Histologic studies of chronic idiopathic urticaria

doi:10.1016/0091-6749(83)90096-9

Journal of Allergy and Clinical Immunology

Volume 71, Issue 2, February 1983, Pages 177-183

https://doi.org/10.1016/0091-6749(83)90096-9 Get rights and content

Abstract

Skin biopsy specimens were obtained from 43 consecutive patients with chronic idiopathic urticaria and from seven normal controls. Of 43 patients, 42 had a non-necrotizing perivascular infiltrate composed primarily of mononuclear cells. There was no evidence of damage to vessel walls, of nuclear debris, or of extravasation of red blood cells, and most cells were seen around vessels rather than within the vessel wall. One patient had vasculitis with a neutrophilic infiltrate, nuclear debris, and positive immunofluorescence. Quantitative cell counts revealed four times the number of mononuclear cells and 10 times the number of mast cells in urticaria biopsy sites vs normal skin. Thus chronic urticaria is characterized by an accumulation of mononuclear cells and mast cells with mast cell degranulation presumably associated with hive formation. In our series, the characteristic lesion is not vasculitic. The stimulus responsible for the infiltration of skin with these cells is unknown.

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Cited by (168)

Chronic urticaria and the pathogenic role of mast cells
2023, Allergology International
The signs and symptoms of chronic urticaria (CU) are caused by the activation and degranulation of skin mast cells (MCs). Recent studies have added to our understanding of how and why skin MCs are involved and different in CU. Also, novel and relevant mechanisms of MC activation in CU have been identified and characterized. Finally, the use of MC-targeted and MC mediator-specific treatments has helped to better define the role of the skin environment, the contribution of specific MC mediators, and the relevance of MC crosstalk with other cells in the pathogenesis of CU. Here, we review these recent findings and their impact on our understanding of CU, with a focus on chronic spontaneous urticaria (CSU). Also, we highlight open questions, issues of controversy, and unmet needs, and we suggest what studies should be performed moving forward.
Autoimmune chronic spontaneous urticaria
2022, Journal of Allergy and Clinical Immunology
Citation Excerpt :
The development of both the wheals and the angioedema in CSU is due to the activation of skin mast cells and release of mediators.1 In addition to mast cells, the pathogenesis of CSU involves an inflammatory infiltrate with interplay of multiple effector cells including T cells, basophils, and eosinophils.8-10 Many patients with CSU report exacerbation of their disease in response to triggers, such as stress, infections, foods, or the intake of nonsteroidal anti-inflammatory drugs.
Chronic spontaneous urticaria (CSU) is a debilitating mast cell–driven disease characterized by recurrent wheals and/or angioedema. Substantial progress has been made in dissecting the 2 main autoimmune mechanisms that drive the pathogenesis of CSU. Type I autoimmune (autoallergic) CSU is associated with IgE antibodies against autoantigens, for example, thyroid peroxidase and IL-24. Type IIb autoimmune CSU is mediated by autoantibodies that activate mast cells, for example, via IgE and FcεRI, and is present in less than 10% of patients with CSU when strict criteria are used, that is, triple positivity of autologous serum skin test, immunoassays for IgG autoantibodies, and basophil activation tests. A subpopulation of patients with CSU has both types. Type IIb autoimmune CSU is characterized by higher disease severity, concomitant autoimmune diseases, low levels of total IgE, elevated levels of IgG-anti–thyroid peroxidase, basopenia, eosinopenia, poor response to antihistamines and to omalizumab, and a good response to cyclosporine. Novel targeted therapies for CSU are under development such as ligelizumab, an anti-IgE, fenebrutinib and remibrutinib, Bruton's tyrosine kinase inhibitors, and dupilumab, an anti–IL-4Rα. Further studies should investigate the overlap between autoallergic and type IIb autoimmune CSU, optimize the diagnosis of both autoimmune endotypes using easy-to-perform, noninvasive, and inexpensive markers, and assess differences in response to therapy.
Skin Biopsy in Chronic Urticaria: When and Where and What to Look for?
2021, Actas Dermo-Sifiliograficas
La urticaria crónica es una entidad relativamente frecuente en la práctica clínica habitual, cuyo diagnóstico se establece de forma clínica. Sin embargo, existen ocasiones en las que está indicada la realización de una biopsia cutánea para confirmar el diagnóstico y diferenciarla de otras patologías que pueden cursar con erupciones urticariformes. En este trabajo revisamos los hallazgos histopatológicos que podemos encontrar tanto en la urticaria crónica como en las patologías que plantean un diagnóstico diferencial. Con base en ello, proponemos un algoritmo que recoge las indicaciones para realizar una biopsia cutánea y la orientación del diagnóstico en función de los hallazgos histopatológicos que encontremos en la misma.
Chronic urticaria is a relatively common condition in dermatology and is usually diagnosed on clinical grounds. Skin biopsy, however, may be indicated in certain cases to confirm diagnosis and rule out other conditions that can cause hive-like rashes. We review histopathologic findings seen in both chronic urticaria and other entities in the differential diagnosis. We then propose an algorithm of indications for skin biopsy in patients with hive-like rashes and suggest possible diagnoses based on the histopathologic findings.
What is neutrophilic urticaria?
2019, Annales de Dermatologie et de Venereologie
L’existence de l’urticaire neutrophilique (UN), en tant qu’entité nosologique, est encore débattue. Pour certains, l’UN est à considérer comme une urticaire banale puisqu’un infiltrat à prédominance de polynucléaires neutrophiles (PNN) existe dans certains cas d’urticaire chronique ou aiguë. Il a d’ailleurs été décrit que l’aspect histologique des urticaires chroniques variait selon le délai entre l’apparition de la plaque et la réalisation de la biopsie : la présence de PNN peut être tardive. D’après la littérature, il ne semble pas exister de caractéristiques cliniques spécifiques associées à la présence de PNN en histologie. La majorité des études mettent en évidence un syndrome inflammatoire biologique modéré. Les données sont contradictoires concernant la réponse au traitement : certaines études ne mettent pas en évidence de différence significative en termes de réponse au traitement par rapport à l’urticaire banale, alors qu’une seule met en évidence une meilleure réponse avec la dapsone en cas d’infiltrat neutrophilique à l’histologie. Il ne semble pas y avoir de pathologie associée plus fréquente en cas d’UN. En conclusion, les données concernant l’UN sont insuffisantes pour affirmer l’existence d’une telle entité. Une étude prospective comparant des biopsies systématiques d’urticaires aiguës et chroniques serait souhaitable afin de mieux caractériser les relations entre l’infiltrat cellulaire et la réponse au traitement.
Some debate continues to surround the existence of neutrophilic urticaria (NU) as a nosological entity. Certain authors consider NU as a banal form of urticaria since an infiltrate predominantly made up of polynuclear neutrophils (PNN) is seen in certain cases of chronic and acute urticaria. Moreover, it has been stated that the histological appearance of chronic urticaria varies according to the time between appearance of the plaque and the performance of biopsy: the presence of PNN may occur later. According to the literature, there appear to be no specific clinical characteristics associated with the presence of PNN at histology. Most cases exhibit moderate laboratory inflammatory syndrome. Data concerning therapeutic response are contradictory: some studies have shown no significant difference in terms of therapeutic response in relation to banal urticaria, while only one study has demonstrated superior response to dapsone in the case of histologically demonstrated neutrophilic infiltrate. There does not appear to be any disease more frequently associated in the event of NU. In conclusion, the available data concerning NU are insufficient to confirm the existence of this condition. A prospective study comparing routine acute and chronic urticaria biopsies would be extremely useful to better characterise the relationships between cellular infiltrate and therapeutic response.
Arterial Injection Treatment
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Association of TG2 from mast cells and chronic spontaneous urticaria pathogenesis
2016, Annals of Allergy, Asthma and Immunology
Mast cells and their mediators play important roles in chronic spontaneous urticaria (CSU) pathogenesis. Transglutaminase 2 (TG2) is expressed in activated mast cells and contributes to airway inflammation in allergic asthma.
To investigate the role of TG2 in CSU.
Patients with CSU (n = 72) and healthy controls (n = 51) were evaluated. Skin biopsy specimens were obtained from 5 patients with CSU and 2 healthy controls. Cord blood–derived human mast cells and peripheral blood–derived human mast cells were activated with IgE. TG2 activity and inflammatory mediators, such as histamine, leukotriene C4, and cytokines, were measured in serum or supernatant from cultured mast cells by enzyme-linked immunosorbent assay. Colocalization of mast cells and TG2 was determined in skin tissues by immunofluorescence.
TG2 activity was significantly higher in serum samples from patients with CSU than in serum samples from healthy controls (P < .001). Colocalization of mast cell surface marker c-kit and TG2 was significantly increased in the lesional skin of patients with CSU compared with that in healthy controls. The levels of histamine, leukotriene C4, tumor necrosis factor α, transforming growth factor β, and interleukins 4, 5, and 6 were significantly higher in patients with CSU than in healthy controls (P < .001). Serum TG2 levels had positive correlations with each inflammatory mediator (P < .001). TG2 activity was increased in cord blood–derived human mast cells (CBMCs) and peripheral blood–derived human mast cells activated with IgE compared with those without activation (P < .05).
Our findings suggest that TG2 expressed in and released from mast cells plays an important role in CSU pathogenesis.

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Original articleHistologic studies of chronic idiopathic urticaria

Abstract

J Allergy Clin Immunol

J Allergy Clin Immunol

J Allergy Clin Immunol

J Invest Dermatol

Lancet

J Invest Dermatol

J Invest Dermatol

Urticaria and angioedema

Hypocomplementemia in chronic idiopathic urticaria

Ann Intern Med

Original article
Histologic studies of chronic idiopathic urticaria