Angioedema: Difference between revisions

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==Risk Factors==
==Risk Factors==
*Common risk factors in the development of [disease name] are [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
*Common risk factors in the development of angioedema are previous history of allergic reactions, family history of allergic reactions, and other autoimmune disorders (atopia, eczema, etc).
   
   
== Natural History, Complications and Prognosis==
== Natural History, Complications and Prognosis==

Revision as of 15:52, 1 November 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Historical Perspective

Historical Perspective

Classification

Classification

Angioedema can be classified into the following types:[3] [4]

  • Allergic angioedema
  • Bradykinin mediated angioedema
    • Drug induced angioedema
    • Hereditary angioedema
      • Type 1 - decreased levels of C1INH (85%);
      • Type 2 - normal levels but decreased function of C1INH (15%);
      • Type 3 - no detectable abnormality in C1INH, occurs in an X-linked dominant fashion and therefore mainly affects women; it can be exacerbated by pregnancy and use of hormonal contraception (originally described by Bork et al in 2000, exact frequency uncertain).It has been linked with mutations in the factor XII gene.
  • Acquired angioedema

Pathophysiology

Allergic reaction is a life-threatening cause of angioedema. Allergic reaction involves detection of a foreign substance by the immune system that results in histamine release into the bloodstream. The cause of angioedema cannot be identified in many cases. The following may cause angioedema:

Hives and angioedema may also occur after infections or with other illnesses (including autoimmune disorders such as lupus, leukemia and lymphoma). A form of angioedema runs in families and has different triggers, complications, and treatments. This is called hereditary angioedema.

Pathophysiology

  • The progression to angioedema usually involves the pathway leading to activation of bradykinin.[6][7]
  • Bradykinin is a molecular peptide that causes vasodialtion. Bradykinin mediated vasodilation results in rapid fluid accumulation in the interstitial space resulting in edema of the underlying tissue. Bradykinin is a known pain mediator and in addition to pain can be released in response to various different stimuli.
  • Angioedema can also be mediated by mechanisms that interfere with bradykinin production or metabolism. ACE is one of the enzymes that degrades bradykinin and is blocked by ACE nhibitors, can result in angioedema as a medication side effect.
  • A hereditary defeciency of C1-esterase inhibitor (C1INH) results in continuous activation of complement system resulting in excess production of bradykinin and kallikrein. C1-esterase inhibitor (C1INH) inhibits the conversion of C1 to C1r and C1s, which in turn activates other proteins of the complement system.
  • Angioedema can also be due to an autoimmune disorder that results in antibody formation against C1INH. This is a type of acquired angioedema and is associated with the development of lymphoma.
  • An episode of angioedema can be triggered in susceptible individuals as a result of consumption of foods that are vasodilators like alcohol and cinnamon. Medication like ibuprofen, acetaminophen and aspirin can increase the probability of an episode in some patients.

Clinical Features

Differentiating [disease name] from other Diseases

  • The following table outlines the differential diagnosis of various types of angioedema:
Concentration of C1-esterase inhibitor Function of C1-esterase inhibitor C4 Tryptase
Hereditary angioedema type I Normal
Hereditary angioedema type II N/ Normal
Hereditary angioedema type III Normal Normal Normal Normal
Acquired Angioedema Normal
ACE inhibitor induced Angioedema Normal Normal Normal Normal
Anaphylaxis Normal Normal Normal N/

Angioedema should be differentiated from:

  • Acute Urticaria
  • Anaphylaxis
  • Food Allergy
  • Drug allergy

Risk Factors

  • Common risk factors in the development of angioedema are previous history of allergic reactions, family history of allergic reactions, and other autoimmune disorders (atopia, eczema, etc).

Natural History, Complications and Prognosis

  • The majority of patients with [disease name] remain asymptomatic for [duration/years].
  • Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
  • If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
  • Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
  • Prognosis is generally [excellent/good/poor], and the [1/5/10­year mortality/survival rate] of patients with [disease name] is approximately [#%].

Diagnosis

Diagnostic Criteria

  • The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met:
  • [criterion 1]
  • [criterion 2]
  • [criterion 3]
  • [criterion 4]

Symptoms

  • [Disease name] is usually asymptomatic.
  • Symptoms of [disease name] may include the following:
  • [symptom 1]
  • [symptom 2]
  • [symptom 3]
  • [symptom 4]
  • [symptom 5]
  • [symptom 6]

Physical Examination

  • Patients with [disease name] usually appear [general appearance].
  • Physical examination may be remarkable for:
  • [finding 1]
  • [finding 2]
  • [finding 3]
  • [finding 4]
  • [finding 5]
  • [finding 6]

Laboratory Findings

  • There are no specific laboratory findings associated with [disease name].
  • A [positive/negative] [test name] is diagnostic of [disease name].
  • An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
  • Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

Imaging Findings

  • There are no [imaging study] findings associated with [disease name].
  • [Imaging study 1] is the imaging modality of choice for [disease name].
  • On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
  • [Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

  • [Disease name] may also be diagnosed using [diagnostic study name].
  • Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].

Treatment

Medical Therapy

  • There is no treatment for [disease name]; the mainstay of therapy is supportive care.
  • The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
  • [Medical therapy 1] acts by [mechanism of action 1].
  • Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].

Surgery

  • Surgery is the mainstay of therapy for [disease name].
  • [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
  • [Surgical procedure] can only be performed for patients with [disease stage] [disease name].

Prevention

  • There are no primary preventive measures available for [disease name].
  • Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
  • Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].

References

  1. Quincke H. Concerning the acute localized oedema of the skin. Monatsh Prakt Derm 1882;1:129-131.
  2. Osler W. Hereditary angio-neurotic oedema. Am J Med Sci 1888;95:362-67.
  3. Bork K, Barnstedt SE, Koch P, Traupe H. Hereditary angioedema with normal C1-inhibitor activity in women. Lancet 2000;356:213-7. PMID 10963200.
  4. Cichon S, Martin L, Hennies HC; et al. (2006). "Increased activity of coagulation factor XII (Hageman factor) causes hereditary angioedema type III". Am. J. Hum. Genet. 79 (6): 1098–104. doi:10.1086/509899. PMID 17186468.
  5. https://www.ncbi.nlm.nih.gov/pubmed/?term=types+of+angioedema. Missing or empty |title= (help)
  6. Kaplan AP (June 2008). "Angioedema". World Allergy Organ J. 1 (6): 103–13. doi:10.1097/WOX.0b013e31817aecbe. PMC 3651192. PMID 23282406.
  7. Champion RH, Roberts SO, Carpenter RG, Roger JH (August 1969). "Urticaria and angio-oedema. A review of 554 patients". Br. J. Dermatol. 81 (8): 588–97. PMID 5801331.

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