Autoimmune urticaria

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Autoimmune urticaria
Urticaria.png
A medical illustration depicting urticaria on the palm, wrist and forearm
Specialty Immunology, dermatology
Symptoms Hives, pruritus
Medication Antihistamines, omalizumab
Frequency0.23% (US) [1]

Autoimmune urticaria, also known as chronic autoimmune urticaria, is a type of chronic urticaria characterized by the presence of autoantibodies in the patient's immune system that target the body's own mast cells, leading to episodes of hives (urticaria). [2] [3] This immunologically distinct type of urticaria is considered autoimmune because the immune system, which normally protects the body from foreign organisms, mistakenly attacks the body's own cells, causing inflammation and other symptoms. [4]

Contents

The condition is chronic, meaning it persists for more than six weeks, and can last for many years. [5] Symptoms include recurrent episodes of hives, which are red, itchy, and swollen areas on the skin. These episodes can be triggered by various factors, including heat, stress, or for no identifiable reason. [6]

Autoimmune urticaria is a relatively rare condition, affecting a small percentage of the population. [1] However, it can significantly impact the quality of life of those affected due to the unpredictability and discomfort of the symptoms. [7] The exact cause of autoimmune urticaria is not fully understood, but it is believed to involve a complex interplay of genetic and environmental factors. [8]

Diagnosis is typically based on the clinical history and physical examination, and confirmed by laboratory tests. [9] [10] Treatment primarily involves managing symptoms and includes the use of antihistamines, corticosteroids, monoclonal antibodies (omalizumab), and in some cases, immunosuppressive drugs. [11] [12]

Despite ongoing research, many aspects of autoimmune urticaria remain poorly understood, and it continues to be a challenging condition to manage. The economic burden is significant, with costs as high as $2050 per year per patient in the United States. [13]

History

Urticaria, commonly known as hives, has been recognized as a medical condition for centuries, with descriptions of the characteristic skin lesions appearing in ancient medical texts. However, the understanding of urticaria as an autoimmune condition is a relatively recent development in medical history. [14]

The term autoimmune urticaria refers to a subset of chronic spontaneous urticaria (CSU) cases where the immune system appears to play a significant role. This understanding began to evolve in the mid to late 20th century as advances in immunology revealed the complex interactions between the immune system and various diseases. [15]

The concept of autoimmunity, where the body's immune system attacks its own cells, was not widely accepted until the 1950s. As the understanding of the immune system and its role in disease evolved, researchers began to explore the possibility that some cases of chronic urticaria could be driven by autoimmune processes. [16] The first article that discussed urticaria as a type I hypersensitivity was in 1962. [17]

In the 1980s and 1990s, researchers discovered that a significant proportion of patients with CSU had circulating autoantibodies, particularly against the high-affinity IgE receptor (FcεRI) and IgE itself. [18] [19] These autoantibodies were found to be capable of activating mast cells and basophils, the key effector cells in urticaria, leading to the release of histamine and other inflammatory mediators that cause the characteristic hives and itching.

One of the key studies that shaped the current understanding of autoimmune urticaria was published by Hide et al. in 1993. [20] This study demonstrated that sera from patients with CSU could induce histamine release from basophils and cutaneous mast cells, and this effect was mediated by IgG autoantibodies against the alpha subunit of the high-affinity IgE receptor (FcεRIα). [20]

Subsequent research has further refined understanding of autoimmune urticaria. For example, a study by Sabroe et al. in 1999 showed that intradermal injection of autologous serum caused a wheal and flare reaction (a hallmark of urticaria) in a majority of patients with CSU, providing further evidence of the role of autoantibodies in this condition. [21]

More recent research has focused on identifying the triggers for the production of these autoantibodies, exploring the role of genetic and environmental factors, and developing new treatments that target the underlying autoimmune process.

Despite these advances, many questions remain about the precise mechanisms underlying autoimmune urticaria, and research in this area is ongoing.[ AI-generated? ]

Pathogenesis

Autoimmune urticaria is characterized by the presence of autoantibodies, which are antibodies that the immune system mistakenly produces against the body's own cells. In the case of autoimmune urticaria, these autoantibodies primarily target the high-affinity IgE receptor (FcεRI) on mast cells and basophils, or less commonly, IgE itself. [22]

In a healthy immune system, antibodies are produced to identify and neutralize foreign bodies such as bacteria and viruses. However, in autoimmune conditions like autoimmune urticaria, the immune system mistakenly identifies its own cells as foreign and produces antibodies against them. This leads to an immune response where the body attacks its own tissues, causing inflammation and damage. [4]

Immune response

In autoimmune urticaria, autoantibodies bind to the FcεRI receptors or IgE on the surface of mast cells and basophils. These autoantibodies cross-link and dimerise FcεRI, leading to mast cell basophil activation which triggers a cascade of events that lead to the degranulation of these cells and the release of histamine and other inflammatory mediators into the surrounding tissues. [22] These mediators include preformed substances like histamine, proteases, interleukin-1, and tumor necrosis factor-α (TNF-α), as well as newly synthesized mediators such as leukotrienes, prostaglandins, cytokines, and chemokines. These substances cause increased expression of cell adhesion molecules by the endothelium of the post capillary venules, leading to leukocyte recruitment, including eosinophils, which characterize the late phase reaction.

Mast cells also have the ability to behave as antigen presenting cells, activating T cells and maintaining the duration of the wheals through an MHC class II-dependent signaling pathway. [23]

Comorbidies

Autoimmune urticaria is often associated with a range of comorbidities. These include other autoimmune diseases and atopic diseases like atopic dermatitis, asthma, and rhino-conjunctivitis. [24] [25] [26] Anti-thyroid and anti-nuclear antibodies (ANAs) are often found as well. As such, thyroid diseases are particularly prevalent, as well as vitiligo. [24] One study found an increased prevalence of gastroesophageal reflux disease in autoimmune urticaria patients. [27]

Psychiatric disorders, including anxiety, depression, and somatoform disorders, are also common among patients, with an overall prevalence of any psychiatric comorbidity estimated at 31.6%. [28] [29] Sleep–wake disorders (especially hypersomnia), mood disorders, and trauma and stressor-related disorders are among the most prevalent psychiatric conditions. [30] [31] As autoimmune urticaria persists, the prevalence of comorbidities such as rheumatic diseases, inflammatory diseases, and psychiatric disorders tends to increase.

Diagnosis and testing

Diagnosing autoimmune urticaria involves a combination of clinical evaluation, diagnostic criteria, and various testing methods. [32] The process aims to confirm the presence of the disease, identify potential triggers, and rule out other conditions that may present with similar symptoms.

Diagnostic criteria

The diagnosis of autoimmune urticaria is primarily based on the clinical presentation and the duration of symptoms. The condition is considered chronic if the hives persist for six weeks or longer. [32] In addition to the clinical presentation, the presence of autoantibodies against the high-affinity IgE receptor (FcεRI) or IgE itself can support the diagnosis of autoimmune urticaria.

Testing methods

Several testing methods can be used to support the diagnosis and identify potential triggers. Skin tests, such as the autologous serum skin test (ASST), can be used to detect the presence of functional autoantibodies. In this test, a small amount of the patient's serum is injected into the skin. A positive reaction, which is the formation of a wheal and flare, indicates the presence of functional autoantibodies. [33]

Blood tests can also be used to detect the presence of autoantibodies. The Enzyme-Linked Immunosorbent Assay (ELISA) is a common method used to detect autoantibodies against FcεRI or IgE in the serum. [34] This test involves adding the patient's serum to a plate coated with the antigen of interest. If the autoantibodies are present, they will bind to the antigen. An enzyme-linked antibody is then added, which binds to the autoantibodies. A substrate is added, which the enzyme converts to produce a color change, indicating the presence of autoantibodies. [34]

Differential diagnosis

The differential diagnosis for autoimmune urticaria includes other conditions that can cause hives or similar skin reactions. [32] These can include allergic reactions, other types of urticaria such as physical urticaria (triggered by physical stimuli such as pressure, cold, or heat), and conditions such as mastocytosis and mast cell activation syndrome. It is also important to rule out systemic diseases that can cause hives, such as vasculitis (urticarial vasculitis), Schnitzler's syndrome, Gleich's syndrome, or thyroid disease. [32] The specific symptoms, triggers, and results of skin and blood tests can help differentiate autoimmune urticaria from these other conditions.

Treatment

The treatment of autoimmune urticaria aims to alleviate symptoms, improve the quality of life, and prevent exacerbations. It involves a combination of pharmacological interventions and lifestyle modifications. The choice of treatment depends on the severity of the symptoms, the patient's response to previous treatments, and the presence of comorbidities.

Goals and strategies

The primary goal of treating autoimmune urticaria is to control the symptoms, which can significantly impact the patient's quality of life. [32] This involves reducing the frequency and severity of hives and itchiness. Another important goal is to prevent exacerbations by identifying and avoiding triggers. The treatment strategy typically involves a stepwise approach, starting with first-line treatments and progressing to more aggressive therapies if the symptoms do not improve. [32]

First-line treatments

First-line treatments for autoimmune urticaria primarily involve the use of antihistamines. [32] These medications work by blocking the action of histamine, a substance in the body that causes allergic symptoms. Antihistamines can be very effective in controlling the symptoms of urticaria and are usually the first choice of treatment. There are two types of antihistamines: first-generation, such as diphenhydramine, which can cause drowsiness, and second-generation, such as cetirizine and loratadine, which are less likely to cause drowsiness. Doxepin is also sometimes used. [35]

Second-line treatments

If antihistamines are not effective, or if the symptoms are severe, second-line treatments may be considered. These can include immunosuppressants and biologics. Immunosuppressants, such as corticosteroids, can reduce inflammation and suppress the immune system's response. [32] However, they can have significant side effects, especially when used long-term, and are usually used for short periods. Biologics, such as omalizumab, which is an anti-IgE antibody, can be used in cases of chronic autoimmune urticaria that do not respond to other treatments. [32] This medication works by reducing the immune system's overreaction to triggers.

Lifestyle modifications

In addition to medication, lifestyle modifications can play a crucial role in managing autoimmune urticaria. This can include avoiding known triggers, such as certain foods (although food allergy is rarely the cause), [36] alcohol, stress, and extreme temperatures. Regular exercise, a healthy diet, and good sleep hygiene can also help manage symptoms and improve overall health. [37]

Prognosis

With appropriate treatment, the prognosis for autoimmune urticaria is generally good. Most patients can achieve good control of their symptoms with first-line treatments. However, some patients may have persistent symptoms despite treatment and may require second-line therapies. [32] Relapse is also common in patients with more severe symptoms. Autoimmune urticaria can be a chronic condition, and managing it may involve addressing not only the physical symptoms but also the emotional and psychological impact of living with a chronic disease.

See also

Related Research Articles

<span class="mw-page-title-main">Allergy</span> Immune system response to a substance that most people tolerate well

Allergies, also known as allergic diseases, are various conditions caused by hypersensitivity of the immune system to typically harmless substances in the environment. These diseases include hay fever, food allergies, atopic dermatitis, allergic asthma, and anaphylaxis. Symptoms may include red eyes, an itchy rash, sneezing, coughing, a runny nose, shortness of breath, or swelling. Note that food intolerances and food poisoning are separate conditions.

<span class="mw-page-title-main">Autoimmunity</span> Immune response against an organisms own healthy cells

In immunology, autoimmunity is the system of immune responses of an organism against its own healthy cells, tissues and other normal body constituents. Any disease resulting from this type of immune response is termed an "autoimmune disease". Prominent examples include celiac disease, post-infectious IBS, diabetes mellitus type 1, Henoch–Schönlein purpura (HSP), systemic lupus erythematosus (SLE), Sjögren syndrome, eosinophilic granulomatosis with polyangiitis, Hashimoto's thyroiditis, Graves' disease, idiopathic thrombocytopenic purpura, Addison's disease, rheumatoid arthritis (RA), ankylosing spondylitis, polymyositis (PM), dermatomyositis (DM), and multiple sclerosis (MS). Autoimmune diseases are very often treated with steroids.

<span class="mw-page-title-main">Basophil</span> Type of white blood cell

Basophils are a type of white blood cell. Basophils are the least common type of granulocyte, representing about 0.5% to 1% of circulating white blood cells. However, they are the largest type of granulocyte and how they work is not fully understood. They are responsible for inflammatory reactions during immune response, as well as in the formation of acute and chronic allergic diseases, including anaphylaxis, asthma, atopic dermatitis and hay fever. They also produce compounds that coordinate immune responses, including histamine and serotonin that induce inflammation, and heparin that prevents blood clotting, although there are less than that found in mast cell granules. Mast cells were once thought to be basophils that migrated from the blood into their resident tissues, but they are now known to be different types of cells.

<span class="mw-page-title-main">Immunoglobulin E</span> Immunoglobulin E (IgE) Antibody

Immunoglobulin E (IgE) is a type of antibody that has been found only in mammals. IgE is synthesised by plasma cells. Monomers of IgE consist of two heavy chains and two light chains, with the ε chain containing four Ig-like constant domains (Cε1–Cε4). IgE is thought to be an important part of the immune response against infection by certain parasitic worms, including Schistosoma mansoni, Trichinella spiralis, and Fasciola hepatica. IgE is also utilized during immune defense against certain protozoan parasites such as Plasmodium falciparum. IgE may have evolved as a defense to protect against venoms.

<span class="mw-page-title-main">Hives</span> Skin disease characterized by red, raised, and itchy bumps

Hives, also known as urticaria, is a kind of skin rash with red, raised, itchy bumps. Hives may burn or sting. The patches of rash may appear on different body parts, with variable duration from minutes to days, and does not leave any long-lasting skin change. Fewer than 5% of cases last for more than six weeks. The condition frequently recurs.

Omalizumab, sold under the brand name Xolair, is a medication to treat asthma, nasal polyps, and urticaria (hives).

<span class="mw-page-title-main">Cold urticaria</span> Allergic reaction to low temperatures

Cold urticaria is a disorder in which large red welts called hives (urticaria) form on the skin after exposure to a cold stimulus. The hives are usually itchy and often the hands and feet will become itchy and swollen as well. Hives vary in size from about 7 mm in diameter to as big as about 27 mm or larger.

Common variable immunodeficiency (CVID) is an immune disorder characterized by recurrent infections and low antibody levels, specifically in immunoglobulin (Ig) types IgG, IgM, and IgA. Symptoms generally include high susceptibility to foreign invaders, chronic lung disease, and inflammation and infection of the gastrointestinal tract. CVID affects males and females equally. The condition can be found in children or teens but is generally not diagnosed or recognized until adulthood. The average age of diagnosis is between 20 and 50. However, symptoms vary greatly between people. "Variable" refers to the heterogeneous clinical manifestations of this disorder, which include recurrent bacterial infections, increased risk for autoimmune disease and lymphoma, as well as gastrointestinal disease. CVID is a lifelong disease.

Autoimmune hemolytic anemia (AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to an insufficient number of oxygen-carrying red blood cells in the circulation. The lifetime of the RBCs is reduced from the normal 100–120 days to just a few days in serious cases. The intracellular components of the RBCs are released into the circulating blood and into tissues, leading to some of the characteristic symptoms of this condition. The antibodies are usually directed against high-incidence antigens, therefore they also commonly act on allogenic RBCs. AIHA is a relatively rare condition, with an incidence of 5–10 cases per 1 million persons per year in the warm-antibody type and 0.45 to 1.9 cases per 1 million persons per year in the cold antibody type. Autoimmune hemolysis might be a precursor of later onset systemic lupus erythematosus.

<span class="mw-page-title-main">Physical urticaria</span> Medical condition

Physical urticaria is a distinct subgroup of urticaria (hives) that are induced by an exogenous physical stimulus rather than occurring spontaneously. There are seven subcategories that are recognized as independent diseases. Physical urticaria is known to be painful, itchy and physically unappealing; it can recur for months to years.

<span class="mw-page-title-main">FCER1</span>

The high-affinity IgE receptor, also known as FcεRI, or Fc epsilon RI, is the high-affinity receptor for the Fc region of immunoglobulin E (IgE), an antibody isotype involved in allergy disorders and parasite immunity. FcεRI is a tetrameric receptor complex that binds Fc portion of the ε heavy chain of IgE. It consists of one alpha, one beta, and two gamma chains connected by two disulfide bridges on mast cells and basophils. It lacks the beta subunit on other cells. It is constitutively expressed on mast cells and basophils and is inducible in eosinophils.

<span class="mw-page-title-main">Solar urticaria</span> Medical condition

Solar urticaria (SU) is a rare condition in which exposure to ultraviolet or UV radiation, or sometimes even visible light, induces a case of urticaria or hives that can appear in both covered and uncovered areas of the skin. It is classified as a type of physical urticaria. The classification of disease types is somewhat controversial. One classification system distinguished various types of SU based on the wavelength of the radiation that causes the breakout; another classification system is based on the type of allergen that initiates a breakout.

<span class="mw-page-title-main">Autoimmune disease</span> Disorders of adaptive immune system

An autoimmune disease is a condition that results from an anomalous response of the adaptive immune system, wherein it mistakenly targets and attacks healthy, functioning parts of the body as if they were foreign organisms. It is estimated that there are more than 80 recognized autoimmune diseases, with recent scientific evidence suggesting the existence of potentially more than 100 distinct conditions. Nearly any body part can be involved.

Schnitzler syndrome or Schnitzler's syndrome is a rare disease characterised by onset around middle age of chronic hives (urticaria) and periodic fever, bone pain and joint pain, weight loss, malaise, fatigue, swollen lymph glands and enlarged spleen and liver.

Autoimmune progesterone dermatitis(APD) occurs during the luteal phase of a woman's menstrual cycle and is an uncommon cyclic premenstrual reaction to progesterone. It can present itself in several ways, including eczema, erythema multiforme, urticaria, angioedema, and progesterone-induced anaphylaxis. The first case of autoimmune progesterone dermatitis was identified in 1964. Reproductive function may be impacted by APD.

One of the most prevalent forms of adverse drug reactions is cutaneous reactions, with drug-induced urticaria ranking as the second most common type, preceded by drug-induced exanthems. Urticaria, commonly known as hives, manifests as weals, itching, burning, redness, swelling, and angioedema—a rapid swelling of lower skin layers, often more painful than pruritic. These symptoms may occur concurrently, successively, or independently. Typically, when a drug triggers urticaria, symptoms manifest within 24 hours of ingestion, aiding in the identification of the causative agent. Urticaria symptoms usually subside within 1–24 hours, while angioedema may take up to 72 hours to resolve completely.

<span class="mw-page-title-main">Acquired C1 esterase inhibitor deficiency</span> Medical condition

Acquired C1 esterase inhibitor deficiency, also referred to as acquired angioedema (AAE), is a rare medical condition that presents as body swelling that can be life-threatening and manifests due to another underlying medical condition. The acquired form of this disease can occur from a deficiency or abnormal function of the enzyme C1 esterase inhibitor (C1-INH). This disease is also abbreviated in medical literature as C1INH-AAE. This form of angioedema is considered acquired due to its association with lymphatic malignancies, immune system disorders, or infections. Typically, acquired angioedema presents later in adulthood, in contrast to hereditary angioedema which usually presents from early childhood and with similar symptoms.

<span class="mw-page-title-main">Chronic spontaneous urticaria</span> Medical condition

Chronic spontaneous urticaria(CSU) also known as Chronic idiopathic urticaria(CIU) is defined by the presence of wheals, angioedema, or both for more than six weeks. Chronic spontaneous urticaria can be characterized by angioedema, excruciatingly itchy recurrent hives, or both. Chronic urticaria patients were found to have a higher prevalence of various autoimmune diseases. Many patients with chronic spontaneous urticaria report that certain triggers, such as stress, infections, specific foods, or nonsteroidal anti-inflammatory drug use, aggravate their condition.

Mast cell activation syndrome (MCAS) is a term referring to one of two types of mast cell activation disorder (MCAD); the other type is idiopathic MCAD. MCAS is an immunological condition in which mast cells inappropriately and excessively release chemical mediators, resulting in a range of chronic symptoms, sometimes including anaphylaxis or near-anaphylaxis attacks. Primary symptoms include cardiovascular, dermatological, gastrointestinal, neurological and respiratory problems.

Immunoglobulin therapy is the use of a mixture of antibodies to treat several health conditions. These conditions include primary immunodeficiency, immune thrombocytopenic purpura, chronic inflammatory demyelinating polyneuropathy, Kawasaki disease, certain cases of HIV/AIDS and measles, Guillain-Barré syndrome, and certain other infections when a more specific immunoglobulin is not available. Depending on the formulation it can be given by injection into muscle, a vein, or under the skin. The effects last a few weeks.

References

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  24. 1 2 Kolkhir, Pavel; Altrichter, Sabine; Asero, Riccardo; Daschner, Alvaro; Ferrer, Marta; Giménez-Arnau, Ana; Hawro, Tomasz; Jakob, Thilo; Kinaciyan, Tamar; Kromminga, Arno; Konstantinou, George N; Makris, Michael; Metz, Martin; Skov, Per Stahl; Staubach, Petra; Sussman, Gordon; Zhang, Ke; Maurer, Marcus (2021). "Autoimmune Diseases Are Linked to Type IIb Autoimmune Chronic Spontaneous Urticaria". Allergy, Asthma & Immunology Research. The Korean Academy of Asthma, Allergy and Clinical Immunology and The Korean Academy of Pediatric Al. 13 (4): 545–559. doi:10.4168/aair.2021.13.4.545. ISSN   2092-7355. PMC   8255350 . PMID   34212543.
  25. ↑ Chiu, Hsien-Yi; Muo, Chih-Hsin; Sung, Fung-Chang (2018-04-16). "Associations of chronic urticaria with atopic and autoimmune comorbidities: a nationwide population-based study". International Journal of Dermatology. Wiley. 57 (7): 822–829. doi:10.1111/ijd.14000. ISSN   0011-9059. PMID   29663342. S2CID   4951610.
  26. ↑ Kolkhir, Pavel; Borzova, Elena; Grattan, Clive; Asero, Riccardo; Pogorelov, Dmitry; Maurer, Marcus (2017). "Autoimmune comorbidity in chronic spontaneous urticaria: A systematic review". Autoimmunity Reviews. Elsevier BV. 16 (12): 1196–1208. doi:10.1016/j.autrev.2017.10.003. ISSN   1568-9972. PMID   29037900.
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  31. ↑ Ates, Hale; Firat, Selma; Buhari, Gozde Koycu; Keren, Metin; Cifci, Bulent; Erkekol, Ferda Öner (2022-04-05). "Relationships between quality of life, sleep problems, and sleep quality in patients with chronic idiopathic urticaria". Journal of Cosmetic Dermatology. Wiley. 21 (9): 4072–4079. doi:10.1111/jocd.14851. ISSN   1473-2130. PMID   35166020. S2CID   246826536.
  32. 1 2 3 4 5 6 7 8 9 10 Zuberbier, Torsten; Abdul Latiff, Amir Hamzah; Abuzakouk, Mohamed; Aquilina, Susan; Asero, Riccardo; Baker, Diane; Ballmer-Weber, Barbara; Bangert, Christine; Ben-Shoshan, Moshe; Bernstein, Jonathan A.; Bindslev-Jensen, Carsten; Brockow, Knut; Brzoza, Zenon; Chong Neto, Herberto Jose; Church, Martin K.; Criado, Paulo R.; Danilycheva, Inna V.; Dressler, Corinna; Ensina, Luis Felipe; Fonacier, Luz; Gaskins, Matthew; Gáspár, Krisztian; Gelincik, Aslı; Giménez-Arnau, Ana; Godse, Kiran; Gonçalo, Margarida; Grattan, Clive; Grosber, Martine; Hamelmann, Eckard; Hébert, Jacques; Hide, Michihiro; Kaplan, Allen; Kapp, Alexander; Kessel, Aharon; Kocatürk, Emek; Kulthanan, Kanokvalai; Larenas-Linnemann, Désirée; Lauerma, Antti; Leslie, Tabi A.; Magerl, Markus; Makris, Michael; Meshkova, Raisa Y.; Metz, Martin; Micallef, Daniel; Mortz, Charlotte G.; Nast, Alexander; Oude-Elberink, Hanneke; Pawankar, Ruby; Pigatto, Paolo D.; Ratti Sisa, Hector; Rojo Gutiérrez, María Isabel; Saini, Sarbjit S.; Schmid-Grendelmeier, Peter; Sekerel, Bulent E.; Siebenhaar, Frank; Siiskonen, Hanna; Soria, Angele; Staubach-Renz, Petra; Stingeni, Luca; Sussman, Gordon; Szegedi, Andrea; Thomsen, Simon Francis; Vadasz, Zahava; Vestergaard, Christian; Wedi, Bettina; Zhao, Zuotao; Maurer, Marcus (2021-10-20). "The international EAACI/GA²LEN/EuroGuiDerm/APAAACI guideline for the definition, classification, diagnosis, and management of urticaria". Allergy. Wiley. 77 (3): 734–766. doi:10.1111/all.15090. hdl: 2434/910992 . ISSN   0105-4538. PMID   34536239. S2CID   237556385.
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  34. 1 2 Jang, Jae-Hyuk; Moon, Jiyoung; Yang, Eun-Mi; Ryu, Min Sook; Lee, Youngsoo; Ye, Young-Min; Park, Hae-Sim (2022-08-19). "Detection of serum IgG autoantibodies to FcεRIα by ELISA in patients with chronic spontaneous urticaria". PLOS ONE. Public Library of Science (PLoS). 17 (8): e0273415. Bibcode:2022PLoSO..1773415J. doi: 10.1371/journal.pone.0273415 . ISSN   1932-6203. PMC   9390921 . PMID   35984815.
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  36. ↑ Zuberbier, T; Chantraine-Hess, S; Hartmann, K; Czarnetzki, B M (1995-11-01). "Pseudoallergen-free diet in the treatment of chronic urticaria. A prospective study". Acta Dermato-Venereologica. Medical Journals Sweden AB. 75 (6): 484–487. doi: 10.2340/0001555575484487 . ISSN   1651-2057. PMID   8651031. S2CID   40198396.
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