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Drug Allergy
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Induction of tolerance can also be performed in the setting of Aspirin-Exacerbated Respiratory Disease (AERD). While protocols for this procedure are similar to that of other agents, the mechanism of reaction is different. The mechanism is believed to be due to an alteration in arachidonic acid metabolism and a shift away from generation of proinflammatory cys-leukotrienes. An example of an aspirin protocol is shown in Table 33.6 (Macy et al. 2007).
Effects of Antithrombotic and Results of Drug Screening
Published in Josef Hladovec, Antithrombotic Drugs in Thrombosis Models, 2020
This classification is rather vague and far from complete. There is much work going on in another direction of arachidonic acid metabolism, i.e., lipoxygenase route. Other agents influence the common portion of both the platelet and endothelial eicosanoid systems, i.e., release of arachidonic acid from membrane phospholipids, activity of various cyclo-oxy-genases, etc. Various kinds of agents affecting one part of the system may possess in the same molecule, activities influencing other parts. Alternatively, various agents may be combined.
Perspective
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
When peptides and polypeptides are discussed in the context of inflammation, it is most often with reference to their proinflammatory effects. Among the earliest and best characterized are activated complement peptides. The complement system, and its component proteins and peptides, play a critical role in the immunological defense against microbial agents. During complement activation, several peptides are generated, especially C3 and C5, which can trigger such features of inflammation as increased vascular permeability; leukocyte activation, chemotoxis, and adhesion; phagocytosis; and activation of the proinflammatory lipoxygenase pathway of arachidonic acid metabolism. The activation of the complement system is closely linked to the pathways leading to activation of blood coagulation, fibrinolysis, and kinin formation (18).
Transcription profiling of cadmium-exposed livers reveals alteration of lipid metabolism and predisposition to hepatic steatosis
Published in Xenobiotica, 2021
Chenghui Ren, Longfei Ren, Jun Yan, Zhongtian Bai, Lei Zhang, Honglong Zhang, Ye Xie, Xun Li
Sonnweber et al. (2018) pointed out that arachidonic acid metabolism plays an important role in cardiovascular and many metabolic diseases including NAFLD, which is consistent with our conclusions. The occurrence of NAFLD is closely related to insulin resistance. The insulin deficiency or insulin resistance causes a decrease in the glucose utilisation in the body. Thus, in order to ensure the body's energy supply, fat catabolism increases relatively, resulting in an increase in free fatty acids levels in the blood. These large amounts of fatty acids are taken up by the liver and accumulated in the form of fat to form fatty liver (Friedman et al.2018). In our research, the KEGG metabolic pathway enrichment analysis of the DEGs showed significant enrichment of the ‘insulin resistance’ pathway.
Nonsteroidal anti-inflammatory drugs in end-stage kidney disease: dangerous or underutilized?
Published in Expert Opinion on Pharmacotherapy, 2021
The predominant mechanism of action of NSAIDs is the inhibition of COX enzymes, prohibiting prostanoid synthesis from arachidonic acid (Figure 1) [1,15,16]. Arachidonic acid metabolism is a multi-step enzymatic process that follows platelet aggregation and activation of membrane phospholipases. Thromboxane A2 (TXA2), a platelet prostanoid product of arachidonic acid metabolism, acts as a vasoconstrictor and platelet aggregant. This platelet-activating cascade is initiated by COX-1, an enzyme that is constituently expressed in mature platelets as well as various organ tissues including the gastric mucosa, kidneys, and vascular endothelium [17]. In contrast, COX-2 is only transiently expressed in immature platelets [18] or in vascular endothelial cells during inflammatory states and is largely involved in the production of prostaglandins, most notably prostacyclin (PGI2). Inhibition of prostacyclin’s vasodilatory and platelet anti-aggregant effects contribute to increased risk for adverse cardiovascular events in patients taking NSAIDs and selective COX-2 inhibitors [19,20].
New and emerging drugs for the treatment of acne vulgaris in adolescents
Published in Expert Opinion on Pharmacotherapy, 2019
Isabel Cristina Valente Duarte De Sousa
Leukotrienes, which are products of arachidonic acid metabolism, are major players in the development of tissue inflammation [182]. Acebilustat, (formerly CTX-4430) [183], is a new once-daily oral anti-inflammatory drug that inhibits leukotriene A4 hydrolase and thus reduces leukotriene B4 (LTB4) production [184]. LTB4 stimulates sebocyte and follicular keratinocyte differentiation, increasing sebum production and comedogenesis as well as the migration of neutrophils to the sebaceous follicles [82,185,186]. Inhibition of leukotriene A4 hydrolase could thus play a role in acne management through LTB4 reduction. The efficacy and safety of acebilustat for the treatment of moderate to severe facial acne vulgaris in patients 16 years of age and older, was assessed in a phase II multicenter, double-blind, randomized, placebo-controlled study completed in 2016. However, official results are not available [187].