Nonallergic rhinitis (NAR) affects an estimated 20%-70% of adults, often beginning after age 20, yet it remains underdiagnosed. Its prevalence appears to be rising alongside urbanization and greater exposure to environmental irritants. More importantly, the condition is now understood less as a simple inflammatory disorder and more as a syndrome of neurogenic hyperreactivity.

Allergic and Nonallergic Overlap

Chronic rhinitis encompasses persistent and heterogeneous inflammatory conditions of the nasal mucosa, the classification of which is based more on the pathophysiologic mechanisms involved than on clinical presentation. “Allergic rhinitis (AR), which is the best characterized, is IgE [immunoglobulin E]-mediated and can be seasonal or perennial,” explained Semia Sahtout Jouini, ENT specialist in Tunis, Tunisia, during a session dedicated to NAR at the Rhinoforum conference from June 18 to 20, 2026, in Bordeaux, France. Infectious forms — whether viral or bacterial — typically involve purulent, discolored secretions and crusts. Nonallergic, noninfectious rhinitis (NANIR) refers to a heterogeneous group of inflammatory conditions not mediated by IgE.

The classification of chronic rhinitis is based on phenotype and endotype, with the latter reflecting the pathophysiologic mechanism. “Three major groups are distinguished, bearing in mind that an allergic component and a nonallergic component frequently coexist in the same patient,” emphasized Sahtout Jouini: IgE-mediated AR, subdivided into seasonal and perennial forms; NANIR, including idiopathic rhinitis (or nonallergic rhinopathy), chronic nonallergic eosinophilic rhinitis (NARES), as well as senile, hormonal, tobacco-related, gustatory, drug-induced, and occupational forms; and finally, mixed rhinitis.

Different Pathophysiologic Pathways

In practice, NAR can be classified into two main, progressive pathophysiologic endotypes. The first is characterized by inflammation that is either type 2 or non-type 2. On the one hand, the type 2 (eosinophilic) profile is based on a response dominated by interleukin (IL)-4, IL-5, and IL-13, associated with NARES. Systemic atopy may be absent. This profile typically responds well to intranasal corticosteroids. It includes NARES, smoker’s, occupational, and hormonal rhinitis. On the other hand, the non-type 2 profile is dominated by neutrophils and may be associated with nasal dysbiosis that promotes biofilm formation and activation of T1/T3 pathways (IL-17, interferon-gamma, and TNF-alpha). This persistent inflammation is often corticosteroid-resistant and notably includes atrophic and drug-induced rhinitis.

Alongside this inflammatory pathway, a second pathophysiologic pathway exists: the neurogenic pathway. “It involves two mechanisms,” explained Sahtout Jouini. “The first stems from an imbalance in the autonomic nervous system (sympathetic/parasympathetic) and includes rhinorrhea in the elderly as well as drug-induced, occupational, and idiopathic rhinitis. The second corresponds to neuroinflammation, found in occupational, gustatory, and idiopathic forms.” Other pathophysiologic mechanisms, as yet unidentified, may also be involved.

NAR

The reflex neurogenic endotype is based on the integration of the sensory and autonomic pathways of the nasal mucosa within a reflex arc that combines a sensory afferent component with a neurovegetative efferent component. In NAR, this nervous hyperreactivity is a central mechanism: Temperature changes, odors, and environmental irritants activate transient receptor potential (TRP) ion channels and trigger symptoms. “This paradigm shift makes the nerve a therapeutic target in its own right, beyond inflammation,” the specialist emphasized, “paving the way for a growing role for neuro-targeted treatments as a complement to conventional anti-inflammatory approaches.”

In addition to this nervous hyperreactivity, there is a neurovascular component within the nasal mucosa linked to dysregulation of the autonomic nervous system, with a relative decrease in sympathetic tone and relatively increased parasympathetic activity. This imbalance leads to intermittent swelling of the nasal mucosa, causing congestion and watery rhinorrhea. Symptoms can be triggered by nonspecific physical stimuli, changes in temperature, atmospheric pressure, and humidity.

Rhinitis Increases Asthma Risk

The prevalence of NAR is increasing, in line with growing urbanization and increased exposure to environmental irritants. Its prevalence is difficult to estimate due to the lack of a uniform definition or international consensus, ranging from 20% to 70% depending on the study. Among the 20,772 participants included in a European analysis, the crude prevalences of AR and NAR were 28% and 10.9%, respectively.

Rhinitis, including NAR, is associated with an increased risk for comorbidities, notably chronic rhinosinusitis, chronic cough, sleep apnea syndrome, and asthma. Thus, the adjusted risk for asthma is 2.71 vs 3.53 for NAR vs AR.

NAR Has Multiple Endotypes

NAR encompasses a variety of endotypes. The idiopathic form is the most common (approximately 40%-50% of cases), followed by drug-induced and occupational forms, and a large proportion of unclassified NAR:

• Local AR (“entopy”) accounts for 10%-45% of chronic rhinitis cases considered nonallergic. It corresponds to an allergic response limited to the nasal mucosa, associated with local IgE production, without detectable systemic sensitization (negative skin tests and serum IgE levels). It is frequently associated with conjunctivitis and asthma. The response to intranasal corticosteroids and allergen immunotherapy is generally favorable. Diagnosis, still limited by available resources, relies on the nasal allergen challenge test. This condition differs from systemic AR in that its IgE-dependent mechanism is exclusively local, despite a comparable clinical presentation.
• First described in 1981, NARES is a particularly severe form of NAR. It combines year-round symptoms with nasal eosinophilia, without systemic atopy. Impaired sense of smell should guide the diagnosis. The response to intranasal corticosteroids is generally favorable. The condition may progress to nasal polyposis or the Widal triad. Some authors suggest that NARES may represent a form of localized AR.
• The spectrum of NAR is broad. The occupational form results from exposure to low-molecular-weight irritants and is often associated with occupational asthma. In the older adults, senile rhinitis is exacerbated by progressive atrophy of the nasal mucosa. Hormonal rhinitis, including pregnancy-related rhinitis, typically begins as early as the second month of pregnancy and resolves after delivery; estrogens are thought to promote an increase in tissue eosinophils and the expression of histamine receptors. As for drug-induced forms, they involve mucosal edema, vasodilation, and the release of inflammatory mediators; the main classes involved are aspirin and nonsteroidal anti-inflammatory drugs, beta-blockers, antihypertensives, psychotropic drugs, contraceptives, and treatments for erectile dysfunction. As for gustatory rhinitis, it manifests as watery rhinorrhea triggered by hot or spicy foods via a “non-adrenergic, non-cholinergic” (NANC) reflex. Finally, tobacco-related rhinitis also constitutes a specific form.
• Last but not least, nonallergic rhinopathy, also known as idiopathic rhinitis, is the most common endotype of NAR (more than 50% of cases). Nasal hyperreactivity, with obstruction and rhinorrhea, is triggered in response to nonspecific stimuli: irritants, temperature changes, fragrances, emotions, and cold, dry air.

It involves hyperactivity of the NANC system combined with overexpression of TRP channels — particularly TRP vanilloid 1 (TRPV1) — in trigeminal sensory fibers. Capsaicin is the primary ligand for TRPV1. “My message in 2026,” stated Sahtout Jouini, “is that the historical term ‘vasomotor rhinitis’ has now been replaced by ‘nonallergic rhinopathy’ to better reflect the role of neurogenic hyperreactivity, neuropeptides, and TRP receptors (TRPV1, TRPA1 [TRP ankyrin1]).

From capsaicin to minimally invasive techniques for posterior nasal nerve ablation (radiofrequency, cryotherapy), several options can offer lasting benefits in refractory cases. The main challenges remain the lack of a consensus definition and standardized diagnostic criteria. The still-limited interventional data (low level of evidence, short follow-up) justify the conduct of high-quality controlled trials.”

This story was translated from Medscape’s French edition.