Immunological effects and potential mechanisms of action of autologous serum therapy in chronic spontaneous urticaria.

BACKGROUND: Autoimmune processes are considered to play a major role in the pathogenesis of chronic spontaneous urticaria (CSU). Very recently, interleukin 24 (IL-24) has been identified as an immunoglobulin E (IgE) autoantigen in CSU. Some studies revealed that notably autologous serum skin test (ASST)-positive CSU patients may benefit from autohemotherapy; however, the mechanisms of action remain unknown. We aimed to investigate the immunological effects of autologous serum injections in ASST-positive CSU patients. METHODS: Sixty-six ASST-positive CSU patients were treated with weekly intramuscular autologous serum injections for 8 weeks and followed up for 12 weeks. Urticaria activity score (UAS7) and Dermatology Life Quality Index (DLQI) were assessed. The ASST was done at baseline, week 9 and week 21. Serum samples (baseline, weeks 9, 13 and/or 21) were analysed for the levels of IgE-anti-IL-24 and immunoglobulin G (IgG)-anti-IL-24 via ELISA and their ability to release histamine in basophils [basophil histamine release assay (BHRA)]. RESULTS: Autologous serum therapy resulted in a substantial improvement in disease activity and quality of life after 8 and 20 weeks. Twenty-eight percent and 34% of patients turned ASST-negative in weeks 9 and 21, respectively, but there was no link between their response to treatment and changes of ASST results. Also, no significant or relevant changes in BHRA were observed. In contrast, autologous serum therapy significantly decreased IgE-anti-IL-24 serum levels, but not IgG-anti-IL-24 serum levels, in responders but not in non-responders. CONCLUSIONS: Our findings suggest that the immunological effects of autologous serum therapy include a reduction in IgE-anti-IL24 autoantibodies, which may contribute to the pathogenesis of CSU.

[Classification and pathophysiology of angioedema]. / Klassifikation und Pathophysiologie von Angioödemen.

BACKGROUND: The classification of angioedema in daily clinical practice is often challenging. OBJECTIVES: The goal is to review the most recent classification of angioedema and to discuss the underlying pathology. MATERIALS AND METHODS: Current guidelines and research on the pathophysiology and classification of angioedema were evaluated. RESULTS: Angioedema is mast cell mediator-induced or bradykinin-mediated. Classic examples for mast cell mediator-induced angioedema are acute angioedema due to allergic reactions or acute urticaria as well as recurrent angioedema in chronic urticaria. Bradykinin-mediated angioedema forms include hereditary angioedema and angiotensin converting enzyme (ACE) inhibitor-induced angioedema. Bradykinin-mediated angioedema is less common than mast cell mediator-induced angioedema and often more severe. The diagnostic workup of angioedema patients includes a good medical history and subsequent laboratory testing. CONCLUSIONS: In most cases, mast cell mediator-induced and bradykinin-mediated forms of angioedema are readily classified clinically and/or by laboratory tests. In very rare cases, however, the cause and mediators of angioedema remain unknown.