History and exam
Key diagnostic factors
common
sneezing
More likely in AR than nonallergic rhinitis.
nasal pruritus
More likely in AR than nonallergic rhinitis.
Other diagnostic factors
common
palate, throat, ear, and eye itching
Usually occurs in the early phase of AR.
eye redness, puffiness, and watery discharge
Usually occurs in the early phase of AR.
fatigue and irritability
May be due to poor quality sleep resulting from nasal congestion.
nasal congestion
Usually occurs in the late phase of AR.
rhinorrhea
Unilateral rhinorrhea should prompt evaluation for cerebrospinal fluid leak. Unilateral disease, with the exception of unilateral nasal congestion due to a deviated septum, should warrant referral to an ear, nose, and throat physician.
allergic shiners
Bluish discoloration in the infraorbital region.
conjunctival injection
May be identified on physical exam of the face.
ocular mucoid discharge
May be identified on physical exam of the face.
nasal crease
A transverse crease on the exterior of the nose resulting from repetitive nose rubbing and manipulation.
pale nasal mucosa
May be identified on physical exam of the nose.
swelling of the nasal mucosa and turbinates
May be identified on physical exam of the nose.
abundant clear nasal secretions
May be identified on physical exam of the nose.
uncommon
Dennie-Morgan lines (creases present under the lower eyelids)
Identified on physical exam of the face, although uncommon. May be due to nasal congestion and poor blood circulation in the ocular region.[59]
Risk factors
strong
other atopic conditions or family history of atopy
The best established risk factor is a family history of atopic disease, especially AR.[30] Various modalities, such as genetic linkage analysis, have been employed to collectively identify a multitude of genetic loci associated with a higher incidence of AR.[31]
The risk of developing atopic disease in the absence of parental family history has been reported to be 13%.[16] The risk increased to 29% if one parent or sibling is atopic, 47% if both parents are atopic, and 72% if both parents have the same atopic manifestation.[16]
age <20 years
exposure to aeroallergens (pollen, molds, house dust mites, pollution)
Epidemiologic studies implicate exposure to aeroallergens, indoor dampness-related exposures, and living in an urban environment.[21][22][23]
A statistically significant correlation has been reported between the incidence and/or prevalence of AR and living in an urban or industrialized environment with associated increased levels of traffic and ambient polycyclic aromatic hydrocarbons.[23][32][33][34]
The International Study of Asthma and Allergies in Childhood established that local environmental or ecologic factors may contribute to the varying prevalence of asthma, rhinoconjunctivitis, and atopic dermatitis.[12]
One meta-analysis demonstrated a modest increased risk of AR associated with exposure to cigarette smoke.[35]
exposure to animal dander
Cat and dog hair are common allergens, and may cause perennial AR symptoms.[36][37]
Exposure to a dog during the first year of life may reduce the risk of AR and asthma.[38][39]
Children of families with exposure to a farming lifestyle (farming animals, unpasteurized milk) in rural areas of Germany, Austria, and Switzerland were less likely to develop allergic sensitization, hay fever, and asthma than children of nonfarmers living in the same localities.[40] Continual long-term exposure to stables until age 5 years was associated with the lowest frequencies of allergic sensitization and disease.[40]
weak
ethnicity
In the US, atopic sensitization (including asthma) appears to be more prevalent among certain ethnic groups, such as African-Americans and Puerto Ricans.[41][42]
In one UK study, significantly more West Indian women consulted primary care physicians for AR compared with the white British population.[43]
positive allergen skin-prick tests
Even though sensitization to a specific allergen does not always equate with clinical disease, allergen reactivity remains one of the strongest risk factors for the presence of upper (as well as lower) allergic respiratory disease. False positive results exist, so it is essential that positive tests of specific allergen reactivity be correlated with the clinical history. Unproven diagnostic tests, such as immunoglobulin G (lgG) or a battery of nonspecific immunoglobulin E (IgE) tests, are not recommended in the evaluation of allergy.[44]
Use of this content is subject to our disclaimer