scholarly journals Synergistic inhibition of type I allergic reactions by leukotriene (LT) D4/E4 and LTB4 receptor antagonists

1998 ◽  
Vol 76 ◽  
pp. 100
Author(s):  
Mamoru Kodani ◽  
Masayoshi Abe ◽  
Tsugutomo Sakurada ◽  
Noriyuki Sakata ◽  
Hiro-o Kamiya ◽  
...  
2020 ◽  
pp. 40-50
Author(s):  
A. Nikitina

Analysis of literature data presented in search engines — Elibrary, PubMed, Cochrane — concerning the risk of developing type I allergic reactions in patients with blood diseases is presented. It is shown that the most common cause of type I allergic reactions is drugs included in the treatment regimens of this category of patients. The article presents statistics on the increase in the number of drug allergies leading to cases of anaphylactic shock in patients with blood diseases. Modern methods for the diagnosis of type I allergic reactions in vivo and in vitro are considered.


Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1615
Author(s):  
Zhongwei Zhang ◽  
Yosuke Kurashima

It is well known that mast cells (MCs) initiate type I allergic reactions and inflammation in a quick response to the various stimulants, including—but not limited to—allergens, pathogen-associated molecular patterns (PAMPs), and damage-associated molecular patterns (DAMPs). MCs highly express receptors of these ligands and proteases (e.g., tryptase, chymase) and cytokines (TNF), and other granular components (e.g., histamine and serotonin) and aggravate the allergic reaction and inflammation. On the other hand, accumulated evidence has revealed that MCs also possess immune-regulatory functions, suppressing chronic inflammation and allergic reactions on some occasions. IL-2 and IL-10 released from MCs inhibit excessive immune responses. Recently, it has been revealed that allergen immunotherapy modulates the function of MCs from their allergic function to their regulatory function to suppress allergic reactions. This evidence suggests the possibility that manipulation of MCs functions will result in a novel approach to the treatment of various MCs-mediated diseases.


1980 ◽  
Vol 2 (3) ◽  
pp. 264 ◽  
Author(s):  
Y. Maruyama ◽  
M. Terasawa ◽  
K. Goto ◽  
Y. Kadobe ◽  
Y. Shiokawa ◽  
...  
Keyword(s):  
Type I ◽  

1993 ◽  
Vol 39 (S1) ◽  
pp. C11-C13 ◽  
Author(s):  
T. D. Penning ◽  
S. W. Djuric ◽  
S. H. Docter ◽  
S. S. Yu ◽  
D. Spangler ◽  
...  

1986 ◽  
Vol 40 ◽  
pp. 229
Author(s):  
Hisashi Kuriki ◽  
Haruhiko Makino ◽  
Taketoshi Saijo ◽  
Yasuko Ashida ◽  
Yoshitaka Maki
Keyword(s):  
Type I ◽  

2014 ◽  
Vol 92 (5) ◽  
pp. 420-424 ◽  
Author(s):  
Boris K. Pliyev ◽  
Tatyana V. Dimitrieva ◽  
Valery G. Savchenko

Diadenosine polyphosphates have been shown to inhibit neutrophil apoptosis, but mechanisms of the antiapoptotic effect are not known. Diadenosine diphosphate (Ap2A) is the simplest naturally occurring diadenosine polyphosphate, and its effect on neutrophil apoptosis has not previously been investigated. Here we report that Ap2A delays spontaneous apoptosis of human neutrophils, and the effect is reversed by the adenosine A2A receptor antagonists SCH442416 and ZM241385. Ap2A induced an elevation of intracellular cAMP and the elevation was blocked by the adenosine A2A receptor antagonists. The antiapoptotic effect of Ap2A was abrogated by 2′,5′-dideoxyadenosine, an inhibitor of adenylyl cyclase, and Rp-8-Br-cAMPS, an inhibitor of type I cAMP-dependent protein kinase A (PKA). Together, these results demonstrate that Ap2A delays neutrophil apoptosis via the adenosine A2A receptor and cAMP/PKA signaling axis.


2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 13574-13574
Author(s):  
M. Suenaga ◽  
N. Mizunuma ◽  
T. Watanabe ◽  
K. Hatake ◽  
T. Muto

13574 Background: Oxaliplatin is a well-known platinum compound as a key agent of FOLFOX regimen, the world standard chemotherapy in colorectal cancer. Allergic reaction due to oxaliplatin is a chronic adverse event regarded as almost type I allergy. In our institute, we have also experienced allergic reaction including severe cases and started to apply practical preventive approach to the patients treated with FOLFOX regimens. Methods: Preventive approach was as follows: 40mg of famotidine and 8mg of dexamethasone before oxaliplatin infusion were given to all patients from the initial cycle and 50mg of diphenhydramine after cycle 4. Further intensive anti-allergic procedure was performed for the patients who showed any allergic reactions against initial preventive approach. Increased dose of dexamethasone to 20mg and diphenhydramine were administered before oxaliplatin infusion and oxaliplatin was prolonged from 2 up to 4 hours for patients with grade 1, 2 allergic reactions (CTCAE v3.0). Treatment was discontinued in patients with severe grade 3 adverse events. Results: 139 patients received FOLFOX regimens during 6 months. 15 patients (10.8%) presented with allergic reaction, 11 (73.3%) of those were grade 1, 2 and the other 4 (26.7%) were grade 3. Immediate discontinuation of oxaliplatin infusion and administration of antihistaminic drugs, steroid or rapid infusion were routine proceeding, and almost of the patients entirely recovered within 2 hours. 9 patients were re-exposed to oxaliplatin using the preventive approach and grade1 reaction appeared in 3 patients (33.3%) again. Conclusions: Our initial preventive approach was effective to reduce the incidence of allergy, severe adverse events. And further intensive anti-allergic procedure contributed to re-expose to oxaliplatin. No significant financial relationships to disclose.


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