVATIVES AS SELECTIVE CYCLOOXYGENASE-2 INHIBITORS

  • Ryu, Hyung-Chul;Park, Sang-Wook;Noh, Ji-Young;Kim, Jong-Hoon;Park, Hyun-Jung;Chung, Young-Mee;Chae, Myeong-Yun;Cho, Il-Hwan
    • Proceedings of the PSK Conference
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    • 2002.10a
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    • pp.355.3-356
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    • 2002
  • Prostaglandins are synthesized by the enzyme cyclooxygenase (COX). Both constitutive (COX-1) and inducible (COX-2) isoforms have been identified. COX-2 expression is stimulated by inflammatory mediators such as growth factors and cytokines. Most non-steroidal anti-inflammatory drugs (NSAIDS) inhibit both isoforms of COX. Recent evidence suggests that selective inhibitors of COX-2 may possess diminished side effects reletive to common NSAIDS. Novel isothiazoles and isoxazoles were identified as selective inhibitiors of cycloxygenase-2(COX-2). (omitted)

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EFFECTS OF INHIBITORY DRUGS ON THE ARACHIDONIC ACID METABOLISM OF PERIODONTAL TISSUE (치은 Arachidonic acid 대사산물의 억제약물에 관한 실험적 연구)

  • Han, Se-Hee;Oh, Kwi-Ok;Kim, Hyung-Seop
    • Journal of Periodontal and Implant Science
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    • v.23 no.2
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    • pp.243-259
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    • 1993
  • The bone resorbing activity of $PGE_2$ and elevated level of prostaglandins(PGs) and thromboxanes (TXs) in inflamed gingiva which are cyclooxygenase(C) metabolites have been well documented. Nonsteroidal anti-inflammatory drugs(NSAIDs) have been known to suppress gingival inflammation and bone resorption through the specific inhibitory action on the C pathway thereby decrease of various C metabolites. Recent studies provide unequivocal results that gingival tissue metabolizes arachidonic acid(AA) mainly through lipoxygenase(L) pathway. And the results of our previous experiments suggest that indomethacin may have inhibitory action on L as well as C. Thus we started this study to show the influences of several C inhibitors on the L activity at therapeutic and toxic dosage. Periodontal tissue samples were obtained from patients with advanced periodontitis and incubated with $^{14}C-AA(0.2{\mu}Ci)$ and various enzyme inhibitors. The tissue lipid extracts were separated by means of thin layer chromatography(TLC) and analyzed by means of autoradiography and TLC analyzer. Our results showed that aspirin inhibited C more selectively than L, however at higher concentration it also decreased HETEs production significantly. Indomethacin showed dose-dependent inhibition of L as well as C and all of the L metabolites were decreased to the same degree by high concentration of indomethacin. AA-861, which is an experimental tool of selective L inhibitor, showed inhibition of HETEs production but no effect on the production of $TXB_2$, PGs and $LTB_4$. Various propionic acid derivatives NSAIDs(ibuprofen, flurbiprofen, naproxen) showed the same patterns of effect on AA metabolism each other that was profound inhibition of PGs production, to the less degree HETEs and $TXB_2$ production, and of no effect on the $LTB_4$ production.

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Optimization of Process Variables for Grinding of Ibuprofen using Response Surface Methodology (반응표면분석법을 이용한 이부프로펜의 분쇄공정변수의 최적화)

  • Sim, Chol-Ho
    • Korean Chemical Engineering Research
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    • v.51 no.6
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    • pp.685-691
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    • 2013
  • Ibuprofen, non-steroidal anti-inflammatory drugs; NSAIDs, is a highly crystalline substance with the pharmaceutical properties of poor solubility and low bioavailability. The size reduction of ibuprofen is needed to improve the solubility. The objective of this study is to optimize the grinding condition of ibuprofen. Grinding of ibuprofen was carried out using a planetary mill. Grinding parameters were optimized using Box-Behnken experimental design method. The physical characteristics of ground ibuprofen were investigated for the particle size by particle size analyzer, for the crystal size by X-ray diffraction (XRD), and for the tensile strength by tensile/compression tester. The optimum conditions for the milling of ibuprofen were 290 rpm of the revolution number of mill, 24.6 g of the weight of sample, and 10 minutes of grinding time. The measured value of the particle size of ground ibuprofen at these optimum conditions was $13.5{\mu}m$. The results showed that the crystal size of ibuprofen was reduced by the planetary milling process. In case the relative density of the tablets formulated of ground ibuprofen was range of 0.85~0.90, the tensile strength of them was range of 1$2{\sim}14Kg_f/cm^2$.

Inhibitory Activities of Natural Products on Lipopolysaccharide Induced Prostaglandin Production in Mouse Macrophages (리포폴리사카라이드에 의해 유도되는 대식세포의 프로스타글란딘 생합성을 저해하는 천연물의 탐색)

  • Noh, Min-Soo;Ha, Jun-Yong;Lee, Chang-Hoon;Lee, Woo-Young;Lee, Soo-Hwan;Lee, Jung-Joon
    • YAKHAK HOEJI
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    • v.42 no.6
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    • pp.558-566
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    • 1998
  • Two isoforms of cyclooxygenase (COX) have been identified - COX-1, which is constitlitively expressed in most tissues, and the inducible form, COX-2, of which expression is induced by inflammatory signals and mitogens. It has been considered that the beneficial effects of NSAIDs are due to the inhibition of COX-2 activity and the side effects are from the inhibition of COX-1 activity. Therefore, it is essential to develop selective COX-2 inhibitor for developing new GI-tolerable NSAIDS. To discover new leads for developing selective COX-2 inhibitors, three-hundred extracts of natural products were primarily screened with the system of prostaglandin accumulation in LPS-stimulated mouse peritoneal macrophages. To identify whether these inhibitory activities of crude extracts on the accumulation of Prostaglandins were derived from direct action against COX-2, the effects of selected extracts on exogenous arachidonic acid-derived production of prostaglandins by LPS-stimulated macrophages were determined. Among them, 5 methanol extracts of natural products, such as Zingiberis Rhizoma, Alpinae Officinarum Rhizoma, Caryophilli Flos, Scutellariae Radix, Dalbergia ordorifera. inhibited more than 70% of the prostaglandin production in LPS-stimulated mouse peritoneal macrophages at a con-centration of 1${\mu}$g/ml.

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Diclofenac Inhibits $IFN-{\gamma}$ Plus Lipopolysaccharide-Induced iNOS Gene Expression via Suppression of $NF-{\kappa}B$ Activation in RAW 264.7 Macrophages

  • Bae, So-Hyun;Ryu, Young-Sue;Hong, Jang-Hee;Park, Jin-Chan;Kim, Yong-Man;Seok, Jeong-Ho;Lee, Jae-Heun;Hur, Gang-Min
    • The Korean Journal of Physiology and Pharmacology
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    • v.5 no.6
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    • pp.521-527
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    • 2001
  • Diclofenac, a phenylacetic acid derivative, is a widely used non-steroidal anti-inflammatory drug (NSAID) to provide effective relief of inflammation and pain. Nitric oxide (NO) synthesized by inducible nitric oxide synthase (iNOS) has been implicated as a mediator of inflammation. We examined the inhibitory effects of diclofenac on the induction of iNOS in RAW 264.7 macrophages which were activated with lipopolysaccharide (LPS) plus interferon-gamma $(IFN-{\gamma}).$ Treatment of RAW 264.7 cells with diclofenac and other NSAIDs (aspirin and indomethacin) significantly inhibited NO production and iNOS protein expression induced by LPS plus $IFN-{\gamma}.$ Also, diclofenac but not aspirin and indomethacin, inhibited iNOS mRNA expression and nuclear factor-kappa B $(NF-{\kappa}B)$ binding activity concentration-dependently. Furthermore, transfection of RAW 264.7 cells with iNOS promoter linked to a CAT reporter gene revealed that only diclofenac inhibited the iNOS promoter activity induced by LPS plus $IFN-{\gamma}$ through the $NF-{\kappa}B$ sites of iNOS promoter. Taken together, these suggest that diclofenac may exert its anti-inflammatory effect by inhibiting iNOS gene expression at the transcriptional level through suppression of $NF-{\kappa}B$ activation.

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A Case of Gouty Arthritis Patient Treated with Collaborative Oriental and Western Medicine with Acute Inflammation and Liver Injury

  • Jeon, Ju-Hyun;Kang, Min-Wan;Kim, Eun-Mi;Song, Hyoun-Gun;Choi, Ka-Won;Kim, Young-Il;Kim, Jung-Ho;Hong, Kwon-Eui;Lee, Hyun;Yim, Yun-Kyoung
    • Journal of Acupuncture Research
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    • v.23 no.2
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    • pp.197-205
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    • 2006
  • Objectives : To examine the effects of the collaborative Oriental and Western medicine, we treated a gouty arthritis patient with acute inflammation and liver injury with a combination of Oriental and Western treatments. Methods : Acupuncture, Bangphungtongsung-San(Fangfengtongsheng-san)', 'Kangwhaljetong-Um(Qianghuochutong-yin)', and 'Sosiho-Tang(Xiaochaihu-tang) were offered to an acute gouty arthritis patient with NSAIDs, Corticosteroids and allopurinol. Laboratory data were observed for the duration of hospital days. Results : In spite of Oriental treatments, NSAIDs administration caused liver injury, but continuous Oriental treatments with small amount of Corticosteroids and allopurinol brought recovery of liver function and gouty arthritis. Confusion : Collaborative treatments of Oriental and Western medicine are better than independent Western treatment for gouty arthritis with acute inflammation and liver injury. Further studies will be required to ascertain the collaborative treatment with Oriental and Western medicine for gouty arthritis and other diseases.

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Early-Onset Postcardiac Injury Syndrome after Percutaneous Coronary Intervention Recovered with Steroids (경피적 관상동맥중재술 후 급성으로 발생한 스테로이드 치료로 회복한 심근 손상 후 증후군)

  • Kim, Min-Jeong;Yoon, Seong-Bo;Lee, Myong Dong;Kim, Si-Ho;Kim, Young Woo
    • The Korean Journal of Medicine
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    • v.93 no.6
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    • pp.565-570
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    • 2018
  • Postcardiac injury syndrome (PCIS) is an inflammatory process that usually occurs within 1 to 6 weeks after an injury to the pericardium, epicardium, or myocardium. As more interventions are performed for complicated coronary artery obstructive lesions, there have been some recent reports on PCIS following percutaneous coronary intervention (PCI). The medical management of PCIS depends on nonsteroidal anti-inflammatory drugs (NSAIDs), in addition to colchicine or steroids. An 80-year-old male patient underwent a PCI. Unfortunately, the guidewire piercing failed but he showed no immediate signs of complication. However, 5 hours after the procedure, he complained of chest discomfort. An electrocardiogram showed widespread ST elevation. Chest X-ray and computed tomography showed pulmonary congestion with pleural effusion, while thoracic echocardiography showed a moderate amount of pericardial effusion. NSAIDs were initiated, but there was no improvement of symptoms. We describe an unusual case of atypical earl onset PCIS after PCI, recovered rapidly by steroids.

Efficacy of topical interventions for temporomandibular disorders compared to placebo or control therapy: a systematic review with meta-analysis

  • Mena, Mariam;Dalbah, Lana;Levi, Lauren;Padilla, Mariela;Enciso, Reyes
    • Journal of Dental Anesthesia and Pain Medicine
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    • v.20 no.6
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    • pp.337-356
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    • 2020
  • This systematic review focused on the efficacy of topical products in reducing temporomandibular joint disorder (TMD)-associated pain, in comparison to placebo or control interventions. The EMBASE, Web of Science, Cochrane Library, and MEDLINE via PubMed databases were searched for randomized controlled trials (RCTs) using topical interventions in adults diagnosed with TMD. The pain intensity was the primary outcome, and other clinical findings were the secondary outcomes. The risk of bias was evaluated according to the Cochrane's handbook. The search up to February 7, 2020 identified a total of 496 unduplicated references. Nine RCTs with 355 adult patients diagnosed with TMD were included. The meta-analysis did not show a significant reduction in baseline pain intensity in the nonsteroidal anti-inflammatory drug (NSAIDs) group, when compared to the placebo group (P = 0.288). One study demonstrated a statistically significant pain score decrease for Theraflex-TMJ compared to placebo after 10 d of treatment (P = 0.003) and follow-up, 5 d after the last application (P = 0.027). Ping On reduced pain at 4 weeks of application (P < 0.001) but not after 7 d of application (P = 0.136). In one study, cannabidiol (CBD) significantly improved the pain intensity compared to placebo (P < 0.001). However, no differences were found with capsaicin in the two studies (P = 0.465). Evidence was of low quality because the studies were considered as having an unclear or a high risk of bias and a small number of studies were analyzed. The evidence is not sufficient to support the use of topical NSAIDs and capsaicin, and limited evidence was found for Threraflex-TMJ, bee venom, Ping On, and CBD, with only one study reporting for each. Additional studies are recommended to validate these results.