"Hay fever" redirects here. For the play, see Hay Fever.

Allergic rhinitis

Pollen grains from a variety of common plants can

cause hay fever. Enlarged 500, ~400 m wide.
ICD-10
J30
ICD-9
477
OMIM
607154
DiseasesDB
31140
MedlinePlus
000813
eMedicine
ent/194 med/104, ped/2560
MeSH
D012221
Allergic rhinitis is an allergic inflammation of the nasal airways. It occurs when an allergen,
such as pollen, dust or animal dander (particles of shed skin and hair) is inhaled by an individual
with a sensitized immune system. In such individuals, the allergen triggers the production of the
antibody immunoglobulin E (IgE), which binds to mast cells and basophils containing histamine.
When caused by pollens of any plants, it is called pollinosis, and if specifically caused by grass
pollens, it is known as hay fever. While symptoms resembling a cold or flu can be produced by
an allergic reaction to pollen from plants and grasses, including those used to make hay, it does
not cause a fever.
IgE bound to mast cells are stimulated by allergens, causing the release of inflammatory
mediators such as histamine (and other chemicals).[1] This usually causes sneezing, itchy and
watery eyes, swelling and inflammation of the nasal passages, and an increase in mucus
production. Symptoms vary in severity between individuals. Very sensitive individuals can
experience hives or other rashes. Particulate matter in polluted air, and chemicals such as
chlorine and detergents, which can normally be tolerated, can greatly aggravate allergic rhinitis.
The physician John Bostock first described hay fever in 1819 as a disease.
Allergies are common. Heredity and environmental exposures may contribute to a predisposition
to allergies. It is roughly estimated that one in three people have an active allergy at any given
time and at least three in four people develop an allergic reaction at least once in their lives. In
Western countries between 1025% of people annually are affected by allergic rhinitis.[2]

Signs and symptoms

Illustration depicting inflammation associated with allergic rhinitis

The characteristic symptoms of allergic rhinitis are: rhinorrhea (excess nasal secretion), itching,
and nasal congestion and obstruction.[3] Characteristic physical findings include conjunctival
swelling and erythema, eyelid swelling, lower eyelid venous stasis (rings under the eyes known
as "allergic shiners"), swollen nasal turbinates, and middle ear effusion.[4]
There can also be behavioural signs; in order to relieve the irritation or flow of mucus, patients
may wipe or rub their nose with the palm of their hand in an upward motion: an action known as
the "nasal salute" or the "allergic salute". This may result in a crease running across the nose,
commonly referred to as the "transverse nasal crease", and can lead to permanent physical
deformity if repeated enough.[5]
Sufferers might also find that cross-reactivity occurs.[6] For example, someone allergic to birch
pollen may also find that they have an allergic reaction to the skin of apples or potatoes.[7] A clear
sign of this is the occurrence of an itchy throat after eating an apple or sneezing when peeling
potatoes or apples. This occurs because of similarities in the proteins of the pollen and the food.[8]
There are many cross-reacting substances.
Some disorders may be associated with allergies: Comorbidities include eczema, asthma and
depression.[citation needed]

Cause
Allergic rhinitis triggered by the pollens of specific seasonal plants is commonly known as "hay
fever", because it is most prevalent during haying season. However, it is possible to suffer from
hay fever throughout the year. The pollen that causes hay fever varies between individuals and
from region to region; generally speaking, the tiny, hardly visible pollens of wind-pollinated
plants are the predominant cause. Pollens of insect-pollinated plants are too large to remain
airborne and pose no risk. Examples of plants commonly responsible for hay fever include:

Trees: such as pine (Pinus), birch (Betula), alder (Alnus), cedar, hazel (Corylus),
hornbeam (Carpinus), horse chestnut (Aesculus), willow (Salix), poplar (Populus), plane
(Platanus), linden/lime (Tilia) and olive (Olea). In northern latitudes birch is considered
to be the most important allergenic tree pollen, with an estimated 1520% of hay fever
sufferers sensitive to birch pollen grains. A major antigen in these is a protein called Bet

V I. Olive pollen is most predominant in Mediterranean regions. Hay fever in Japan is

caused primarily by sugi (Cryptomeria japonica) and hinoki(Chamaecyparis obtusa) tree
pollen.
o "Allergy friendly" trees include: ash (female only), red maple, yellow poplar,
dogwood, magnolia, double-flowered cherry, fir, spruce and flowering plum.[9]

Grasses (Family Poaceae): especially ryegrass (Lolium sp.) and timothy (Phleum
pratense). An estimated 90% of hay fever sufferers are allergic to grass pollen.

Weeds: ragweed (Ambrosia), plantain (Plantago), nettle/parietaria (Urticaceae), mugwort

(Artemisia Vulgaris), Fat hen (Chenopodium) and sorrel/dock (Rumex)

The panallergen concept encompasses families of related proteins, which are involved in
general vital processes and thus, widely distributed throughout nature. Plant panallergens
share highly conserved sequence regions, structure, and function. They are responsible for
many IgE cross-reactions even between unrelated pollen and plant food allergen sources.
Although usually considered as minor allergens, sensitization to panallergens might be
problematic as it bears the risk of developing multiple sensitizations. Clinical
manifestations seem to be tightly connected with geographical and exposure factors. Future
population- and disease-based screenings should provide new insights on panallergens and
their contribution to disease manifestations. Such information requires molecule-based
diagnostics and will be valuable for developing patient-tailored prophylactic and
therapeutic approaches. In this article, we focus on profilins, non-specific lipid transfer
proteins, polcalcins, and Bet v 1-related proteins and discuss possible consequences of
panallergen sensitization for the allergic patient. Based on their pattern of IgE crossreactivity, which is reflected by their distribution in the plant kingdom, we propose a novel
classification of panallergens into ubiquitously spread "real panallergens" (e.g. profilins)
and widespread "eurallergens" (e.g. polcalcins). "Stenallergens" display more limited
distribution and cross-reactivity patterns, and "monallergens" are restricted to a single
allergen source.

IgE
Immunoglobulin E (IgE) is a class of antibody (or immunoglobulin (Ig) "isotype") that has
been found only in mammals. IgE exists as monomers consisting of two heavy chains ( chain)
and two light chains, with the chain containing 4 Ig-like constant domains (C1-C4).[1] IgE's
main function is immunity to parasites such as parasitic worms[2] like Schistosoma mansoni,
Trichinella spiralis, and Fasciola hepatica.[3][4][5] IgE may also be important during immune
defense against certain protozoan parasites such as Plasmodium falciparum.[6]
IgE also plays an essential role in type I hypersensitivity,[7] which manifests various allergic
diseases, such as allergic asthma, allergic rhinitis, food allergy, and some types of chronic
urticaria and atopic dermatitis. IgE also plays a pivotal role in allergic conditions, such as
anaphylactic reactions to certain drugs, bee stings, and antigen preparations used in specific
desensitization immunotherapy.
Although IgE is typically the least abundant isotype - blood serum IgE levels in a normal ("nonatopic") individual are only 0.05% of the Ig concentration,[8] compared to 10 mg/ml for the IgGs
(the isotypes responsible for most of the classical adaptive immune response) - it is capable of
triggering the most powerful inflammation reactions.
IgE was discovered in 1966 by the Japanese scientist couple Teruko and Kimishige Ishizaka.[9]

Physiology

There is much speculation into what physiological benefits IgE contributes, and, so far,
circumstantial evidence in animal models and statistical population trends have hinted that IgE
may be beneficial in fighting gut parasites such as Schistosoma mansoni, but this has not been
conclusively proven in humans. It is most likely beneficial in removal of hookworms from the
lung.
Although it is not yet well understood, IgE may play an important role in the immune systems
recognition of cancer,[10] in which the stimulation of a strong cytotoxic response against cells
displaying only small amounts of early cancer markers would be beneficial. If this were the case,
anti-IgE treatments such as omalizumab (for asthma) might have some undesirable side effects.
However, a recent study, which was performed based on pooled analysis using comprehensive
data from 67 phase I to IV clinical trials of omalizumab in various indications, concluded that a
causal relationship between omalizumab therapy and malignancy is unlikely.[11]
Role in disease

Atopic individuals can have up to 10 times the normal level of IgE in their blood (as do sufferers
of hyper-IgE syndrome). However, this may not be a requirement for symptoms to occur as has
been seen in asthmatics with normal IgE levels in their blood - recent research has shown that
IgE production can occur locally in the nasal mucosa.[12]
IgE that can specifically recognise an "allergen" (typically this is a protein, such as dust mite Der
p 1, cat Fel d 1, grass or ragweed pollen, etc.) has a unique long-lived interaction with its highaffinity receptor FcRI so that basophils and mast cells, capable of mediating inflammatory
reactions, become "primed", ready to release chemicals like histamine, leukotrienes, and certain
interleukins. These chemicals cause many of the symptoms we associate with allergy, such as
airway constriction in asthma, local inflammation in eczema, increased mucus secretion in
allergic rhinitis, and increased vascular permeability, it is presumed, to allow other immune cells
to gain access to tissues, but which can lead to a potentially fatal drop in blood pressure as in
anaphylaxis. Although the mechanisms of each response are fairly well understood, why some
allergics develop such drastic sensitivities when others merely get a runny nose is still one of
science's hot topics.
IgE is known to be elevated in various autoimmune disorders such as Lupus(SLE), Rheumatoid
Arthritis(RA) & psoriasis, and is theorized to be of pathogenetic importance in RA and SLE by
eliciting a hypersensitivity reaction. [13][14]
Regulation of IgE levels through control of B cell differentiation to antibody-secreting plasma
cells is thought to involve the "low-affinity" receptor FcRII, or CD23.[15] CD23 may also allow
facilitated antigen presentation, an IgE-dependent mechanism whereby B cells expressing

CD23 are able to present allergen to (and stimulate) specific T helper cells, causing the
perpetuation of a Th2 response, one of the hallmarks of which is the production of more
antibodies.[16]