Effects of Helicobacter Pylori on the Pathogenesis of Chronic Urticaria

• Main Author: Bakos, Noémi
• Format: Dissertation
• Language: English
• Published: ProQuest Dissertations & Theses 01-01-2003
• Subjects: Antigens; Autoimmune diseases; Bacteria; Bacterial infections; Biopsy; Cytokines; Food allergies; Histamine; Histology; Hypothyroidism; Immunology; Infections; Inflammation; Lipoproteins; Medicine; Pathogenesis; Pathology; Patients; Permeability; Public health; Thyroid diseases; Ulcers; Urticaria; Womens health
• ISBN: 9798381042009

The role of Helicobacter pylori in the pathogenesis of chronic urticaria (CU) has been questioned until recently. It is tempting to speculate that it triggers urticaria by means of an immunoglobulin E (IgE)-mediated pathway. H. pylori-specific IgE and consecutive mast cell and eosinophil activation take part in a local inflammatory process due to infection and in H. pylori-associated gastritis and ulcer. I have demonstrated an elevated total serum IgE level as compared with that in seronegative CU patients (I). Nevertheless, H. pylori-specific IgE is not common in CU, and there might not be a link between H. pyloriand CU.My findings have strengthened a beneficial effect of eradication therapy on the course of CU (I). After a follow-up of 12 weeks, there was a significant difference in the symptoms of previously seropositive, but eradicated and seronegative chronic idiopathic patients. The resolution of chronic inflammation in H. pylorigastritis is slow, and the healing takes several months. This explains the observation that the healing or improvement of CU occurred within 3-12 weeks after successful eradication.Thes data support the hypothesis that H. pyloricould play an indirect role as a triggering factor in the pathogenesis of CU.H. pylori has several immunoreactive proteins, which take part in humoral and cellular immunoreactivity. Antigastric antibodies play a role in the pathogenesis of gastric mucosal atrophy and gastritis. Type A gastritis (corpus-restricted autoimmune gastritis) is often associated with pernicious anaemia, an autoimmune disease. Immunoreactivity against some H. pylori proteins, mainly structural proteins and products, leads to cross-reactivity between essential human and H. pyloriproteins, which gives rise to extradigestive autoimmune diseases.Previous studies have demonstrated a relation between the results of autologous serum tests and H. pylori, which suggests its role in autoimmune urticaria. I have found a connection between autoimmune urticaria and the most frequent organ-specific autoimmune disorder, autoimmune thyroiditis. The association was modified by the presence of H. pylori(II).A further possible link might be a H. pylori-specific 20 kD lipoprotein. Lipoprotein may act as an autoimmune target protein in several autoimmune diseases (systemic lupus erythematosus and rheumatoid arthitis). I have demonstrated a significant difference in immunoreactivity against lipoprotein20 between CU and non-CU patients (III).In conclusion, my findings support the hypothesis that H. pylori infection may be involved in the pathogenesis of CU. However, it may be not the primary cause of CU, but rather a triggering factor involved in several different pathways. Accordingly, the eradication of H. pyloriinfection is required in seropositive patients because this may have a beneficial role in the course of CU.