Poster: Idiopathic Angioedema: A Subtle Presentation

Velen Tat; Christopher Forest

Poster: Idiopathic Angioedema: A Subtle Presentation

Velen Tat, Christopher Forest

California State University, Monterey Bay

Research output: Contribution to conference › Presentation

Abstract

      Idiopathic Allergic Angioedema (AE)     is the most common form and is a diagnosis of exclusion 
   §    Focal swelling develops rapidly and peak in 5 hours 
   §    Mostly affects the face while sparing the gastrointestinal and laryngeal mucosa4 
   §    Ig-E-mediated Type 1 reaction; mast cells release histamine or vasoactive mediators 
   §    Antihistamine and corticosteroids are the mainstay treatment of idiopathic AE 
 
      C1 esterase inhibitor deficiency    (C1-INH) is the most common form of hereditary AE  
   §    Abnormal complement cascade resulting in unregulated activity of vasoactive mediators bradykinin, kallikreins and plasmin.  
   §    Prevalence: 1/10,000 – 100,000.3 
   §    Bradykinin causes skin, upper respiratory airways and gastrointestinal tract symtpoms 
   §    Order C1 INH and C4 for patients with family history of AE or suspect C1-INH deficiency 
   §    Antihistamines, glucocorticosteroids, and epinephrine have little to no effect hereditary AE 
   §    Treatment of choice is plasma-derived C1-INH concentrate 
 
   ACEI AE is a well-documented pharmaceutical side effect that initiates unregulated bradykinin production causing edema in the face, lips, eyelids, tongue, neck and upper airways with airway obstruction dangers. The incidence is highest (25%) within the first month of starting medication but may present years after use.2ACEI AE occurs in less than 1% patients taking ACEI therapy.4 Epinephrine is used for laryngeal edema and anaphylaxis. Definite treatment is the discontinuation of the offending agent.  
 
   Successful AE management requires detection and avoidance of triggers, early recognition of acute attacks, and aggressive airway management. The most common type of AE is idiopathic and responds to antihistamine and corticosteroids. If the patient is not responding to treatment, consider hereditary or medication induced AE.  

Original language	American English
State	Published - May 2016
Event	American Academy of Physician Assistants / 40th Annual Conference - San Antonio, TX Duration: May 1 2016 → …

Conference

Conference	American Academy of Physician Assistants / 40th Annual Conference
Period	5/1/16 → …

Keywords

ACE Inhibitor
Angioedema
Dermatology

Disciplines

Medicine and Health Sciences

Access to Document

201600083 Tat Forest Angioedema.pdfFinal published version, 479 KBLicense: Unspecified

Cite this

@conference{1c4df9dba70e484a9cbd7a587f2b1d5f,

title = "Poster: Idiopathic Angioedema: A Subtle Presentation",

abstract = " Idiopathic Allergic Angioedema (AE) is the most common form and is a diagnosis of exclusion § Focal swelling develops rapidly and peak in 5 hours § Mostly affects the face while sparing the gastrointestinal and laryngeal mucosa4 § Ig-E-mediated Type 1 reaction; mast cells release histamine or vasoactive mediators § Antihistamine and corticosteroids are the mainstay treatment of idiopathic AE C1 esterase inhibitor deficiency (C1-INH) is the most common form of hereditary AE § Abnormal complement cascade resulting in unregulated activity of vasoactive mediators bradykinin, kallikreins and plasmin. § Prevalence: 1/10,000 – 100,000.3 § Bradykinin causes skin, upper respiratory airways and gastrointestinal tract symtpoms § Order C1 INH and C4 for patients with family history of AE or suspect C1-INH deficiency § Antihistamines, glucocorticosteroids, and epinephrine have little to no effect hereditary AE § Treatment of choice is plasma-derived C1-INH concentrate ACEI AE is a well-documented pharmaceutical side effect that initiates unregulated bradykinin production causing edema in the face, lips, eyelids, tongue, neck and upper airways with airway obstruction dangers. The incidence is highest (25%) within the first month of starting medication but may present years after use.2ACEI AE occurs in less than 1% patients taking ACEI therapy.4 Epinephrine is used for laryngeal edema and anaphylaxis. Definite treatment is the discontinuation of the offending agent. Successful AE management requires detection and avoidance of triggers, early recognition of acute attacks, and aggressive airway management. The most common type of AE is idiopathic and responds to antihistamine and corticosteroids. If the patient is not responding to treatment, consider hereditary or medication induced AE. ",

keywords = "ACE Inhibitor, Angioedema, Dermatology",

author = "Velen Tat and Christopher Forest",

year = "2016",

month = may,

language = "American English",

note = "American Academy of Physician Assistants / 40th Annual Conference ; Conference date: 01-05-2016",

}

TY - CONF

T1 - Poster: Idiopathic Angioedema: A Subtle Presentation

AU - Tat, Velen

AU - Forest, Christopher

PY - 2016/5

Y1 - 2016/5

N2 - Idiopathic Allergic Angioedema (AE) is the most common form and is a diagnosis of exclusion § Focal swelling develops rapidly and peak in 5 hours § Mostly affects the face while sparing the gastrointestinal and laryngeal mucosa4 § Ig-E-mediated Type 1 reaction; mast cells release histamine or vasoactive mediators § Antihistamine and corticosteroids are the mainstay treatment of idiopathic AE C1 esterase inhibitor deficiency (C1-INH) is the most common form of hereditary AE § Abnormal complement cascade resulting in unregulated activity of vasoactive mediators bradykinin, kallikreins and plasmin. § Prevalence: 1/10,000 – 100,000.3 § Bradykinin causes skin, upper respiratory airways and gastrointestinal tract symtpoms § Order C1 INH and C4 for patients with family history of AE or suspect C1-INH deficiency § Antihistamines, glucocorticosteroids, and epinephrine have little to no effect hereditary AE § Treatment of choice is plasma-derived C1-INH concentrate ACEI AE is a well-documented pharmaceutical side effect that initiates unregulated bradykinin production causing edema in the face, lips, eyelids, tongue, neck and upper airways with airway obstruction dangers. The incidence is highest (25%) within the first month of starting medication but may present years after use.2ACEI AE occurs in less than 1% patients taking ACEI therapy.4 Epinephrine is used for laryngeal edema and anaphylaxis. Definite treatment is the discontinuation of the offending agent. Successful AE management requires detection and avoidance of triggers, early recognition of acute attacks, and aggressive airway management. The most common type of AE is idiopathic and responds to antihistamine and corticosteroids. If the patient is not responding to treatment, consider hereditary or medication induced AE.

AB - Idiopathic Allergic Angioedema (AE) is the most common form and is a diagnosis of exclusion § Focal swelling develops rapidly and peak in 5 hours § Mostly affects the face while sparing the gastrointestinal and laryngeal mucosa4 § Ig-E-mediated Type 1 reaction; mast cells release histamine or vasoactive mediators § Antihistamine and corticosteroids are the mainstay treatment of idiopathic AE C1 esterase inhibitor deficiency (C1-INH) is the most common form of hereditary AE § Abnormal complement cascade resulting in unregulated activity of vasoactive mediators bradykinin, kallikreins and plasmin. § Prevalence: 1/10,000 – 100,000.3 § Bradykinin causes skin, upper respiratory airways and gastrointestinal tract symtpoms § Order C1 INH and C4 for patients with family history of AE or suspect C1-INH deficiency § Antihistamines, glucocorticosteroids, and epinephrine have little to no effect hereditary AE § Treatment of choice is plasma-derived C1-INH concentrate ACEI AE is a well-documented pharmaceutical side effect that initiates unregulated bradykinin production causing edema in the face, lips, eyelids, tongue, neck and upper airways with airway obstruction dangers. The incidence is highest (25%) within the first month of starting medication but may present years after use.2ACEI AE occurs in less than 1% patients taking ACEI therapy.4 Epinephrine is used for laryngeal edema and anaphylaxis. Definite treatment is the discontinuation of the offending agent. Successful AE management requires detection and avoidance of triggers, early recognition of acute attacks, and aggressive airway management. The most common type of AE is idiopathic and responds to antihistamine and corticosteroids. If the patient is not responding to treatment, consider hereditary or medication induced AE.

KW - ACE Inhibitor

KW - Angioedema

KW - Dermatology

M3 - Presentation

T2 - American Academy of Physician Assistants / 40th Annual Conference

Y2 - 1 May 2016

ER -