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An overview of angioedema: Pathogenesis and causes

An overview of angioedema: Pathogenesis and causes
Author:
Bruce Zuraw, MD
Section Editor:
Sarbjit Saini, MD
Deputy Editor:
Anna M Feldweg, MD
Literature review current through: Jan 2024.
This topic last updated: Jun 29, 2023.

INTRODUCTION — Angioedema is self-limited, localized swelling of the skin or mucosal tissues, which results from extravasation of fluid into the interstitium due to a loss of vascular integrity. Angioedema may occur in isolation, accompanied by urticaria, or as a component of anaphylaxis.

The pathogenesis and causes of angioedema will be reviewed here. The clinical features, diagnosis, differential diagnosis, and management of acute angioedema are discussed separately. (See "An overview of angioedema: Clinical features, diagnosis, and management".)

EPIDEMIOLOGY — Data regarding the epidemiology of angioedema are limited, although it affects both adults and children and is not a rare disorder. In a retrospective review of all hospital admissions in New York State over 13 years, angioedema was the second most common "allergic" disease to necessitate hospitalization, exceeded only by asthma [1]. In this study, the number of angioedema hospitalizations per year more than doubled during the study period, suggesting that the prevalence may be increasing.

African Americans were disproportionately affected as they accounted for 42 percent of the admissions for angioedema but only 16 percent of the state's population.

The epidemiology of specific forms of angioedema, such as hereditary angioedema (HAE) due to C1 inhibitor (C1INH) deficiency, is discussed separately. (See "Hereditary angioedema: Epidemiology, clinical manifestations, exacerbating factors, and prognosis".)

PATHOGENESIS — Angioedema results from a loss of vascular integrity that allows fluid to move into tissues. Exposure of the vasculature to inflammatory mediators causes dilation and increased permeability of capillaries and venules. Fluid collects asymmetrically in the areas in which the vasculature has been altered, and these areas (eg, face, larynx, bowel wall) are not typically gravitationally dependent. Angioedema differs from the edema associated with cardiovascular, kidney, and liver disease (eg, heart failure, kidney failure, venous obstruction). Edema is usually due to an alteration in Starling's forces, such as an increase in intracapillary pressure or a reduction in the plasma oncotic pressure (ie, any cause of severe hypoalbuminemia) in the presence of normal vasculature. Edema affects gravitationally dependent parts of the body, and fluid collects symmetrically in those areas. (See "Pathophysiology and etiology of edema in adults".)

CAUSES — The known causes of angioedema can be subdivided into three groups, depending on the underlying mechanism (table 1):

Mast cell-mediated etiologies, in which angioedema results from release of mast cell-derived mediators that increase vascular permeability. Mast cell-mediated angioedema is associated with urticaria and/or pruritus in most cases.

Bradykinin-mediated etiologies, in which angioedema results from the generation of bradykinin, leads to increased vascular permeability. These forms of angioedema are not associated with urticaria and/or pruritus and are diagnosed and treated differently from other types of angioedema. (See "An overview of angioedema: Clinical features, diagnosis, and management".)

Etiologies of unknown mechanism.

Mast cell-mediated etiologies — Mast cell-mediated angioedema is associated with urticaria and/or pruritus in many instances. This form of angioedema is pathologically similar to urticaria, although it takes place in the deeper levels of the dermis and subcutaneous tissues, most often involving the face or mouth. Mast cells can be activated via several mechanisms (table 2). Activated mast cells release inflammatory mediators, including histamine, heparin, leukotriene C4, and prostaglandin D2, which cause dilation of venules in the dermis and enhance venule permeability with resultant tissue edema. (See "Mast cells: Development, identification, and physiologic roles" and "Mast cells: Surface receptors and signal transduction" and "Mast cell-derived mediators".)

Acute mast cell-mediated angioedema is treated with antihistamines and with epinephrine, if severe and accompanied by symptoms in other organ systems beyond the skin. The treatment of mast cell-mediated angioedema is discussed in detail separately. (See "An overview of angioedema: Clinical features, diagnosis, and management".)

Allergic reactions — Acute angioedema, with or without other symptoms of allergic reactions, may be triggered by foods, drugs, latex, exercise, the stings of various insects, and a growing list of other uncommon allergens (table 3). Angioedema is a common component of anaphylaxis, and, since anaphylaxis is treated differently from isolated angioedema (ie, with epinephrine), the clinician must be vigilant for other signs and symptoms of anaphylaxis (such as urticaria, pruritus, flushing, throat tightness, bronchospasm, and hypotension) in patients presenting with angioedema.

The classic type of allergic reaction results from immunoglobulin E (IgE) mediated, Gell and Coombs type I hypersensitivity (table 4). The reaction typically occurs within minutes to two hours following exposure to the trigger. However, some IgE-mediated allergic reactions are delayed in onset, such as allergic reactions to certain meats (lamb, beef, and/or pork) that can lead to reactions with prominent angioedema beginning two to six hours after ingestion [2]. (See "Anaphylaxis: Acute diagnosis" and "Food-induced anaphylaxis" and "Allergy to meats".)

Isolated angioedema is a relatively uncommon presentation of an allergic reaction. In a series of 112 patients with penicillin allergy confirmed by skin testing, only 1 patient had experienced isolated angioedema without urticaria during the presenting allergic reaction [3]. However, it can occur. Examples include reactions to nonsteroidal antiinflammatory drugs (NSAIDs). (See 'Aspirin and NSAIDs' below.)

Direct mast cell release — Mast cells can be nonspecifically stimulated to release their proinflammatory mediators by certain medications and pharmaceuticals, such as opiates and radiocontrast media. This type of angioedema is accompanied by urticaria in most cases. IgE is not involved, and skin testing or in vitro testing is rarely helpful. (See "Diagnosis and treatment of an acute reaction to a radiologic contrast agent".)

Aspirin and NSAIDs — Nonsteroidal antiinflammatory drugs (NSAIDs), such as aspirin and ibuprofen, can cause acute urticaria/angioedema and can exacerbate chronic urticaria/angioedema. There are six known types of hypersensitivity reactions to NSAIDs, which are often difficult to distinguish from one another based on clinical history alone (table 5). (See 'Chronic urticaria with or without angioedema' below and "NSAIDs (including aspirin): Allergic and pseudoallergic reactions".)

The more common type of NSAID reaction is believed to be due to the pharmacologic properties of the medications on mast cells. NSAIDs inhibit the enzyme cyclooxygenase 1 (COX-1), which mediates the generation of prostaglandins from arachidonic acid within mast cells and other leukocytes. NSAID administration results in increased formation of proinflammatory mediators, leading to angioedema in susceptible individuals. NSAIDs that nonselectively inhibit both COX-1 and COX-2 enzymes (aspirin, ibuprofen, and most others) can potentially induce this effect, and patients often react to multiple agents. Selective COX-2 inhibitors, such as celecoxib, are tolerated by most patients who have reacted to nonselective NSAIDs [4], although rare exceptions are reported [5]. Management of patients with these reactions is reviewed separately. (See "NSAIDs (including aspirin): Allergic and pseudoallergic reactions", section on 'Types 1 to 4: Treatment options'.)

NSAIDs can also cause rare IgE-mediated allergic reactions, which are typically triggered by a single agent. The diagnostic approach to NSAID reactions is reviewed separately. (See "NSAIDs (including aspirin): Allergic and pseudoallergic reactions".)

Chronic urticaria with or without angioedema — Chronic urticaria refers to urticaria that continues to recur for a period of six weeks or longer [6]. Angioedema is present in at least one-half of patients with chronic urticaria [7].

Chronic urticaria may persist over months to years and is more common in females, particularly between the ages of 40 and 50 years. In most cases of chronic urticaria/angioedema, a specific cause cannot be identified. This disorder is reviewed in more detail separately. (See "Chronic spontaneous urticaria: Clinical manifestations, diagnosis, pathogenesis, and natural history" and "Chronic spontaneous urticaria: Standard management and patient education".)

Bradykinin-mediated etiologies — Angioedema can occur due to vasodilation and increased vascular permeability resulting from other inflammatory mediators, especially bradykinin. Angioedema can result from either overproduction of bradykinin or inhibition of bradykinin degradation. Mast cells are not believed to be involved in this form of angioedema, and pruritus and urticaria are absent. Bradykinin-mediated angioedema, unlike histamine-mediated angioedema, frequently affects the gastrointestinal mucosa, leading to bowel wall edema and presenting with episodes of abdominal pain, nausea, vomiting, and/or diarrhea.

Perturbations in kinin pathways resulting directly from the actions of medications (eg, angiotensin-converting enzyme [ACE] inhibitors) or from deficiencies of C1 inhibitor (C1INH) are the main recognized causes of bradykinin-mediated angioedema. The treatment of bradykinin-induced angioedema is discussed separately. (See "An overview of angioedema: Clinical features, diagnosis, and management".)

Bradykinin-mediated angioedema does not respond to epinephrine, antihistamines, or glucocorticoids. Instead, this type of angioedema is treated with drugs that act on the bradykinin pathway (eg, icatibant, ecallantide, lanadelumab), preparations of C1INH concentrate (human), or plasma replacement (depending on the cause).

ACE inhibitors — Angiotensin-converting enzyme (ACE) inhibitors account for approximately 30 percent of all angioedema cases presenting to emergency departments in both community and tertiary care settings [8,9]. ACE inhibitors impair degradation of multiple peptides, including bradykinin and substance P (figure 1). Angioedema related to ACE inhibitors most often affects the lips, tongue, mouth, larynx, pharynx, and subglottic tissues. Urticaria and itching are absent. ACE inhibitors can also cause intestinal edema, and the sudden onset of abdominal pain, nausea, and sometimes vomiting in an older adult should prompt inquiries about the use of ACE inhibitors. The epidemiology, pathophysiology, diagnosis, and management of patients with ACE inhibitor-induced angioedema is discussed separately. (See "ACE inhibitor-induced angioedema".)

The risk of angioedema with the use of angiotensin II receptor blockers (ARBs), such as losartan, valsartan, and telmisartan, appears to be considerably lower than with ACE inhibitors [10-12]. The development of angioedema following therapy with ARBs is surprising since these drugs are not thought to affect kinin metabolism directly (figure 1). The administration of ARBs to a patient with past ACE inhibitor-induced angioedema is discussed separately. (See "ACE inhibitor-induced angioedema".)

ACE inhibitors and ARBs may also unmask deficiencies of C1INH [13-16].

DPP-4 inhibitors — Dipeptidyl peptidase 4 (DPP-4) inhibitors (ie, gliptins) can also inhibit degradation of bradykinin and substance P and have been associated with an increased risk of angioedema, especially when used together with immunosuppressive drugs or ACE inhibitors [17]. (See "ACE inhibitor-induced angioedema", section on 'Dipeptidyl peptidase-4 inhibitors'.)

Hereditary and acquired angioedema due to C1 inhibitor deficiency — Angioedema can occur in patients with abnormalities in the level or function of the regulatory serpin C1INH (previously referred to as C1 esterase inhibitor), leading to increased generation of bradykinin due to contact system (also known as plasma kallikrein-kinin system) activation. Angioedema in these disorders typically asymmetrically affects the face, lips, tongue, throat, ears, hands and feet, bowel wall, and genitalia and does not characteristically occur in dependent parts of the body. Clinical manifestations and diagnosis are reviewed in detail separately. (See "Hereditary angioedema: Epidemiology, clinical manifestations, exacerbating factors, and prognosis" and "Acquired C1 inhibitor deficiency: Clinical manifestations, epidemiology, pathogenesis, and diagnosis".)

Summarized briefly, both hereditary and acquired forms of C1INH deficiency exist, with similar clinical manifestations. The main differences between the two conditions are the age of presentation and the underlying health of the patient:

Patients with hereditary angioedema (HAE) typically present in childhood or early adolescence with angioedema, including recurrent abdominal attacks. Angioedema may follow trauma, infection, dental procedures, or emotional stress. There is typically an increasing frequency and severity of episodes with the onset of puberty. Exposure to estrogens, either through contraception, hormone replacement therapy, or pregnancy, may trigger attacks. These patients are otherwise healthy.

In contrast, the acquired form typically occurs at an older age, and most patients have an associated lymphoproliferative disorder or autoimmune diathesis. (See "Acquired C1 inhibitor deficiency: Clinical manifestations, epidemiology, pathogenesis, and diagnosis", section on 'Associated disorders'.)

The swelling with both forms of C1INH deficiency can range in severity during a given episode from a minor inconvenience to life-threatening laryngeal edema. Overall, there is a significant risk of morbidity and mortality from angioedema attacks.

Hereditary angioedema with normal C1 inhibitor — Familial angioedema with an autosomal dominant inheritance pattern but normal C1INH levels has been identified [18]. The clinical presentation of angioedema in these patients resembles but is subtlety different than HAE due to C1INH deficiency. (See "Hereditary angioedema with normal C1 inhibitor".)

Specifically, these patients tend to be somewhat older at onset of swelling and have a greater ratio of orofacial swelling to abdominal swelling than HAE due to C1INH deficiency. Several subtypes of HAE with normal C1INH have been identified:

HAE-FXII, defined by mutations involving coagulation factor XII

HAE-Plasminogen, defined by a mutation in the plasminogen gene

HAE-Angiopoietin-1, defined by a mutation in the angiopoietin-1 gene

HAE-Kininogen, defined by a mutation in the kininogen gene

HAE-Myoferlin, defined by a mutation in the myoferlin gene

HAE-HS3ST6, defined by a mutation in the heparan sulfate-glucosamine 3-O-sulfotransferase 6 gene

HAE-Unknown, which is the terminology used when patients meet the HAE with normal C1 inhibitor diagnostic criteria but have no recognized mutation

Fibrinolytic agents — Angioedema without urticaria has been reported following fibrinolysis with streptokinase and alteplase in patients treated acutely for stroke and thrombosis [19,20]. The swelling associated with fibrinolytic agents is likely bradykinin mediated as plasmin has been reported to activate coagulation factor XII of the contact system [21]. This complication is discussed separately. (See "Intravenous thrombolytic therapy for acute ischemic stroke: Therapeutic use", section on 'Angioedema'.)

Etiologies of unknown mechanism — There are several recognized causes of angioedema for which mechanisms are not defined (table 1). The treatment of these disorders is reviewed separately. (See "An overview of angioedema: Clinical features, diagnosis, and management".)

Idiopathic angioedema — "Idiopathic angioedema" is the term applied to recurrent episodes of angioedema without urticaria for which no explanation can be found after a thorough evaluation to exclude allergic disorders, drug reactions, and defects in complement pathways. Idiopathic angioedema may be divided into idiopathic histaminergic angioedema and idiopathic nonhistaminergic angioedema. The diagnosis and management of idiopathic angioedema are presented separately. The former is often associated with chronic spontaneous urticaria or inducible forms of urticaria (ie, physical urticaria). Idiopathic histaminergic angioedema without hives may have distinct pathophysiology compared with chronic spontaneous urticaria with or without angioedema [22]. Idiopathic nonhistaminergic angioedema may represent new probands with HAE-Unknown because the penetrance of HAE with normal C1INH can be relatively low. (See "An overview of angioedema: Clinical features, diagnosis, and management", section on 'Recurrent, idiopathic angioedema'.)

Infections — Infections have been associated with angioedema in children [23]. In a prospective study of 95 consecutive children with isolated angioedema (without urticaria or anaphylaxis) referred to an allergy clinic, angioedema was associated with infection in 19 (21 percent) [24]. Identified infections included the common cold (17 patients), streptococcal pharyngitis, and urinary tract infection. Infection was the most commonly associated disorder, followed by allergic etiologies. The association between angioedema and infections is not reported as regularly in adults. (See 'Children' below.)

Calcium channel blockers — Both dihydropyridines (eg, amlodipine, nifedipine) and nondihydropyridines (eg, diltiazem and verapamil) have been associated with angioedema, either of the skin or small bowel [25-29]. However, no mechanism has been proposed.

Other drugs — Other drugs that have been reported to cause angioedema without urticaria include sirolimus, everolimus, amiodarone, metoprolol, risperidone, paroxetine, and etanercept and other biologic agents [30-38]. Inhaled cocaine has been implicated in uvular angioedema [39-42].

Herbal medicines — Several herbal medicines have been associated with angioedema, including garlic, sanyak, and Ecballium elaterium [43-45].

Other rare causes — Other rare causes of angioedema include selected disorders with eosinophilia and urticarial vasculitis.

Disorders with eosinophilia – Angioedema is associated with a peripheral eosinophilia in two disorders, the hypereosinophilic syndromes (HES) and Gleich syndrome.

Approximately 15 percent of patients with the HES have angioedema, and this diagnosis should be considered in patients with dramatic elevations in peripheral eosinophil counts (eg, ≥1500 eosinophils/microliter) [46,47]. The mechanisms of the angioedema in this disorder may involve the direct release of vasodilatory mediators from eosinophils or may reflect the activation of cutaneous mast cells by eosinophil-derived mediators. (See "Hypereosinophilic syndromes: Clinical manifestations, pathophysiology, and diagnosis".)

The entity of episodic angioedema with eosinophilia (Gleich syndrome) is characterized by recurrent episodes of angioedema, urticaria, pruritus, fever, weight gain, elevated serum immunoglobulin M (IgM), and leukocytosis with marked blood eosinophilia [48-51]. The level of blood eosinophilia parallels disease activity. The etiology of this syndrome is unknown but has been associated with upregulation of C5a receptors on eosinophils during episodes of disease [52]. Gleich syndrome is now considered a type of HES, although the absence of cardiac damage or other end-organ involvement and the episodic nature of the symptoms distinguish this condition from other forms of HES. (See "Hypereosinophilic syndromes: Clinical manifestations, pathophysiology, and diagnosis", section on 'Episodic angioedema with eosinophilia (Gleich syndrome)'.)

Urticarial vasculitis – Angioedema may be observed in patients with hypocomplementemic urticarial vasculitis, in which immunoglobulin G (IgG) anti-C1q is often identified [53,54]. The urticarial lesions of urticarial vasculitis are variably painful, ecchymotic, and purpuric and often leave residual bruising upon resolution. Systemic disease and fever may be present. (See "Urticarial vasculitis".)

CHILDREN — There are very few studies of angioedema in children (other than hereditary angioedema [HAE]), and isolated angioedema (ie, without urticaria or anaphylaxis) appears to be uncommon in this age group. One study reported on 95 children referred to an allergy clinic and followed prospectively [24]. Most had more than one episode. In 51 percent, no cause could be identified. In the remaining one-half, the most common associations were common infections (21 percent), followed by various allergic disorders (14 percent), the presence of thyroid autoimmunity with normal thyroid function (8 percent), and nonsteroidal antiinflammatory drugs (NSAIDs; 6 percent). One-third of the children required ongoing treatment with antihistamines, and all improved with this intervention. (See 'Infections' above.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Urticaria and angioedema (excluding hereditary angioedema)".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Angioedema (The Basics)" and "Patient education: Angioedema caused by ACE inhibitor medicines (The Basics)")

SUMMARY

Definition and pathogenesis – Angioedema is self-limited, localized swelling of the skin or mucosal tissues. The presence of inflammatory mediators leads to a loss of vascular integrity, which allows fluid to move into the interstitial tissues. Angioedema may occur in isolation, accompanied by urticaria, or as a component of anaphylaxis. (See 'Pathogenesis' above.)

Three groups of etiologies – The causes of angioedema can be divided into three groups based on the underlying mechanism (table 1) (see 'Causes' above):

Mast cell mediated – Mast cell-mediated angioedema, such as that seen in allergic reactions and reactions to nonsteroidal antiinflammatory drugs (NSAIDs). (See 'Mast cell-mediated etiologies' above.)

Bradykinin mediated – Bradykinin-mediated angioedema, such as that induced by angiotensin-converting enzyme (ACE) inhibitors or hereditary or acquired C1 inhibitor (C1INH) deficiency. (See 'Bradykinin-mediated etiologies' above.)

Unknown mechanism – Causes with unknown mechanisms, such as idiopathic angioedema and angioedema associated with viral infections in children. (See 'Etiologies of unknown mechanism' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge Clifton O Bingham, III, MD, who contributed to earlier versions of this topic review.

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Topic 8099 Version 26.0

References

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