Helicobacter pylori and skin autoimmune diseases

Autoimmune skin diseases are characterized by dysregulation of the immune system resulting in a loss of tolerance to skin self-antigen(s). The prolonged interaction between the bacterium and host immune mechanisms makes Helicobacter pylori(H. pylori) a plausible infectious agent for triggering autoimmunity. Epidemiological and experimental data now point to a strong relation of H. pylori infection on the development of many extragastric diseases, including several allergic and autoimmune diseases. H. pylori antigens activate cross-reactive T cells and induce autoantibodies production. Microbial heat shock proteins(HSP) play an important role of in the pathogenesis of autoimmune diseases because of the high level of sequence homology with human HSP. Eradication of H. pylori infection has been shown to be effective in some patients with chronic autoimmune urticaria, psoriasis, alopecia areata and Schoenlein-Henoch purpura. There is conflicting and controversial data regarding the association of H. pylori infection with Beh et's disease, scleroderma and autoimmune bullous diseases. No data are available evaluating the association of H. pylori infection with other skin autoimmune diseases, such as vitiligo, cutaneous lupus erythematosus and dermatomyositis. The epidemiological and experimental evidence for a possible role of H. pylori infection in skin autoimmune diseases are the subject of this review.

Helicobacter pylori infection in patients with selective immunoglobulin E deficiency

AIM: To investigate the prevalence and clinical characteristics of Helicobacter pylori(H.pylori)-infected dyspeptic patients with selective immunoglobulin E deficiency(IgE d).METHODS: All individuals who underwent serum totalimmunoglobulin E(Ig E) measurement at the Leumit Healthcare Services(Israel) in 2012 were identified in an electronic database search(n = 18487).From these,selected case group subjects were ≥ 12 years of age and had serum total Ig E < 2 k IU/L(n = 158).The control group was selected from a random sampling of the remaining subjects ≥ 12 years of age to obtain a case-control ratio of 1:20(n = 3160).Dyspeptic diseases,diagnosed no more than 5 years before serum total Ig E testing,were identified and retrieved from the electronic database using specific International Classification of Diseases diagnostic codes.Results of C13-urea breath tests were used to identify subjects infected with H.pylori.Categorical variables between case and control subjects were analyzed using Fisher's exact tests,whereas continuous variables were analyzed using χ2 tests.RESULTS: Dyspepsia was present in 27.2%(43/158) of case subjects and 22.7%(718/3160) of controls.Of these,significantly more case subjects(32/43,74.4%) than controls(223/718,31.1%) were positive for H.pylori(P < 0.01).Esophagogastroduodenoscopy was performed in 19 case and 94 control subjects,revealing that gastritis was more prevalent in IgE d case subjects than in controls(57.9% vs 29.8%,P < 0.05).Furthermore,a significantly greater proportion of case subjects presented with peptic duodenal ulcers(63.2% vs 15.9%,P < 0.01).Histopathologic examination showed marked chronic inflammation,lymphoid follicle formation and prominent germinal centers,with polymorphonuclear cell infiltration of gastric glands,that was similar in case and control biopsy tissues.Finally,Ig Ed case subjects that underwent esophagogastroduodenoscopy were more likely to exhibit treatment-refractory H.pylori infections that require second-line triple antibiotic therapy(47.4% vs 11.7%,P < 0.01).CONCLUSION: IgE d is associated with higher rates ofH.pylori-associated gastritis and peptic duodenal ulcers.

Possible therapeutic role of Ig E blockade in irritable bowel syndrome

Omalizumab is a humanized monoclonal antibody that binds to the high-affinity type-I Ig E Fc receptors on mast cells(MCs) and basophils, inhibiting the Ig E immune pathway. Irritable bowel syndrome(IBS) is the most common functional gastrointestinal disorder, and dysregulation of the immune system likely contributes to its etiology and/or symptomatology. Colonic biopsies from patients with IBS demonstrate considerable increase in the number of degranulating MCs releasing histamine in proximity to nerves, and this event may underlie the common IBS symptom of abdominal pain. Pharmacologic control of MC activation and mediator release is a current area of active interest in the field of IBS research. Recently, we and Pearson et al described 2 cases of patients with IBS with diarrhea(IBS-D) showing positive clinical response to omalizumab. In both cases, the female patients had severe, long-lasting IBS-D and achieved an almost complete resolution of IBS symptoms. Both patients were also able to discontinue all IBS medications after commencing the anti-Ig E therapy. For both patients, the omalizumab treatment showed a relatively rapid onset of action, resembling the efficacy observed in and previously reported for patients with chronic spontaneous urticaria. In this Editorial, we discuss the possible biological mechanisms that may underlie the clinical efficacy of omalizumab in IBS. We suggest that there is a need for a well-designed prospective study to investigate the therapeutic effects of anti-Ig E in IBS.