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The diagnosis and management of preterm labor with intact membranes
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Roberto Romero, Tinnakorn Chaiworapongsa, Francesca Gotsch, Lami Yeo, Ichchha Madan, Sonia S. Hassan
Prostaglandins are considered the universal mediators of labor and can induce uterine contractility and cervical ripening. The therapeutic target is the cyclooxygenase (COX) enzyme, which catalyzes the conversion of arachidonic acid to the intermediate product of prostaglandins, PGH. There are two COX enzymes, COX-1 and COX-2. The former is the constitutive enzyme, and the second is the inducible enzyme. Indomethacin is a non-specific inhibitor of COX, while nimesulide is a specific inhibitor of COX-2. One of the randomized clinical trials in which indomethacin was compared with placebo concluded that indomethacin resulted in a reduction in the rate of preterm birth (defined as <37 gestational weeks) (328,329). However, this trial included only 36 women, and there was no difference in neonatal outcome. Comparative trials (with either beta-adrenergic agents or magnesium sulfate) show that COX inhibitors reduced the rate of preterm birth before 37 weeks and the frequency of adverse events (329). However, there was no demonstrable improvement in neonatal outcome. Two studies comparing non-selected COX inhibitors versus COX-2 inhibitors did not demonstrate differences in maternal and neonatal outcome (329–331). It is recognized that the trials have been of small sample size.
Suprofen
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
Suprofen is a nonsteroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic and antipyretic activities. It binds to the cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) isoenzymes, preventing the synthesis of prostaglandins and reducing the inflammatory response. Currently, it appears not to be used systemically, but suprofen is utilized in eye drops to inhibit the miosis (pupil constriction) that may occur during ocular surgery (1). It is also available since 1989 in Japan in an ointment containing 1% suprofen (1,3). All reports of (photo)contact allergy thus far have come from Japan, with the exception of one patient who was sensitized during a clinical trial (12).
Proinflammatory Peptides in Relation to Other Inflammatory Mediators
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
Pierangelo Geppetti, Costanza Emanueli, Michela Figini, Domenico Regoli
The role of prostaglandins in the activation of sensory nerves induced by kinins merits specific attention. Three issues appear of particular relevance: first, bradykinin releases large amounts of prostaglandins from a variety of cells; second, prostaglandins are known to sensitize sensory nerves to the excitatory action of different mediators including kinins (25); and third, sensory neuropeptide release induced by bradykinin is markedly inhibited by indomethacin (26,27). Therefore, it appears that kinins and prostaglandins act synergistically to activate the dual afferent (pain transmission) and efferent functions (neuropeptide release) of primary sensory neurons. The ionic basis and the mechanism of release of sensory neuropeptides by prostaglandins and bradykinin has been reviewed recently (15). Kinins and prostaglandins are involved in the pathogenesis of painful and inflammatory diseases, including migraine and arthritis. In these pathologies, cyclooxygenase inhibitors have a major therapeutic impact. The therapeutic potential of the new peptide and nonpeptide antagonists of bradykinin B2 receptors will reflect the pathogenetic role played by kinins, but also how much of this role is independent from prostaglandin release.
Artificial intelligence-assisted development of in situ forming nanoparticles for arthritis therapy via intra-articular delivery
Published in Drug Delivery, 2022
Ahmed S. Yacoub, Hussein O. Ammar, Magdy Ibrahim, Suzan M. Mansour, Nada M. El Hoffy
NSAIDs are the corner stone in the management of various chronic inflammatory conditions as rheumatoid arthritis (RA). Through hindering cyclo-oxygenase (COX) enzymes that are responsible for inflammation and synthesis of prostaglandins which are part of the in normal physiological operations. The major adverse effects experienced with the clinical use of NSAIDs are mainly the overdose toxicity. It is believed that the more advanced COX-2-selective moieties better inhibit the inducible form of COX rather than the enzyme's other forms (Bertolini et al., 2002). Oral administration of these agents is the most common, but systemic side effects may be associated with them. Localized application of these compounds is drawing ultimate attention to solve these side effects (Izar et al., 2016).
Experimental in vivo model to evaluate the impact of Cernitin™ on pain response on induced chronic bladder inflammation
Published in Scandinavian Journal of Urology, 2022
Céline Augé, Nishtman Dizeyi, Lena Ramnemark, Philippe Lluel, Magnus Grabe
Cyclophosphamide-induced BPS in rodents is a well-characterized model [11–13]. Systemic CYP is metabolized in the liver but eliminated primarily through the kidneys. CYP’s major uro-toxic metabolite is acrolein, which causes mucosal inflammation as indicated by microscopic changes in the bladder and the presence of inflammatory cell infiltrations as well as visceral pain [2,14]. This experimental model makes CYP-induced BPS the optimal choice to elucidate mechanisms, identify specific biomarkers related to this chronic condition and subsequently finding effective therapeutic options. A chronic condition, inducing inflammation and tissue damage, can change the properties of sensory pathways leading to a reduction in pain threshold (allodynia) and an amplification of painful sensations (hyperalgesia) [2]. Furthermore, chronic CYP-induced BPS may involve alterations in neurotrophic factors, chemokines [12,15] and cytokines [16]. The presence of pro-inflammatory cytokines can induce cyclooxygenase-2 (COX-2) enzyme, an inflammatory early response gene [17] and generate prostaglandins, a substance that plays a role in the inflammation process. In this study, we hypothesize that CYP-induced BPS upregulates COX-2 [18] and prostanoids [19] in the urinary bladder, which contributes to altered urodynamic function. Cyclooxygenase-2 has also been reported to have a nociceptive (analgesic) effect in both the central and peripheral nervous systems. They show the improvement in bladder function with administration of a specific COX-2 inhibitor [20] suggesting the pivotal role of COX-2 and prostanoids in BPS.
Multimodal analgesia in neurosurgery: a narrative review
Published in Postgraduate Medicine, 2022
Caterina Aurilio, Maria Caterina Pace, Pasquale Sansone, Luca Gregorio Giaccari, Francesco Coppolino, Vincenzo Pota, Manlio Barbarisi
It is now understood that there are two forms of cyclooxygenase, termed cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). COX-1 is a constitutive isoform found in normal tissues, while COX-2 is induced in settings of inflammation and is constitutively expressed in certain areas of brain. NSAIDs are usually classified as mild analgesics, but it is important to consider the type of pain and its intensity in the assessment of analgesic efficacy. In postoperative pain, the NSAIDs may be superior to the opioids because they are particularly effective in different contests in which inflammation has caused sensitization of pain receptors [16]. The inhibition of COX-1 correlates with the inhibition of endogenous prostaglandins that impairs platelet function and promotes the ability of these drugs to increase the perioperative bleeding time. Probably for this reason, there are few clinical studies on the use of NSAIDs in brain surgery. In a Cochrane review, six studies were included in a meta-analysis on 742 patients to assess acute postoperative intensity of pain in brain surgery [10,17,18].