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Journal articles on the topic 'Nonsteroidal anti-inflammatory agents'

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Published: 4 June 2021

Last updated: 1 March 2023

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1

Morris, John L., David A. Rosen, and Kathleen R. Rosen. "Nonsteroidal Anti-Inflammatory Agents in Neonates." Pediatric Drugs 5, no. 6 (2003): 385–405. http://dx.doi.org/10.2165/00128072-200305060-00004.

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2

Olkkola, Klaus T., Aurora V. Brunetto, and Mauri J. Mattila. "Pharmacokinetics of Oxicam Nonsteroidal Anti-Inflammatory Agents." Clinical Pharmacokinetics 26, no. 2 (February 1994): 107–20. http://dx.doi.org/10.2165/00003088-199426020-00004.

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3

Nichols, John, and Robert W. Snyder. "Topical nonsteroidal anti-inflammatory agents in ophthalmology." Current Opinion in Ophthalmology 9, no. 4 (August 1998): 40–44. http://dx.doi.org/10.1097/00055735-199808000-00007.

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4

Biederman, Ross E. "Pharmacology in Rehabilitation: Nonsteroidal Anti-inflammatory Agents." Journal of Orthopaedic & Sports Physical Therapy 35, no. 6 (June 2005): 356–67. http://dx.doi.org/10.2519/jospt.2005.35.6.356.

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5

Goodwin, James S. "Immunologic Effects of Nonsteroidal Anti-inflammatory Agents." Medical Clinics of North America 69, no. 4 (July 1985): 793–804. http://dx.doi.org/10.1016/s0025-7125(16)31019-7.

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6

Nawaz, Fareha A., Christopher P. Larsen, and Megan L. Troxell. "Membranous Nephropathy and Nonsteroidal Anti-inflammatory Agents." American Journal of Kidney Diseases 62, no. 5 (November 2013): 1012–17. http://dx.doi.org/10.1053/j.ajkd.2013.03.045.

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7

Ongini, Ennio, and Manlio Bolla. "Nitric-oxide based nonsteroidal anti-inflammatory agents." Drug Discovery Today: Therapeutic Strategies 3, no. 3 (September 2006): 395–400. http://dx.doi.org/10.1016/j.ddstr.2006.09.004.

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8

Arnaud, Alain. "Allergy and intolerance to nonsteroidal anti-inflammatory agents." Clinical Reviews in Allergy and Immunology 13, no. 3 (September 1995): 245–51. http://dx.doi.org/10.1007/bf02771764.

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9

Kaidbey, K. H. "Photosensitizing potential of certain nonsteroidal anti-inflammatory agents." Archives of Dermatology 125, no. 6 (June 1, 1989): 783–86. http://dx.doi.org/10.1001/archderm.125.6.783.

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10

Gutch, C. F. "Nonsteroidal anti-inflammatory agents and acute renal failure." Archives of Internal Medicine 156, no. 21 (November 25, 1996): 2414. http://dx.doi.org/10.1001/archinte.156.21.2414.

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11

Kaidbey, Kays H. "Photosensitizing Potential of Certain Nonsteroidal Anti-inflammatory Agents." Archives of Dermatology 125, no. 6 (June 1, 1989): 783. http://dx.doi.org/10.1001/archderm.1989.01670180055005.

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12

Kollenberg, LO, EO Hudyma, and JM Robbins. "Nonsteroidal anti-inflammatory agents. A review of the literature." Journal of the American Podiatric Medical Association 75, no. 10 (October 1, 1985): 517–22. http://dx.doi.org/10.7547/87507315-75-10-517.

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13

Chan, A., and V. Ramachandra. "Comparing the analgesic effect of nonsteroidal anti-inflammatory agents." Anaesthesia 48, no. 12 (February 22, 2007): 1117. http://dx.doi.org/10.1111/j.1365-2044.1993.tb07569.x.

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14

Savage, Michael G., and Michael A. Henry. "Preoperative nonsteroidal anti-inflammatory agents: Review of the literature." Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 98, no. 2 (August 2004): 146–52. http://dx.doi.org/10.1016/j.tripleo.2004.01.012.

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15

Grob, J. J., A. M. Collet, and J. J. Bonerandi. "Dermatomyositis-Like Syndrome Induced by Nonsteroidal Anti-Inflammatory Agents." Dermatology 178, no. 1 (1989): 58–59. http://dx.doi.org/10.1159/000248390.

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16

Yousfi, Mahmoud M., Giovanni De Petris, Jonathan A. Leighton, Virender K. Sharma, Barbara A. Pockaj, Dawn E. Jaroszewski, Russell I. Heigh, Nizar N. Ramzan, and David E. Fleischer. "Diaphragm Disease After Use of Nonsteroidal Anti-inflammatory Agents." Journal of Clinical Gastroenterology 38, no. 8 (September 2004): 686–91. http://dx.doi.org/10.1097/01.mcg.0000135367.66159.87.

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17

Wallace, John L. "The 1994 Merck Frosst Award. Mechanisms of nonsteroidal anti-inflammatory drug (NSAID) induced gastrointestinal damage—potential for development of gastrointestinal tract safe NSAIDs." Canadian Journal of Physiology and Pharmacology 72, no. 12 (December 1, 1994): 1493–98. http://dx.doi.org/10.1139/y94-215.

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Nonsteroidal anti-inflammatory drugs are widely used for the treatment of osteoarthritis and rheumatoid arthritis, but their ability to cause gastrointestinal bleeding is a significant limitation to this use. A better understanding of the pathogenesis of gastric and intestinal injury induced by these agents will permit the rational design of anti-inflammatory drugs that spare the gastrointestinal tract. In this review, the mechanisms through which nonsteroidal anti-inflammatory drugs are believed to cause gastrointestinal ulceration are reviewed. Several strategies that are being employed to develop gastrointestinal-sparing drugs are outlined.Key words: nonsteroidal anti-inflammatory drugs, ulcer, cyclooxygenase, nitric oxide, gastrointestinal, prostaglandins.

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18

Tenenbaum, Jerry. "The Epidemiology of Nonsteroidal Anti-Inflammatory Drugs." Canadian Journal of Gastroenterology 13, no. 2 (1999): 119–22. http://dx.doi.org/10.1155/1999/361651.

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Nonsteroidal anti-inflammatory drug (NSAID) use has increased dramatically in the past two decades. A large proportion of the elderly population (more than 65 years of age) holds a current or recent NSAID prescription, accounting for approximately 90% of all NSAID prescriptions. Despite studies that advise finding alternatives for NSAIDs for the management of osteoarthritis, physicians often prescribe NSAIDs first for such common musculoskeletal conditions. Despite being identified as risk factors for gastrointestinal complications, the simultaneous use of two NSAIDs and the coadministration of NSAIDs with corticosteroids and with coumadin continue to occur. The point prevalence of NSAID-induced ulcers is 10% to 30%, and 15% to 35% of all peptic ulcer complications are caused by NSAIDs. The increased risk of gastrointestinal complications when NSAIDs are used is 3% to 5%. This risk increases with other identified risk factors (eg, older age, previous gastrointestinal history, comorbid diseases and poor health). Gastrointestinal causes of hospitalization (eg, gastrointestinal hemorrhage and perforation) and death have increased in parallel to increased NSAID use. ‘Antiulcer’ agents are prescribed twice as often in NSAID users, and the economic impact (eg, diagnostic tests and hospitalization) is that about one-third of the arthritis budget has been dedicated to deal with gastrointestinal side effects of NSAIDs. Misoprostol and omeprazole have been shown to be cytoprotective for the gastroduodenal mucosa when NSAIDs are used, and misoprostol has been shown to reduce the risk of gastroduodenal ulcer complications. Economic evaluations have suggested that these agents are a cost effective means of dealing with such NSAID-associated problems. Although no NSAID is totally safe, a number of studies have demonstrated that NSAIDs may be ranked according to relative gastrointestinal toxicity. The role ofHelicobacter pyloriin NSAID-associated problems remains uncertain.

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19

Miranda, H. F., F. Sierralta, and G. Pinardi. "Carbachol interactions with nonsteroidal anti-inflammatory drugs." Canadian Journal of Physiology and Pharmacology 80, no. 12 (December 1, 2002): 1173–79. http://dx.doi.org/10.1139/y02-145.

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The inhibition of cyclooxygenase enzymes by nonsteroidal anti-inflammatory drugs (NSAIDs) does not completely explain the antinociceptive efficacy of these agents. It is known that cholinergic agonists are antinociceptive, and this study evaluates the interactions between carbachol and some NSAIDs. Antinociceptive activity was evaluated in mice by the acetic acid writhing test. Doseresponse curves were constructed for NSAIDs and carbachol, administered either intraperitoneally (i.p.) or intrathecally (i.t.). The interactions of carbachol with NSAIDs were evaluated by isobolographic analysis after the simultaneous administration of fixed proportions of carbachol with each NSAID. All of the drugs were more potent after spinal than after systemic administration. The combinations of NSAIDs and carbachol administered i.p. were supra-additive; however, the i.t. combinations were only additive. Isobolographic analysis of the coadministration of NSAIDs and carbachol and the fact that atropine antagonized the synergistic effect suggest that carbachol may strongly modulate the antinociceptive activity of NSAIDs; thus, central cholinergic modulation would be an additional mechanism for the antinociceptive action of NSAIDs, unrelated to prostaglandin biosynthesis inhibition.Key words: antinociception, nonsteroidal anti-inflammatory drugs, cholinergic, carbachol, writhing test.

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20

Sun, Yaying, Jiwu Chen, Hong Li, Jia Jiang, and Shiyi Chen. "Steroid Injection and Nonsteroidal Anti-inflammatory Agents for Shoulder Pain." Medicine 94, no. 50 (December 2015): e2216. http://dx.doi.org/10.1097/md.0000000000002216.

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21

Bartley, George B., and Roger A. Warndahl. "Surgical Bleeding Associated With Aspirin and Nonsteroidal Anti-Inflammatory Agents." Mayo Clinic Proceedings 67, no. 4 (April 1992): 402–3. http://dx.doi.org/10.1016/s0025-6196(12)61566-3.

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22

Matzke, Gary R. "Nonrenal toxicities of acetaminophen, aspirin, and nonsteroidal anti-inflammatory agents." American Journal of Kidney Diseases 28, no. 1 (July 1996): S63—S70. http://dx.doi.org/10.1016/s0272-6386(96)90571-5.

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23

Thaller, John, Matthew Walker, Alex J Kline, and D. Greg Anderson. "The Effect of Nonsteroidal Anti-Inflammatory Agents on Spinal Fusion." Orthopedics 28, no. 3 (March 1, 2005): 299–303. http://dx.doi.org/10.3928/0147-7447-20050301-15.

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24

Hanson, Curtis A., Paul S. Weinhold, Hessam M. Afshari, and Laurence E. Dahners. "The Effect of Analgesic Agents on the Healing Rat Medial Collateral Ligament." American Journal of Sports Medicine 33, no. 5 (May 2005): 674–79. http://dx.doi.org/10.1177/0363546504269722.

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Background Studies have suggested that some nonselective nonsteroidal anti-inflammatory drugs, including piroxicam, may improve ligament healing, whereas other nonsteroidal anti-inflammatory drugs, including ibuprofen and the cyclooxygenase-2 inhibitor celecoxib, may have no effect on the mechanical properties or may even deter the healing process. These results might reflect variations in cyclooxygenase enzyme selectivity by different drugs or, alternatively, may be related to their analgesic properties because it is generally accepted that early activity improves ligament healing. Hypothesis Nonselective nonsteroidal anti-inflammatory drugs improve ligament healing, whereas other analgesics provide lesser degrees of improvement, and cyclooxygenase-2 inhibitors are detrimental. Study Design Controlled laboratory study. Methods One hundred fifty-five Sprague-Dawley rats were divided into 7 treatment groups (piroxicam, naproxen, rofecoxib, butorphanol, 2 doses of acetaminophen, and control). The right medial collateral ligament of each rat was transected, and the drugs were administered postoperatively on days 1 to 6. On day 14, the rats were sacrificed, and mechanical testing was performed on the medial collateral ligament. Results The piroxicam group demonstrated significantly greater load to failure (27%) compared with the control. No significant differences were observed between other groups. Conclusions Piroxicam improves ligament healing, but this effect cannot be attributed to all nonselective nonsteroidal anti-inflammatory drugs. Opiate analgesics, acetaminophen, and cyclooxygenase-2 inhibitors do not appear to categorically affect ligament healing. Clinical Relevance In the treatment of ligament injury, piroxicam may be a drug of choice.

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25

Abe, David O., Arvin Eskandari, and Kogularamanan Suntharalingam. "Diflunisal-adjoined cobalt(iii)-polypyridyl complexes as anti-cancer stem cell agents." Dalton Transactions 47, no. 39 (2018): 13761–65. http://dx.doi.org/10.1039/c8dt03448f.

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26

Thoo, Sophie, Sudha Cugati, Andrew Lee, and Celia Chen. "Successful treatment of fingolimod-associated macular edema with intravitreal triamcinolone with continued fingolimod use." Multiple Sclerosis Journal 21, no. 2 (April 2, 2014): 249–51. http://dx.doi.org/10.1177/1352458514528759.

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The occurrence of macular edema as an adverse effect of fingolimod is well documented. Treatment modalities used to manage fingolimod-associated macular edema (FAME) have included nonsteroidal anti-inflammatory agents and sub-tenon injection. We describe two cases where intravitreal injection is used to successfully treat FAME in patients who were previously unsuccessfully treated with topical nonsteroidal anti-inflammatories.

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27

Nelson, Robert P., John J. Stablein, and Richard F. Lockey. "Asthma Improved by Acetylsalicylic Acid and Other Nonsteroidal Anti-Inflammatory Agents." Allergy and Asthma Proceedings 7, no. 2 (March 1, 1986): 117–21. http://dx.doi.org/10.2500/108854186779047717.

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28

Feeney, Michelle, Maria Giannuzzo, Patrizia Paolicelli, and Maria Antonietta Casadei. "Hydrogels of Dextran Containing Nonsteroidal Anti-Inflammatory Drugs as Pendant Agents." Drug Delivery 14, no. 2 (January 2007): 87–93. http://dx.doi.org/10.1080/10717540600740003.

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29

Tuomanen, E., B. Hengstler, R. Rich, M. A. Bray, O. Zak, and A. Tomasz. "Nonsteroidal Anti-Inflammatory Agents in the Therapy for Experimental Pneumococcal Meningitis." Journal of Infectious Diseases 155, no. 5 (May 1, 1987): 985–90. http://dx.doi.org/10.1093/infdis/155.5.985.

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30

Gross, Nicholas J., Nathaniel O. Holloway, and K. Roy Narine. "Effects of Some Nonsteroidal Anti-Inflammatory Agents on Experimental Radiation Pneumonitis." Radiation Research 127, no. 3 (September 1991): 317. http://dx.doi.org/10.2307/3577947.

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31

Sandler, Robert S., Joseph C. Galanko, Sharon C. Murray, James F. Helm, and John T. Woosley. "Aspirin and nonsteroidal anti-inflammatory agents and risk for colorectal adenomas." Gastroenterology 114, no. 3 (March 1998): 441–47. http://dx.doi.org/10.1016/s0016-5085(98)70526-8.

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32

Wu, Christopher L., Kethy M. Jules-Elysee, Meghan A. Kirksey, and Gregory A. Liguori. "Perioperative Nonsteroidal Anti-Inflammatory Agents in the COVID-19 Orthopedic Patient." HSS Journal ® 16, S1 (September 14, 2020): 97–101. http://dx.doi.org/10.1007/s11420-020-09783-3.

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33

Gaudreault, Pierre. "Nonsteroidal Anti-Inflammatory Agents in the Treatment of Asthma in Children." Canadian Respiratory Journal 2, suppl a (1995): 24A—31A. http://dx.doi.org/10.1155/1995/956715.

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The increasing scientific information clearly demonstrates the important role of inflammation in asthma. This evidence has led physicians to focus their treatment on the elimination of inflammation instead of working solely against bronchoconstriction. Steroids and nonsteroidal agents are currently used to prevent this inflammatory component. This paper focuses only on nonstcroidal anti-inflammatory agents such as sodium cromoglycate, nedocromil sodium and ketotifen and their use in pediatric asthma. The discussion on each medication addresses its mechanism of action, the evidence concerning its efficacy in pediatrics (ie, clinical pharmacology, acute bronchial challenge, late asthmatic response, bronchial hyperrcactivity, clinical efficacy) and the pediatric dose.

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34

O’MALLEY, PATRICIA. "The Risks and Benefits of Nonsteroidal Anti-inflammatory Agents for Pain." Clinical Nurse Specialist 16, no. 5 (September 2002): 270–73. http://dx.doi.org/10.1097/00002800-200209000-00011.

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35

Yücesoy, M., I. M. A. Öktem, and Z. Gülay. "In-VitroSynergistic Effect of Fluconazole with Nonsteroidal Anti-Inflammatory Agents AgainstCandida albicansStrains." Journal of Chemotherapy 12, no. 5 (January 2000): 385–89. http://dx.doi.org/10.1179/joc.2000.12.5.385.

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36

DIRIKOLU, L., W. E. WOODS, J. BOYLES, A. F. LEHNER, J. D. HARKINS, M. FISHER, D. J. SCHAEFFER, and T. TOBIN. "Nonsteroidal anti-inflammatory agents and musculoskeletal injuries in Thoroughbred racehorses in Kentucky." Journal of Veterinary Pharmacology and Therapeutics 32, no. 3 (June 2009): 271–79. http://dx.doi.org/10.1111/j.1365-2885.2008.01038.x.

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37

Thun, M. J., S. J. Henley, and C. Patrono. "Nonsteroidal Anti-inflammatory Drugs as Anticancer Agents: Mechanistic, Pharmacologic, and Clinical Issues." JNCI Journal of the National Cancer Institute 94, no. 4 (February 20, 2002): 252–66. http://dx.doi.org/10.1093/jnci/94.4.252.

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38

IRANI, J., V. RAVERY, J. L. PARIENTE, E. CHARTIER-KASTLER, E. LECHEVALLIER, M. SOULIÉ, D. CHAUTARD, et al. "Effect of Nonsteroidal Anti-Inflammatory Agents and Finasteride on Prostate Cancer Risk." Journal of Urology 168, no. 5 (November 2002): 1985–88. http://dx.doi.org/10.1016/s0022-5347(05)64277-2.

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39

Yiannakopoulou, Eugenia. "Pharmacogenomics of acetylsalicylic acid and other nonsteroidal anti-inflammatory agents: clinical implications." European Journal of Clinical Pharmacology 69, no. 7 (February 24, 2013): 1369–73. http://dx.doi.org/10.1007/s00228-013-1477-9.

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40

Gomes, Francisco Isaac Fernandes, Maria Gerusa Brito Aragão, Vicente de Paulo Teixeira Pinto, Delane Viana Gondim, Francisco Cesar Barroso, Antonio Alfredo Rodrigues e. Silva, Mirna Marques Bezerra, and Hellíada Vasconcelos Chaves. "Effects of Nonsteroidal Anti-inflammatory Drugs on Osseointegration: A Review." Journal of Oral Implantology 41, no. 2 (April 1, 2015): 219–30. http://dx.doi.org/10.1563/aaid-joi-d-13-00125.

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The purpose of this study was to review the effects of nonsteroidal anti-inflammatory drugs on osseointegration and determine whether they cause failures in dental implants and whether patients who use them chronically can receive dental implants safely. A bibliographic electronic search was performed using the Cochrane Library, PubMed, and Medline databases, selecting articles published between January 1982 and December 2012. The search included the following keywords, either alone or combined: “nonsteroidal anti-inflammatory drugs,” “dental implants,” “bone healing,” and “osteoprogenitor cells.” The inclusion criteria were the following: randomized, double-blind, placebo-controlled clinical studies, in vivo animal model studies of osseointegration, and in vitro studies of the effects of these agents on osteoprogenitor cells. The literature search revealed 360 references. A total of 31 articles met the inclusion criteria, including 2 clinical trials, 20 animal studies, and 9 osteoprogenitor cell studies. The clinical trials revealed that cyclooxygenase-1 (COX-1) inhibitors did not impair osseointegration. The animal studies showed that any drug that is capable of inhibiting COX-2 may impair the osseointegration process. The in vitro studies showed that COX-2 inhibitors are the most potent depressors of osseointegration at the cellular level. Caution must be taken when selecting COX-2 nonsteroidal anti-inflammatory drugs during the postoperative period.

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41

Fajardo, Alexandra M., and Gary A. Piazza. "Chemoprevention in gastrointestinal physiology and disease. Anti-inflammatory approaches for colorectal cancer chemoprevention." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 2 (July 15, 2015): G59—G70. http://dx.doi.org/10.1152/ajpgi.00101.2014.

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Colorectal cancer (CRC) is one of the most common human malignancies and a leading cause of cancer-related deaths in developed countries. Identifying effective preventive strategies aimed at inhibiting the development and progression of CRC is critical for reducing the incidence and mortality of this malignancy. The prevention of carcinogenesis by anti-inflammatory agents including nonsteroidal anti-inflammatory drugs (NSAIDs), selective cyclooxygenase-2 (COX-2) inhibitors, and natural products is an area of considerable interest and research. Numerous anti-inflammatory agents have been identified as potential CRC chemopreventive agents but vary in their mechanism of action. This review will discuss the molecular mechanisms being studied for the CRC chemopreventive activity of NSAIDs (i.e., aspirin, sulindac, and ibuprofen), COX-2 inhibitors (i.e., celecoxib), natural products (i.e., curcumin, resveratrol, EGCG, genistein, and baicalein), and metformin. A deeper understanding of how these anti-inflammatory agents inhibit CRC will provide insight into the development of potentially safer and more effective chemopreventive drugs.

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42

Antman, Elliott M. "Evaluating the Cardiovascular Safety of Nonsteroidal Anti-Inflammatory Drugs." Circulation 135, no. 21 (May 23, 2017): 2062–72. http://dx.doi.org/10.1161/circulationaha.117.027288.

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Some drugs used to treat noncardiovascular conditions may adversely impact the cardiovascular status of individuals both with and without known cardiovascular disease. When the US Food and Drug Administration judges the potential cardiovascular safety signal to be of sufficient concern, it may require the pharmaceutical manufacturer of the drug in question to conduct a postmarketing (phase 4) randomized controlled trial (RCT). Although historically many phase 4 RCTs focused on efficacy (using a superiority design), contemporary phase 4 RCTs often are focused on safety and use a noninferiority design. The choices made by investigators during the planning stage of a postmarketing phase 4 RCT dedicated to the evaluation of cardiovascular safety can influence the ability to compare the standard and test agents. Multiple factors reflecting the conduct of a phase 4 RCT for a general medical condition may influence interpretation of a cardiovascular safety signal. The higher the rates of failure to adhere to the protocol and dropout from the study, the greater the risk of bias. Trials evaluating the cardiovascular safety of nonsteroidal anti-inflammatory drugs (NSAIDs) when used for arthritis are difficult to conduct and even more challenging to interpret. Concerns include the comparison of drug regimens that do not provide comparable analgesic efficacy and problems with adherence to the protocol and retention in the study. On the basis of phase 4 RCTs of NSAIDs to date, it appears that a comparatively low dose of celecoxib administered to low-risk subjects is associated with approximately the same cardiovascular risk as NSAIDs with less cyclooxygenase-2 inhibitory activity, but at the cost of not controlling arthritic pain as effectively.

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43

Rao, Praveen, and Edward E. Knaus. "Evolution of Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Cyclooxygenase (COX) Inhibition and Beyond." Journal of Pharmacy & Pharmaceutical Sciences 11, no. 2 (September 20, 2008): 81. http://dx.doi.org/10.18433/j3t886.

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Purpose. NSAIDs constitute an important class of drugs with therapeutic applications that have spanned several centuries. Treatment of inflammatory conditions such as rheumatoid arthritis (RA) and osteoarthritis (OA) starting from the classic drug aspirin to the recent rise and fall of selective COX-2 inhibitors has provided an enthralling evolution. Efforts to discover an ultimate magic bullet to treat inflammation continues to be an important drug design challenge. This review traces the origins of NSAIDs, their mechanism of action at the molecular level such as cyclooxygenase (COX) inhibition, development of selective COX-2 inhibitors, their adverse cardiovascular effects, and some recent developments targeted to the design of effective anti-inflammatory agents with reduced side effects. Methods. Literature data is presented describing important discoveries pertaining to the sequential development of classical NSAIDs and then selective COX-2 inhibitors, their mechanism of action, the structural basis for COX inhibition, and recent discoveries. Results. A brief history of the development of NSAIDs and the market withdrawal of selective COX-2 inhibitors is explained, followed by the description of prostaglandin biosynthesis, COX isoforms, structure and function. The structural basis for COX-1 and COX-2 inhibition is described along with methods used to evaluate COX-1/COX-2 inhibition. This is followed by a section that encompasses the major chemical classes of selective COX-2 inhibitors. The final section describes briefly some of the recent advances toward developing effective anti-inflammatory agents such as nitric oxide donor NO-NSAIDs, dual COX/LOX inhibitors and anti-TNF therapy. Conclusions. A great deal of progress has been made toward developing novel anti-inflammatory agents. In spite of the tremendous advances in the last decade, the design and development of a safe, effective and economical therapy for treating inflammatory conditions still presents a major challenge.

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44

Lyalina, V. V., S. V. Borisovskaya, E. A. Skripnichenko, O. A. Ettinger, T. M. Padzheva, and I. G. Nikitin. "Perioperative Management of Patients with Rheumatic Diseases: Glucocorticoids, DMARDs, Biological Agents and NSAIDs." Russian Archives of Internal Medicine 12, no. 1 (January 31, 2022): 22–34. http://dx.doi.org/10.20514/2226-6704-2022-12-1-22-34.

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The rheumatic patients are characterized by various structural and functional changes, caused by chronic disease the necessity of constant medication intake, including anti-inflammatory drugs and immunosuppressants. In this regard, the rheumatic patients have an increased risk of intraoperative and postoperative complications. The purpose of this publication is to review current recommendations on the topic of perioperative management of rheumatic patients. The publication consists of two parts. In the first part we review the issues of perioperative administration of steroids, disease-modifying antirheumatic drugs, biologics and nonsteroidal anti-inflammatory drugs.

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45

Askonas, Leslie J., and Trevor M. Penning. "Development of affinity labeling agents based on nonsteroidal anti-inflammatory drugs: labeling of the nonsteroidal anti-inflammatory drug binding site of 3.alpha.-hydroxysteroid dehydrogenase." Biochemistry 30, no. 49 (December 10, 1991): 11553–60. http://dx.doi.org/10.1021/bi00113a010.

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46

Hassan, Ghaneya S., Gehan H. Hegazy, Noha M. Ibrahim, and Samar H. Fahim. "New ibuprofen derivatives as H2S and NO donors as safer anti-inflammatory agents." Future Medicinal Chemistry 11, no. 23 (December 2019): 3029–45. http://dx.doi.org/10.4155/fmc-2018-0467.

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Aim: Nonsteroidal anti-inflammatory drugs are expansively used worldwide. However, their prolonged administration is associated with serious side effects, especially gastrointestinal ulceration. Materials & methods: New ibuprofen derivatives hybridized with H2S- or NO-donating moieties were synthesized and evaluated for their anti-inflammatory activity and ulcerogenic effect. COX-1/COX-2 isozymes selectivity test for the most promising derivatives was performed. Molecular docking studies were performed. Results: Most of the compounds showed promising anti-inflammatory activity comparable to that of ibuprofen (% edema inhibition = 76.6 and ulcer index = 21.26) with much better gastrointestinal tract tolerance (ulcer indices ranging from 0 to 14.67), especially compound 2 -H2S donor- (% edema inhibition = 75.5 and ulcer index = 11.75) and compound 16 -NO donor- (% edema inhibition = 65.4 and ulcer index = 8.66).

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Kyle, Meghann E., James C. Wang, and Jennifer J. Shin. "Impact of Nonaspirin Nonsteroidal Anti-inflammatory Agents and Acetaminophen on Sensorineural Hearing Loss." Otolaryngology–Head and Neck Surgery 152, no. 3 (January 5, 2015): 393–409. http://dx.doi.org/10.1177/0194599814564533.

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Abel, Robert, and Ari D. Abel. "Perioperative antibiotic, steroid, and nonsteroidal anti-inflammatory agents in cataract intraocular lens surgery." Current Opinion In Ophthalmology 8, no. 1 (February 1997): 29–32. http://dx.doi.org/10.1097/00055735-199702000-00007.

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Abel, Robert, and Ari D. Abel. "Perioperative antibiotic, steroid, and nonsteroidal anti-inflammatory agents in cataract intraocular lens surgery." Current Opinion In Ophthalmology 8, no. 1 (February 1997): 29–32. http://dx.doi.org/10.1097/00055735-199708010-00007.

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Khalil, Viviane, Wei Wang, Lauren Charlson, and Samantha Blackley. "Evaluation of prescribing patterns of nonsteroidal anti-inflammatory agents in a tertiary setting." International Journal of Evidence-Based Healthcare 17, no. 3 (September 2019): 164–72. http://dx.doi.org/10.1097/xeb.0000000000000173.

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