Early Giant Cell Arteritis Identifying duration from symptoms to diagnosis, possible therapies and clinically-relevant cell dynamics

• Published in: Zdravniški vestnik (Ljubljana, Slovenia : 1992) Vol. 87; no. 7-8
• Main Authors: Burja, Blaž, Hočevar, Alojzija, Šemrl, Snežna Sodin, Lakota, Katja, Rotar, Žiga, Rok Ješe, Žigon, Polona, Čučnik, Saša, Nadkarni, Suchita, Peretti, Mauro, Praprotnik, Sonja, Tomšič, Matija
• Format: Journal Article
• Language: Slovenian
• Published: Ljubljana ZDRAVNISKI VESTNIK - SLOVENIAN MEDICAL JOURNAL 01.07.2018
• Subjects: Arthritis; Autoimmune diseases; Kinases; Lymphocytes; Vein & artery diseases; Veins & arteries
• ISSN: 1318-0347; 1581-0024
• DOI: 10.6016/ZdravVestn.2642

Giant cell arteritis (GCA) is the most prevalent primary systemic vasculitis in adults over 50 in Europe. It affects large and medium sized arteries; the inflammatory process can ultimately lead to stenosis or occlusion of arterial lumen resulting in severe clinical complications. In the last decade imaging in diagnostics has importantly shortened the time to disease recognition (e.g. early GCA). Fast track clinics have led to a decrease in appearance of the most severe ischemic disease complications and lower costs of therapy. In spite of fast access to appropriate therapy, the disease is chronic and patients can experience relapses, which together with glucocorticoid therapy may lead to organ and tissue damage. Therefore, viable molecular and cellular target therapies are intensely explored. The major aims of our review were to: a) identify studies with indicated time from symptom development to diagnosis, b) explore promising molecular targets for GCA therapy and c) identify clinically-relevant cellular phenotypes. Most promising molecular targets are IL-6, IL-12/IL-23, cytotoxic T–lymphocyte-associated protein-4, while therapies against TNF-α showed limited value and no clinical studies with sekukimumab targeting IL-17 in GCA have been reported to date. Potential future therapeutic targets have been discussed, including targets in signalling pathways.