scholarly journals ALLERGIC RHINITIS AND ASTHMA CO-MORBIDITY

2019 ◽  
Vol 72 (4) ◽  
pp. 622-626
Author(s):  
Victoria S. Sukhan

Introduction: The combination of asthma and allergic rhinitis can affect the mutual encumbrance to which other pathogenetic mechanisms join, which worsen the course of both diseases. The aim of work is to analyze the features of the genotype and phenotype in patients with a co-morbidity of asthma and allergic rhinitis. Materials and methods: In order to detect the features of asthma and allergic rhinitis, 115 patients were examined. Patients were divided into two groups: the first included 58 patients with allergic asthma and allergic rhinitis co-morbidity, the second – 57 patients with non-allergic asthma morbidity. Results: For the group of patients with allergic asthma with concomitant allergic rhinitis, the first manifestation of allergy in childhood is characteristic (allergic rhinitis, hay fever, atopic dermatitis). For this group of patients characterized by a heavy family allergic history. Symptoms of allergic rhinitis aggravate the course of asthma. Characteristic correlation of symptoms of allergic rhinitis with distal obstruction and pronounced lability of bronchi. In these patients, the total increase in IgE and blood eosinophilia, in 1,5 times increased blood histamine and the level of exhaled NO2 have been increased. Also, asthma control with concomitant allergic rhinitis was significantly worse than in an isolated asthma group (p <0.05). Conclusion: The obtained data allow to distinguishing the phenotype of patients with asthma and allergic rhinitis co-morbidity.

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Chris RuiWen Kuo ◽  
Rory Chan ◽  
Brian Lipworth

AbstractThe concept of the unified allergic airway disease (UAD) recognises the association between allergic inflammation in the upper and lower airways. Patients with asthma and concomitant allergic rhinitis experience more asthma-related primary and secondary care visits. We therefore aimed to determine differences in asthma control (asthma control questionnaire ACQ-6), lung function (spirometry) and T2 biomarkers (FeNO and Eos) in relation to the presence of allergic rhinitis in patients with allergic asthma. Retrospectively, we evaluated a cohort of 60 consecutive patients with persistent asthma attending our research unit for screening into clinical trials. All included subjects were receiving inhaled corticosteroids (ICS) and had a positive skin prick test (SPT) to at least one common aeroallergen to fulfil the criterion of allergic asthma. Patients with UAD had a diagnosis of allergic asthma in addition to established concomitant allergic rhinitis. T2 biomarkers were significantly higher in patients with allergic rhinitis in contrast to those without. FEV1 % predicted and FEF25-75 % predicted were also significantly lower in patients with concomitant allergic rhinitis. However, there was no difference in ACQ-6 observed between groups. In summary, patients with allergic asthma, the presence of concomitant allergic rhinitis is associated with worse lung function and higher type 2 biomarkers.


2007 ◽  
Vol 9 (9) ◽  
pp. 1-13 ◽  
Author(s):  
Saffron A.G. Willis-Owen ◽  
Nilesh Morar ◽  
Charles A. Willis-Owen

Atopic dermatitis (AD) is a strongly heritable, chronic relapsing dermatosis that frequently co-occurs with other atopic phenotypes including asthma and allergic rhinitis (the so-called atopic triad disorders). However, despite high levels of co-morbidity, relatively low levels of genomic co-incidence have been observed between atopic triad disorders. Conversely, current mapping data have revealed a striking pattern of co-localisation between AD disease loci and those mapped using another chronic dermatological disease – psoriasis. In this review, we examine the evidence for co-localisation between AD and a range of atopic, infectious, inflammatory and autoimmune diseases, and consider the implications of these data for the AD disease concept and future research in the field.


Author(s):  
E.L. Savlevich ◽  
M.E. Dyneva ◽  
L.E. Gaganov ◽  
V.I. Egorov ◽  
A.N. Gerasimov ◽  
...  

Обоснование, Хронический полипозный риносинусит (ПРС) отличается широкой вариабельностью клинических проявлений. Для практического врача важно прогнозировать развитие заболевания, оценить риск рецидива и подобрать наиболее эффективный способ лечения в каждом конкретном случае. В настоящий момент отсутствуют стандартизированные, валидизированные диагностические биомаркеры, которые можно использовать в качестве предикторов клинического течения ПРС. Цель, Разработать алгоритм диагностики и лечения разных фенотипов ПРС на основе клинических и лабораторных показателей. Материалы и методы, Пациенты с ПРС были разделены на 3 группы: 1-я группа - ПРС без аллергии и бронхиальной астмы (БА), 2-я группа - ПРС в сочетании с аллергическим ринитом (АР) и/или аллергической БА (аБА), 3-я группа - ПРС в сочетании с неаллергической БА (нБА). Всем пациентам проводилась эндоскопия полости носа и взятие биопсии ткани носовых полипов, аллергологическое обследование, гистологическое исследование стромы полипов с определением степени выраженности лейкоцитарной инфильтрации и эозинофильно-нейтрофильного индекса. Результаты, Фенотипы ПРС достоверно различаются между собой по выраженности клинических проявлений риносинусита (р0,005), уровню эозинофилов крови (р0,001) и степени лейкоцитарной инфильтрации стромы полипов (р0,004). При этом при сочетании ПРС с АР, аБА и нБА отмечался более выраженный воспалительный ответ, что подтверждает факт взаимного влияния этих патологических процессов друг на друга. Также установлено, что абсолютное содержание эозинофилов в периферической крови не коррелирует с выраженностью эозинофильно-клеточной инфильтрации стромы носовых полипов, а следовательно, не несет клинически значимой информации об интенсивности локального воспалительного процесса в отличие от доказанной ранее взаимосвязи уровня эозинофилов в крови и в мокроте у больных БА. Заключение, Показана целесообразность фенотипирования ПРС в зависимости от сопутствующей патологии, что является необходимым инструментом при подборе терапии в каждом конкретном случае. Поэтому для улучшения контроля и предупреждения рецидива ПРС предложен лечебно-диагностический алгоритм ведения пациентов в зависимости от фенотипа заболеванияChronic rhinosinusitis with nasal polyps (CRSwNP) may vary in clinical manifestations and can often be associated with a number of comorbid diseases. For a practitioner it is important to forecast the development of the disease, evaluate the risk of relapse and select the most efficient method of treatment in each clinical case. At present, there are no standardized and validated diagnostic biomarkers that could be used as predictors of CRSwNP clinical course. Purpose of the study: to develop diagnostic and treatment algorithm for varies CRSwNP phenotypes based on clinical and laboratory parameters. Materials and methods, CRSwNP patients were split into 3 groups: group 1 - CRSwNP without allergy and asthma group 2 - CRSwNP with allergic rhinitis and/or allergic asthma group 3 - CRSwNP with non-allergic asthma. All patients were subjected to nasal cavity endoscopy and nasal polyps biopsy, allergological examination, histological analysis of polyp stroma to detect the leukocytes infiltration and eosinophil-neutrophil index (ENI). Results, CRSwNP phenotypes show significant difference in clinical manifestations of rhinosinusitis (p0.005), eosinophil blood count (p0.001), and polyps stroma leukocytes infiltration (p0.004). At the same time, the combination of CRSwNP with allergic rhinitis, allergic and non-allergic asthma showed a more pronounced inflammatory response, which once again confirms the fact of the mutual influence of these pathological processes on each other. It was also found that the absolute eosinophil blood in peripheral blood does not correlate with the severity of eosinophilic cell infiltration degree in nasal polyps stroma, and, consequently, does not have correlate clinically relevant information on intensity of the local inflammatory response, contrary to previously proven relation between eosinophil count in blood and sputum in patients with asthma. Conclusion, Our study showed the feasibility of phenotyping CRSwNP depending on the comorbidity, which is a necessary tool in the selection of therapy in each case. Therefore, to improve the control and prevention of relapse of CRSwNP, a diagnostic and treatment algorithm for the management of patients depending on the phenotype of the disease is proposed.


Author(s):  
Kate W. Sjoerdsma ◽  
W. James Metzger

Eosinophils are important to the pathogenesis of allergic asthma, and are increased in bronchoalveolar lavage within four hours after bronchoprovocation of allergic asthmatic patients, and remain significantly increased up to 24 hours later. While the components of human eosinophil granules have been recently isolated and purified, the mechanisms of degranulation have yet to be elucidated.We obtained blood from two volunteers who had a history of allergic rhinitis and asthma and a positive skin test (5x5mm wheal) to Alternaria and Ragweed. Eosinophils were obtained using a modification of the method described by Roberts and Gallin.


2019 ◽  
Vol 1 (7) ◽  
pp. 29-32 ◽  
Author(s):  
L. S. Kruglova ◽  
E. M. Gensler

Over the past decades, the first breakthrough milestone in the treatment of severe forms of atopic dermatitis (AD) has been targeted therapy aimed at inhibiting IL-4 and IL-13. This was made possible thanks to advances in the understanding of the pathogenesis of AD, the driver of which is the Th2-type immune response, which also underlies such manifestations of atopy as bronchial asthma, allergic rhinitis, and polynosis. In the case of the Th2-type immune response, cytokines IL-4 and IL-13 are secreted, which are the main promoters of the inflammatory response in AD. Inhibition of IL-4 and IL-13 leads to the prevention of inflammation and is an effective approach to therapy. The use of therapy aimed at inhibition of cytokines allows you to effectively cope with the manifestations of severe and moderately severe blood pressure.


2021 ◽  
Vol 147 (2) ◽  
pp. AB28
Author(s):  
Jonathan Spergel ◽  
Michael Blaiss ◽  
Peter Lio ◽  
Aharon Kessel ◽  
Liza Takiya ◽  
...  

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Qixue Du ◽  
Wei Meng ◽  
Seyyed Shamsadin Athari ◽  
Renzhong Wang

Abstract Background Allergic asthma is an inflammatory disease resulting from continued or intermittent allergen exposure, and allergic rhinitis can be trigger of asthma. The main mechanism of these disease is allergic reaction and immune response dysregulation. Co-Q10 is an enzyme cofactor in mitochondria can control asthma and allergic rhinitis symptoms. In the present study, we determined that the CoQ10-induced anti-allergic effects were mediated by up-regulation of Nrf2. Methods Animal models of allergic rhinitis and allergic asthma were produced and treated with Co-Q10, Co-Q10 and O-3, Co-Q10 and Mg-S. Bronchoalveolar lavage fluid was collected from animal models, and IL-4, 5, 13, INF-y, Eicosanoids, IgE, EPO, and histamine production were measured. Also, COX-2, CCL24, CCL11, Nrf2, Eotaxin, Cytb, COX1 and ND1 genes expressions and histopathology were studied. BALf's cells were collected by tracheostomy and used in slide producing by cytospine. Cytokines, Eicosanoids, IgE, EPO, and histamine were measured by ELISA method. Gene expression was done by Real-time PCR. Results Co-Q10 with two supplementation (Mg-S and O-3) modulate MRC, BALf eosinophils, eosinophilic inflammation related genes (eotaxin, CCL11 and CCL24), peribronchial and perivascular inflammation, EPO, type 2 cytokines (IL-4, 5 and 13), IgE, histamine, Cyc-LT and LTB4 as main allergic bio-factors. Importantly, Co-Q10 treatment increased Nrf2 expression and Nrf2 induced antioxidant genes, glutathione redox and inhibited inflammation, oxidative stress injury, Th2 cytokines production and attenuated allergic inflammatory responses. Conclusion Nrf2 is activated in response to allergen, induces resistance against the rhinitis and asthma development and plays an essential role in broncho-protection. Co-Q10 increases the Nrf2 expression and the Nrf2 over-expression has strong effect in control of type2 cytokines, allergic mediators and inflammatory factors that lead to harnessing of allergy and asthma. Graphic abstract


2018 ◽  
Vol 44 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Martín Bedolla-Barajas ◽  
Norma Angélica Pulido-Guillén ◽  
Bolívar Vivar-Aburto ◽  
Jaime Morales-Romero ◽  
José Raúl Ortiz-Peregrina ◽  
...  

ABSTRACT Objective: To investigate whether there is an association between suicidal ideation (SI) and allergic diseases in adults. Methods: This was a comparative cross-sectional study involving individuals ranging from 20 to 50 years of age recruited from a university hospital in the city of Guadalajara, Mexico. We included patients with a confirmed diagnosis of allergic asthma, those with a confirmed diagnosis of allergic rhinitis, and healthy controls. All subjects completed the Beck Depression Inventory-II (BDI-II), which includes an item that evaluates the presence of suicidal thoughts or desires within the last two weeks, in order to identify SI. Results: The sample comprised 115 patients with allergic asthma, 111 patients with allergic rhinitis, and 96 healthy controls. The number of individuals identified with SI in the three groups were, respectively, 17 (14.8%), 13 (11.7%), and 8 (8.3%). Regarding the presence of SI, no statistically significant association was found in the allergic asthma group (OR = 1.98; 95% CI: 0.78-4.64; p = 0.154) or in the allergic rhinitis group (OR = 1.46; 95% CI: 0.58-3.68; p = 0.424) when they were compared with the control group. However, the presence of depression was associated with SI in the three groups: allergic asthma (OR = 12.36; 95% CI: 2.67-57.15; p = 0.001); allergic rhinitis (OR = 6.20; 95% CI: 1.66-23.14; p = 0.006); and control (OR = 21.0; 95% CI: 3.75-117.36; p < 0,001). Conclusions: In comparison with the control group, no association was found between SI and the groups with allergic diseases. In contrast, there was association between SI and depression in the three groups.


2018 ◽  
Vol 32 (6) ◽  
pp. 502-517 ◽  
Author(s):  
Nuray Bayar Muluk ◽  
Fazilet Altın ◽  
Cemal Cingi

Objectives Our intention was to review all material published to date regarding superantigens (SAgs) and allergy from an otorhinolaryngological viewpoint to understand this association more clearly. Methods We identified all materials published mentioning both SAg and allergic rhinitis (AR), chronic sinusitis, asthma, and atopic dermatitis (AD) that are indexed on PubMed, Google, or the ProQuest Central databases. Results Staphylococcus aureus is a significant bacterial pathogen in humans and has the ability to produce enterotoxins with superantigenic features. The inflammatory response in allergy seen in both B cell and T cell may be attributed to SAgs. Sufferers of both allergic asthma with rhinitis and AR alone produce serological evidence of immunoglobulin E formation to SAgs produced by S. aureus. Perennial AR sufferers carry S. aureus more frequently and the presence of the organism within the nasal cavity may exacerbate perennial AR. SAg produced by S. aureus potentially worsens the asthmatic inflammatory response within the airway and may lead to the airways becoming hyperresponsive, as well as possibly activating T cells if asthmatic control is poor. Staphylococcal SAgs potentially increase the risk of developing chronic rhinosinusitis with nasal polyposis, additionally being a marker for more severe disease. If SAgs bring about chronic inflammatory responses in the nose and sinuses, then T cells excreting interferon-gamma may be a crucial mediator. In allergic dermatitis, S. aureus could be a key player in exacerbation of the condition. Even in younger pediatric patients with allergic dermatitis, allergic hypersensitivity to SAgs is frequent and may be a factor explaining how severe the condition becomes. Conclusion Just as SAgs are known to feature in many allergic conditions, they play their part in AR, chronic rhinosinusitis, asthma, and AD. Further research is required before the relationship between SAgs and allergy can be adequately explained.


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