State of the art paper Does aspirin-induced oxidative stress cause asthma exacerbation?

Abstract

Aspirin-induced asthma (AIA) is a distinct clinical syndrome characterized by severe asthma exacerbations after ingestion of aspirin or other non-steroidal anti-inflammatory drugs. The exact pathomechanism of AIA remains unknown, though ongoing research has shed some light. Recently, more and more attention has been focused on the role of aspirin in the induction of oxidative stress, especially in cancer cell systems. However, it has not excluded the similar action of aspirin in other inflammatory disorders such as asthma. Moreover, increased levels of 8-isoprostanes, reliable biomarkers of oxidative stress in expired breath condensate in steroid-naïve patients with AIA compared to AIA patients treated with steroids and healthy volunteers, has been observed. This review is an attempt to cover aspirin-induced oxidative stress action in AIA and to suggest a possible related pathomechanism.

Evaluation of selected parameters of the coagulation system during the perioperative period in patients undergoing endoscopic surgery of the paranasal sinuses

“…In recent years, newer non-vitamin K dependent anticoagulants (NOACs) have appeared that provide an effective and comfortable alternative to VKAs [22]. Acetylsalicylic acid is also a common drug in use today [23]. All of them pose a challenge for the operating surgeons, as well as for the attending internists, cardiologists or neurologists.…”

Effects of Medium Molecular Weight Heparinyl Phenylalnine on Superoxide Dismutase Activity in Mice

“…Recently, participation of free radicals is reported in several diseases, such as in the cardiovascular system (14), Alzheimer's disease (15), arteriosclerosis (16), myocardial infarction (17), cerebral infarction (18), Parkinson's disease (19), pancreatitis (20), glomerulonephritis (21), diabetes (22), cirrhosis (23), stomach ulcers (24), atopic dermatitis (25) and asthma (26,27). Although the research on EC-SOD is advanced and several radical scavengers are under in vivo 30: 841-844 (2016) development, the number of ethical drugs is few.…”

What we know about nonsteroidal anti-inflammatory drug hypersensitivity

“…NHS reactions can be subdivided as cross-reactive, in which the cyclooxygenase 1 (COX-1) pathway is inhibited, or selective, resulting from an immunological (allergic) reaction to the drugs and characterized by IgE-mediated (acute) or T cell-mediated (delayed) reactions [ 2 , 11 - 13 ]. In addition, novel mechanisms related to oxidative stress and platelet activation that could contribute to the pathogenesis of NHS have been reported [ 14 - 17 ].…”

“…By suppressing COX-1 activity, aspirin and some classical NSAIDs inhibit the synthesis of PGs, especially PGE 2 ; thereby, increasing the production of CysLTs (LTA 4 , LTB 4 , LTC 4 , LTD 4 ) [ 2 , 17 , 23 , 24 ]. PGEE 2 has a protective effect against bronchoconstriction, releases inflammatory mediators from mast cells, and recruits immune cells to inflammatory sites [ 25 , 26 ].…”

“…For example, Antczak et al [ 44 ] showed that the levels of 8-isoprostanes, metabolized products from AA that are induced by reactive oxygen species, are increased in the exhaled breath condensate of patients with NERD [ 45 ], suggesting a role of oxidative stress in NHS. Moreover, aspirin can trigger apoptosis by inducing oxidative stress as well as by inhibiting expression of the anti-apoptotic protein, Beclin-2 (Bcl2) [ 17 ]. NSAIDs may reduce Bcl2 expression by blocking the IL6-IL6R-STAT3 signaling pathway.…”