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Introduction: Asthma and chronic urticaria (CU) are two high prevalent diseases and often coexist. The underlying relationship and potential immunological mechanism between the two diseases are still unclear. The objective of this study was to investigate the clinical and immunological feature of asthma comorbid with CU. Methods: A retrospective study was conducted. Fifty patients with asthma comorbid CU, 50 patients with asthma, and 50 patients with CU alone were included. Age and sex of the patients enrolled were matched. Data of demographic characteristics, clinical manifestations including disease severity (frequency of symptoms, age of onset, disease duration, symptom score, complication with allergic rhinitis) as well as serum immunological index including total IgE (tIgE), allergen-specific IgE (sIgE), and food-specific IgG4 (FS-IgG4), were collected and analyzed. Results: No significant differences in the frequency of symptoms, age of onset, and disease duration were found among the three groups. The score of asthma control test (ACT) in patients with asthma comorbid CU was significantly lower than that of asthma (p = 0.005); however, compared with patients with CU, the 7-day urticaria activity score (UAS7) of patients with asthma comorbid CU did not show obvious differences. Immunological index showed that the positive rates of tIgE, house dust mite (HDM)-sIgE, and FS-IgG4 were different among the three groups (p < 0.05). Patients with asthma comorbid CU had the highest rate of positive tIgE, moderate and severe positive sIgE to HDM. Egg-specific IgG4 (egg-sIgG4) had the highest positive rate in all groups. Patients of asthma comorbid CU obtained the highest rate of severe positive of egg-sIgG4. Conclusion: Our results demonstrated that patients with asthma comorbid CU have lower control level of asthma symptoms, higher tIgE and HDM-sIgE level, and highest rate of severe positive egg-sIgG4. These results indicate that comorbidity of CU in asthma obviously increases the severity of allergens. [ABSTRACT FROM AUTHOR]

Introduction: The purpose of this study was to assess the clinical effectiveness and safety profile of omalizumab as a therapeutic intervention for chronic urticaria (CU). Methods: From March 1, 2023, to September 30, 2023, data on a cohort comprising 96 patients with CU, who underwent treatment with omalizumab at our medical institution's allergy clinic, were systematically compiled. Subsequent to the administration of omalizumab, the therapeutic efficacy was assessed utilizing the 7-day urticaria activity score and the urticaria control test. Results: Based on the statistical analysis, the mean duration of therapeutic intervention was 2.4 ± 1.3 months, with a corresponding mean cumulative dosage of 765 ± 450 mg. Of the subset of 42 patients with CU who were subjected to a follow-up period exceeding 3 months, it was observed that the treatment led to complete symptom remission, and no instances of recurrence were documented. Notably, there were statistically significant differences in the treatment duration and the cumulative dosage between patients who experienced co-morbid conditions and those who did not (p < 0.01, 95% CI: 0.280–1.326; p < 0.01, 95% CI: 0.597–2.997). Furthermore, there were significant differences in the treatment duration and cumulative dosage between patients in the combined allergic rhinitis group and those in the non-combined allergic rhinitis group (p < 0.01, 95% CI: 0.204–1.305; p = 0.01, 95% CI: 0.326–2.860). Conclusion: Omalizumab demonstrates efficacy in the management of CU among Chinese patients by exerting effective symptom control and facilitating the regression of skin lesions. The assessment of its therapeutic efficacy typically requires a 12-week treatment period. Moreover, the co-occurrence of CU with other allergic disorders serves as a pertinent consideration for the adjustment of omalizumab dosing regimens. [ABSTRACT FROM AUTHOR]

Introduction: Chronic urticaria (CU) is a common skin condition that can be divided into chronic spontaneous urticaria (CSU) and chronic inducible urticaria (CIndU). Omalizumab is one treatment option for CU, but currently there are limited clinical studies of omalizumab's efficacy for treating CU in Chinese patients. This study sought to investigate the efficacy and safety of omalizumab treatment for CU patients in a Chinese patient population. Specifically, we aimed to compare the differential efficacy of omalizumab for CSU and CIndU patients and predict risk factors for recurrence. Methods: We completed a retrospective clinical data review of 130 CU patients who received omalizumab treatment from August 2020 to May 2022, with a maximum follow-up period of 18 months. Results: A total of 108 CSU patients and 22 CIndU patients were included in the study. After treatment with omalizumab, the response rate in the CSU group was higher than that in the CIndU group (93.5% vs. 68.2%), and CSU patients accounted for a higher proportion of responders and early responders (responders: 87.1% vs. 12.9%, p < 0.001; early responders: 95.7% vs. 4.3%, p = 0.001). Nonresponders had lower total immunoglobulin E (IgE) levels (75.0 vs. 167.5 IU/mL, p = 0.046) and a relatively shorter duration of treatment (1.0 vs. 3.0 months, p = 0.009) compared to responders. Early responders had shorter disease duration (1.0 vs. 3.0 years, p = 0.028), higher baseline UCT (4.0 vs. 2.0, p = 0.034), lower baseline DLQI (18.0 vs. 18.5, p = 0.026), and shorter total treatment time (2.0 vs. 4.0 months, p < 0.001) compared to late responders. All adverse events reported during treatment were mild. Seventy-four patients with CU discontinued the drug after achieving complete disease control, of which 26 (35.1%) relapsed for 2.0 months (interquartile range: 1.0–3.0 months). Compared with nonrelapsed patients, relapsed patients often had other allergic diseases (42.3% vs. 18.8%, p = 0.029), higher basal levels of total IgE (263.0 vs. 140.0 IU/mL, p = 0.033), and longer disease duration (4.2 vs. 1.0 years, p = 0.002). Relapsed patients could still achieve good disease control after restarting omalizumab therapy. Conclusion: Omalizumab was effective and safe for CSU and CIndU patients. Patients with CSU responded more quickly to omalizumab and showed a relatively better treatment effect. However, there was a possibility of relapse after discontinuation of omalizumab after complete control of CU, and in these cases, restarting omalizumab treatment after relapse was effective. [ABSTRACT FROM AUTHOR]

Background: Allergic diseases are a public health problem with the largest number of patients and the widest age distribution. Chronic urticaria (CU) is a common clinical allergic disease. Bilastine is effective in the treatment of CU, especially skin wind masses and erythema. The purpose of this study was to systematically evaluate the efficacy and safety of Bilastine in the treatment of CU symptoms and to provide an evidence-based reference for clinical rational drug use. Methods: PubMed, Scopus, the Cochrane Library, Embase, EBSCO, and other databases were searched by computer to collect the trials on the effect of bilastine on patients with CU. The retrieval time limit was established until November 2021. Two researchers independently screened the literature, extracted data, and evaluated the risk of bias in the included study. Meta-analysis was performed using RevMan5.4 software. Results: A total of 7 studies were included, including 975 patients. Meta-analysis results showed that compared to the control group, bilastine significantly improved the skin quality of life index, Total Symptom Score (TSS), and weekly urticaria activity score. The skin quality of life index DLQI score (MD = −4.98, 95% CI: −8.09 to −1.86, p = 0.002), skin symptom score TSS (MD = −1.62, 95% CI −2.29 to −0.94, p < 0.00001), the number of hives in a week UAS-7 score (MD = −25.28, 95% CI −32.36 to −18.19, p < 0.00001), and the differences were statistically significant. Conclusions: Bilastine has a better therapeutic effect on CU and can also significantly improve the clinical symptoms and quality of life of CU. [ABSTRACT FROM AUTHOR]

Background: Chronic urticaria (CU) has been associated with several systemic and autoimmune disorders. The association with atopic disorders is however controversial. The objective of this study was to perform a systematic review and meta-analysis to assess the association between CU and the atopic disorders: atopic dermatitis (AD), asthma, and allergic rhinoconjunctivitis (ARC). Methods: Search hits from PubMed, Embase, Cochrane Library, and Web of Science were systematically reviewed. English papers from 2000 to present, containing original data of the association (prevalence, incidence, or risk) between CU and any atopic disorder(s), were included. Pooled point prevalence and OR with 95% confidence intervals were calculated with a random effects model. Results: A total of 8,108 search hits were screened and reviewed. Thirty-eight studies met all inclusion criteria. The estimated pooled point prevalence of AD, asthma, and ARC in CU was 7% (5–11%, I2 = 99%), 12% (9–15%, I2 = 100%), and 22% (16–29%, I2 = 100%), respectively. Pooled ORs were estimated to 2.75 (2.05–3.68, I2 = 94%) for AD, 1.87 (1.01–3.45, I2 = 100%) for asthma, and 2.94 (1.84–4.68, I2 = 100%) for ARC. Conclusion: Pooled point prevalences of atopic disorders in CU were comparable to the general population. However, studies that compared prevalences with controls from the same population all found a significantly increased risk of atopic disorders in CU. Results should however be interpreted with caution as high heterogeneity was found in all analyses. [ABSTRACT FROM AUTHOR]

Introduction: This study aimed to evaluate factors affecting drug survival and treatment response in patients with chronic urticaria treated with omalizumab in clinical practice. Methods: This study included 386 patients with chronic urticaria. Demographic characteristics, clinical features, laboratory parameters, and omalizumab treatment data were analyzed retrospectively. The 7-day urticaria activity score (UAS7) and urticaria control test (UCT) were used to assess disease severity and treatment responses. Results: Well-controlled disease (UAS7 ≤6) was achieved in 59.3% of patients at a median of 2 months. Complete response was significantly higher in patients treated with omalizumab for ≥12 months (p < 0.001). Family history of asthma (p = 0.01) was less frequent, and disease duration (p = 0.041) was shorter in patients with well-controlled disease. Total treatment duration was longer in patients with relapse (p < 0.001) and serum Helicobacter pylori IgA positivity (p = 0.029). Discussion/Conclusion: Treatment response is better in patients treated with omalizumab for ≥12 months. However, prolonged treatment does not prevent relapse. Our findings suggest that continuous or intermittent therapy is an appropriate alternative treatment option in patients with severe chronic urticaria; however, continuous therapy can be preferred to maintain the patient's quality of life. [ABSTRACT FROM AUTHOR]

Chronic urticaria is a dermatological condition characterized by the appearance of wheals or angioedema longer than 6 weeks. It could cause serious complications such as laryngeal edema, vasculitis, and diarrhea. However, the pathologic changes of the ocular fundus caused by chronic urticaria are rarely reported. In this study, we described the pathologic changes of ocular fundus in a patient with history of chronic urticaria and central serous chorioretinopathy. A 28-year-old female was presented with blurred vision and distorted images in her right eye for 6 days. The patient was diagnosed with choroidal neovascularization. She received an intravitreal injection of conbercept (0.5 mg/eye/time) monthly. Finally, no abnormality was found in her ocular examination after 4 months of first injection. In conclusion, chronic urticaria could cause central serous chorioretinopathy, leading to choroidal neovascularization. Intravitreal conbercept injection showed an excellent local therapeutic efficacy for this eye condition. [ABSTRACT FROM AUTHOR]

Background: Anaphylaxis is a life-threatening systemic allergic reaction. Omalizumab (OMA) is an established treatment in chronic urticaria (CU), but experience in anaphylaxis is limited. Objectives: The objective was to evaluate the efficacy and safety of OMA on anaphylaxis in patients with CU who are resistant to antihistamine therapy and have a history of anaphylaxis. Method: Patients with antihistamine-resistant CU and a history of anaphylaxis were eligible. OMA was given 300 mg/150 mg every 4 weeks. Urticaria control test (UCT) scores, the episodes of anaphylaxis, and adverse events were recorded during the OMA treatment. Results: A total of 7 adults were included. After starting OMA, all of them achieved a complete control (UCT = 16) after 3 months of OMA treatment; 6 of them did not suffer any attack of anaphylaxis in the follow-up periods (5 patients for more than 12 months and 1 patient for 4 months). No adverse events were observed. Conclusion: The study indicated the efficacy and safety of OMA for antihistamine-resistant CU patients with a history of anaphylaxis and its potential as a prevention option for anaphylaxis. [ABSTRACT FROM AUTHOR]

Background: Some forms of chronic urticaria (CU) can be specifically attributed to a response to a definite trigger, referred to as chronic inducible urticaria (CIndU). We aimed to assess the demographics, clinical characteristics, comorbidities, natural history, and management of pediatric patients with CIndU. Methods: Over a 6-year period, children presenting to the allergy clinic at the Montreal Children's Hospital (MCH) with CIndU were prospectively recruited. CU was defined as the presence of wheals and/or angioedema, occurring for at least 6 weeks. A standardized diagnostic test was used to establish the presence of a specific form of urticaria. Resolution was defined as the absence of hives for 1 year without treatment. Results: Sixty-four patients presented with CIndU, of which 51.6% were male, with a median age of 12.5 (interquartile range 7.3, 15.9) years. Cold CU and cholinergic CU were the most common subtypes (60.3 and 41.3%, respectively). Basophil counts were undetectable in 48.4% of the cases, and C-reactive protein levels were elevated in 7.8% of patients. Of all cases, 71.4% were controlled with second-generation antihistamines. The resolution rate was of 45.3% (95% confidence interval 33.1–57.5%), based on per-protocol population within the 6-year course of the study. Resolution was more likely in patients who presented with well-controlled urticaria control test scores and elevated CD63 counts and in those suffering from thyroid comorbidity. Conclusion: The natural history of CIndU resolution in pediatric patients was relatively low and was associated with elevated CD63 levels, as well as thyroid comorbidity. [ABSTRACT FROM AUTHOR]

Omalizumab is approved for use in chronic spontaneous urticaria (CSU); however, it is not approved for chronic inducible urticaria (CIndU). The aim of the present study was to assess the effectiveness of omalizumab in treating CSU and CIndU in Italy. This is a multicentre prospective observational real-life study involving patients with severe urticaria capable of undergoing omalizumab therapy. We enrolled 127 patients (59.1% females), ranging in age from 15 to 83 years, 69.3% had CSU alone, 26.8% had CSU and CIndU, and 3.9% had only CIndU (30.8% delayed pressure, 35.9% dermographic, 15.3% cholinergic, 12.8% cold, 5.1% aquagenic). After the first cycle of omalizumab (300 mg every 4 weeks for 24 weeks), 16 CSU patients and 10 patients (20.5%) with CIndU with or without CSU did not require a second cycle of omalizumab (300 mg every 4 weeks for 20 weeks). The patient with aquagenic urticaria achieved remission after the first cycle. None showed a lack of response to the second cycle of omalizumab. Omalizumab is a promising drug for both spontaneous and inducible chronic urticaria. Current evidence indicates that omalizumab may be approved also for CIndU. [ABSTRACT FROM AUTHOR]

The etiology of chronic urticaria (CU) remains elusive. Histamine-releasing factor (HRF) is reported to have a proinflammatory role in asthma and immediate hypersensitivity of the skin. The aim of this study was to examine the role of HRF in the pathogenesis of CU. Forty patients with CU were enrolled and their serum HRF concentrations were determined by ELISA. The results demonstrated that the concentrations of HRF and HRF-reactive IgE in the CU group were significantly higher than those in the control group, and there was a significant linear correlation between HRF and HRF-reactive IgE concentrations (r = 0.859, p < 0.001) in CU patients. Additionally, the HRF-reactive IgE concentration was significantly correlated with the disease activity (r = 0.693, p < 0.0001). HRF and HRF-reactive IgE alone failed to activate LAD2 cells. After being primed by the patient sera with the highest IgE concentrations and stimulated by HRF, ß-hexosaminidase can be released from LAD2 cells. Our findings suggest that the synergistic actions of HRF and HRF-reactive IgE may play important roles in the pathogenesis of CU. [ABSTRACT FROM AUTHOR]

Omalizumab is very effective in the majority of patients with severe chronic spontaneous urticaria (CSU), but its mechanism of action is still unclear. In CSU the coagulation cascade is activated with an intensity that parallels the disease severity, and elevated plasma D-dimer levels are associated with a poor response to both antihistamines and cyclosporin. We measured D-dimer plasma levels before and after the first administration of omalizumab in 32 patients with severe CSU. A number of clinical and laboratory parameters were recorded, including the urticaria activity score, presence of angioedema, disease duration, C-reactive protein, anti-nuclear, and anti-thyroid antibodies. Baseline D-dimer levels were elevated in 19 (59%) cases. Omalizumab induced a complete response in 25 patients (78%), in most cases already after the first administration. At baseline, 14/25 responders had increased D-dimer plasma levels versus 5/7 non-responders. All responders showed a dramatic decrease of D-dimer plasma levels after the first administration of the drug (from 1,024 ± 248 [mean ± SE] to 251 ± 30 ng/mL; p = 0.003). In contrast, non-responders did not show any reduction in D-dimer levels after omalizumab administration (from 787 ± 206 to 1,230 ± 429 ng/mL; p = ns). In conclusion, plasma levels of D-dimer are frequently elevated in patients with severe CSU before omalizumab administration and decrease according to the clinical response of the disease to the drug, suggesting a possible effect of omalizumab on coagulation activation and fibrin degradation in a subset of CSU patients. [ABSTRACT FROM AUTHOR]

Background: Chronic spontaneous urticaria (CSU) is an idiopathic condition that seriously affects quality of life. It is well known that oxidative stress and nitrosative stress (NS) are generally involved in many chronic inflammatory diseases. This study aimed to evaluate the possible role of NS in the pathogenesis of CSU. Methods: Thirty-two children with CSU and 22 healthy control subjects were enrolled in the study. Demographic and clinical features were defined, and disease activity was quantified using the urticaria activity score (UAS). Serum NS was assessed by the plasma levels of total nitric oxide (NOx) metabolites and nitrite and nitrate measurements using a Griess method-based commercial kit. Results: Plasma NOx levels were 82.5 ± 11.3 µmol/L in the CSU group and 50.9 ± 9.4 µmol/L in the control group. The difference was statistically significant (p < 0.001). CSU patients also had higher plasma nitrite levels than controls (53.3 ± 13.8 vs. 30.2 ± 10.1 µmol/L, respectively, p < 0.001). The median values of plasma nitrate were 27.5 µmol/L (IQR 19.1-35.5) in CSU patients and 20.9 µmol/L (IQR 17.9-23.2) in the control group, and the difference was statistically significant (p = 0.009). In addition, plasma NOx and nitrite levels were positively correlated with the UAS (rho = 0.512, p = 0.03 and rho = 0.452, p = 0.011, respectively). Conclusion: Plasma NS is elevated and positively correlated with disease activity in children with CSU. [ABSTRACT FROM AUTHOR]

Background: Increasing evidence suggests that adipokines affect immune responses and chronic urticaria (CU) is associated with an altered immune response related to chronic systemic inflammation. Our objectives were to investigate whether adipokines are involved in CU pathogenesis and to outline relationships between adipokines and urticaria severity and quality of life. Methods: Serum adiponectin, leptin, lipocalin-2 (LCN2), interleukin (IL)-10, IL-6, and tumor necrosis factor (TNF)-α concentrations were measured by enzyme-linked immunosorbent assays in 191 CU patients and 89 healthy controls. The effect of LCN2 on N-formyl-methionine-leucine-phenylalanine (fMLP)-induced neutrophil chemotaxis was assessed using migration assays. CU severity was assessed based on the urticaria activity score (UAS). To explore relationships between adipokines and UAS and the chronic urticaria-specific quality of life (CU-QoL) questionnaire, a structural equation model was used. Results: Mean levels of serum LCN2, TNF-α, IL-6, and IL-10 were significantly higher in CU patients than in controls. Adiponectin levels were significantly lower in patients with CU than in controls. While serum IL-6 levels were significantly higher in refractory CU patients, compared to responsive CU individuals, LCN2 levels were significantly lower. LCN2 inhibited fMLP-induced neutrophil migration. LCN2 showed a direct relationship with UAS (β = -0.274, p < 0.001), and UAS was found to contribute to CU-QoL (β = 0.417, p < 0.001). Conclusions: Our results highlighted an imbalance in pro- and anti-inflammatory adipokines in CU patients. We suggest that LCN2 could be a differential marker for disease activity and the clinical responses to antihistamine treatment in CU patients. Modulation of systemic inflammation may be a therapeutic strategy for treating severe, refractory CU. [ABSTRACT FROM AUTHOR]

Background: The basophil activation test (BAT) using CD63 expression is a sensitive and specific tool for the diagnostic workup of autoimmune chronic spontaneous urticaria (CSU). The definition of a positive BAT is directly dependent on the reference range and the cutoff values established in control populations. As of now, the pediatric reference range and cutoff values of the CD63 BAT remain to be established. Methods: In this study, we analyzed CD63 expression in 80 children (1-17 years old) without chronic urticaria (i.e., controls) and compared the values to those of a pediatric cohort of 105 CSU patients and 23 physical urticaria (PU) patients. Results: Based on the log-normal distribution of CD63 values in control subjects, the reference range and the cutoff for positive CD63 BAT values was established to be 1.2-1.8% (95% CI) and 1.8%, respectively. Children with CSU showed significantly elevated and significantly increased BAT values compared to healthy controls (Wilcoxon rank test p value <0.001). In contrast, no difference was found between BAT results in controls and PU patients. In pediatric CSU patients, a higher disease activity was associated with higher BAT values. Conclusions: Our study provides, for the first time, reference and cutoff values for the CD63 BAT in children. Our findings show that positive CD63 BAT are common in children with CSU and linked to a high disease activity. [ABSTRACT FROM AUTHOR]

Background: Platelets are implicated in many pathophysiological processes, including inflammation and immunity. Ever-growing evidence suggests the active involvement of platelets in the pathogenesis of various inflammatory disorders, including cutaneous inflammatory diseases. A limited number of studies have investigated the role of platelets in chronic urticaria (CU). In this review, we summarize the current knowledge regarding the role of platelets in chronic spontaneous and inducible urticarias. Methods: A literature search was performed using PubMed and Google Scholar, and the references of relevant literature were reviewed. Results: Overall, in CU patients, conflicting results have been obtained from the assessment of platelet indices, such as mean platelet volume, platelet count and distribution width, as well as markers of platelet aggregation and activation. Nevertheless, a few studies showed significant changes of such parameters in CU patients compared to controls, in apparent correlation with clinical severity, autoreactivity and/ or inflammatory status. Conclusions: In the absence of definitive conclusions, the pathogenic role of platelets in CU needs to be further explored. Platelets might represent a link between inflammation, coagulation and histamine release in the pathophysiological network of CU. [ABSTRACT FROM AUTHOR]

Background: Patients with chronic urticaria (CU) in the UK could be referred to health care professionals (HCPs) with diverse specialties using different guidelines. The aims of the present study were to determine which CU guidelines HCPs in the UK use, which tests they use for the diagnosis of CU, and how they manage CU. Methods: In this UK-wide survey, we designed a questionnaire covering the diagnosis and management of CU based on current guidelines. The link to the questionnaire was sent to the British Society for Allergy and Clinical Immunology (BSACI), the British Association of Dermatologists (BAD), the British Society of Immunology (BSI), and the Food Allergy and Intolerance Specialist Group (FAISG) of the British Dietetic Association (BDA), who distributed the link to their members. Results: The questionnaire was completed by 55 allergists/immunologists, 64 dermatologists, and 43 dietitians. More dermatologists used the BAD guidelines in comparison with allergists and immunologists (93.6 vs. 12.5%; p < 0.001). On the other hand, the BSACI guidelines (83.3 vs. 14.9%; p < 0.001) and the European Academy of Allergy and Clinical Immunology (EAACI)/Global Allergy and Asthma European Network (GA2LEN)/European Dermatology Forum (EDF)/World Allergy Organization (WAO) guidelines (2013) (52.1 vs. 10.6%; p < 0.001) were used by more allergists and immunologists compared to dermatologists. Differences were found between allergists/immunologists and dermatologists with regard to guidelines used, investigations performed, preference of first-line antihistamine, and prescription of alternative treatment methods. Conclusion: In conclusion, differences in the diagnosis and management of CU between HCPs of diverse specialties were identified, which reflected differences among the guidelines used. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Chronic urticaria (CU) is a common disease characterized by recurrent itchy wheals and/or angioedema for more than 6 weeks. We aimed to investigate the potential involvement of chemotactic mediators and soluble adhesion molecules as markers of endothelial dysfunction in the pathogenesis of chronic spontaneous urticaria (CSU). The potential relevance of these soluble mediators in the evaluation of disease activity was also investigated. Methods: We measured the levels of CCL5/RANTES, CXCL8/IL-8, sVCAM-1, and sICAM-1 in the sera of 87 patients with CSU and 61 normal healthy subjects (NHS) using ELISA assays. According to the results of autologous serum skin tests (ASST), CSU patients were classified into ASST-positive and ASST-negative subgroups. Furthermore, we investigated in 4 patients whether H1-antihistamine therapy decreases sVCAM-1 and sICAM-1 levels. Results: We detected a significantly higher concentration of CCL5/RANTES (p < 0.0001) but not of CXCL8/IL-8 in CSU patients compared to NHS. The serum levels of sICAM-1 and sVCAM-1 were significantly increased in CSU patients compared to NHS (p = 0.0121 and p = 0.0043, respectively). No difference in chemokine or soluble adhesion molecule levels was detected between the ASST-positive and ASST-negative subgroups. A positive correlation was found between sICAM-1 and sVCAM-1 (p = 0.0022) but not between these and CCL5/RANTES. After H1-antihistamine therapy, sVCAM-1 and sICAM-1 levels did not decrease in the 4 CSU patients tested. Conclusions: Our study suggests that CCL5/RANTES, sICAM-1, and sVCAM-1 play a potential role in the pathogenesis of CSU but they do not parallel disease activity and are not predictive of the response to H1-antihistamine therapy. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Chronic urticaria (CU) appears to be of autoimmune origin in about half of all patients, since several autoreactive immunoglobulin Gs (IgGs), such as anti-FcεRIα and anti-IgE, are detected in the sera of such patients. However, whether autoreactive IgE is associated with CU remains unclear. In this study, we attempted to identify autoreactive IgE antibodies in sera from patients with CU. Methods: Sera were collected from 67 normal subjects, 85 patients with CU and 28 patients with atopic dermatitis (AD). An autologous serum skin test (ASST) was performed on 27 of the CU patients. Autoreactive IgE and IgG levels against self-antigens were measured using enzyme-linked immunosorbent assays. The basophils were activated with dsDNA, and the CD63 expression level was examined using a fluorescence-activated cell sorter. Results: The anti-dsDNA IgE levels were significantly higher in patients with CU and AD than in normal subjects, but no differences in the anti-dsDNA IgG levels were seen. The levels of thioredoxin-, peroxiredoxin- and thyroglobulin-reactive IgE and IgG were not significantly higher in the CU patients than in the other 2 groups. There was no significant difference in the levels of anti-dsDNA IgE between ASST-positive and ASST-negative patients. The basophils from 2 out of 9 CU patients exhibited degranulation in response to dsDNA. Conclusions: Our data suggest that anti-dsDNA IgE is involved in the pathogenesis of some cases of CU. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Chronic urticaria is associated with an immune dysregulation usually mediated by T lymphocytes. Recently, Th17 and Tc17 have been implicated in autoimmune diseases; however, their role in urticaria is not clear yet. Methods: For the study we recruited 20 patients [10 of them had autoreactive chronic spontaneous urticaria (positive autologous intradermal serum test response, ASST+), and the other 10 were nonautoreactive chronic spontaneous urticaria patients (ASST-)] and 17 healthy age- and gender-matched controls (HG). The frequency and functional activity of Th17/Tc17 and Th1/Tc1 cells were evaluated by flow cytometry and type 2 cytokine mRNA by real-time PCR. Results: Our results demonstrated a significant decrease in Th17 frequency in both chronic urticaria groups compared to HG; regarding the amount of IL-17, at the single cell level, it was reduced in ASST- compared to HG. Concerning the Th1 and Th17 cells producing IFN-γ, IL-2, and TNF-α, a lower frequency was noted in chronic urticaria patients compared to HG. In contrast, a significantly increased frequency of Tc1 cells producing these cytokines was noted in ASST+ compared to HG and ASST-. Also, the frequency of Tc17 cells producing TNF-α was increased in ASST+ compared to HG; however, with respect to the amount of TNF-α, at the single cell level, we found a decrease in ASST+ compared to HG. Regarding type 2 cytokine mRNA, a higher expression was verified in ASST+ compared to HG. Conclusion: Our data suggest a probable involvement of cytotoxic T cells, mainly the Tc1 and Tc17 subsets, in chronic urticaria, particularly in the ASST+ group. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Chronic urticaria (CU) may affect up to 1% of the general population. Anisakis simplex hypersensitivity is frequent in areas where raw fish is consumed and A. simplex allergy represents a relevant cause of acute urticaria. We as-sessed the possible association between CU and A. simplex sensitization in an area where marinated fish is very fre-quently eaten. Methods: A thorough history of CU was sought in 919 adults seen at the Allergy Center, Bari. CU pa-tients and 187 controls underwent skin-prick testing with a commercial extract of A. simplex, and reactors were recom-mended a 6-month raw-fish-free diet regimen. Responders were followed after a further 3 months. Results: Of 919 sub-jects, 213 (23%) met the criteria for CU and 106/213 (49.7%) were sensitized to A. simplex with a significant difference be-tween patients aged >65 or <65 years (56 vs. 41%, respec-tively; p < 0.05). All patients hypersensitive to A. simplex were regular consumers of marinated fish. In a control population without CU, the prevalence of A. simplex sensitization was 16% (p < 0.001). The 6-month diet regimen led to the disap-pearance of urticaria in 82/106 cases (77%) versus 1/42 (2%) subjects who did not change their dietary habits (p < 0.001). All nonresponders were sensitized to house-dust mites. Of 75 responders who were followed-up after 3 months, CU re-lapsed In 88% of those who had reintroduced raw fish versus 14% of those who were still on the diet (p < 0.001). Conclu-sion: In areas where raw or marinated fish Is frequently eat-en, A. simplex hypersensitivity is a frequent cause of CU. [ABSTRACT FROM AUTHOR]

Background: Mugwort pollen is known to cross-react with a variety of spices and vegetables that are typically part of elimination diets used in the treatment of chronic urticaria (CU). Objective: We sought to investigate the association between CU and allergic sensitization to mugwort pollen. Methods: We conducted 2 case-control studies comparing aeroallergen skin prick test results between patients with and without CU and with or without allergic rhinitis (total n = 202). Results: CU patients with coexisting allergic rhinitis were more than twice as likely to be sensitized to mugwort as subjects not suffering from CU (67 vs. 30%; p = 0.004). Ragweed, cat, rat and mite sensitization were also significantly associated with CU. Overall, patients with CU had more positive aeroallergen skin tests than patients without CU (p < 0.005). Conclusion: Mugwort sensitization was associated with CU, possibly contributing to beneficial effect of elimination diets. [ABSTRACT FROM AUTHOR]

We report on a 24-year-old male, with exercise-induced asthma and intermittent abdominal pain since puberty, who suffered from recurrent anaphylactic reactions. He also complained of occasional headaches. After extensive studies he was eventually diagnosed with idiopathic anaphylaxis, once the following diagnoses had been excluded: allergic origin [foods (including ω5-gliadin), latex and drugs], hydatidosis, carcinoid syndrome, systemic mastocytosis, autonomic epilepsy, hereditary angioedema, pheocromocitoma, Meckel diverticle, medullar thyroid carcinoma, leukemia, hyper-IgE and hypereosinophilic syndromes. Given the frequency and severity of the attacks, we started off-label treatment with omalizumab, initially well tolerated. Some days after the second dose the patient started to develop recurrent urticaria. Because of these new symptoms, blood work was repeated, and elevated TSH, decreased T4, positive antithyroid antibodies and decreased cortisol levels with normal ACTH were found. The antiadrenal autoantibodies were negative. The MRI showed a slight thickening of the infundibulum, without pituitary adenoma. Suspecting an autoimmune hypophysitis, we looked for antipituitary antibodies; the result was positive. A clinical picture of recurrent anaphylactic reactions, the result of complicated adrenal crises in an asthmatic patient, was a manifestation of lymphocytic hypophysitis, a rare chronic inflammatory disease of autoimmune etiology. One year after replacement therapy had been started, the patient remained asymptomatic. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: The association of chronic urticaria (CU) with autoimmune disorders is relatively well proved. Protein tyrosine phosphatase-22 (PTPN22) is considered to be one of the strongest genetic factors for human autoimmunity. We decided to evaluate whether additional, non 1858C>T, PTPN22 variants are independent contributors to the risk of CU occurrence in the Polish population. Methods: A total of 91 CU patients with a positive result of autologous serum skin test and 100 healthy volunteers were enrolled in the study. The Urticaria Activity Score was used in disease intensity assessment. In all subjects rs3811021, rs1310182 and rs2488457 polymorphisms were genotyped. Results: We found a higher prevalence of -1123 C allele among CU patients. No differences in the allele and genotype distribution were found in the other analyzed polymorphisms. Haplotype construction of the three SNPs revealed statistically significant CU association of rs2488457C, rs1310182T and rs3811021T. Conclusions: Contrary to previous findings, the contribution of PTPN22 to disease susceptibility is suggested. We can speculate that CU is a genetically complex disease and that its occurrence needs multiple genetic and environmental risk factors. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Chronic spontaneous urticaria (CSU) is the most common form of chronic urticaria. A considerable amount of data supports an immunological basis for CSU. Some research has focused on the association between chronic urticaria and specific human leukocyte antigen (HLA) alleles. The aim of this study was to investigate the HLA status of Polish patients diagnosed with CSU. Methods: The standard complement-dependent microlymphocytotoxicity assay and PCR amplification with sequence-specific primers were used to analyze HLA alleles in 115 patients diagnosed with CSU, and the results were compared to those from 162 healthy, genetically unrelated individuals. Results: Among the HLA-A alleles, A-33 occurred significantly more often in the control group (p < 0.01). Analysis of the HLA-B allele frequencies revealed the prevalence of the B44 antigen in the study group (p < 0.0001). Frequencies of HLA-C alleles and HLA-DQ did not differ significantly between the groups. Among the HLA class II alleles, DRB1*04 was observed significantly more often in the study population (p < 0.001), mainly in the autoimmunological subtype of urticaria. Conclusion: HLA alleles may be involved in CSU development or play a protective role in CSU. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Elevated IgE levels in patients with chronic urticaria have been noted previously, but the significance of these findings has not been appreciated. Objective: To measure the IgE levels in such patients and to examine the relationship between these levels and urticarial severity, autologous serum skin test, anti-thyroid antibodies and duration. Methods: Serum total IgE levels from 203 patients with chronic urticaria were measured and compared with nonatopic individuals. Additionally, patients were assessed for urticarial severity, the presence of autologous serum skin test and anti-thyroid antibodies. Results: Of the chronic urticaria patients, 47 (23.2%) were classified as mild, whereas 67 (33%) were classified as having moderate and 89 (43.8%) as having severe chronic urticaria. Total IgE levels were elevated, above 175 U/ml, in 69/203 (34%) of patients, compared with 7/81 (8.6%) of healthy controls (p < 0.001). A significant association between increased total IgE and chronic urticaria severity was found. Whereas 93% of patients with increased level of total IgE suffered from moderate-to-severe chronic urticaria, this was observed in only 69% of patients with normal IgE (p < 0.0001). Autologous serum skin test and anti-thyroid antibodies were positive in 59/163 (36%) and 28/189 (15%) patients, respectively. A significant association between increased total IgE levels and the presence of autologous serum skin test, anti-thyroid antibodies and urticarial duration lasting more than 25 months (p < 0.0001, p < 0.0001 and p = 0.021, respectively) was also detected. Conclusions: Total serum IgE levels are frequently elevated in patients with chronic urticaria and these are associated with disease severity and duration. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Chronic urticaria (CU) patients often present activation of the coagulation cascade and fibrinolysis whose markers correlate with disease severity. Aim: We evaluated whether CU patients with elevated plasma D-dimer have a poor response to antihistamines, and anticoagulation and inhibition of fibrinolysis may be beneficial in these patients. Methods: Sixty-eight consecutive patients with CU were prescribed cetirizine 10 mg daily for 2 weeks; plasma D-dimer was measured. Non-responders were given cetirizine 30 mg daily for 1 week and subsequently, in case of failure, systemic steroids. Patients with persistent uncontrolled CU and elevated D-dimer plasma levels were offered subcutaneous nadroparin 11,400 IU once a day and oral tranexamic acid 1 g three times a day for 2 weeks. Results: D-dimer levels were elevated in 14/68 (20.6%) patients (range 306–7,317 ng/ml; normal values <278 ng/ml) and were associated with a more severe disease. Twelve of 14 patients with elevated D-dimer levels did not respond to antihistamine treatment (p = 0.0001). On the whole, 14 patients reported a poor or absent response to cetirizine 10 mg daily and only 1 of these responded satisfactorily to cetirizine 30 mg daily. Eight patients with elevated D-dimer and whose disease was not satisfactorily controlled by prednisone received nadroparin and tranexamic acid. A marked improvement of symptoms was observed in 5/8 cases. Conclusion: Our findings indicate that CU patients with elevated D-dimer often present a more severe disease with reduced response to antihistamines. Based on this short pilot study, some of these patients may benefit from treatment with nadroparin and tranexamic acid. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: The coexistence of allergic diseases and chronic urticaria (CU) is not uncommon. Our aim was to show the prevalence of allergic diseases in chronic urticaria patients and whether possible risk factors precipitate the development of these conditions. Methods: The data of 953 patients diagnosed with CU in our adult allergy clinic between January 1991 and June 2006 were retrospectively evaluated. Results: The mean ages of the CU patients with and without non-steroidal anti-inflammatory drug hypersensitivity (NSAIDH) were 39.0 ± 11.8 and 36.7± 12.3, respectively (p = 0.014). There was a female predominance in both groups (74.6 and 68.2%, respectively, p = 0.06). Apparently, some conditions occurred significantly more often in CU patients with NSAIDH compared to those without NSAIDH: 16.4 and 8.4% for asthma (p < 0.001), 4.2 and 0.8% for nasal polyps (p < 0.01), 20.8 and 7.3% for antibiotic hypersensitivity (p < 0.001), 21.6 and 12.3% for metal sensitization (p < 0.01), and 8 and 0.6% for familial NSAIDH (p < 0.001), respectively. Dermographism was more common in CU patients without NSAIDH compared to those with NSAIDH (29.4 and 21.2%, respectively; p < 0.05). NSAIDH increased the risk of asthma and rhinitis development [odds ratios: 52.9 (18.1–154.6) and 5.2 (2.0–13.4)]. Conclusion: Based on our data, the incidence rates of asthma, nasal polyps, antibiotic hypersensitivity, metal sensitization and familial NSAIDH are increased in patients with CU with NSAIDH compared to those with CU only. Coexistence of NSAIDH and CU increases the risk of developing asthma and rhinitis. Copyright © 2009 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Although several cases of chronic urticaria (CU) are currently regarded as autoimmune in origin, associated with histamine-releasing autoantibodies, an activation of blood coagulation via tissue factor (TF) and a strong expression of TF in lesional skin have been described. Eosinophils, which are involved in CU skin lesions, have recently been demonstrated as the major source of TF in human blood. We assessed whether eosinophils are the cellular source of TF in CU skin lesions. Methods: Twenty patients with severe CU were studied. Skin biopsy specimens were taken from wheals. The control group consisted of specimens of perilesional normal skin from different types of skin tumours (10) and various skin disorders with non-eosinophilic infiltrates, including leukocytoclastic vasculitis (7), lichen planus (8) and mastocytosis (3). TF expression was evaluated by immunohistochemical methods using an anti-TF monoclonal antibody. Co-localization of TF and eosinophil cationic protein, a classic cell marker of eosinophils, was investigated by double-staining studies using 2 specific monoclonal antibodies in the 4 specimens showing the highest TF reactivity scores. Results: All specimens from patients with CU clearly showed TF expression that was absent in all normal control specimens (p = 0.0001) and in the skin disorders with non-eosinophilic infiltrates (p = 0.001–0.0001). The double-staining experiments for TF and eosinophil cationic protein clearly showed that the TF-positive cells were eosinophils. Conclusions: Eosinophils are the main source of TF in CU lesional skin. This finding highlights the role of these cells in the pathophysiology of CU and might pave the way for new therapeutic strategies. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Objectives: Chronic urticaria (CU) is a common disease in which pathogenesis is unclear and which is resistant to therapy. Recent investigations have indicated that autoimmunity plays a role in nearly one third of CU patients. The present study aimed to investigate the relationship between human leukocyte antigen (HLA) class I and class II antigens and immune pathogenesis of CU. Methods: HLA class I and class II antigens were investigated in 40 patients diagnosed with CU, utilizing serologic techniques and polymerase chain reactions. The study was performed between October 2005 and May 2006. Further HLA typing in patient subsets was done depending on the response of patients to intradermal injection of autologous serum. About 30 healthy and genetically unrelated individuals formed the control group for evaluation. Results: The results revealed that HLA-B44 frequency was significantly higher (25%) in the patient group as compared with the matched control group (3.33%) (p = 0.033, OR = 9.667). There was no significant difference in HLA-A allelic distribution between the patient and control groups. In the genotyping of class II HLA alleles, HLA-DRB1*01 (25%) (p = 0.033, OR = 9.667) and HLA-DRB*15 (25%) (p = 0.033, OR = 9.667) were predominant alleles in the patient group. Conclusion: The association ofHLA-B44, HLA-DRB1*01 and HLA-DRB*15 alleles with idiopathic CU suggests that there is a genetic component in the pathogenesis of CU. Copyright © 2008 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: The presence of autoantibodies reacting with the high affinity IgE receptor (FcεRIα) usually indicates a more severe form of chronic urticaria (CU). Previously, we showed an increased lymphocyte reactivity in CU patients; however, the relation between enhanced cellular immunity and the presence of anti-FcεRIα-specific autoantibodies has not been investigated. Methods: Cellular and humoral immune reactivity of 50 CU patients and 28 healthy controls was studied.Serum sIL-2R, neopterin, and tryptase levels were measured to assess T-cell, monocyte/macrophage and mast cell activity, respectively. Helicobacter pylori (HP)-specific IgG antibody, and IgE levels were also tested. Anti-FcεRIα-specific autoantibody was determined by Western blotting. In vivo histamine-releasing activity of patients’ sera was assessed by the autologous serum skin test (AST). Results: 17/50 CU patients, who both had IgG-type anti-FcεRIα-antibodies by Western blotting and a positive AST response, were classified as autoimmune CU. All patients with CU had significantly higher serum sIL-2R and tryptase levels than healthy controls (p = 0.000257, p = 0.000166, respectively), indicating T-cell and mast cell activation. Patients with higher sIL-2R levels also had higher tryptase levels; the strongest correlation was shown in the autoimmune subgroup of patients (ρ = 0.688, p = 0.002). There was a tendency towards higher tryptase levels in the autoimmune subgroup, as compared to the nonautoimmune CU patients. While the serum IgE was significantly lower in autoimmune than in nonautoimmune CU (p = 0.000836), there was no significant difference in their sIL-2R, neopterin and HP-specific IgG antibody levels. CU patients with a positive AST response (38/50) had significantly higher tryptase levels (p = 0.0107) when compared to the negative skin test group. Conclusions: The significant correlation between sIL-2R and tryptase levels in patients with CU indicates that T cell activation is proportional to mast cell degranulation in these patients. The increased level of tryptase in autoimmune CU may suggest more severe disease.Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: An association between Helicobacter pylori and chronic urticaria has been suspected previously. An IgE-mediated pathway might be a possible link between H. pylori infection and chronic urticaria, and therefore we wanted to prepare an optimal H. pylori antigen to detect H. pylori-specific IgE antibodies in chronic urticaria patients. Methods:H. pylori antigen extracts were prepared in different ways to find the optimal antigen extract to be used in the assays. Immunoblotting was used to detect IgE-binding bands. The results were applied in an H. pylori RAST assay for specific H. pylori IgE antibodies in patient sera. Results: In immunoblotting, the largest number of IgE-stained bands were visualized in the washing fluids and sonicated extracts, while strong heating and denaturing treatments destroyed the epitopes for IgE binding, suggesting that they belonged to the flagellar structures of H. pylori. However, in H. pylori-specific RAST analysis, specific IgE was found only in 1 of 25 H. pylori-infected patients. Conclusions: Our findings suggest that although IgE-binding epitopes were found in H. pylori, H. pylori-specific IgE antibodies are not common in chronic urticaria, and the clinical significance of the IgE response is unclear.Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background:Helicobacter pylori, the most important etiologic factor of gastritis and peptic ulcer, has recently been associated with several extradigestive diseases. Previous studies reported conflicting results on H. pylori eradication in chronic urticaria, in that some studies showed a benefit, while others found no effect. Methods: Peripheral blood mononuclear cells of 24 chronic urticaria patients (13 seropositive/11 seronegative for H. pylori) and 18 healthy controls (9 seropositive/9 seronegative) were stimulated with whole heat-inactivated H. pylori (8 × 10[sup 5] , 8 × 10[sup 6 ] and 8 × 10[sup 7] bacteria/well), phytohemagglutinin (2 μg/ml) and pokeweed mitogen (5 μg/ml). The proliferative response was determined by [sup 3] H-thymidine incorporation. Helicobacter-specific IgG antibody response was determined by ELISA. Results: There were significantly higher proliferative responses to various concentrations of whole heat-inactivated H. pylori antigen in 6- to 7-day cultures of peripheral blood mononuclear cells of chronic urticaria patients compared to healthy controls. We found a tendency to exhibit a higher proliferative response to either Helicobacter antigens or mitogens in seropositive compared to seronegative patients. Conclusion: Our results support the hypothesis that there is an increased lymphocyte reactivity in chronic urticaria, perhaps further enhanced by the presence of H. pylori which, therefore, may be involved as a trigger in the pathogenesis of chronic urticaria.Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Chronic urticaria and concurrent angioedema are frustrating problems for both physicians and patients. Methods: 100 patients with chronic urticaria (mean duration 33.3±48.2 months) attending the urticaria consulting hour of our Department of Dermatology within 1 year were carefully analyzed for pathogenesis to avoid extensive unnecessary diagnostic approach in the future. Results: In 43 cases a potential infectious trigger could be identified, 35 were of idiopathic origin, and 15 demonstrated pseudoallergic reactions to acetylsalicylic acid or food additives, 5 had antibodies to thyroid gland, and 2 had malignant diseases. Of patients with foci, 26 had Helicobacter pylori–associated gastritis, 9 chronic tonsillitis or sinusitis, 4 infections with Epstein–Barr virus or cytomegalovirus, 2 dental focal infections and 2 suffered from Yersinia infection. High prevalence of H. pylori gastritis was found since 47% of patients showed elevated H. pylori–specific IgA and/or IgG antibodies. 27 patients underwent endoscopy and in all but 1 (96%) antral H. pylori infection was found. In contrast, a prevalence rate of 37% among asymptomatic adults has been published. Disappearance (67%) or improvement of urticaria (24%) occurred in most antimicrobially treated patients after 3–12 weeks. In contrast, only 50% of untreated H. pylori–seropositive patients with chronic urticaria showed spontaneous remission or improvement within 12 weeks. Prevalence of H. pylori infection may even be underestimated since only 27/100 patients underwent endoscopy. It is suggested that H. pylori infection may be present at least in all seropositive subjects (47%). Moreover, we found H. pylori infection in 2 seronegative subjects demonstrating gastric complaints. Conclusions: Thus, measurement of H. pylori–specific antibodies and/or gastroscopy should be included in the diagnostic management of chronic urticaria to identify patients who may profit from eradication treatment with disappearance of long–standing and annoying urticaria symptomatology. [ABSTRACT FROM AUTHOR]

No abstract available Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]