PMID- 36610760
OWN - NLM
STAT- MEDLINE
DCOM- 20230110
LR  - 20230208
IS  - 2213-2201 (Electronic)
VI  - 11
IP  - 1
DP  - 2023 Jan
TI  - Urticaria and Angioedema: Understanding Complex Pathomechanisms to Facilitate 
      Patient Communication, Disease Management, and Future Treatment.
PG  - 94-106
LID - S2213-2198(22)01192-8 [pii]
LID - 10.1016/j.jaip.2022.11.006 [doi]
AB  - Chronic spontaneous urticaria (CSU) is primarily a T2-dominant disease with a 
      complex genetic background. Skin mast cell activation can be induced not only via 
      the IgE-FcepsilonRI axis but also from several other distinct mechanisms, molecules, 
      and receptors involved in CSU onset, persistence, and exacerbation. These include 
      autoallergy, autoimmunity, central or peripheral neuroimmune dysregulation, 
      activation of both extrinsic and intrinsic coagulation pathways, and microbial 
      infections. Besides mast cells, recent reports suggest the active and direct 
      involvement of basophils and eosinophils. Several biological characteristics or 
      biomarkers have been linked with CSU's known endotypes and may help forecast 
      therapeutic responses. The introduction of biologic therapy for CSU has been a 
      major advance in the last 10 years. The cornerstone of angioedema (AE) 
      pathogenesis is increased vascular permeability and plasma leakage into the 
      deeper dermis and subcutis, either mediated by histamine or bradykinin (BK). 
      C1-inhibitor deficiency, hereditary or acquired, is the primary cause of 
      BK-mediated AE due to increased plasma BK concentration. Other complex conditions 
      have been identified, with some likely involving contact system dysregulation and 
      other putative mechanisms related to vascular endothelial dysfunction. The 
      approval of multiple hereditary-AE-specific therapies for both prevention and 
      acute attacks has revolutionized treatment of this disease. Any new knowledge of 
      the pathogenesis of CSU and AE offers the opportunity to improve patient 
      information, physician-patient communication, prediction of therapeutic 
      responses, selection of precise tailor-made treatment for each patient, and 
      exploration of novel treatment options for those who do not achieve disease 
      control with current medications.
CI  - Copyright (c) 2022 American Academy of Allergy, Asthma & Immunology. Published by 
      Elsevier Inc. All rights reserved.
FAU - Konstantinou, George N
AU  - Konstantinou GN
AD  - Department of Allergy and Clinical Immunology, 424 General Military Training 
      Hospital, Thessaloniki, Greece. Electronic address: gnkonstantinou@gmail.com.
FAU - Riedl, Marc A
AU  - Riedl MA
AD  - US HAEA Angioedema Center, Division of Rheumatology, Allergy and Immunology, 
      University of California San Diego, La Jolla, Calif.
FAU - Valent, Peter
AU  - Valent P
AD  - Department of Internal Medicine I, Division of Hematology and Hemostaseology, 
      Medical University of Vienna, Vienna, Austria; Ludwig Boltzmann Institute for 
      Hematology and Oncology, Medical University of Vienna, Vienna, Austria.
FAU - Podder, Indrashis
AU  - Podder I
AD  - Department of Dermatology, College of Medicine and Sagore Dutta Hospital, 
      Kolkata, West Bengal, India.
FAU - Maurer, Marcus
AU  - Maurer M
AD  - Institute of Allergology, Charite-Universitatsmedizin Berlin, corporate member of 
      Freie Universitat Berlin and Humboldt-Universitat zu Berlin, Berlin, Germany; 
      Fraunhofer Institute for Translational Medicine and Pharmacology ITMP, 
      Allergology and Immunology, Berlin, Germany.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Allergy Clin Immunol Pract
JT  - The journal of allergy and clinical immunology. In practice
JID - 101597220
RN  - S8TIM42R2W (Bradykinin)
SB  - IM
MH  - Humans
MH  - *Urticaria/drug therapy
MH  - *Angioedema/therapy
MH  - *Angioedemas, Hereditary
MH  - *Chronic Urticaria
MH  - Bradykinin/therapeutic use/metabolism
MH  - Communication
MH  - Disease Management
MH  - Chronic Disease
OTO - NOTNLM
OT  - Angioedema
OT  - Autoallergy
OT  - Autoimmunity
OT  - Basophils
OT  - Bradykinin
OT  - C1-inhbitor
OT  - Coagulation
OT  - Communication
OT  - Cytokines
OT  - Eosinophils
OT  - Hereditary
OT  - Histamine
OT  - Management
OT  - Mast cells
OT  - Mediators
OT  - Mutations
OT  - Neuroinflammation
OT  - Novel
OT  - Pathogenesis
OT  - Urticaria
EDAT- 2023/01/08 06:00
MHDA- 2023/01/11 06:00
CRDT- 2023/01/07 20:56
PHST- 2022/09/08 00:00 [received]
PHST- 2022/10/29 00:00 [revised]
PHST- 2022/11/01 00:00 [accepted]
PHST- 2023/01/07 20:56 [entrez]
PHST- 2023/01/08 06:00 [pubmed]
PHST- 2023/01/11 06:00 [medline]
AID - S2213-2198(22)01192-8 [pii]
AID - 10.1016/j.jaip.2022.11.006 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol Pract. 2023 Jan;11(1):94-106. doi: 
      10.1016/j.jaip.2022.11.006.