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Atopic dermatitis (AD) is a chronic inflammatory heterogenous skin condition marked by immune dysregulation and impaired skin barrier function.1,2 For healthcare professionals seeking to understand the immunologic drivers of AD, the OX40L signaling axis has emerged as a key pathway involved in T-cell activation and chronic inflammation.2,3
Atopic dermatitis (AD) is a chronic inflammatory condition caused by complex underlying pathophysiology, driven by genetic, immunologic and environmental factors and triggers that collectively disrupt the epidermis.1-3 Despite the range of treatment options available, patients continue to experience fluctuations in disease activity due to the heterogeneity of AD.4-6 There remains an unmet need to develop a deeper understanding of the diverse immune dysregulation profiles found in patients with AD and determine optimal treatment on a more personalized basis.4,6
Atopic dermatitis (AD) is a heterogenous disease defined by contributions from multiple distinct inflammatory pathways.1 Although type 2 inflammation‘s role in AD pathogenesis is well-characterized, other non-type 2 T cell-mediated pathways also play a role in AD chronicity.1,2 For healthcare professionals seeking to understand the diversity of immune signatures in their AD patients, looking beyond Th2 cytokines is essential.1
Atopic dermatitis (AD) is a chronic, immune-mediated inflammatory disease that often begins in early infancy and persists into adulthood.1-3 While symptoms such as the intense itch that disrupts the lives of patients are well known, AD also imposes a profound chronic ‘hidden burden’ that extends far beyond visible skin lesions, significantly impairing patients' mental health, relationships, and daily productivity.1-11 This burden can be compounded by the treatment regimens themselves, which can be time-consuming, economically straining, and limited by low patient satisfaction and patient phobias of treatments and their side effects.12-14
Hemophilia is an inherited bleeding disorder caused by a deficiency of either clotting factor VIII (hemophilia A) or IX (hemophilia B), leading to impaired blood clotting and an increased risk of prolonged or spontaneous bleeding. Clotting factor therapy, which involves intravenous administration of factor VIII or IX, restores the clotting and remains a cornerstone of hemophilia management.1,2 While other treatments are available, this article focuses specifically on clotting factor replacement delivered through intravenous infusion.
Pharmacokinetic (PK) testing with accurate Factor VIII assays may help personalize hemophilia A treatment.1,2 This article reviews one-stage and chromogenic methods and their clinical use.
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MAT-US-2405607-v1.0-06/2024
