Acetylsalicylic acid challenge optimal dose in nonsteroidal anti‐inflammatory drugs hypersensitivity diagnosis

Allergy ◽  
2020 ◽  
Vol 75 (6) ◽  
pp. 1501-1503 ◽  
Author(s):  
Natalia Pérez‐Sánchez ◽  
José Antonio Cornejo‐García ◽  
Gádor Bogas‐Herrera ◽  
María José Torres Jaén ◽  
Inmaculada Doña Díaz
2020 ◽  
Vol 4 (01) ◽  
pp. 135-143
Author(s):  
Ulrike Förster-Ruhrmann ◽  
Anne-Kristin Tietz ◽  
Jonghui Kim ◽  
Uta Liebers ◽  
Agnieszka J. Szczepek ◽  
...  

2020 ◽  
Vol 145 (2) ◽  
pp. AB92
Author(s):  
Natalia Perez-Sanchez ◽  
Francisca Gomez Perez ◽  
Raquel Jurado Escobar ◽  
Maria Auxiliadora Guerrero ◽  
Jose Cornejo-Garcia ◽  
...  

2021 ◽  
Vol 23 (3) ◽  
Author(s):  
V. V. Buheruk ◽  
O. B. Voloshyna ◽  
L. I. Kovalchuk ◽  
I. V. Balashova ◽  
O. V. Naidionova

The aim of this review is to analyze and summarize the existing evidence regarding the possibilities of using acetylsalicylic acid (ASA) and other non-steroidal anti-inflammatory drugs (NSAIDs) to reduce cancer risk. Conclusions. Chronic inflammation facilitates the onset and progress of tumour growth. Anti-cancer properties of acetylsalicylic acid and other non-steroidal anti-inflammatory drugs are mediated via cyclooxygenase COX-dependent mechanisms, as well as other tumorigenic pathways. Current systematic review addresses potential role of ASA and other NSAIDs in reduction of cancer risk for the following localizations: head and neck, lungs, gastrointestinal tract, breast, ovaries, prostate, and skin. The role of ASA in primary prevention of colorectal cancer in specific populations is presented in 2016 U. S. Preventive Services Task Force guidelines. Studies indicate heterogeneous protective potential of ASA against different cancer types, depending on studied population, duration of intake and dose. Influence of non-aspirin NSAIDs on cancer morbidity and mortality is more controversial.


1994 ◽  
Vol 22 (2) ◽  
pp. 100-106 ◽  
Author(s):  
G Hasçelik ◽  
B ŞLener ◽  
Z Hasçelik

The effects of piroxicam, tenoxicam, diclofenac sodium, acetylsalicylic acid and tiaprofenic acid on the chemotaxis and random migration of human polymorphonuclear leukocytes were investigated, using zymosan-activated serum as chemo-attractant, with a modified Boyden chamber technique. All five compounds significantly reduced chemotaxis. The random migration of polymorphonuclear leukocytes was inhibited by piroxicam, diclofenac sodium and tiaprofenic acid but not by tenoxicam or acetylsalicylic acid. The inhibitory effect of these non-steroidal anti-inflammatory drugs on polymorphonuclear leukocyte chemotaxis and on random migration was generally dose-dependent. The results suggest that the drugs studied may have a direct effect on polymorphonuclear leukocyte chemotaxis and that this activity may contribute to their anti-inflammatory properties.


2012 ◽  
Vol 108 (07) ◽  
pp. 183-190 ◽  
Author(s):  
Andreas Kurth ◽  
Andreas Clemens ◽  
Herbert Noack ◽  
Bengt Eriksson ◽  
Joseph Caprini ◽  
...  

SummaryPatients undergoing total hip or knee arthroplasty should receive anticoagulant therapy because of the high risk of venous thromboembolism. However, many are already taking non-steroidal anti-inflammatory drugs (NSAIDs) or acetylsalicylic acid (ASA) that can have antihaemostatic effects. We assessed the bleeding risk in patients treated with thromboprophylactic dabigatran etexilate, with and without concomitant NSAID or ASA. A post-hoc analysis was undertaken of the pooled data from trials comparing dabigatran etexilate (220 mg and 150 mg once daily) and enoxaparin. Major bleeding event (MBE) rates were determined and odds ratios (ORs) generated for patients who received study treatment plus NSAID (half-life ≤12 hours) or ASA (≤160 mg/day) versus study treatment alone. Relative risks were calculated for comparisons between treatments. Overall, 4,405/8,135 patients (54.1%) received concomitant NSAID and 386/8,135 (4.7%) received ASA.ORs for the comparison with/without concomitant NSAID were 1.05 (95% confidence interval [CI] 0.55–2.01) for 220 mg dabigatran etexilate; 1.19 (0.55–2.55) for 150 mg; and 1.32 (0.67–2.57) for enoxaparin. ORs for the comparison with/without ASA were 1.14 (0.26–5.03); 1.64 (0.36–7.49); and 2.57 (0.83–7.94), respectively. For both NSAIDs and ASA there was no significant difference in bleeding between patients with and without concomitant therapy in any treatment arm. Patients concomitantly taking NSAIDs or ASA have a similar risk of MBE to those taking dabigatran etexilate alone. No significant differences in MBE were detected between dabigatran etexilate and enoxaparin within comedication subgroups, suggesting that no increased major bleeding risk exists when dabigatran etexilate is administered with NSAID or ASA.Investigation performed at multiple centres participating in the RE-MODEL™, RE-NOVATE®, and RE-MOBILIZE® trials.


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