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Amaç: Blastocystosis diyare, karin agrisi, gaz hissi gibi non-spesifik belirtilerle iliskilendirilmektedir. Bu çalismada, blastocystosisin ürtiker ve gastrointestinal sistem yakinmalari ile olan iliskisinin arastirilmasi amaçlanmistir.

Chronic spontaneous urticaria (csU), which is characterized by recurrent episodes of mast cell-driven wheal and flare-type skin reactions, is often associated with elevated total IgE levels and thyroid autoimmunity. We speculate that some csU patients express IgE autoantibodies against thyroid antigens such as thyroid peroxidase (TPO), which could bind to skin mast cells and induce their activation. We developed and used a site-directed human IgE capture ELISA to quantify IgE-anti-TPO. We used this assay and investigated csU patients (n = 478) and healthy control subjects (n = 127) for IgE-anti-TPO and then assessed IgE-anti-TPO-positive and -negative csU patients for clinical and serological differences. CsU patients were found to express more than 2fold higher IgE-anti-TPO serum levels as compared to healthy control subjects (p<0.001). 54% of csU patients had serum levels higher than the cut off ( = 5 IU/ml). By distribution analyses we identified two distinct subpopulations of csU patients: 1) IgE-anti-TPO(low) ( = 39%, IgE-anti-TPO: median 2.17 interquartile range 0.86-5.44,  =  comparable to healthy controls) and 2) IgE-anti-TPO(high) ( = 61%, IgE-anti-TPO: median 6.67, interquartile range 5.39-8.24). IgE-anti-TPO-positive and -negative csU patients had very similar distributions of age and gender as well as disease activity and duration. IgE-anti-TPO-positive csU patients exhibited significantly higher IgG-anti-TPO levels and lymphocyte counts as well as decreased C4 complement levels. Our findings show that a sizeable subgroup of csU patients expresses IgE antibodies against thyroid peroxidase. These autoantibodies could cause \"autoallergic\" mast cell activation, a novel pathomechanism of chronic spontaneous urticaria.

Oral H 1 -antihistamines (AHs) are the most commonly used therapy to treat allergic rhinitis and chronic urticaria. Older, first-generation AHs (e.g. diphenhydramine, hydroxyzine) have significant and common side effects including sedation, impairment with decreased cognitive function, poor sleep quality, dry mouth, dizziness, and orthostatic hypotension. These drugs have also been found to result in death from accidents, intentional or unintentional overdoses, and sudden cardiac death. The unfavourable risk–benefit profile of first-generation AHs led to the development of newer, less-sedating second- and third-generation AHs, which first became available in Canada in the 1980s. High-quality trials have proven that newer generation AHs are superior in safety compared to older first-generation AHs. On average, they have improved potency and efficacy. Second- and third-generation AHs are the recommended first-line treatment for mild allergic rhinitis and acute and chronic urticaria. Despite this evidence, older first-generation AHs continue to be over-utilized because of their over-the-counter (OTC) status and long history of use. The Canadian Society of Allergy Clinical Immunology (CSACI) recommends that newer generation AHs should be preferred over first-generation AHs for the treatment of allergic rhino-conjunctivitis and urticaria. To promote this recommendation, education of health professionals and the public is necessary. Further, given the dangers of older first-generation AHs, we believe they should be used only as a last resort with eventual consideration given to having them only available behind the counter in pharmacies.

The aim of this guidance is to provide recommendations to clinicians and other interested parties on chronic urticaria in children. The Italian Society for Pediatrics (SIP), the Italian Society for Allergy and Immunology (SIAIP), the Italian Society for Pediatric dermatology (SIDerP) convened a multidisciplinary panel that prepared clinical guidelines for diagnosis and management of chronic urticaria in childhood. Key questions on epidemiology, natural history, diagnosis, and management were developed. The literature was systematically searched and evaluated, recommendations were rated and algorithms for diagnosis and treatment were developed. The recommendations focus on identification of diseases and comorbidities, strategies to recognize triggering factors, improvement of treatment by individualized care.

Background Dermatological illness can affect the quality of life and may coexist with psychiatric disorders. Objective The aim of this review was to systematically evaluate the published evidence of any psychiatric disorders that may coexist with chronic urticaria (CU) and any effect psychiatric interventions may have on CU. Methods Following the Cochrane guidance, we conducted a systematic literature search using web-based search engines provided by PubMed (for Medline database), Google Scholar and Scopus for studies that have investigated the existence of psychiatric comorbidity in patients with CU. To be included, a study had to possess features, such as: (1) distinction between chronic urticaria and allergic conditions, (2) direct collection of diagnostic psychiatric data by using clinical interview and standardized questionnaires, (3) International Classification of Disorders criteria or the Diagnostic and Statistical Manual of Mental Disorders criteria for the diagnosis of mental disorders, and (4) manuscripts written or published in the English language. Unpublished research and research in progress were not included. All the eligible studies were scrutinized for any reported psychiatric interventions that had any effect on CU. The systematic review has been registered on PROSPERO (registration number CRD42019122811) and was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA). Results Twenty-five studies were identified. Almost one out of three CU patients have at least one underlying psychiatric disorder. None of the studies clarified whether the psychiatric disorders pre-existed the CU onset, and no association was found between CU severity and duration, and psychological functioning. Only one case report and two case series mentioned that treatment of psychiatric disorders with either anti-depressants, anti-anxiety drugs or psychological interventions might result in improvement of urticaria. Conclusions Patients with CU frequently experience psychiatric disorders. This highlights the need for a multidisciplinary therapeutic approach involving prompt recognition and management of any potential psychiatric disorder in addition to urticaria treatment. Further studies are needed to assess whether psychiatric disorders coexist with CU independently or follow urticaria onset and whether any psychological or psychiatric intervention may help in CU control.

Background/Aims: There is increasing evidence that exposure to air pollutants, including particulate matter (PM 2.5 , PM 10 ), nitrogen dioxide (NO 2 ), and sulfur dioxide (SO 2 ), might aggravate preexisting skin diseases such as eczema and urticaria. Here we investigated if a possible link exists between air pollution and acne vulgaris. We assessed the association between ambient air pollutant concentrations and the number of visits of patients for acne vulgaris to a dermatological outpatient clinic in Beijing, China, from April 1, 2012 to April 30, 2014. Methods: In this time period, 59,325 outpatient visits were recorded because of acne vulgaris. Daily air pollution parameters for PM 10 , PM 2.5 , SO 2 , and NO 2 were obtained from the Beijing Municipal Environmental Monitoring Center. Results: Increased concentrations of ambient PM 2.5 , PM 10 , and NO 2 were significantly associated with increased numbers of outpatient visits for acne vulgaris over the 2 years. These effects could be observed for NO 2 in a single-pollutant model and for PM 2.5 , PM 10 , and NO 2 in 2-pollutant models, which are closer to real-life exposure. Of note, these effects were specific because they were not observed for increased SO 2 concentrations, which even showed negative correlations in all test models. Conclusion: This study provides indirect evidence for a link between acne vulgaris and air pollution.

Chronic spontaneous urticaria (CSU) is defined by the appearance of wheals and a variable presence of angioedema which persists for at least 6 weeks. It represents the most common subtype of chronic urticaria and is gaining importance in civil society because of its association with impaired quality of life. Moreover, CSU has a growing impact on national health systems representing a great burden due to its variable rate of response to the approved therapies. In this scenario, the identification of clinical and molecular biomarkers is of pivotal importance. Some groups are trying to detect molecules which would be able to help clinicians in reaching a proper diagnosis; additionally, the opportunity to describe disease severity which leads to cluster patients in different groups could fill the gap in the numerous unmet clinical needs. Several biomarkers are currently being studied with the purpose to predict the response to a defined therapy; unfortunately, none of them are ready to be translated from bench to bedside.

Anaphylaxis is the most serious of all allergic reactions and can be fatal. The diagnosis is frequently delayed, and misdiagnosis often occurs with asthma or urticaria. Biomarkers such as tryptase are not routinely checked, and appropriate treatment with epinephrine is not administered in a majority of cases, increasing the risk of poor outcomes. The objective of this review is to provide a better understanding of the pathophysiology of anaphylaxis with a description of phenotypes, endotypes, and biomarkers available in both the clinical and research settings. Expanding knowledge with regard to the presentation, causes, and triggers for anaphylaxis among health care providers will improve its diagnosis and management, increase patient safety, and decrease morbidity and mortality.

Chronic spontaneous urticaria (CSU) is often associated with organ specific autoimmunity but is rarely caused by food allergy. Colourings and preservatives in pre-packaged foods, so called pseudoallergens, have also been implicated. Factors that promote inflammation or reduce anti-inflammatory mechanisms may however, predispose susceptible individuals to CSU. Chronic underlying infection and mental and emotional stress can sometimes precede the onset of CSU and once established can exacerbate the symptoms. There is early evidence of dysbiosis within the gastrointestinal tract in people with CSU and reduced levels of vitamin D are also evident. The latter may be related to the importance of vitamin D3 in increasing T regulatory function which can control a tendency to autoimmunity. It is quite possible that a state of on-going chronic inflammation with reduced anti-oxidant mechanisms may underlie the not infrequent association between CSU and metabolic syndrome. Effective treatment of CSU should involve the use of anti-histamines, intermittent steroids and anti-IgE therapy. For recalcitrant disease immune modulatory therapy has a place. However, talking therapies that reduce stress and anxiety, vitamin D3 supplementation, correction of intestinal dysbiosis and treatment of any chronic infection should also be considered.

Omalizumab is an anti-IgE monoclonal antibody (mAb) approved for the treatment of severe asthma and chronic spontaneous urticaria. Use of omalizumab is associated with reported side effects ranging from local skin inflammation at the injection site to systemic anaphylaxis. To date, the mechanisms through which omalizumab induces adverse reactions are still unknown. Here, we demonstrated that immune complexes formed between omalizumab and IgE can induce both skin inflammation and anaphylaxis through engagement of IgG receptors (Fc[gamma]Rs) in Fc[gamma]R- humanized mice. We further developed an Fc-engineered mutant version of omalizumab, and demonstrated that this mAb is equally potent as omalizumab at blocking IgE-mediated allergic reactions, but does not induce Fc[gamma]R-dependent adverse reactions. Overall, our data indicate that omalizumab can induce skin inflammation and anaphylaxis by engaging Fc[gamma]Rs, and demonstrate that Fc-engineered versions of the mAb could be used to reduce such adverse reactions.