Chronic spontaneous urticaria

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Chronic spontaneous urticaria
Other namesChronic idiopathic urticaria, CIU, and CSU. [1]
Chronic spontaneous urticaria.jpg
Typical presentation of chronic spontaneous urticaria.
Symptoms Urticaria, angioedema, headache, fatigue, joint pain or swelling, gastrointestinal symptoms flushing, wheezing, and palpitations. [2]
Usual onsetThird to fifth decades of life. [2]
DurationEpisodic. [2]
Causes NSAIDs, heat, tight clothing or straps, stress, variations in diet, and alcohol. [2]
Risk factors Allergic diseases, autoimmune conditions, and thyroid disorders. [2]
Diagnostic method Clinical findings, complete blood count with differential, CRP or ESR, and skin biopsy. [2]
Differential diagnosis Urticarial vasculitis, lupus, cryoglobulinemia, Schnitzler syndrome, mast cell disorders, polymorphic eruption of pregnancy, hypereosinophilic syndrome, and Cryopyrin-associated periodic syndromes. [2]
TreatmentAvoidance of exacerbating factors, and antihistamines. [3]
Medication Cetirizine, Levocetirizine, Fexofenadine, Loratadine, and Desloratadine. [3]
Prognosis Spontaneous remission in 30-50% of cases. [2]
Frequency1% of the general population in the United States. [2]

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. [4] Chronic spontaneous urticaria can be characterized by angioedema, excruciatingly itchy recurrent hives, or both. [5] Chronic urticaria patients were found to have a higher prevalence of various autoimmune diseases. [6] 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. [7]

Contents

Wheals and angioedema appear to be caused by the degranulation of skin mast cells in CSU. These cells secrete proteases, histamine, and cytokines, as well as platelet-activating factors and other arachidonic acid metabolites. [8] Several theories exist regarding the pathophysiology of chronic urticaria, none of which has been proven beyond a reasonable doubt. [9] Studies have been conducted to investigate the validity of serologic testing [10] in order to establish an autoimmune basis for disease as well as the autoimmune theory of illness. [11] Other hypotheses include additional serologic factors, [12] [13] tissue mast cell abnormalities, [14] [15] and basophils. [16] [17]

The standard workup for CSU differs in different parts of the world. However, most doctors agree on the importance of having a detailed history. [18] The main goal is to identify any urticaria-inducing factors because eliminating them is the most straightforward course of treatment. [19] Basic laboratory tests, such as C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and possibly a complete blood count (CBC) with differential, are critical for detecting signs of systemic inflammation and ruling out autoinflammatory conditions as well as urticarial vasculitis with systemic involvement. [5]

For the treatment of chronic spontaneous urticaria, a two-pronged strategy has been proposed. The underlying cause(s) and/or eliciting trigger(s) must first be identified and eliminated. The second approach is pharmacotherapy, which aims to alleviate symptoms. Although eliminating the source of the problem is the ideal solution, it does not appear to be feasible in many cases. [20] A therapeutic approach should be implemented in three steps, according to current guidelines: (1) taking a second-generation antihistamine once daily; (2) increasing the second-generation antihistamine's daily dose up to four times; and (3) pursuing off-label therapy with cyclosporine A or montelukast or add-on therapy with omalizumab, which is an approved treatment option for CSU. [21]

Signs and symptoms

Angioedema, excruciatingly itchy recurrent wheals, or both can be signs of chronic spontaneous urticaria. [5] Between 40 and 50 percent of CSU patients experience angioedema. [22] However, angioedema is the main symptom reported by about 10% of patients. [8]

Usually, urticarial lesions or hives are elevated, erythematous plaques with a defined perimeter. If a patient is taking antihistamines, these lesions may appear flattened and take on a range of sizes. It can affect any part of the body, including parts where clothing might press against the skin. Lesions typically do not last more than 24 hours. The degree of pruritus can interfere with everyday activities and sleep. [9]

Angioedema is characterized by sporadic, asymmetrical submucosal or subcutaneous edema. It is more common to experience paresthesia, such as tingling or numbness, than the pruritus associated with urticaria. Often affected body parts are the lips, eyes, cheeks, and limbs. [9] Urticaria and angioedema typically coexist, but in a small percentage of cases, angioedema may be the only symptom. [23]

Causes

Individuals with chronic urticaria have been found to have a higher prevalence of various autoimmune diseases. [6] Many patients with chronic spontaneous urticaria report that certain triggers, like stress, infections, certain foods, or nonsteroidal anti-inflammatory drug consumption, cause their disease to worsen. [7]

Risk factors

There is evidence that individuals with chronic urticaria are more likely to have a variety of autoimmune diseases. [6] Researchers found that patients with systemic lupus erythematosus, rheumatoid arthritis, thyroid issues, celiac disease, Sjögren syndrome, and type 1 diabetes had higher rates of these conditions than those with chronic urticaria in a study involving a database of 13,000 patients compared to 10,000 control subjects. [24]

Triggers

The majority of patients with chronic spontaneous urticaria frequently linked multiple triggers to flare-ups. [25] However, the suspected trigger does not always result in symptoms, so patients frequently subject themselves to needless limitations and lifestyle modifications. [26]

In one study, the most common type of idiopathic urticaria among CSU patients was symptomatic dermographism. The second most common physical trigger that was reported was pressure. The third most commonly reported trigger was cold. [26]

The majority of guidelines discourage food as the cause of chronic urticaria; nonetheless, patients frequently believe that certain foods aggravate their condition or are the cause of it. Between 13 and 80% of people self-report that food triggers their CSU episodes. [27]

A contributing factor to the exacerbation of chronic spontaneous urticaria in certain patients may be stress. On the other hand, urticaria is most likely one of the main sources of stress. [20]

Mechanism

Two mast cells in bone marrow at 1000x magnification after Wright staining. Mast cells in bone marrow.jpg
Two mast cells in bone marrow at 1000x magnification after Wright staining.

The degranulation of skin mast cells in CSU appears to be involved in wheals and angioedema. These cells release proteases, histamine, and cytokines along with platelet-activating factors and other metabolites of arachidonic acid. [8] These mediators cause swelling, redness, and itching by stimulating sensory nerve endings, increasing vascular permeability, and inducing vasodilatation. [28] Edema, mast cell degranulation, and a perivascular infiltrate of cells, including CD4ξ lymphocytes, monocytes, neutrophils, eosinophils, and basophils, are the hallmarks of a lesion site, also known as a wheal. [29] [30] This infiltrate bears resemblance to the infiltrate observed in the allergen late-phase reaction. [31] T-cell expression of IL-4, IL-5, and IFN-g is evident in the lesion cytokine profile, indicating a mixed TH1/TH2 response. [32] The dermis of lesion skin contains epithelial-derived cytokines that support the TH2 profile, such as IL-33, IL-25, and thymic stromal lymphopoietin, as well as the vasoactive agents calcitonin gene-related peptide and vascular endothelial growth factor. [33] These factors were not present in the skin that is not affected. [34] The pathophysiology of chronic urticaria is the subject of several theories, none of which has been proven beyond a reasonable doubt. [9] Research has looked at the validity of serologic testing [10] to establish an autoimmune basis for disease as well as the autoimmune theory of illness. [11] Other theories include additional serologic factors, [12] [13] abnormalities of tissue mast cells, [14] [15] and basophils. [16] [17]

Diagnosis

Chronic spontaneous urticaria is defined by the presence of wheals, angioedema, or both for more than six weeks. [4]

In various areas of the world, the standard workup is different. A very comprehensive history is something that is universally agreed upon. [18] The main goal is to identify any urticaria-inducing factors, as the most straightforward course of treatment is to eliminate them, including physical provocation factors, food allergies, etc. Provocations such as double-blinded, placebo-controlled food provocation, pressure, heat, cold, and others should be used if an eliciting factor is suspected in order to confirm if it is an eliciting factor. Because chronic as well as recurrent infections are known to cause urticaria, only differential blood counts and CRP or ESR are advised if no symptom-inducing factor can be found. [19]

Urticarial autoinflammatory diseases and urticarial vasculitis (UV) are uncommon but should be taken into consideration in patients who experience recurrent wheals. [35] [36] Doctors should ask about the duration as well as resolution of each wheal as well as the presence of any other signs and symptoms, such as fever episodes or musculoskeletal pain, in addition to itchy wheals or angioedema, in order to rule out both conditions. Extended periods of time exceeding twenty-four hours and a gradual resolution of individual wheals indicate UV exposure; further indications of systemic inflammation may indicate autoinflammatory disease as well as other autoimmune disorders. A skin biopsy should be part of the diagnostic process if UV as well as an autoinflammatory disease is suspected. This is so that neutrophilic infiltrates or vascular destruction can be checked for. [4] It could be challenging to differentiate UV from CSU because there are currently no established standardized histopathologic criteria for UV. [37] Basic laboratory tests, which include inflammatory markers C-reactive protein (CRP) as well as erythrocyte sedimentation rate (ESR) and possibly complete blood count (CBC) with differential, are crucial to detect signs of systemic inflammation and rule out autoinflammatory conditions as well as UV with systemic involvement. However, these results can also be influenced by other comorbidities and can be seen in CSU. [5]

Patients with recurrent wheals need to have a number of other conditions taken into consideration. Certain conditions, like hypereosinophilic syndromes and Wells syndrome, are uncommon. [36] The primary skin lesions in these patients vary, ranging from permanent maculopapular lesions to long-lasting plaque-like lesions, even though they may also present with urticarial lesions. Patients with coexisting wheals and plaques and who are pregnant are said to have pruritic urticarial papules and plaques of pregnancy (also called polymorphic eruption in pregnancy). A skin biopsy is necessary to confirm premonitory bullous pemphigoid in the elderly when there is no sign of vesicles or bullae. [38]

Bradykinin-mediated disorders, such as angiotensin-converting enzyme (ACE) inhibitor-induced angioedema, hereditary angioedema, as well as angioedema due to acquired C1 inhibitor deficiency, must be taken into consideration in patients presenting with frequent angioedema without wheals. [39] Here, the doctor should closely examine the patient's history, age at symptom onset, duration of attacks, presence of abdominal angioedema episodes, use of concurrent medications (particularly ACE inhibitor intake), lack of response to antihistamines or corticosteroids, and prodromal symptoms. Laboratory evaluation must involve complement C4 levels, C1 inhibitor concentration, and function in every patient with frequent angioedema in whom hereditary angioedema as well as an acquired C1 inhibitor deficiency cannot be ruled out in order to rule out or confirm hereditary angioedema due to C1 inhibitor deficiency. [4]

Classification

According to recent data, there are three subgroups of CSU: autoimmunity type I (CSUaiTI, also known as "autoallergic CSU"), autoimmunity type IIb (CSUaiTIIb), and CSU with an unidentified cause (CSUuc). [40] [41] Type I and type IIb autoimmunity may coexist in some cases. [42] The underlying pathomechanism in the majority of CSU patients is thought to be CSUaiTI, with IgE autoantibodies to autoallergens. [11] IgG or IgM autoantibodies directed against mast cell receptors that are activated cause mast cell activation and degranulation in CSUaiTIIb. [43] Other mechanisms that are currently unknown have significance for the degranulation of skin mast cells in CSUuc. Furthermore, modulating factors like medications, stress, or infections can change how sensitive skin mast cells are to degranulators, which can lead to increased disease activity and/or exacerbation of the disease. [4]

Treatment

A two-pronged strategy has been proposed for the treatment of chronic spontaneous urticaria. First, the underlying cause(s) and/or eliciting trigger(s) must be established and eliminated. Pharmacotherapy is the second, and its goal is to relieve symptoms. Although removing the cause is the ideal course of action, this may not be feasible in many situations. [20] According to current guidelines, a therapeutic approach should be implemented in three steps: (1) taking a second-generation antihistamine once daily; (2) increasing the daily dose of the second-generation antihistamine up to four times; and (3) pursuing off-label therapy with cyclosporine A or montelukast or add-on therapy with omalizumab, which is an approved treatment option for CSU. [21]

Omalizumab works well even in the most difficult, resistant situations. [44] Despite having nearly as good of an efficacy as omalizumab, cyclosporine is regarded as third line because it carries a much higher risk of side effects. [45] Long-term use of corticosteroids is not advised because the side effects increase with dosage and duration and eventually result in greater disability than CSU. However, until other treatments take effect, acute symptoms can be managed with a brief course of steroids. [8]

Outlook

According to one study examining the course of urticaria in the general population, 50% of patients with chronic urticaria had no symptoms after three months, and 80% had no symptoms after twelve months. Still, 11% experienced urticaria after five years. [46]

Epidemiology

It has been discovered by American authors that approximately one in five individuals will at some point in their lives suffer from urticaria of any kind. [47] Similar figures were discovered in a recent Spanish study. [46] Nonetheless, studies conducted in Europe suggest a lower lifetime prevalence, or the prevalence observed throughout one's lifetime up until the investigation, of approximately 8–10%. [48] [49] There is less information on nonacute urticaria. A study conducted forty years ago in Sweden found a point prevalence of about 0.1% in the population overall, [50] and a different study conducted in Spain more recently reported a point prevalence of 0.6% in the population. [46]

See also

Related Research Articles

<span class="mw-page-title-main">Mast cell</span> Cell found in connective tissue

A mast cell is a resident cell of connective tissue that contains many granules rich in histamine and heparin. Specifically, it is a type of granulocyte derived from the myeloid stem cell that is a part of the immune and neuroimmune systems. Mast cells were discovered by Paul Ehrlich in 1877. Although best known for their role in allergy and anaphylaxis, mast cells play an important protective role as well, being intimately involved in wound healing, angiogenesis, immune tolerance, defense against pathogens, and vascular permeability in brain tumors.

<span class="mw-page-title-main">Hypereosinophilic syndrome</span> Unexplained chronic eosinophila

Hypereosinophilic syndrome is a disease characterized by a persistently elevated eosinophil count in the blood for at least six months without any recognizable cause, with involvement of either the heart, nervous system, or bone marrow.

<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.

<span class="mw-page-title-main">Omalizumab</span> Monoclonal antibody medication

Omalizumab, sold under the brand name Xolair, is an injectable medication to treat severe persistent allergic forms of asthma, nasal polyps, urticaria (hives), and immunoglobulin E-mediated food allergy.

<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.

Aquagenic urticaria, also known as water allergy and water urticaria, is a rare form of physical urticaria in which hives develop on the skin after contact with water, regardless of its temperature. The condition typically results from contact with water of any type, temperature or additive. In rare cases, it is internal rather than external and causes ones body to let water enter the lungs, leading to drowning symptoms and/or pneumonia

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.

Adrenergic urticaria is a skin condition characterized by an eruption consisting of small (1-5mm) red macules and papules with a pale halo, appearing within 10 to 15 min after emotional upset. There have been 10 cases described in medical literature, and involve a trigger followed by a rise in catecholamine and IgE. Treatment involves propranolol and trigger avoidance.

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

Pressure urticaria or delayed pressure urticaria is a physical urticaria caused by pressure applied to the skin, and is characterized by the development of swelling and pain that usually occurs 3 to 12 hours after local pressure has been applied.

Pseudoallergy, sometimes known as nonallergic hypersensitivity, is a clinical mimic of immediate-type allergic reactions that lacks underlying immunological mechanisms.

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Autoimmune enteropathy is a rare autoimmune disorder characterized by weight loss from malabsorption, severe and protracted diarrhea, and autoimmune damage to the intestinal mucosa. Autoimmune enteropathy typically occurs in infants and younger children however, adult cases have been reported in literature. Autoimmune enteropathy was first described by Walker-Smith et al. in 1982.

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.

NSAIDhypersensitivity reactions encompass a broad range of allergic or allergic-like symptoms that occur within minutes to hours after ingesting aspirin or other NSAID nonsteroidal anti-inflammatory drugs. Hypersensitivity drug reactions differ from drug toxicity reactions in that drug toxicity reactions result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual. Hypersensitivity reactions are idiosyncratic reactions to a drug. Although the term NSAID was introduced to signal a comparatively low risk of adverse effects, NSAIDs do evoke a broad range of hypersensitivity syndromes. These syndromes have recently been classified by the European Academy of Allergy and Clinical Immunology Task Force on NSAIDs Hypersensitivity.

Exercise-induced anaphylaxis is a rare condition in which anaphylaxis, a serious or life-threatening allergic response, is brought on by physical activity. Approximately 5–15% of all reported cases of anaphylaxis are thought to be exercise-induced.

<span class="mw-page-title-main">Mosquito bite allergy</span> Excessive reactions to mosquito bites

Mosquito bite allergies, also termed hypersensitivity to mosquito bites, are excessive reactions of varying severity to mosquito bites. They are allergic hypersensitivity reactions caused by the non-toxic allergenic proteins contained in the saliva injected by a female mosquito at the time it takes its blood meal, and are not caused by any toxin or pathogen. By general agreement, mosquito bite allergies do not include the ordinary wheal and flare responses to these bites although these reactions are also allergic in nature. Ordinary mosquito bite allergies are nonetheless detailed here because they are the best understood reactions to mosquito bites and provide a basis for describing what is understood about them.

<span class="mw-page-title-main">Autoimmune urticaria</span> Autoimmune disease causing hives and itching

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). 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.

Ucenprubart (LY3454738) is a monoclonal antibody that acts as an agonist at CD200R1 and is developed by Eli Lilly and Company for atopic dermatitis and other autoimmune diseases.

References

  1. ↑ "Chronic idiopathic urticaria (HPO)". Monarch Initiative. Retrieved December 20, 2023.
  2. 1 2 3 4 5 6 7 8 9 "Chronic spontaneous urticaria: Clinical manifestations, diagnosis, pathogenesis, and natural history". UpToDate. Retrieved December 20, 2023.
  3. 1 2 "Chronic spontaneous urticaria: Standard management and patient education". UpToDate. Retrieved December 20, 2023.
  4. 1 2 3 4 5 Metz, Martin; Altrichter, Sabine; Buttgereit, Thomas; Fluhr, Joachim W.; Fok, Jie Shen; Hawro, Tomasz; Jiao, Qingqing; Kolkhir, Pavel; Krause, Karoline; Magerl, Markus; Pyatilova, Polina; Siebenhaar, Frank; Su, Huichun; Terhorst-Molawi, Dorothea; Weller, Karsten; Xiang, Yi-Kui; Maurer, Marcus (2021). "The Diagnostic Workup in Chronic Spontaneous Urticaria—What to Test and Why". The Journal of Allergy and Clinical Immunology: In Practice. 9 (6). Elsevier BV: 2274–2283. doi:10.1016/j.jaip.2021.03.049. ISSN   2213-2198. PMID   33857657. S2CID   233257578.
  5. 1 2 3 4 Zuberbier, T.; Aberer, W.; Asero, R.; Abdul Latiff, A. H.; Baker, D.; Ballmer‐Weber, B.; Bernstein, J. A.; Bindslev‐Jensen, C.; Brzoza, Z.; Buense Bedrikow, R.; Canonica, G. W.; Church, M. K.; Craig, T.; Danilycheva, I. V.; Dressler, C.; Ensina, L. F.; Giménez‐Arnau, A.; Godse, K.; Gonçalo, M.; Grattan, C.; Hebert, J.; Hide, M.; Kaplan, A.; Kapp, A.; Katelaris, C. H.; Kocatürk, E.; Kulthanan, K.; Larenas‐Linnemann, D.; Leslie, T. A.; Magerl, M.; Mathelier‐Fusade, P.; Meshkova, R. Y.; Metz, M.; Nast, A.; Nettis, E.; Oude‐Elberink, H.; Rosumeck, S.; Saini, S. S.; Sánchez‐Borges, M.; Schmid‐Grendelmeier, P.; Staubach, P.; Sussman, G.; Toubi, E.; Vena, G. A.; Vestergaard, C.; Wedi, B.; Werner, R. N.; Zhao, Z.; Maurer, M. (June 25, 2018). "The EAACI/GA²LEN/EDF/WAO guideline for the definition, classification, diagnosis and management of urticaria". Allergy. 73 (7). Wiley: 1393–1414. doi: 10.1111/all.13397 . hdl: 10230/35554 . ISSN   0105-4538. PMID   29336054.
  6. 1 2 3 Kozel, Martina M.A.; Bossuyt, Patrick M.M.; Mekkes, Jan R.; Bos, Jan D. (2003). "Laboratory tests and identified diagnoses in patients with physical and chronic urticaria and angioedema: A systematic review". Journal of the American Academy of Dermatology. 48 (3). Elsevier BV: 409–416. doi:10.1067/mjd.2003.142. ISSN   0190-9622.
  7. 1 2 Kolkhir, Pavel; Muñoz, Melba; Asero, Riccardo; Ferrer, Marta; Kocatürk, Emek; Metz, Martin; Xiang, Yi-Kui; Maurer, Marcus (2022). "Autoimmune chronic spontaneous urticaria". Journal of Allergy and Clinical Immunology. 149 (6). Elsevier BV: 1819–1831. doi: 10.1016/j.jaci.2022.04.010 . ISSN   0091-6749. PMID   35667749.
  8. 1 2 3 4 Saini, Sarbjit S.; Kaplan, Allen P. (2018). "Chronic Spontaneous Urticaria: The Devil's Itch". The Journal of Allergy and Clinical Immunology: In Practice. 6 (4). Elsevier BV: 1097–1106. doi:10.1016/j.jaip.2018.04.013. ISSN   2213-2198. PMC   6061968 . PMID   30033911.
  9. 1 2 3 4 Saini, Sarbjit S. (2014). "Chronic Spontaneous Urticaria". Immunology and Allergy Clinics of North America. 34 (1). Elsevier BV: 33–52. doi:10.1016/j.iac.2013.09.012. ISSN   0889-8561.
  10. 1 2 Schmetzer, Oliver; Lakin, Elisa; Topal, Fatih A.; Preusse, Patricia; Freier, Denise; Church, Martin K.; Maurer, Marcus (2018). "IL-24 is a common and specific autoantigen of IgE in patients with chronic spontaneous urticaria". Journal of Allergy and Clinical Immunology. 142 (3). Elsevier BV: 876–882. doi: 10.1016/j.jaci.2017.10.035 . ISSN   0091-6749.
  11. 1 2 3 Kolkhir, Pavel; Church, Martin K.; Weller, Karsten; Metz, Martin; Schmetzer, Oliver; Maurer, Marcus (2017). "Autoimmune chronic spontaneous urticaria: What we know and what we do not know". Journal of Allergy and Clinical Immunology. 139 (6). Elsevier BV: 1772–1781.e1. doi: 10.1016/j.jaci.2016.08.050 . ISSN   0091-6749. PMID   27777182.
  12. 1 2 Bossi, F.; Frossi, B.; Radillo, O.; Cugno, M.; Tedeschi, A.; Riboldi, P.; Asero, R.; Tedesco, F.; Pucillo, C. (2011). "Mast cells are critically involved in serum-mediated vascular leakage in chronic urticaria beyond high-affinity IgE receptor stimulation: Mast cells and vascular leakage in chronic urticaria". Allergy. 66 (12): 1538–1545. doi:10.1111/j.1398-9995.2011.02704.x. S2CID   5181903.
  13. 1 2 Cugno, M; Tedeschi, A; Frossi, B; Bossi, F; Marzano, AV; Asero, R (October 19, 2016). "Detection of Low-Molecular-Weight Mast Cell–Activating Factors in Serum From Patients With Chronic Spontaneous Urticaria". Journal of Investigational Allergology and Clinical Immunology. 26 (5). Esmon Publicidad, SA: 310–313. doi: 10.18176/jiaci.0051 . ISSN   1018-9068. PMID   27763857.
  14. 1 2 JACQUES, P; LAVOIE, A; BEDARD, P; BRUNET, C; HEBERT, J (1992). "Chronic idiopathic urticaria: Profiles of skin mast cell histamine release during active disease and remission". Journal of Allergy and Clinical Immunology. 89 (6). Elsevier BV: 1139–1143. doi:10.1016/0091-6749(92)90297-f. ISSN   0091-6749. PMID   1376735.
  15. 1 2 Nettis, E.; Dambra, P.; Loria, M. P.; Cenci, L.; Vena, G. A.; Ferrannini, A.; Tursi, A. (2001). "Mast‐cell phenotype in urticaria". Allergy. 56 (9). Wiley: 915. doi:10.1034/j.1398-9995.2001.00296.x. ISSN   0105-4538. S2CID   13293117.
  16. 1 2 Vonakis, Becky M; Saini, Sarbjit S (2008). "New concepts in chronic urticaria". Current Opinion in Immunology. 20 (6). Elsevier BV: 709–716. doi:10.1016/j.coi.2008.09.005. ISSN   0952-7915. PMC   2610333 . PMID   18832031.
  17. 1 2 Borriello, Francesco; Granata, Francescopaolo; Marone, Gianni (2014). "Basophils and Skin Disorders". Journal of Investigative Dermatology. 134 (5). Elsevier BV: 1202–1210. doi: 10.1038/jid.2014.16 . ISSN   0022-202X. PMID   24499736.
  18. 1 2 Vestergaard, Christian; Deleuran, Mette (2015). "Chronic spontaneous urticaria: latest developments in aetiology, diagnosis and therapy". Therapeutic Advances in Chronic Disease. 6 (6): 304–313. doi:10.1177/2040622315603951. ISSN   2040-6223. PMC   4622315 . PMID   26568807.
  19. 1 2 Zuberbier, T.; Aberer, W.; Asero, R.; Bindslev‐Jensen, C.; Brzoza, Z.; Canonica, G. W.; Church, M. K.; Ensina, L. F.; Giménez‐Arnau, A.; Godse, K.; Gonçalo, M.; Grattan, C.; Hebert, J.; Hide, M.; Kaplan, A.; Kapp, A.; Abdul Latiff, A. H.; Mathelier‐Fusade, P.; Metz, M.; Nast, A.; Saini, S. S.; Sánchez‐Borges, M.; Schmid‐Grendelmeier, P.; Simons, F. E. R.; Staubach, P.; Sussman, G.; Toubi, E.; Vena, G. A.; Wedi, B.; Zhu, X. J.; Maurer, M. (April 30, 2014). "The <scp>EAACI</scp>/<scp>GA</scp>2<scp>LEN</scp>/<scp>EDF</scp>/<scp>WAO</scp> Guideline for the definition, classification, diagnosis, and management of urticaria: the 2013 revision and update". Allergy. 69 (7). Wiley: 868–887. doi:10.1111/all.12313. ISSN   0105-4538.
  20. 1 2 3 Maurer, M.; Weller, K.; Bindslev-Jensen, C.; Giménez-Arnau, A.; Bousquet, P. J.; Bousquet, J.; Canonica, G. W.; Church, M. K.; Godse, K. V.; Grattan, C. E. H.; Greaves, M. W.; Hide, M.; Kalogeromitros, D.; Kaplan, A. P.; Saini, S. S.; Zhu, X. J.; Zuberbier, T. (2011). "Unmet clinical needs in chronic spontaneous urticaria. A GA2LEN task force report1: Unmet clinical needs in chronic urticaria". Allergy. 66 (3): 317–330. doi: 10.1111/j.1398-9995.2010.02496.x . PMID   21083565.
  21. 1 2 Termeer, Christian; Staubach, Petra; Kurzen, Hjalmar; Strömer, Klaus; Ostendorf, Rolf; Maurer, Marcus (2015). "Chronic spontaneous urticaria – a management pathway for patients with chronic spontaneous urticaria". JDDG: Journal der Deutschen Dermatologischen Gesellschaft. 13 (5): 419–428. doi: 10.1111/ddg.12633 . ISSN   1610-0379. PMID   25918085.
  22. ↑ Maurer, Marcus; Costa, Celia; Gimenez Arnau, AnaMaria; Guillet, Gerard; Labrador‐Horrillo, Moises; Lapeere, Hilde; Meshkova, Raisa; Savic, Sinisa; Chapman‐Rothe, Nadine (September 3, 2020). "Antihistamine‐resistant chronic spontaneous urticaria remains undertreated: 2‐year data from the AWARE study". Clinical & Experimental Allergy. 50 (10). Wiley: 1166–1175. doi: 10.1111/cea.13716 . hdl: 1854/LU-8714221 . ISSN   0954-7894. PMID   32735720.
  23. ↑ Zingale, L. C.; Beltrami, L.; Zanichelli, A.; Maggioni, L.; Pappalardo, E.; Cicardi, B.; Cicardi, M. (October 24, 2006). "Angioedema without urticaria: a large clinical survey". Canadian Medical Association Journal. 175 (9). CMA Joule Inc.: 1065–1070. doi:10.1503/cmaj.060535. ISSN   0820-3946. PMC   1609157 . PMID   17060655.
  24. ↑ Confino-Cohen, Ronit; Chodick, Gabriel; Shalev, Varda; Leshno, Moshe; Kimhi, Oded; Goldberg, Arnon (2012). "Chronic urticaria and autoimmunity: Associations found in a large population study". Journal of Allergy and Clinical Immunology. 129 (5). Elsevier BV: 1307–1313. doi:10.1016/j.jaci.2012.01.043. ISSN   0091-6749. PMID   22336078.
  25. ↑ Trevisonno, Jordan; Balram, Bhairavi; Netchiporouk, Elena; Ben-Shoshan, Moshe (May 10, 2015). "Physical urticaria: Review on classification, triggers and management with special focus on prevalence including a meta-analysis". Postgraduate Medicine. 127 (6). Informa UK Limited: 565–570. doi:10.1080/00325481.2015.1045817. ISSN   0032-5481. PMID   25959894. S2CID   205452082.
  26. 1 2 Sánchez, Jorge; Amaya, Emerson; Acevedo, Ana; Celis, Ana; Caraballo, Domingo; Cardona, Ricardo (2017). "Prevalence of Inducible Urticaria in Patients with Chronic Spontaneous Urticaria: Associated Risk Factors". The Journal of Allergy and Clinical Immunology: In Practice. 5 (2). Elsevier BV: 464–470. doi:10.1016/j.jaip.2016.09.029. ISSN   2213-2198. PMID   27838325.
  27. ↑ Sánchez, Jorge; Sánchez, Andres; Cardona, Ricardo (June 19, 2018). "Dietary Habits in Patients with Chronic Spontaneous Urticaria: Evaluation of Food as Trigger of Symptoms Exacerbation". Dermatology Research and Practice. 2018. Hindawi Limited: 1–6. doi: 10.1155/2018/6703052 . ISSN   1687-6105.
  28. ↑ KAPLAN, A; HORAKOVA, Z; KATZ, S (1978). "Assessment of tissue fluid histamine levels in patients with urticaria". Journal of Allergy and Clinical Immunology. 61 (6). Elsevier BV: 350–354. doi:10.1016/0091-6749(78)90113-6. ISSN   0091-6749. PMID   659726.
  29. ↑ SMITH, C; KEPLEY, C; SCHWARTZ, L; LEE, T (1995). "Mast cell number and phenotype in chronic idiopathic urticaria". Journal of Allergy and Clinical Immunology. 96 (3). Elsevier BV: 360–364. doi: 10.1016/s0091-6749(95)70055-2 . ISSN   0091-6749.
  30. ↑ ELIAS, J; BOSS, E; KAPLAN, A (1986). "Studies of the cellular infiltrate of chronic idiopathic urticaria: Prominence of T-lymphocytes, monocytes, and mast cells". Journal of Allergy and Clinical Immunology. 78 (5). Elsevier BV: 914–918. doi: 10.1016/0091-6749(86)90240-x . ISSN   0091-6749. PMID   3491100.
  31. ↑ Sabroe, Ruth A.; Poon, Eric; Orchard, Guy E.; Lane, David; Francis, David M.; Barr, Robert M.; Black, Martin M.; Black, Anne Kobza; Greaves, Malcolm W. (1999). "Cutaneous inflammatory cell infiltrate in chronic idiopathic urticaria: Comparison of patients with and without anti-FcϵRI or anti-IgE autoantibodies". Journal of Allergy and Clinical Immunology. 103 (3). Elsevier BV: 484–493. doi: 10.1016/s0091-6749(99)70475-6 . ISSN   0091-6749. PMID   10069884.
  32. ↑ Ying, Sun; Kikuchi, Yoko; Meng, Qiu; Kay, A.Barry; Kaplan, Allen P. (2002). "TH1/TH2 cytokines and inflammatory cells in skin biopsy specimens from patients with chronic idiopathic urticaria: Comparison with the allergen-induced late-phase cutaneous reaction". Journal of Allergy and Clinical Immunology. 109 (4). Elsevier BV: 694–700. doi: 10.1067/mai.2002.123236 . ISSN   0091-6749. PMID   11941321.
  33. ↑ Kay, A.B.; Clark, P.; Maurer, M.; Ying, S. (April 12, 2015). "Elevations in T-helper-2-initiating cytokines (interleukin-33, interleukin-25 and thymic stromal lymphopoietin) in lesional skin from chronic spontaneous ('idiopathic') urticaria". British Journal of Dermatology. 172 (5). Oxford University Press (OUP): 1294–1302. doi: 10.1111/bjd.13621 . ISSN   0007-0963. PMID   25523947. S2CID   207072761.
  34. ↑ Kay, A. B.; Ying, S.; Ardelean, E.; Mlynek, A.; Kita, H.; Clark, P.; Maurer, M. (2014). "Calcitonin gene‐related peptide and vascular endothelial growth factor are expressed in lesional but not uninvolved skin in chronic spontaneous urticaria". Clinical & Experimental Allergy. 44 (8): 1053–1060. doi:10.1111/cea.12348. ISSN   0954-7894. PMID   24902612. S2CID   204981933.
  35. ↑ Brodell, Lindsey A.; Beck, Lisa A. (2008). "Differential diagnosis of chronic urticaria". Annals of Allergy, Asthma & Immunology. 100 (3). Elsevier BV: 181–188. doi:10.1016/s1081-1206(10)60438-3. ISSN   1081-1206. PMID   18426134.
  36. 1 2 Peroni, Anna; Colato, Chiara; Zanoni, Giovanna; Girolomoni, Giampiero (2010). "Urticarial lesions: If not urticaria, what else? The differential diagnosis of urticaria". Journal of the American Academy of Dermatology. 62 (4). Elsevier BV: 557–570. doi:10.1016/j.jaad.2009.11.687. ISSN   0190-9622. PMID   20227577.
  37. ↑ Bonnekoh, H.; Scheffel, J.; Maurer, M.; Krause, K. (November 28, 2017). "Use of skin biomarker profiles to distinguish Schnitzler syndrome from chronic spontaneous urticaria: results of a pilot study". British Journal of Dermatology. 178 (2). Oxford University Press (OUP): 561–562. doi:10.1111/bjd.15705. ISSN   0007-0963. PMID   28580686. S2CID   46821999.
  38. ↑ Peroni, Anna; Colato, Chiara; Schena, Donatella; Girolomoni, Giampiero (2010). "Urticarial lesions: If not urticaria, what else? The differential diagnosis of urticaria". Journal of the American Academy of Dermatology. 62 (4). Elsevier BV: 541–555. doi:10.1016/j.jaad.2009.11.686. ISSN   0190-9622. PMID   20227576.
  39. ↑ Wu, Maddalena Alessandra; Perego, Francesca; Zanichelli, Andrea; Cicardi, Marco (2016). "Angioedema Phenotypes: Disease Expression and Classification". Clinical Reviews in Allergy & Immunology. 51 (2): 162–169. doi:10.1007/s12016-016-8541-z. ISSN   1080-0549. PMID   27113957. S2CID   26721778.
  40. ↑ de Montjoye, L.; Darrigade, A.S.; Gimenez Arnau, A.; Herman, A.; Dumoutier, L.; Baeck, M. (2021). "Correlations between disease activity, autoimmunity and biological parameters in patients with chronic spontaneous urticaria". European Annals of Allergy and Clinical Immunology. 53 (2). Edra SpA: 55. doi: 10.23822/eurannaci.1764-1489.132 . ISSN   1764-1489. PMID   31965967.
  41. ↑ Schoepke, Nicole; Asero, Riccardo; Ellrich, André; Ferrer, Marta; Gimenez‐Arnau, Ana; E. H. Grattan, Clive; Jakob, Thilo; Konstantinou, George N.; Raap, Ulrike; Skov, Per Stahl; Staubach, Petra; Kromminga, Arno; Zhang, Ke; Bindslev‐Jensen, Carsten; Daschner, Alvaro; Kinaciyan, Tamar; Knol, Edward F.; Makris, Michael; Marrouche, Nadine; Schmid‐Grendelmeier, Peter; Sussman, Gordon; Toubi, Elias; Church, Martin K.; Maurer, Marcus (2019). "Biomarkers and clinical characteristics of autoimmune chronic spontaneous urticaria: Results of the PURIST Study" (PDF). Allergy. 74 (12): 2427–2436. doi:10.1111/all.13949. ISSN   0105-4538. S2CID   195298843.
  42. ↑ Asero, R; Marzano, A V; Ferrucci, S; Lorini, M; Carbonelli, V; Cugno, M (March 17, 2020). "Co-occurrence of IgE and IgG autoantibodies in patients with chronic spontaneous urticaria". Clinical and Experimental Immunology. 200 (3). Oxford University Press (OUP): 242–249. doi: 10.1111/cei.13428 . ISSN   0009-9104. PMC   7231996 .
  43. ↑ Altrichter, Sabine; Zampeli, Vasiliki; Ellrich, André; Zhang, Ke; Church, Martin K; Maurer, Marcus (June 18, 2020). "IgM and IgA in addition to IgG autoantibodies against FcɛRIα are frequent and associated with disease markers of chronic spontaneous urticaria". Allergy. 75 (12). Wiley: 3208–3215. doi: 10.1111/all.14412 . ISSN   0105-4538. PMID   32446275.
  44. ↑ Kaplan, Allen P.; Joseph, Kusumam; Saini, Sarbjit S. (2015). "How omalizumab came to be studied as a therapy for chronic spontaneous/idiopathic urticaria". The Journal of Allergy and Clinical Immunology: In Practice. 3 (4). Elsevier BV: 648. doi:10.1016/j.jaip.2015.04.008. ISSN   2213-2198. PMID   26164583.
  45. ↑ Kulthanan, Kanokvalai; Chaweekulrat, Pichanee; Komoltri, Chulaluk; Hunnangkul, Saowalak; Tuchinda, Papapit; Chularojanamontri, Leena; Maurer, Marcus (2018). "Cyclosporine for Chronic Spontaneous Urticaria: A Meta-Analysis and Systematic Review". The Journal of Allergy and Clinical Immunology: In Practice. 6 (2). Elsevier BV: 586–599. doi:10.1016/j.jaip.2017.07.017. ISSN   2213-2198. PMID   28916431.
  46. 1 2 3 Gaig, P; Olona, M; Muñoz Lejarazu, D; Caballero, M T; Domínguez, F J; Echechipia, S; García Abujeta, J L; Gonzalo, M A; Lleonart, R; Martínez Cócera, C; Rodríguez, A; Ferrer, M (2004). "Epidemiology of urticaria in Spain" (PDF). Journal of Investigational Allergology & Clinical Immunology. 14 (3): 214–220. PMID   15552715 . Retrieved 22 December 2023.
  47. ↑ Sheldon, John M.; Mathews, Kenneth P.; Lovell, Robert G. (1954). "The vexing urticaria problem: Present concepts of etiology and management". Journal of Allergy. 25 (6). Elsevier BV: 525–560. doi:10.1016/s0021-8707(54)90034-9. ISSN   0021-8707. PMID   13211146.
  48. ↑ Bakke, P.; Gulsvik, A.; Eide, G. E. (1990). "Hay fever, eczema and urticaria in southwest Norway". Allergy. 45 (7). Wiley: 515–522. doi:10.1111/j.1398-9995.1990.tb00527.x. ISSN   0105-4538. PMID   2252162. S2CID   37734944.
  49. ↑ Zuberbier, T.; Balke, M.; Worm, M.; Edenharter, G.; Maurer, M. (April 26, 2010). "Epidemiology of urticaria: a representative cross-sectional population survey". Clinical and Experimental Dermatology. 35 (8). Oxford University Press (OUP): 869–873. doi:10.1111/j.1365-2230.2010.03840.x. ISSN   0307-6938. PMID   20456386. S2CID   41062673.
  50. ↑ HELLGREN, LARS (1972). "The Prevalence of Urticaria in the Total Population". Allergy. 27 (3). Wiley: 236–240. doi:10.1111/j.1398-9995.1972.tb01420.x. ISSN   0105-4538. PMID   4678809. S2CID   45351511.

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