Pathogenesis Of Chronic Urticaria Research Articles

Identification of key genes and molecular mechanisms of chronic urticaria based on bioinformatics.

Chronic urticaria (CU) is characterized by persistent skin hives, redness, and itching, enhanced by immune dysregulation and inflammation. Our main objective is identifying key genes and molecular mechanisms of chronic urticaria based on bioinformatics. We used the Gene Expression Omnibus (GEO) database and retrieved two GEO datasets, GSE57178 and GSE72540. The raw data were extracted, pre-processed, and analyzed using the GEO2R tool to identify the differentially expressed genes (DEGs). The samples were divided into two groups: healthy samples and CU samples. We defined cut-off values of log2 fold change ≥1 and p<.05. Analyses were performed in the Kyoto Encyclopaedia of Genes and Genomes (KEGG), theDatabasefor Annotation, Visualization and Integrated Discovery (DAVID), Metascape, Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and CIBERSOFT databases. We obtained 1613 differentially expressed genes. There were 114 overlapping genes in both datasets, out of which 102 genes were up-regulated while 12 were down-regulated. The biological processes included activation of myeloid leukocytes, response to inflammations, and response to organic substances. Moreover, the KEGG pathways of CU were enriched in the Nuclear Factor-Kappa B (NF-kB) signaling pathway, Tumor Necrosis Factor (TNF) signaling pathway, and Janus kinase/signal transducers and activators of transcription (JAK-STAT) signaling pathway. We identified 27 hub genes that were implicated in the pathogenesis of CU, such as interleukin-6 (IL-6), Prostaglandin-endoperoxide synthase 2 (PTGS2), and intercellular adhesion molecule-1 (ICAM1). The complex interplay between immune responses, inflammatory pathways, cytokine networks, and specific genes enhances CU. Understanding these mechanisms paves the way for potential interventions to mitigate symptoms and improve the quality of life of CU patients.

Atopy in chronic urticaria: an important yet overlooked issue.

Chronic urticaria (CU) is one of the most common dermatological diseases and has a significant impact on the quality of life of patients. However, the pathogenesis of this disease remains unclear. Autoimmunity in chronic spontaneous urticaria (CSU) has received considerable attention and has been studied previously. Atopy is an important characteristic of CU; however, it has not been fully recognized. Atopy predisposes individuals to immune responses to allergens, leading to type 2 inflammation and immunoglobulin E (IgE) overproduction. Compared with healthy individuals, patients with CU have a higher proportion of atopy, and an atopic background is correlated with the clinical characteristics of CU. The total IgE levels in patients with CU is significantly higher than those in healthy individuals. Although its level is not higher than that in classic allergic diseases, it is closely related to CU. Exogenous allergens, auto-allergens, and specific IgEs, which are closely related to atopy, have been reported, and their roles in CU pathogenesis are also being studied. Local and systemic atopic inflammation is present in patients with CU. This review summarizes the current knowledge regarding atopy and CU, speculating that there are CU subtypes, such as atopic CSU or atopic chronic inducible urticaria (CIndU) and that atopy may be involved in the pathogenesis of CU. These findings provide a new perspective for a comprehensive understanding of the clinical features of CU and further research regarding its pathogenesis.

Современные представления о патогенезе хронической крапивницы. Эффективные методы лечения

Современные представления о патогенезе хронической крапивницы. Эффективные методы лечения

Research progress in the pathogenesis of chronic urticaria.

Chronic urticaria is very common in clinic, but its pathogenesis is not fully elucidated. Most patients can't find the exact cause, resulting in misdiagnosis or delayed treatment. Previous studies have found that mast cell activation is the central link in the pathogenesis of chronic urticaria. Genetics, autoimmune, coagulation disorders, and infection may also be involved in the pathophysiological process of chronic urticaria. With the deepening of research, more immune and non-immune mechanisms have been gradually revealed in the pathogenesis of chronic urticaria, such as the interaction of immune cells in the microenvironment of urticaria, intestinal flora and metabolism, neuroimmunity, environmental factors and hormones. Clarifying the pathogenesis of chronic urticaria will help to find more treatment targets and provide more diversified ideas for clinical diagnosis and treatment.

Fisetin alleviates chronic urticaria by inhibiting mast cell activation via MRGPRX2.

The activation of mast cell (MC) plays an important part in the pathogenesis of chronic urticaria (CU), and the expression of MRGPRX2 (Mas-related G-protein coupled receptor X2) and the circulating levels of SP (substance P) in skin MC of CU patients increased. Fisetin is a natural flavonoid with anti-inflammatory and antiallergic pharmacological effects. This study aimed to investigate the inhibitory effect of fisetin on CU via MRGPRX2 and its possible molecular mechanisms. OVA/SP co-stimulated and SP-stimulated CU like murine models were used to evaluate the effect of fisetin on CU. MRGPRX2/HEK293 cells and LAD2 cells were used to perform the antagonism effect of fisetin on MC via MRGPRX2. The results indicated that fisetin prevented urticaria-like symptoms in murine CU models, and inhibited MCs activation by suppressing calcium mobilization and degranulation of cytokines and chemokines via binding to MRGPRX2. The bioinformatics analysis showed that fisetin might have an interaction relationship with Akt in CU. The western blotting experiments showed that fisetin downregulated the phosphorylation levels of Akt, P38, NF-κB, and PLCγ in C48/80 activated LAD2 cells. Fisetin alleviates CU progression by inhibiting mast cell activation via MRGPRX2, which may be a novel therapeutic candidate for CU.

Mast cell silencing: A novel therapeutic approach for urticaria and other mast cell-mediated diseases.

Chronic urticaria (CU) is a mast cell (MC)-dependent disease with limited therapeutic options. Current management strategies are directed at inhibiting IgE-mediated activation of MCs and antagonizing effects of released mediators. Due to the complexity and heterogeneity of CU and other MC diseases and mechanisms of MC activation-including multiple activating receptors and ligands, diverse signaling pathways, and a menagerie of mediators-strategies of MC depletion or MC silencing (i.e., inhibition of MC activation via binding of inhibitory receptors) have been developed to overcome limitations of singularly targeted agents. MC silencers, such as agonist monoclonal antibodies that engage inhibitory receptors (e.g., sialic acid-binding immunoglobulin-like lectin8 -[Siglec-8] [lirentelimab/AK002], Siglec-6 [AK006], and CD200R [LY3454738]), have reached preclinical and clinical stages of development. In this review, we (1) describe the role of MCs in the pathogenesis of CU, highlighting similarities with other MC diseases in disease mechanisms and response to treatment; (2) explore current therapeutic strategies, categorized by nonspecific immunosuppression, targeted inhibition of MC activation or mediators, and targeted modulation of MC activity; and (3) introduce the concept of MC silencing as an emerging strategy that could selectively block activation of MCs without eliciting or exacerbating on- or off-target, immunosuppressive adverse effects.

Effect of Puberty, Menstruation, Pregnancy, Lactation and Menopause on Chronic Urticaria Activity.

Chronic urticaria (CU) is a systemic disorder which is characterized by recurrent wheals and/or angioedema lasting more than 6 weeks. Sex hormones have been suggested to play a role in CU pathogenesis, however, their clinical implications have not been adequately described in the literature. To determine whether conditions that change sex hormone levels such as puberty, menstruation, pregnancy, breastfeeding, and menopause affect the course of CU. This cross-sectional questionnaire study was conducted on female CU patients at Okmeydani Training and Research Hospital UCARE Center between 2016 and 2017. The open-ended questionnaire consisted of questions evaluating the effects of hormonal changes on disease course. A total of 111 female CU patients were included in the analysis. During the perimenstrual period, CU symptoms worsened in 29% of patients but improved in 4.8%. The disease course did not change in the majority of patients during puberty, pregnancy, lactation, or menopause (100%, 96%, 83.8%, and 95.6%, respectively). Contrary to expectations, a change in sex hormone levels had no effect on the course of CU in the majority of cases. However, disease activity increased in one-third of CU patients during the perimenstrual period.

Role of substance P in the pathogenesis of chronic urticaria

Chronic urticaria (CU) is a serious issue in clinical allergology. Exact pathogenesis of diseases is unknown despite a fairly large number of studies. From clinical view, CU manifests as wheals and/or angioedema, lasting for more than 6 weeks. It is classified into spontaneous (without obvious triggers) and induced CU (in cases of evident physical and chemical stimuli). It is quite difficult to reveal its cause. Most often, the patients refer to specific foods as a trigger factor. Stress is the second leading cause of CU after breaking the diet. Mental or emotional stress has been shown to cause degranulation of mast cells (MC) and histamine release. Substance P (SP) is a neurotransmitter, which underlies neuroimmune inflammation, being considered the most informative marker of CU. The purpose of our study was to assess a role of SP in the CU pathogenesis and to determine the relationship of SP with known urticaria triggers and comorbidities.&#x0D; We examined 97 patients with CU and 68 apparently healthy individuals matched by sex and age. The levels of histamine and substance P (SP) were determined in blood serum by enzyme immunoassay. The patients were classified into groups, depending on the history of food and drug intolerance, presence of concomitant autoimmune thyroiditis (AIT), influence of stress as a trigger for CU.&#x0D; When analyzing the average levels of histamine and SP in the group of patients suffering from CU, compared with the control group, no significant correlations were found. We detected an almost 3-fold increase of histamine levels in the patients suffering from AIT (28.25 ng/mL versus 83.61 ng/mL). However, when assessing the level of histamine in patients with CU and with a history of food and drug intolerance, trigger stress and AIT, the average values of the indicator did not show significant differences. Meanwhile, when assessing the SP index in patients with a history of drug, food intolerance, AIT and stress as a trigger for CU, we have found a significant increase in SP in the patients when compared with control group (p 0.05).&#x0D; Our results confirm the neuroimmune inflammation system to be involved in genesis of mast cell activation in CU patients. Further studies are required in order to discern a specific phenotype of stress-induced CU and determine the opportunities for its psychopharmacological correction.

Circulating microRNA signatures in patients with chronic Urticaria.

Background: Chronic Urticaria (CU) is a complex skin disease that appears as recurrent raised itchy rash/angioedema or both for more than six weeks. The pathophysiology of CU is complex and has yet to be understood entirely. It is predominantly a mast cell-driven disease with the possible involvement of type 2 inflammation. Current evidence largely favors mast cell activation by an IgE-mediated autoallergic mechanism or an autoimmune mechanism by IgG autoantibodies to IgE/ high-affinity receptor of IgE. MicroRNAs (miRNA) are small coding RNAs regulating gene expression at the post-transcription level. This study aimed to investigate the circulating miRNA as potential biomarkers in CU patients compared to healthy controls. Methods: The miRNA gene expression was done in seven patients with CU and seven healthy controls. The expression of miRNA is done using TaqMan openArray human advanced miRNA Panel. ExpressionSuite Software (Thermo Fischer Scientific, Waltham, MA, USA) is used for data analysis to quantify the miRNA expressions. P<0.05 is considered to be statistically significant. Results: A significant upregulation (p<0.05) in the miR-451a, miR-9-5p, miR-150-5p, miR-296-5p, and miR-182-5p was observed in CU compared to controls. Dysregulation of miR-451a is identified as an early biomarker in allergic diseases. Functional enrichment analysis with the KEGG pathway and disease ontology databases showed that these miRNAs were associated with skin diseases and inflammation. The differentially expressed miRNAs contribute to determining the genes regulated in CU. miRNA-based therapies that target different genes in a given pathway might be a potential candidate for treating CU. Conclusion: miRNA field has grown steadily over the past few years, but the role of circulating miRNAs in CU remains relatively unexplored. This study showed that the upregulated circulating miRNA might play an essential role in CU pathogenesis and inflammation. Also, our study highlights the importance of miRNAs as a future biomarker and potential therapeutic target to be investigated.

Immunological signature of chronic spontaneous urticaria (Review).

Chronic urticaria (CU) is a condition characterized by intensely pruritic, edematous, erythematous papules lasting for more than 6 weeks. Over half of the cases have concomitant swelling of deeper tissues, known as angioedema. The socio-economic burden of the disease is significant. Unfortunately, patients with severe CU, refractory to conventional treatment, have limited and expensive therapeutic options. The pathogenesis of CU is not yet completely understood. Therefore, elucidating the pathophysiological mechanisms involved would potentially identify new therapeutic targets. It has been accepted in recent years that mast cells and their activation, followed by excessive degranulation represent the key pathophysiological events in chronic spontaneous urticaria (CSU). The triggering events and the complexity of the effector mechanisms, however, remain intensely debated topics with conflicting studies. One pathogenetic mechanism incriminated in chronic spontaneous urticaria is the response mediated by the high-affinity receptor for IgE (FcεRI) expressed on mast cells. Increasing recognition of chronic spontaneous urticaria as an autoimmune disease linked to the cytokine-chemokine network imbalance resulting from alteration of innate immune response is another pathogenetic explanation. It is likely that these different pathological mechanisms are more interconnected, both acting synergistically, rather than separately, to produce the clinical expression of CU. The discovery and understanding of pathogenic mechanisms represent the premise for the development of safe and effective immunomodulators and targeted biological treatment for severe, refractory CU.

Circulatory EVs as a predictor of chronic urticarial activity.

Background: Chronic urticaria (CU) is a common and complex disorder that occurs without any identifiable provoking factor. The mechanisms underlying CU pathogenesis are still not fully understood. The autoimmune theory of IgG autoantibodies to IgE/high-affinity receptor of IgE on mast cells and mast cell activation and autoallergy (IgE-mediated disease) might contribute to CU pathogenesis. Extracellular vesicles (EVs) are membranous vesicles released from apoptotic or activated cells of different types. In this study, we aimed to investigate circulating EVs as potential biomarkers in patients with CU compared with that in healthy controls. Methods: We studied 15 patients with CU and 16 healthy controls. Circulatory EVs (plasma) were characterized by the presence of externalized phosphatidylserine (annexin V staining). An unpaired t-test was used, and P < 0.05 was considered statistically significant. Results: We did not find significant differences in the total number of EVs in patients with CU. A significant decrease in the levels of T-cells (CD3) and endothelial cells (CD146) (P < 0.05) in these patients than in controls was found. No significant differences were observed between patients with CU and healthy controls in terms of platelets, macrophages, PECAM-1, B cells, and tissue factors. Conclusion: Endothelial cells have been shown to contribute to the pathogenesis of CU and are also targeted by mediators released by mast cells and other cellular infiltrates. We identified that circulatory endothelial and T-cell EVs might play an important role in CU pathogenesis. In addition, our study highlights the importance of EVs as future therapeutic targets to be investigated.

Association between Chronic Urticaria and Helicobacter pylori Infection among Patients Attending a Tertiary Hospital in Tanzania.

Background Chronic urticaria (CU) is a common skin disease; however, its etiology is rarely recognized. Infection due to Helicobacter pylori (H. pylori) has been shown in some studies to play a significant role in the pathogenesis of CU. Objective This study was conducted to determine the association between CU and H. pylori infection among patients attending the Regional Dermatology Training Center, Northern Tanzania, from October 2018 to April 2019. Methodology. A matched case-control study that included 55 cases and 55 controls matched by age and sex was conducted. Data were collected through direct interviews, and the results of laboratory investigations were recorded in the extraction sheet. An enzyme-linked immunosorbent assay test was used to detect H. pylori antigen in the stool samples. Conditional logistic regression was used to measure the association between CU and H. pylori. Results The total number of participants in this study was 110 patients (55 cases and 55 controls), whereby the median age was 31 (IQR 27–45) among controls versus 34 (IQR: 22–46) years among the cases. Both cases and controls had the same number of females and males. There was no significant association between CU and baseline characteristics of the participants. There was an association between CU and H. pylori infection, such that subjects with CU had a higher number of positive H. pylori test (15/55 = 27%) versus controls (6/55 = 10.1%) (p = 0.0225). The adjusted odds of CU among patients who were positive for H. pylori were sixfolds higher (OR = 6.9; CI: 1.3–36.2; p = 0.021) than those of patients who were negative for H. pylori.Conclusion There was a strong and significant association between CU and H. pylori infection. We recommend investigating for H. pylori in all cases of CU and conducting further trials on H. pylori eradication.

Altered Gut Microbiota Diversity and Composition in Chronic Urticaria.

Background The pathogenesis of chronic urticaria (CU) is closely related to imbalances in immunity. The gastrointestinal microflora provides a vast and continuous stimulation for the immune system. However, the composition and diversity of gut microflora in CU patients are rarely reported. Methods 10 CU patients and 10 healthy individuals were selected in this study, and their intestinal microbiome was detected by 16S rRNA sequencing. The data were analyzed using R language software. Results 392 bacterial OTUs were common in the CU and healthy groups, but there were 159 OTUs particularly existing in the CU group, while 87 OTUs only were observed in healthy individuals. The bacterial diversity was reduced in CU patients compared with healthy individuals. The principal component analysis (PCA) and principal coordinate analysis (PCoA) revealed that the bacterial cluster in CU patients and the healthy controls were divided into different branches. Pathogenic strains including Escherichia coli were significantly higher in CU, while Faecalibacterium prausnitzii, Prevotella copri, and Bacteroides sp. were significantly lower in CU when compared with the healthy controls. CU patients with a high abundance of Escherichia coli had no ideal effect for probiotic therapy. Conclusion Our results demonstrated that the microbial composition was significantly different between CU patients and the healthy individual, which may be the reason leading to the various outcomes of probiotic treatment.

Role of Helicobacter Pylori in Chronic Urticaria among Egyptian Patients with Dyspepsia: A case–control study

Chronic urticaria is one of the most frequent skin diseases and still its etiology is recognized only in a minority of cases. Some recent studies point out to infections due to Helicobacter Pylori as being of major importance in the pathogenesis of chronic urticaria. This study aimed to find out the association of chronic urticaria with H. pylori

Advances in Chronic Urticaria

In recent years, there have been important advances in our knowledge and management of chronic urticaria, a frequently debilitating disease. This review will be an update on the significant progress made in diagnostic and therapeutic procedures, as well as the classification, pathophysiology and assessment tools available for urticaria. Some of the latest advances will be detailed, including new findings that shed light on the mechanism of chronic urticaria. Updated information on optimal management of chronic urticaria will be discussed, including evidence on newer therapy, primarily the humanized monoclonal anti-IgE antibody, omalizumab. This is now considered to be third-line therapy after licensed doses of antihistamines and unlicensed updosing of antihistamines fourfold. Further understanding of the pathogenesis of chronic urticaria may help explain the mechanisms involved in the action of treatments. This would then aid the clinician with the appropriate diagnostic tests and therapeutic options. Extensive research on the administration of omalizumab has determined optimal dosage, the interval and duration of treatment. Recent studies have significantly advanced the treatment of chronic urticaria refractory to antihistamines, and the stepwise treatment algorithm has been updated in accordance with new evidence. Biomarkers, such as the basophil histamine release assay and autologous skin serum test, have been useful to identify chronic autoimmune urticaria, a subset of chronic urticaria, and may aid selection of third-line therapy, as well as predict speed of response and prognosis.

Biological agents in the treatment of chronic urticaria

Chronic urticaria is a common and recurrent allergic disease in dermatology. Antihistamines are the first-line treatment of chronic urticaria, but nearly half of patients show poor responses to antihistamines. Complicated pathogenesis of chronic urticaria, including imbalance of Th1/Th2 cell subsets and abnormality of inflammatory mediators, IgE and anti-FceRⅠ antibody, may be one of the important reasons why chronic urticaria is hard to cure. Biological agents can selectively regulate or inhibit immune abnormality, and have become a new approach to the treatment of chronic urticaria and other urticaria-related skin diseases. Related biological agents mainly include BCG-polysaccharide nucleic acid, gamma globulins, tumor necrosis factor (TNF) -α inhibitors, interleukin (IL) -1 blockers, rituximab, omalizumab, and so on, and play important roles in the treatment of chronic urticaria. Omalizumab, a kind of anti-IgE monoclonal antibody, has a favorable benefit/risk ratio and good tolerability, and is considered to be one of the ideal biological agents for the treatment of chronic urticaria. Key words: Urticaria; Biological agents; Antibodies, monoclonal; Rituximab; Omalizumab

Synergistic Actions of Histamine-Releasing Factor and Histamine Releasing Factor-Reactive IgE in Chronic Urticaria

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, β-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.

Altered Systemic Adipokines in Patients with Chronic Urticaria

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.

Correlation between dehydroepiandrosterone and occurrence of chronic urticaria

Chronic urticaria (CU) is a common skin disease with complex etiology and pathogenesis, and its cause is unclear in about 80% of patients. In clinic, there are many problems with CU, such as complicated condition, frequent recurrence, poor therapeutic effect of antihistamines, and so on, which seriously affect life quality of patients. In recent years, neuroendocrine-immune system dysfunction has got more and more attention, and has been suggested to play an important role in the pathogenesis of CU. Dehydroepiandrosterone (DHEA) and its sulfate derivative (DHEA-S) , which are secreted and regulated by the nervous system, participate in the process of neuroimmune regulation, and are regarded as potential factors regulating immune homeostasis. It has been reported that serum levels of DHEA and DHEA-S markedly decrease in patients with CU. It is unclear whether the decrease of DHEA and DHEA-S circulation concentrations is a primary cause or just a concomitant symptom of CU, and what role it plays in the development of CU. Key words: Dehydroepiandrosterone sulfate; Urticaria; Neuroendocrinology; Incidence; Severity of illness

Association of chronic urticaria with Helicobacter Pylori infection in Erbil: A case-control study

Background and objective: Chronic urticaria is one of the most frequent skin diseases and still its etiology is recognized only in a minority of cases. Some recent studies point out to infections due to Helicobacter Pylori as being of major importance in the pathogenesis of chronic urticaria. This study aimed to find out the association of chronic urticaria with H. pylori. Methods: A case-control study was conducted in Erbil city within the period of April 1st, 2013 to January 1st, 2014. The study included 55 cases with chronic urticaria and 55 controls that were free from features of chronic urticaria. Data was collected through direct interview and the results of laboratory investigations were recorded in a specially designed questionnaire. Enzyme-linked immunosorbent assay test was used for detection of Helicobacter pylori antigen in the stool sample. Results: The age of the 55 cases and 55 controls enrolled ranged from 13 to 65 years. Stool for Helicobacter pylori antigen test was positive in 69.1% of cases and 29.1% of controls (OR = 5.44, P ˂0.001). The mean age ± SD of positive Helicobacter pylori patients were 35.75 ± 12.64 years, with male to female ratio 1:2.8. No statistically significant association was found between Helicobacter Pylori infection with dyspepsia and duration of urticaria. Conclusions: There was a strong association of chronic urticaria with Helicobacter pylori infection. Investigating for Helicobacter pylori in all cases of chronic urticaria and conducting further trials on Helicobacter pylori eradication is recommended.