Allergic rhinitis (AR) affects 10% to 40% of the population. It reduces quality of life and school and work performance and is a frequent reason for office visits in general practice. Medical costs are large, but avoidable costs associated with lost work productivity are even larger than those incurred by asthma. New evidence has accumulated since the last revision of the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines in 2010, prompting its update. We sought to provide a targeted update of the ARIA guidelines. The ARIA guideline panel identified new clinical questions and selected questions requiring an update. We performed systematic reviews of health effects and the evidence about patients' values and preferences and resource requirements (up to June 2016). We followed the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) evidence-to-decision frameworks to develop recommendations. The 2016 revision of the ARIA guidelines provides both updated and new recommendations about the pharmacologic treatment of AR. Specifically, it addresses the relative merits of using oral H1-antihistamines, intranasal H1-antihistamines, intranasal corticosteroids, and leukotriene receptor antagonists either alone or in combination. The ARIA guideline panel provides specific recommendations for the choice of treatment and the rationale for the choice and discusses specific considerations that clinicians and patients might want to review to choose the management most appropriate for an individual patient. Appropriate treatment of AR might improve patients' quality of life and school and work productivity. ARIA recommendations support patients, their caregivers, and health care providers in choosing the optimal treatment.

Allergic and nonallergic rhinitis affect approximately 30% of the U.S. population. Although allergic rhinitis has a clear definition and its pathophysiology has been thoroughly investigated, nonallergic rhinitis remains poorly defined and understood. There is consensus, however, that nonallergic rhinitis consists of a variety of heterogeneous conditions. In allergic rhinitis, the process of allergen sensitization involves the participation of antigen-presenting cells, T lymphocytes, and B lymphocytes and depends on environmental allergen exposure. Sensitization results in the generation of allergen-specific IgE that circulates in the peripheral blood and attaches itself on the surface of all mast cells and basophils including those that home to the nasal mucosa. Subsequent nasal exposure to allergen activates these cells and, through the release of the classic mediators of the allergic reaction, produces acute nasal symptoms. Over a short period of time, these symptoms become indolent, whereas inflammatory and immune cell infiltrate, including eosinophils, basophils, neutrophils, T lymphocytes, and monocytes, characterizes the late stages of the allergic response. In parallel, and probably as a result of the development of mucosal inflammation, the nose becomes primed to allergen and reacts more vigorously to subsequent allergen exposure but also becomes hyperresponsive to irritants and to changes in atmospheric conditions. In nonallergic rhinitis, several conditions may have been identified that are of interest for further research and phenotyping. These include a group of patients with apparent hyperresponsiveness of the C-fiber sensory nerves with no inflammatory changes in the nasal mucosa and a group with mucosal eosinophilia who may have allergic sensitization to common aeroallergens that is, however, manifested only in the nasal mucosa.

Asthma, rhinitis, and atopic dermatitis (AD) are interrelated clinical phenotypes that partly overlap in the human interactome. The concept of “one‐airway‐one‐disease,” coined over 20 years ago, is a simplistic approach of the links between upper‐ and lower‐airway allergic diseases. With new data, it is time to reassess the concept. This article reviews (i) the clinical observations that led to Allergic Rhinitis and its Impact on Asthma (ARIA), (ii) new insights into polysensitization and multimorbidity, (iii) advances in mHealth for novel phenotype definitions, (iv) confirmation in canonical epidemiologic studies, (v) genomic findings, (vi) treatment approaches, and (vii) novel concepts on the onset of rhinitis and multimorbidity. One recent concept, bringing together upper‐ and lower‐airway allergic diseases with skin, gut, and neuropsychiatric multimorbidities, is the “Epithelial Barrier Hypothesis.” This review determined that the “one‐airway‐one‐disease” concept does not always hold true and that several phenotypes of disease can be defined. These phenotypes include an extreme “allergic” (asthma) phenotype combining asthma, rhinitis, and conjunctivitis. Rhinitis alone and rhinitis and asthma multimorbidity represent two distinct diseases with the following differences: (i) genomic and transcriptomic background (Toll‐Like Receptors and IL‐17 for rhinitis alone as a local disease; IL‐33 and IL‐5 for allergic and non‐allergic multimorbidity as a systemic disease), (ii) allergen sensitization patterns (mono‐ or pauci‐sensitization versus polysensitization), (iii) severity of symptoms, and (iv) treatment response. In conclusion, rhinitis alone (local disease) and rhinitis with asthma multimorbidity (systemic disease) should be considered as two distinct diseases, possibly modulated by the microbiome, and may be a model for understanding the epidemics of chronic and autoimmune diseases.