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Nasal Polyposis
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Patients should have a trial of medical therapy first unless histology is required. Medical management includes: Intra-nasal corticosteroids (INCS).Short courses of systemic corticosteroids in more extensive polyposis.Antihistamines help only if allergy is present.Leukotriene inhibitors may help patients with coexisting asthma and/or aspirin sensitivity.
The Role of Platelet-Activating Factor in Endotoxin-Related Disease
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Taco W. Kuijpers, Tom van der Poll
Within the GPCR superfamily, inflammation can be mediated through lipid metabolites other than PAF, e.g., the aforementioned leukotrienes, thromboxanes, and prostaglandins (14). For instance, the leukotrienes are biologically active 5-lipoxygenase products of arachidonic acid metabolism involved in the mediation of many of the inflammatory disorders in which PAF is believed to act. Leukotriene B4 is generated by many cell types and is a chemoattractant for granulocytes. The sulfidopeptide leukotrienes C4, D4, and E4 have been incriminated in allergic reactions and increase vascular permeability and constrict smooth muscle. Leukotrienes also exert their biological actions through specific GPCR interactions (see Table 1).
Immunomodulating Agents in Gastrointestinal Disease
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Samir A. Shah, Athos Bousvaros, A. Christopher Stevens
Since cyclooxygenase blockade did not alleviate colonic inflammation in patients, attention shifted to the lipoxygenase pathway of arachidonic acid metabolism [13]. Azulfidine and 5-ASA inhibit both 5-lipoxygenase- and lipoxygenase-activating protein (FLAP) [14,15]. This action blocks the production of leukotrienes, which function as chemotactic factors for neutrophils. In particular, mucosal levels of leukotriene B4 directly correlate with active inflammation in inflammatory bowel disease patients. Preliminary animal and human trials with lipoxygenase inhibitors were promising, but subsequent prospective randomized double-blinded clinical trials have not demonstrated a significant clinical response (see Section VII. D) [16–18].
Silicone hydrogel contact lenses retain and document ocular surface lipid mediator profiles
Published in Clinical and Experimental Optometry, 2023
Karsten Gronert, Arnav Modi, Kaleb Asfaha, Sharon Chen, Elizabeth Dow, Scott Joslin, Mike Chemaly, Zohra Fadli, Leilani Sonoda, Bailin Liang
Silicone hydrogel lenses from several subjects contained significant levels of the eicosanoids lipoxin A4, leukotriene B4 and/or prostaglandin E2, which in animal models are markers and mediators of inflammation, leukocyte activation, epithelial injury and changes in ocular surface homoeostasis.7 Lipoxin A4, leukotriene B4, and prostaglandin E2 are clinically relevant eicosanoids whose receptors are expressed in corneal and conjunctival epithelial cells, fibroblast, corneal nerves, endothelial cells, and recruited leukocytes and lymphocytes.3,4,11,12,33–35 Additional studies, in subjects with adverse events are required to determine if cell-specific formation of these lipid mediators is an early biomarker of infection, epithelial stress, presence of tear neutrophils or corneal nerve activation due to contact lens wear.
The pharmacological management of asthma-chronic obstructive pulmonary disease overlap syndrome (ACOS)
Published in Expert Opinion on Pharmacotherapy, 2020
Timothy E. Albertson, James A. Chenoweth, Skyler J. Pearson, Susan Murin
Leukotriene pathway modifiers including both leukotriene synthesis inhibitors and receptor antagonists are widely available and used in asthma and other atopic diseases. The cysteinyl leukotrienes (cys-LT) which include C4, D4 and E4 are formed by arachidonic acid precursors acted on by 5-lipoxygenase enzyme activity that then attract eosinophils and interact at cys-LT receptors on the outer plasma membrane of monocytes, macrophages, eosinophils, mast cells and smooth muscle cells of the airway [106]. Two agents that antagonize the cys-LT receptor (LRA) are available in the US and Europe (montelukast and zafirlukast) and pranlukast is also available in Japan. The second class of leukotriene pathway modulators is an inhibitor of the 5-lipoxygenase enzyme that inhibits the synthesis of both cysteinyl leukotrienes (LTC4, LTD4, and LTE4) and leukotriene B4 (LTB4) (zileuton).
Investigational drugs in phase II clinical trials for acute coronary syndromes
Published in Expert Opinion on Investigational Drugs, 2020
Amit Rout, Ajaypaul Sukhi, Rahul Chaudhary, Kevin P Bliden, Udaya S Tantry, Paul A Gurbel
Leukotrienes are mainly derived from arachidonic acid via the 5- lipoxygenase (5-LO) pathway in leukocytes. 5-LO, along with 5-lipooxygenase activating protein (FLAP), initially leads to the formation of precursor leukotriene A4. Leukotriene B4 (LTB4) is a potent leukocyte activator and chemokine. The cysteinyl leukotrienes (LTC4, LTD4, and LTE4) are potent vasoactive and inflammatory mediators [5,6]. Coronary artery disease (CAD) is an atheroinflammatory condition involving endothelial dysfunction, infiltration of inflammatory cells, and platelets into the arterial vessel wall, smooth muscle proliferation, and atherogenesis. 5-LO pathway mediators and products are increasingly expressed in the unstable atherosclerotic lesions and play a significant role in inflammation and progression of CAD and ACS [5,6].