CHRONIC AUTOIMMUNE URTICARIA IN CHILDREN

• Main Authors: Lana Stergar, Anja Koren Jeverica, Štefan Blazina
• Format: Article
• Language: Slovenian
• Published: The Society for Children with Metabolic Disorders 2021-03-01
• Series: Slovenska pediatrija
• Subjects: urticaria; child; chronic urticaria; autoinflamma-tory disease; treatment; omalizumab
• Online Access: http://www.slovenskapediatrija.si/Portals/0/Clanki/2021/Slovpediatr-2021-1-04en.pdf

Urticaria is a common disease in childhood, characterised by the appearance of a transient itchy nettle rash on the skin, which may be accompanied by angioedema. In most cases, the rash stops appearing within a few days or weeks, but occasionally it can last longer. When it persists most days of the week for at least six weeks, it is by definition chronic urticaria. Chronic urticaria can be divided into two main types, chronic inducible urticaria, where a specific trigger factor is known and chronic spontaneous urticaria, in which the trigger factor is unknown. One of the mechanisms in chronic spontaneous urticaria is autoreactivity with functional autoantibodies directed usually against the high-affinity IgE receptor, or more rarely autoantibodies, directed against IgE immunoglobulins. Nettle rash (hives) can also occur as part of some other diseases, such as maculopapular cutaneous mastocytosis, bradykinin-mediated angioedema, urticaria vasculitis, systemic mastocytosis and some autoinflammatory syndromes. These conditions are rare and for this reason, are often recognised late in the course of the disease. The delay in treatment can cause irreparable damage, e.g., renal failure in urticaria vasculitis. Some of the diseases accompanied by chronic urticaria can be treated with targeted therapy, for example, interleukin - 1 blockers in autoinflammatory conditions. Chronic spontaneous urticaria is treated with antihistamines. Omalizumab can be added if higher doses of antihistamines are ineffective. If the chronic hives persist, other immunosuppressive agents may be added.