Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by intense pruritus, eczematous lesions, and relapsing course. It presents with great clinical heterogeneity, while underlying pathogenetic mechanisms involve a complex interplay between a dysfunctional skin barrier, immune dysregulation, microbiome dysbiosis, genetic and environmental factors. All these interactions are shaping the landscape of AD endotypes and phenotypes. In the “era of allergy epidemic”, the role of food allergy (FA) in the prevention and management of AD is a recently explored “era”. Increasing evidence supports that AD predisposes to FA and not vice versa, while food allergens are presumed as one of the triggers of AD exacerbations. AD management should focus on skin care combined with topical and/or systemic treatments; however, in the presence of suspected food allergy, a thorough allergy evaluation should be performed. Food-elimination diets in food-allergic cases may have a beneficial effect on AD morbidity; however, prolonged, unnecessary diets are highly discouraged since they can lead to loss of tolerance and potentially increase the risk of IgE-mediated food allergy. Preventive AD strategies with the use of topical emollients and anti-inflammatory agents as well as early introduction of food allergens in high-risk infants seem promising in managing and preventing food allergy in AD patients. The current review aims to overview data on the complex AD/FA relationship and provide the most recent developments on whether food allergy interventions change the AD course and vice versa.
Allergic asthma is the most common asthma phenotype and is characterized by IgE sensitization to airborne allergens and subsequent typical asthmatic symptoms after exposure. A form of type 2 (T2) airway inflammation underlies allergic asthma. It usually arises in childhood and is accompanied by multimorbidity presenting with the occurrence of other atopic diseases, such as atopic dermatitis and allergic rhinitis. Diagnosis of the allergic endotype is based on in vivo (skin prick tests) and/or in vitro (allergen-specific IgE levels, component-resolved diagnosis (CRD)) documentation of allergic sensitization. Biomarkers identifying patients with allergic asthma include total immunoglobulin E (IgE) levels, fractional exhaled nitric oxide (FeNO) and serum eosinophil counts. The treatment of allergic asthma is a complex procedure and requires a patient-tailored approach. Besides environmental control involving allergen avoidance measurements and cornerstone pharmacological interventions based on inhaled drugs, allergen-specific immunotherapy (AIT) and biologics are now at the forefront when it comes to personalized management of asthma. The current review aims to shed light on the distinct phenotype of allergic asthma, ranging over its current definition, clinical characteristics, pathophysiology and biomarkers, as well as its treatment options in the era of precision medicine.
Chronic Urticaria (CU) is a chronic inflammatory, predominantly mast cell-driven disease, characterized by the development of wheals and/or angioedema for more than 6 weeks. It affects approximately 1%–5% of the total population worldwide and imposes a substantial burden on health-related quality of life, significantly affecting patients' daily life. The economic impact on the health system is also not negligible, with an estimated cost per patient per year of approximately 2.000 $ in the United States. Although the underlying pathophysiology is not fully explored, autoimmune mechanisms have been proposed, including type I (“autoallergy” by means of autoantibodies to self-antigens) and type IIb (autoimmunity). Atopic, autoimmune, and psychiatric disorders are prevalent comorbidities in both children and adults with Chronic Spontaneous Urticaria (CSU). Although malignancies, cardiovascular diseases and other comorbidities have also been reported as associated diseases in patients with CSU, data remain scarce. It is still unknown whether the aforementioned comorbidities share common pathophysiological mechanisms with specific endotypes of CSU. The current review aims to overview current data on comorbidities of CU, and furthermore to comment on the potential linked pathways underlying these diseases.
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