Rhinitis:
allergic, atopic or specific nasal hyperactivity
pseudo allergic rhinitis with eosinophilia, cause unknown
Non-allergic or vasomotor rhinitis, non-specific nasal hyperactivity, impaired
vasomotion nasal
Genesis in infectious rhinitis: a) virus, b) bacterial
Other forms: a) to iatrogenic drug abuse vasoconstrictors, b) pregnant, c)
hypothyroidism d) mechanical, eg. and adenoids) septal deviation.
Predisposing factors and etiology
Allergic rhinitis usually affects atopic individuals or those with a family
history in which they reported symptoms similar or closely related and with a
history of allergic reactions that can be represented by atopic dermatitis,
dall'orticaria and / or asthma .
Symptoms usually appear before the fourth decade of life and therefore tend to
decrease gradually in intensity with age, although a complete spontaneous
remission is quite uncommon. There is a relatively small number of shrubs,
grasses and trees which depends on pollination by wind and air currents rather
than by insects, so these plants are major producers of pollen dispersed widely
and easily carried by the wind: these were the pollen can trigger seasonal
allergic rhinitis. The time of year is the pollination of these species usually
has a defined minimum annual variations in the region, but may be quite
different in other climatic zones. In temperate regions of North America, the
pollination period is typically from March to May for the trees, from June to
early July for grass, from mid-August to the beginning of October for ragweed.
The molds, which are widely found in nature, being in the soil and decaying
organic matter, spread the spores in different ways according to different
climatic conditions. Perennial allergic rhinitis occurs in response to allergens
that are present throughout the year, such as desquamation of the epithelium
found in pet dandruff, flaking in some insects, chemicals or other equipment or
materials used in industrial plants and 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 either alone
or together. Dust mites feed on human skin flaking and cover with the proteins
they produce the digested material, which is then excreted in the form of fecal
bolus. Dust mites are constantly in hot and humid climates, but in colder areas
their presence decreases in winter because of the lack of humidity in the home.
Some patients with perennial rhinitis are sensitive only to house dust. In more
than two thirds of patients with perennial rhinitis are unable to demonstrate
clearly the causative allergen. The ability of allergens to induce rhinitis
rather than asthma symptoms may depend on their size (ranging from 10 to 100
microns) and, consequently, the different possibilities to cross the airway or
be stuck in the nose.
.
.
.
Clinical manifestations and pathophysiology
The episodes of nasal hypersecretion, sneezing and nasal obstruction, with
lacrimation and itching of the conjunctiva, nasal and oropharyngeal mucosa are
the most salient clinical aspects of allergic rhinitis. The nasal mucosa is pale
and soft, but the nostrils are not reddened or excoriated. The conjunctiva may
be edematous and congested, and the pharynx has no remarkable changes, except an
occasional hyperemia. Edema of the turbinates and mucous membranes with
obstruction of the hosts, sinuses and Eustachian tube may facilitate the
accumulation of secondary infections, respectively, of the paranasal sinuses and
middle ear, frequent occurrence in the form of perennial rhinitis and rather
rare, but in the form of the season. Because of edema and sinus infections,
nasal polyps can often be that tend to exacerbate obstructive symptoms.
The nose has a large mucosal surface that extends in the loops of the turbinates,
which serves to regulate temperature and humidity and to filter the inhaled
particles. The convoluted passages inside the nose facilitate the trapping of
particles larger than 10 μm by simple impact with the mucous lining: At this
point the action of the cilia push the trapped particles toward the pharynx. The
trapping of the pollen and the digestion of the outer layers of the pollen grain
by enzymes present in the mucosa, including lysozyme, causes the release of
allergenic proteins in the molecular weight between 10000 and 40000. Although
the initial interaction occurs between allergen and its intraepithelial mast
cells sensitized by specific IgE, most mast cells remained in the deeper layers
of the mucosal surface and is recruited at a later time. During the season of
symptoms, when the mucosa is almost completely swollen and hyperemic, we are
seeing an increase in seasonal pollen reactivity not only to pollen but also
antigenically different, in respect of which there is hypersensitivity. This
ease of initiation is attributed to the easier penetration of allergens that
come into contact with the perivascular mast cells of deeper layers. In the
nasal mucosa biopsy specimens taken during a crisis there was an allergic deep
submucosal edema with infiltration consisting mainly of eosinophils, although
they may be present in polymorphonuclear leukocytes. The polyps, a feature of
perennial rhinitis, are merely protrusions of the mucosa with edematous fluid
containing mostly consists of eosinophil infiltration present in variable
quantities.
The fluids present on mucosal surfaces contain not only IgA (immunoglobulin A
class, ie, molecules of protein nature that produce defense-lymphocytes),
present in large quantities because with secretory component, but also IgE (also
called immunoglobulins or reagins) which come to you, apparently by diffusion,
by plasma cells distributed in the vicinity of the mucosal surfaces. The IgE
antibodies attach themselves to mast cells in the mucosa and submucosa and the
intensity of the clinical response to inhaled allergens is proportional to the
amount of pollen in the air naturally occurring or experimentally dosed.
Specific IgE bind to mast cells not only tissue but also at the level of
leukocytes basophils, and patients with the most severe form of the disease have
basophils that release histamine in vitro in response to allergen concentrations
much lower than those necessary to obtain a similar release from the cells of
patients with a milder form of the disease. 1 nasal polyps of susceptible
individuals, stimulated in vitro with the determinants of ragweed allergen, they
release histamine. peptides acting chemotactic for eosinophils and leukotriene
spasmogenici. In sensitive individuals, the introduction of the allergen in the
nose causes sneezing, "stuffy nose" and hyper-nasal mucus contains histamine,
PGD2, and leukotrienes. The mast cells of the polyp mucosa and submucosa of the
nose are then able to produce and release mediators after IgE-mediated reaction
that causes tissue edema and infiltration of eosinophils. In fact, when an
antigen reacts with IgE antibodies that are linked to surface receptors on mast
cells and basophils are important triggers the synthesis of inflammatory
mediators, as mentioned above, and activate the so-called cascade of arachidonic
acid, synthesized from the activation of phospholipase. These products are
formed by the effect played by the cyclooxygenase and lipoxygenase arachidonic
acidity. The way of lipoxygenase stimulates the formation of leukotrienes, both
of which play a role in new drug molecules, the monteluskat, leukotrienes
responsible for the induction of vasodilation, edema and contraction muscolare.L
'chronic inflammation typical of asthma is associated with an increased number
of eosinophils, mast cells and T cells in the airways, partially reducible by
treatment with inhaled corticosteroids (CSI). This process takes place in
inflammation when it becomes chronic, the interleukins, particularly where the
IL-5, is activated for determine the production, activation and proliferation of
eosinophils. The CSI, however, do not act effectively on cysteinyl leukotrienes
(cysJs) which play a key role in inflammation and in the pathophysiology of
asthma General (recruitment of eosinophils, mucus hypersecretion, airway
hyperresponsiveness, bronchoconstriction).
Diagnosis
It is based on the patient's history (history): assessing the family history,
that is if there is no history of allergy in the blood relatives, it is also
important to the work history, such as where there is occupational exposure to
some inhalants, the medical history remote, disease, past medical history and
recent symptoms next. Then follows the ENT examination, that the visit ENT (otorhinolaryngology).
The specialist may supplement the examination with a fiberoptic, that can use a
special instrument, an endoscope with a camera or optical fibers, which show the
inside of the nasal cavity with fiber optic instruments and video systems (video
endoscopy) The examination indicated the diagnosis of diseases of the nose,
paranasal sinuses and nasopharynx, assesses the inside of the nasal cavity and
nasopharynx by using fiber optic (flexible or rigid endoscopes). The test is an
outpatient and is completely painless. Is performed after the introduction of
small flaps in the nasal swab solution of anesthetics and vasoconstrictors (decongestants),
which are left in situ for about ten minutes. Removed the anesthetic medication
is introduced endoscope to perform the examination. The technique can be
performed at any age: even three or four years to evaluate the adenoids. Being
an examination of a cruelty has virtually no contra ..
X-ray examinations: standard radiographs of the skull, CT scans (in the
evaluation of complications sinusitiche).
Cultural examination of the nasal mucus running with susceptibility: Using a
cotton ball mounted on a small device that is introduced into the nasal cavities,
then remove the nasal mucus that coats the walls of the nasal cavity. The
material is seeded in a culture medium and, after a certain period of time,
considering whether there has been a growth of bacteria or fungi. In the event
that the colonies have developed, they are subjected to the action of certain
antibiotics to assess the activity (susceptibility).
Microscopic examination of nasal smear: is done to assess the number of
eosinophils in nasal secretions (rinocitogramma).
Allergy testing
· Prick test: Inject intradermally, into the skin of the arm, aqueous
suspensions of the test substances (pollens, mites, animal dander). We evaluate
the reactions of the skin (redness, swelling).
Specific nasal provocation test: are you the patient to inhale through the nose
powder suspensions for testing of substances (pollens, mites). We evaluate the
response (onset of nasal obstruction, itching, sneezing and secretion).
Test serum: you run through a blood test. With them you can evaluate:
Total IgE (Pristo) measures the total amount of allergy antibodies (IgE).
.......
e- mail E-MAIL here
>>>see first page
>>>see also RICERCA