Multiple reasons underlaying uncontrolled disease in the majority of chronic rhinosinusitis patients

BackgroundUp to 40% of patients with chronic rhinosinusitis (CRS) remain uncontrolled despite guidelines of care being available, with an enormous socio-economic impact. The reasons for uncontrolled disease can be arbitrarily divided into disease-related, diagnosis-related, treatment-related, and patient-related factors. The relative contribution of each factor in uncontrolled CRS remains speculative. This explorative study aimed at determining the factors responsible for uncontrolled CRS in a tertiary care center, thereby identifying the most commons reasons for uncontrolled disease in CRS.MethodsPatients with uncontrolled CRS (n = 187) were asked to fill out a questionnaire and underwent a clinical examination at the outpatient clinic of the University Hospital of Leuven, Belgium. Two independent physicians evaluated the (multiple) reason(s) for uncontrolled disease.ResultsIn uncontrolled CRS, 66% of patients showed two or more reasons for uncontrolled disease according to the physicians' evaluation. Disease-related factors (70%) were most often considered the reason for uncontrolled disease, followed by treatment- (45%), patient- (42%), and diagnosis- (32%) related factors.ConclusionIn case of uncontrolled CRS, the different contributing factors to the uncontrolled nature need to be carefully addressed during diagnostic and therapeutic actions in order to define strategies to improve CRS care. Most uncontrolled CRS patients have multiple reasons contributing to their disease status, with disease-related factors being the most common factor

Monoclonal antibody or aspirin desensitization in NSAID-exacerbated respiratory disease (N-ERD)?

Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is a clinical syndrome characterized by nasal polyposis, asthma, and intolerance to aspirin/NSAID. It affects approximately 15% cases of severe asthma, 10% of nasal polyps and 9% of rhinosinusitis. N-ERD results in associated asthma exacerbations, oral corticosteroids bursts, corticosteroid-dependent disease, and multiple endoscopic sinus surgeries. Unknown influences cause polyp epithelium to release alarmins, such as IL-33 and TSLP. These cytokines activate lymphoid cells, both Th2 and ILC2, to release cytokines such as IL5, IL4 and IL13, resulting in complex type 2 inflammation involving mast cells, eosinophils and platelets. Arachidonic acid released from such cells is metabolized into mediators. N-ERD is characterized by an imbalance in eicosanoid levels, especially CysLTs, PDG and PGE2. Patients with N-ERD present nasal symptoms (congestion, hyposmia/anosmia, nasal discharge) and lower airways symptoms (cough, sneezing, shortness of breath, chest tightness), anosmia, severe hyposmia as well as severe asthma which impacts the quality of life in this disease and leads to safety concerns in patients daily lives. Despite the variety of treatment strategies, the likelihood of recurrence of symptoms is high in patients with N-ERD. The most important strategies for treating N-ERD are listed as following: drug therapies, aspirin desensitization, monoclonal antibodies and other therapies associated. N-ERD treatment remains a major challenge in the current situation. Selecting the appropriate patient for aspirin desensitization, monoclonal antibodies or both is essential. This review provides an overview on aspirin desensitization and biologics in N-ERD and might help in decision making from both the perspective of the physician and patient. Patient characteristics, safety, efficacy, health care costs, but also patient preferences are all factors to take into account when it comes to a choice between biologics or aspirin desensitization

Realising the potential of mHealth to improve asthma and allergy care : how to shape the future

Non peer reviewe

Evaluation of skin prick location on the forearm using a novel skin prick automated test device

BackgroundThe skin prick test (SPT) is the gold standard for identifying allergic sensitization in individuals suspected of having an inhalant allergy. Recently, it was demonstrated that SPT using a novel skin prick automated test (SPAT) device showed increased reproducibility and tolerability compared to the conventional SPT, among other benefits.ObjectiveThis study aimed to evaluate prick location bias using the novel SPAT device.MethodsA total of 118 volunteers were enrolled in this study and underwent SPATs with histamine (nine pricks) and glycerol control (one prick) solutions on the volar side of their forearms. Imaging of the skin reactions was performed using the SPAT device, and the physician determined the longest wheal diameter by visually inspecting the images using a web interface. Prick location bias was assessed along the medial vs. lateral and proximal vs. distal axes of the forearm.ResultsIn total, 944 histamine pricks were analyzed. Four medial and four lateral histamine pricks were grouped, and wheal sizes were compared. The longest wheal diameters were not significantly different between the medial and lateral prick locations (p = 0.41). Furthermore, the pricks were grouped by two based on their position on the proximal–distal axis of the forearm. No significant difference was observed among the four groups of analyzed prick locations (p = 0.73).ConclusionThe prick location on the volar side of the forearm did not influence wheal size in SPAT-pricked individuals

Mometasone furoate and fluticasone furoate are equally effective in restoring nasal epithelial barrier dysfunction in allergic rhinitis

Rinitis alérgica; Integridad epitelial; Furoato de mometasonaRinitis al·lèrgica; Integritat epitelial; Furoat de mometasonaAllergic rhinitis; Epithelial integrity; Mometasone furoateTight junction defects (TJ) have been associated with a defective epithelial barrier function in allergic rhinitis (AR). Intranasal corticosteroids are potent drugs frequently used to treat AR and are shown to restore epithelial integrity by acting on TJs and by reducing type 2 cytokine production. However, the effect of different classes of intranasal corticosteroids on the epithelial barrier has not been studied. Therefore, we compared the effect of 2 intranasal corticosteroids, ie, fluticasone furoate (FF) and mometasone furoate (MF) on epithelial barrier function. Both FF and MF similarly increased trans-epithelial electrical resistance of primary nasal epithelial cell cultures from AR patients. In a house dust mite-induced allergic asthma mouse model, FF and MF had similar beneficial effects on fluorescein isothiocyanate–dextran 4 kDa mucosal permeability, eosinophilic infiltration and IL-13 levels. Both molecules increased mRNA expression of the TJ proteins occludin and zonula occludens-1, thereby restoring epithelial barrier function. Lastly, we showed that long-term FF treatment also increased expression of occludin in AR patients compared to controls. In conclusion, both FF and MF effectively restore epithelial barrier function by increasing expression of TJ proteins in AR patients.This work was supported by an unrestricted grant from GSK. BS is supported by the Fund for Scientific Research Flanders (FWO), Belgium

A common language to assess allergic rhinitis control : results from a survey conducted during EAACI 2013 Congress

Peer reviewedPublisher PD

Role of Echocardiography in Percutaneous Mitral Valve Interventions

Intraprocedural imaging continues to evolve in parallel with advances in percutaneous mitral valve interventions. This didactic review uses several illustrations and rich intraprocedural videos to further describe and demonstrate the role of the most up-to-date echocardiographic and advanced imaging technologies in the patient selection and intraprocedural guidance of percutaneous mitral valve interventions. We will focus on 3 interventions: 1) percutaneous balloon mitral valvuloplasty for mitral stenosis; 2) transcatheter edge-to-edge repair of mitral valve regurgitation; and 3) transcatheter closure of periprosthetic mitral regurgitation. In addition, we discuss potential pitfalls of 3-dimensional transesophageal echocardiography and show examples of this technique