notes by dr Claudio Italiano
cf >> Allergy management guidelines
Allergic rhinitis, the anteroom of bronchial asthma, is
characterized by sneezing, rhinorrhea, nasal obstruction, conjunctival pruritus
and pharyngeal and tearing that occur as a result of exposure to the allergen.
Although the most common form of allergic rhinitis is seasonal, closely related
to the concentration of pollen in the air, clinical manifestations can occur
throughout the year, especially as a result of chronic exposure to environmental
antigens. The incidence of allergic rhinitis in North America is about 7% and
the frequency is higher among children and adolescents.
- Allergic, atopic or specific nasal hyperactivity
- Eosinophilic rhinitis from pseudo allergy, unknown cause
- Non-allergic or vasomotor refinitis, non-specific nasal hyperactivity, impaired
nasal vasomotility
- Infectious reminence in genesis: a) viral, b) bacterial
-Other forms: a) iatrogenic for abuse of vasoconstrictive drugs, b) pregnancy, c)
hypothyroidism d) mechanical, es. adenoids e) deviation of the septum.
Allergic rhinitis generally affects atopic individuals, ie subjects with a family history in which similar or closely related symptoms are reported and with a personal anamnesis of collateral allergic manifestations that may be represented by atopic dermatitis, urticaria and / or asthma . Symptoms usually appear before the fourth decade of life and therefore tend to gradually decrease in intensity with age, even if complete spontaneous remission is rather infrequent. There is a relatively small number of shrubs, grasses and trees whose pollination depends on wind and air currents rather than insects; therefore these plants produce large quantities of pollen, widely airborne and easily transported by the wind: these are the pollens that can trigger seasonal allergic rhinitis. The period of the year in which pollination occurs in these species generally has minimal annual variations in a delimited region, but may be quite different in other climatic zones. In the temperate regions of North America the pollination period typically goes from March to May for the trees, from June to the beginning of July for the grasses, from the middle of August to the beginning of October for the ambrosia. Molds, which are widely diffused in nature, found in the soil and in decomposing organic substances, diffuse the spores differently depending on the different climatic conditions. Perennial allergic rhinitis occurs in response to allergens that are present throughout the year, such as in the desquamation epithelium present in the dandruff of domestic animals, in the desquamation of some insects, in chemicals or other processing products used in industrial plants , as well as in the dust that accumulates in the workplace and in homes. The powder contains various allergens, including mites Dermatophagoides pteronyssinus and D. farinae, which may be present alone or together. Dust mites feed on the desquamation of human skin and cover the digested material with protein substances produced by them, which is subsequently excreted in the form of a fecal bolus. Dust mites are constantly present in hot-humid climates, but in colder areas their presence decreases in winter due to the lack of humidity in the home environment. Some patients with perennial rhinitis are only sensitive to house dust. In more than two thirds of patients with perennial rhinitis, the triggering allergen can not be clearly demonstrated. The ability of allergens to induce rhinitis rather than asthma symptoms may depend on their size (varying from 10 to 100 μm) and, consequently, on the different possibility of crossing the airways or being blocked at the nasal level.
The episodes of nasal hypersecretion, sneezing and obstruction of the nasal passages, with tearing and itching of the conjunctiva, of the nasal and oropharyngeal mucosa, are the most salient clinical aspects of allergic rhinitis. The nasal mucosa is pale and soft, but the nostrils are neither reddened nor excoriated. The conjunctiva can be congested and edematous, while the pharynx does not show remarkable alterations, except for an occasional hyperemia. An edema of the turbinates and mucous membranes with obstruction of osti, sinuses and Eustachian tubes can facilitate the overlapping of secondary infections, respectively of the paranasal sinuses and the middle ear, frequent occurrence in the form of perennial and rather rare rhinitis, instead , in the seasonal form. Because of edema and infections of the paranasal sinuses, nasal polyps can often form that tend to accentuate the obstructive symptoms. The nose is provided with a large mucous surface that extends in the loops of the turbinates and which serves to regulate the temperature and humidity of the inhaled air and to filter the solid particles.
The convoluted passages inside the nose facilitate the trapping of particles larger than 10 μm by simple impact with the mucosal lining: at this point the action of the cilia pushes the trapped particles towards the pharynx. The entrapment of pollen and the digestion of the outer layers of the pollen grain by enzymes present in the mucosa, including lysozyme, determines the release of allergenic proteins with a molecular weight of between 10000 and 40000. Even if the initial interaction is its own check between allergen and intraepithelial mast cell sensitized by specific IgE, the majority of mast cells remains in the deeper layers of the mucosal surface and is only recruited at a later time. During the season of symptoms, when the mucosa is almost completely oedematous and hyperemic, there is an increase in reactivity not only to seasonal pollens but also to antigenically different pollens, in comparison of which there is hypersensitivity. This ease of priming is attributed to the easier penetration of allergens that come into contact with the perivascular mast cells of the deeper layers. In the biopsy samples of nasal mucosa taken during an allergic crisis there is a deep submucosal edema with infiltrate consisting mainly of eosinophils, although polymorphonuclear leukocytes may be present. The polyps, a feature of perennial rhinitis, are nothing more than protrusions of the mucosa containing mainly edematous fluid with an infiltrate consisting of eosinophils present in variable amounts. The fluids present on the mucosal surfaces contain not only IgA (class A immunoglobulins, ie defense proteins of a protein nature that produce the lymphocytes), present in large quantities precisely because they have the secretory component, but also IgE (or immunoglobulins also called reagine) which are received, apparently by diffusion, from the plasma cells distributed near the mucosal surfaces. IgE attaches to the mucosa and submucosa mast cells and the intensity of the clinical response to inhaled allergens is proportional to the amount of pollen naturally present in the air or experimentally measured.
Specific IgE are fixed not only to tissue mast cells, but also to circulating basophilic leukocytes; patients with the most severe form of the disease have basophils that release histamine in vitro in response to concentrations of allergens much lower than those needed to obtain a similar release from the cells of patients with a milder form of the disease. Nasal polyps of susceptible individuals, stimulated in vitro with the allergenic determinants of ambrosia, release histamine. peptides with a chemotactic action for eosinophils and spasmogenic leukotrienes. In susceptible individuals, the introduction of the allergen into the nose causes sneezing, "stuffy nose" and nasal hypersecretion; the mucus contains histamine, PGD2 and leukotrienes. Mast cells of the mucosal mucosa and submucosa of the nose are then able to produce and release mediators following an IgE-mediated reaction that causes tissue edema and eosinophil infiltrate. In fact, when an antigen reacts with the IgE that are bound to the surface of the receptors present on mast cells and basophils, the synthesis of important inflammation mediators is triggered, as already mentioned, and the so-called arachidonic acid cascade is activated, synthesized from from the activation of the phospholipase. These products are formed by the effect of cyclooxygenase and lipoxygenase on arachidonic acid. The pathway of lipoxygenase stimulates the formation of leukotrienes, at the level of which new pharmacological molecules play a role, monteluskat, responsible for the leukotrienes of induction of vasodilation, edema and muscle contraction. The chronic inflammation typical of asthma is associated with an increased number of eosinophils, mast cells and T lymphocytes in the airways, partially reducible by treatment with inhaled corticosteroids (CSI). This process occurs in inflammation when it is chronic, where interleukins and in particular IL-5 intervene for to determine the production, activation and multiplication of eosinophils. However, CSIs do not act effectively on cysteinyl leukotrienes (cysJs), which play a key role in the inflammation and general pathophysiology of asthma (recruitment of eosinophils, mucosal hypersecretion, hyperresponsiveness, bronchoconstriction).
It is based on the patient's history (anamnesis): the family anamnesis is
evaluated, that is if there is a history of allergy in the blood relatives; the
medical history is also important, for example if there is professional exposure
to some inhalants; the remote pathological anamnesis, the previous illnesses and
the pathological anamnesis next the recent symptoms. Then the ENT target
examination, ie the ENT examination (ENT). The specialist can integrate the
examination with a fibroscopy, that is, he can use a special instrument, an
endoscope, equipped with a camera or optical fibers, with which to visualize the
inside of the nasal cavities with optical fiber instruments and video systems
(video endoscopy) The examination, indicated in the diagnosis of diseases of the
nose, paranasal sinuses and nasopharynx, evaluates the inside of the nasal
cavities and of the nasopharynx through the use of optical fiber instruments (rigid
or flexible endoscopes). The test is outpatient and is completely painless. It
is performed after having introduced into the nasal cavities small layers of
cotton soaked in solution of anesthetics and vasoconstrictors (decongestants),
which are left "in situ" for about ten minutes. Once the anesthetic dressing has
been removed, the endoscope is introduced to perform the examination. The
technique can be performed at any age: even at three to four years to evaluate
the adenoids. Being a non-gory examination, it has practically no
contraindication.
X-ray examinations: standard radiographic examination of the skull, TAC (in the
evaluation of sinusitis complications).
Cultivation examination on the nasal mucus with antibiogram execution: through a
cotton pad mounted on a small instrument that is introduced into the nasal
cavities, the nasal mucus that covers the walls of the nasal cavities is removed.
The material is sown in a culture medium and, after a certain period of time, it
is evaluated if a development of bacteria or fungi has occurred. In the event
that colonies are developed, they are subjected to the action of some
antibiotics to evaluate their activity (antibiogram).
Microscopic examination of the nasal smear: this is performed to evaluate the
number of eosinophils in the nasal secretions (rhinocytogram).
- Prick test: intradermal injecting, in the skin of the arm, aqueous suspensions
of the substances to be tested (pollens, mites, epidermal derivatives of animals).
Skin reactions (redness, swelling) are evaluated.
-
Specific nasal provocation test: the patient is inhaled by powder suspension of
the substances to be tested (pollen, mites). Reactions are evaluated (appearance
of nasal obstruction, pruritus, sneezing and secretion).
-
Serum tests: they are performed by means of a blood sample. With them we can
evaluate:
-
Total IgE (PRIST): measures the total amount of allergy antibodies (IgE).
-
Specific IgE (RAST): measures the amount of antibodies (IgE) for each individual
substance (inhalants, food, drugs).
>>> Rhinitis therapy