Date of Presentation
5-2-2024 12:00 AM
College
Rowan-Virtua School of Osteopathic Medicine
Poster Abstract
Angioedema is defined as a non-pitting edema that involves the subcutaneous layer and additionally may include submucosal layers of tissue which pertain to the face, oral cavity, larynx, lips, extremities and gastrointestinal tract; this becomes a life-threatening situation particularly when there is involvement of the larynx. Angioedema may be classified as either histamine-mediated or bradykinin-mediated. Histamine-mediated, associated with mast-cell and basophil activation, is the most common. Bradykinin-mediated (secondary to hereditary, acquired C1-inhibitor deficiency, ACEI-associated angioedema) occur when an allergic reaction and hives will not trigger this reaction. The C1-inhibitor is a regular of the complement system and either dysfunction or lack thereof of the inhibitor itself will result in an excess of kallikrein, which results in the proteolysis of high-molecular-weight kininogen and bradykinin; this cascade leads to increased edema and vascular permeability. Associated angioedema results from the decreased degradation of bradykinin. This spiral cascade involving plasmin, XIIa and kallikrein leads to generation of bradykinin and edema. Since this process is not clearly a distinct disease, nor simply a syndrome, we refer to it as a phenomenon.
Keywords
Quincke's Edema, Angioedema, Angiotensin-Converting Enzyme Inhibitors, ACE Inhibitors, Uvula, Adverse Drug Reaction
Disciplines
Emergency Medicine | Medicine and Health Sciences | Pathological Conditions, Signs and Symptoms | Pharmaceutical Preparations | Stomatognathic System
Document Type
Poster
Included in
Emergency Medicine Commons, Pathological Conditions, Signs and Symptoms Commons, Pharmaceutical Preparations Commons, Stomatognathic System Commons
Quincke’s Phenomenon – The ACE Inhibitor Culprit
Angioedema is defined as a non-pitting edema that involves the subcutaneous layer and additionally may include submucosal layers of tissue which pertain to the face, oral cavity, larynx, lips, extremities and gastrointestinal tract; this becomes a life-threatening situation particularly when there is involvement of the larynx. Angioedema may be classified as either histamine-mediated or bradykinin-mediated. Histamine-mediated, associated with mast-cell and basophil activation, is the most common. Bradykinin-mediated (secondary to hereditary, acquired C1-inhibitor deficiency, ACEI-associated angioedema) occur when an allergic reaction and hives will not trigger this reaction. The C1-inhibitor is a regular of the complement system and either dysfunction or lack thereof of the inhibitor itself will result in an excess of kallikrein, which results in the proteolysis of high-molecular-weight kininogen and bradykinin; this cascade leads to increased edema and vascular permeability. Associated angioedema results from the decreased degradation of bradykinin. This spiral cascade involving plasmin, XIIa and kallikrein leads to generation of bradykinin and edema. Since this process is not clearly a distinct disease, nor simply a syndrome, we refer to it as a phenomenon.