Allergo Journal International最新文献

Background

Omalizumab is recommended as adjunctive therapy for antihistamine-refractory chronic spontaneous urticaria (CSU). However, its long-term effectiveness is understudied. The systemic immune-inflammation index (SII) and the systemic inflammatory response index (SIRI) have shown prognostic value in cancer, strokes, and other diseases.

Objectives

This study aimed to evaluate the long-term effectiveness of omalizumab in CSU patients while investigating potential associations of SII and SIRI with the drug survival of omalizumab.

Methods

A retrospective study was conducted using patient data from the electronic hospital database, including patients with CSU treated with omalizumab between January 2018 and May 2021. Drug survival curves were visualized using Kaplan-Meier survival analysis. and Cox regression was utilized to assess potential associations.

Results

A total of 109 CSU treated with omalizumab at the University Hospital of Zurich were included. The mean drug survival was 13.6 ± 10.9 months. The mean SII and SIRI were 796.1 ± 961.3 and 2.1 ± 3.1, respectively. The multivariate model revealed that SIRI (p = 0.098) was a more robust predictor of omalizumab’s drug survival than SII (p = 0.367), while concurrent autoimmune disease or baseline immunoglobulin E (IgE) levels showed no significant impact.

Conclusion

This study suggests the potential utility of SIRI as a superior predictive indicator for omalizumab’s drug survival in CSU patients compared to SII. Concomitant autoimmune disease or baseline IgE levels did not significantly affect the drug’s effectiveness.

Background

Medical devices are not subject to any legal obligation to declare ingredients. With an increasing number of available medical devices, increasing reports of contact allergies to these devices result in a more difficult, delayed or lack of diagnosis of the trigger.

Methods

Elaborate chemical methods, such as gas chromatography–mass spectroscopy, were able to detect novel contact allergens in medical devices.

Results

Diabetic patients requiring insulin benefit from sophisticated glucose sensor measurement systems and insulin pump systems, but are limited in their choices by the development of contact allergy. Potential contact allergens in medical adhesives, plasters, and wound dressings require extensive diagnostic testing. Contact allergic reactions to cardiac electronic implants are rare. The potential relevance of a contact allergic reaction to endoluminal stents to restenosis of the treated vascular territory is discussed. Contact dermatitis to medical gloves is usually due to the vulcanization accelerators. Mouth–nose protective or FFP2 mask-associated eczema is often irritant, very rarely allergic in origin.

Conclusion

With continued development of medical devices, new contact allergens are introduced. The declaration of their ingredients is necessary for rapid diagnosis and future prevention.

Background

Inflammation is central to the initiation of immune responses and to the pathogenesis of many diseases such as allergic contact dermatitis (ACD). ACD is an inflammatory skin disease caused by low molecular weight organic chemicals and metal ions. The immune system plays a decisive role. After protein binding, the triggering chemicals act as contact allergens that are recognized by specific T cells. Before this can happen, however, the chemicals must trigger inflammation in the skin, without which the adaptive immune system in particular is not activated.

Methods

In recent years, the inflammatory mechanisms of contact allergy have been studied at the cellular and molecular level in vivo and in vitro.

Results

Contact allergens activate the innate immune system and additionally cellular stress responses, which in interaction are responsible for skin inflammation. In this context, inflammation is required for both initial sensitization and elicitation of ACD.

Conclusion

Skin inflammation in ACD is orchestrated by the interplay of the innate immune system and cellular stress responses.

Urticaria is a common inflammatory dermatosis characterized by transient, usually intensely itching wheals mediated by mast cells. Urticarial lesions can also be mimicked by other skin diseases. Differential diagnoses of urticaria should be considered if the single urticarial skin lesion persists for more than 24 h, if hyperpigmentation, scaling, or blistering occurs, if the lesions are not itching, or if fever or arthralgias are reported. In these cases, histologic examination and thorough serologic diagnostic may help to differentiate other dermatoses, such as vasculitis, autoimmune bullous skin diseases, drug reactions, or autoinflammatory syndromes. This article summarizes common differential diagnoses of urticaria.

Background

Sensitization to epoxy resin is mostly acquired occupationally, with those employed in the construction industry being particularly affected. Cases of non-occupational epoxy resin allergy are observed less frequently. In the literature, an association between epoxy resin allergy and fragrance allergy is postulated.

Methods

Analysis of corresponding data from the Information Network of Departments of Dermatology (IVDK); literature review.

Results

In the IVDK 2013–2022, the rate of positive reactions to epoxy resin in patients with occupational dermatitis (OD) was 2.4–4.0%, in patients without OD 0.8–1.5%. Accompanying reactions to reactive diluents and hardeners prove an exposure to epoxy resins also in patients without OD. Patients sensitized to epoxy resin have an increased risk of reactions to other baseline series allergens. Case reports of non-occupational epoxy resin allergy concern work with casting resins. However, epoxy resin exposure is also possible, for example, from three-dimensional (3D) printing finishes or products for hoof repair in horses.

Discussion

Non-occupational epoxy resin allergy may be acquired not only from do-it-yourself activities in the narrow sense, which should be considered when taking the medical history. The association between epoxy resin and fragrance allergy does not go beyond the general level of associations between contact allergies with each other.

Chronic spontaneous urticaria (CsU) is a chronic inflammatory dermatosis whose etiology is not yet fully understood. In affected patients, it is often associated with a high limitation of health-related quality of life, which necessitates effective therapeutic management. Different immune cell populations such as mast cells, eosinophilic and basophilic granulocytes, and T cells are involved in the pathogenesis of CsU, whereby mast cells playing a key role. In addition, type I autoallergic reactions with auto IgE antibodies or type IIb autoimmune reactions with auto IgG antibodies have been identified in a proportion of patients. The current international guideline initially recommends the use of second-generation H1 antihistamines, first in standard, then in off-label quadruple dosing. Subsequently, the anti-IgE antibody omalizumab should be added. However, this therapy algorithm does not lead to freedom from manifestations in all patients. Therefore, various targeted therapies are currently being evaluated for their efficacy in CsU, such as off-label use of the anti-interleukin receptor alpha (IL4Rα) antibody dupilumab, the anti-IL-17A antibody secukinumab, or interleukin‑5 blockade using mepolizumab, reslizumab, or benralizumab. In addition, new promising compounds such as the Bruton tyrosine kinase (BTK) inhibitors remibrutinib and fenebrutinib, the anti-cKIT antibody barzolvolimab, the anti-SIGLEC8 antibody lirentelimab, the anti-TSLP antibody tezepelumab, the anti-C5aR1 antibody advoralimab, or the topical application of Syk kinase inhibitors are being tested, which were developed according to new insights into the pathogenesis of CsU. The BTK inhibitor fenebrutinib is currently not being pursued due to a less favorable side effect profile compared to remibrutinib, as well as the anti-IgE antibody ligelizumab, which was inferior to omalizumab therapy in a phase 3 study. Overall, there is a high need for new therapeutic strategies to better treat CsU both symptomatically and curatively. This requires a more comprehensive understanding of pathogenesis of the disease in order to develop new targeted therapies.

Summary

Urticaria can manifest at any age, including infants and young children. Urticaria is one of the most prevalent skin diseases in childhood. As in adults, a distinction is made between acute and chronic urticaria, with chronic urticaria further classified into chronic spontaneous urticaria and inducible urticaria. According to the current German S3 guideline for classification, diagnosis, and treatment of urticaria, existing literature suggests that the prevalence, disease characteristics, causes, and also the response to treatment are very similar in children and adults. The clinical hallmark of urticaria is the subjective sensation of itch. In young children who may have difficulty expressing itching, it is crucial to observe their scratching behavior during clinical examinations. Particularly in children, mastocytosis and autoinflammatory syndromes (cryopyrin-associated periodic syndromes [CAPS], especially Muckle–Wells syndrome and childhood Still’s disease) are important differential diagnoses. Autoinflammatory syndromes are characterized by additional symptoms such as fever, bone pain, muscle pain, and joint complaints. Cryopyrin-associated periodic syndromes usually manifest in infancy, so that these diseases must be considered, especially if cold-associated urticarial skin lesions are present. Appropriate and early treatment can prevent serious sequelae. In maculopapular mastocytosis (urticaria pigmentosa), reddish macules are characteristic for the disease; especially after elicitation of the Darier’s sign, differentiation from urticaria can be difficult, but the macules are permanent. Clinically, wheals and/or angioedema are found similarly to adults, indicating that mast cell-induced angioedema is also associated with childhood urticaria. In the case of exclusive angioedema, hereditary angioedema must also be considered, which usually manifests for the first time during puberty, often linked to hormone preparation usage.