With sinusitis, you and almost 30 million people feel unhappy every year. The combination of facial pressure, headache, fatigue, sneezing, runny nose, drainage of thick, colored mucus from the nose and severe nasal congestion contributes to misery. The worst thing is that it is often difficult to treat, for many people it is very slow to improve and reproduce frequently. The chronic recurring disease known as chronic sinusitis or rhinosinusitis is a mystery. We don't really understand all of the factors that promote the symptoms that make you so prone to relapse.
Although the causes are not understood, some theories and observations are unclear. This is clearly a stubborn condition that often dissolves slowly. Infections are a common component, but not the only piece of the puzzle. Research suggests that the sinuses and nasal passages have some swelling and inflammation that causes blockage of the airways and connections between the sinuses. Whenever there is a warm, damp room in the human body, this is predisposed to problems. Many factors can cause swelling and inflammation. Environmental allergies are common triggers and are likely to be underestimated in the inflammatory response. The presence of certain types of bacteria without actually causing an infection can also irritate the immune system and cause inflammation. Structural abnormalities of the septum or polyps, which are also due to chronic inflammation, can also block the nasal passages. Other diseases can be part of the problem. This can range from simple allergies, acid reflux from the stomach to the nasal passages during sleep, cystic fibrosis or any chronic illness that affects the response of the immune system. The need to identify chronic sinusitis and initiate treatment can contribute to greater comfort and avoid serious complications.
History and clinical results are most helpful in identifying this condition. Diagnostic tests can include nasal cultures or imaging tests such as X-rays or MRI. If allergies are suspected, further allergy tests can be helpful to identify the triggers. Treatment should actively fight infections if they are present. With so many clues pointing to the role of inflammation, nasal sprays have become a cornerstone of management. There are several non-sedative antihistamines that are available without a prescription and are effective for allergies. Many people find it beneficial to perform daily saline irrigation with a Neti pot or an inexpensive watering bottle. Regular use of a simple salt spray is also very helpful to open the nasal passages and provide them with moisture. Non prescription decongestants such as Sudafed or Afrin nasal spray should be avoided. Although they provide quick, short-term relief, they also become less effective quickly and can actually stimulate a rebound overload. This means that they are part of the problem rather than the solution. The operation should only be left as a last resort for extreme cases where all other measures have failed.
Chronic sinusitis is undoubtedly a persistent and all too common problem. Although we don't fully understand why, there are many treatment options. Contact your doctor to find the right diet for your needs. Do not ignore it and continue to suffer. There is help!
Allergic respiratory diseases such as allergic rhinitis and asthma are characterized by local muscle damage and organ dysfunction in the upper and reduced airways, which are due to an abnormal hypersensitivity immune response to generally harmless environmental allergens and are ubiquitous. The allergens that cause respiratory diseases are mainly seasonal pollen from trees, grass and weeds or perennial inhalants (e.g. mite, cockroach, mold, animal hair and some professional protein antigens). ,
Sensitized diseases are a typical trigger for acute and chronic problems of the cervical muscles in children and adults. Sensitive rhinitis and asthma are responsible for significant morbidity, and the prevalence of atopic diseases has increased more than in recent decades. In a Danish survey, the prevalence of skin sensitized rhinitis in 15- to 41-year-olds increased from 12.9% in 1990 to 22.5% in 1998.
Allergic rhinitis is discussed here as a model for the pathophysiology of IgE-sensitive neck muscle disease. Sensitized rhinitis implies the presence of immediate type I hypersensitivity (mediated by IgE) to environmental allergens that directly affect the mucosa of the upper respiratory tract.
Particles that are larger than 5 μm are almost completely filtered by the nasal mucosa. Since most pollen grains are at least that size, some intact particles should get into the narrowed airways when the nose is functioning normally. The sensitized or atopic condition is characterized by an innate tendency to produce IgE antibodies against certain environmental allergens and the physiological reactions that result from the inflammation mediators that are released after the interaction of the allergen with IgE that is bound to mast cells.
The clinical appearance of sensitized rhinitis includes itching in the nose, eye and palate, paroxysmal sneezing, rhinorrhea and nasal congestion. An individual or family history of other allergic diseases such as asthma or neurodermatitis supports the diagnosis of an allergy. Evidence of eosinophilia or basophilia of the sinuses by swabbing or scraping the sinuses can also be helpful in diagnosis.
Confirmation of sensitized rhinitis requires the detection of specific IgE antibodies against common allergens by in vitro controls such as the radioallergosorbent test or the in vivo test (skin) in persons with a history of signs and symptoms with relevant exposures. Inflammatory changes in the airways are recognized as critical functions in sensitized rhinitis and chronic asthma.
The cross-linking of IgE, which is bound to the surface by the antigen, activates the tissue mast tissue and the basophils and induces the immediate discharge of the preformed mediators and the synthesis of the newly created mediators. Mast cells and basophils also have the ability to synthesize and excrete pro-inflammatory cytokines, growth, and regulatory elements that interact in complex networks.
The interaction of mediators with many organs and target cells of the neck muscles can trigger a biphasic allergic reaction: an early phase, which is mainly mediated by the release of histamine and other stored mediators (tryptase, chymase, heparin, chondroitin sulfate and TNF), during late phases -Indications after the formation of arachidonic acid metabolites (leukotrienes and prostaglandins), the platelet-activating aspect and the de novo synthesis of cytokines.
The early phase reaction occurs within minutes of being covered with antigen. After intranasal provocation or exposure to the respective allergen in the area, the person begins to sneeze and develops an improvement in nasal secretion. After about five minutes, the subject develops primary swelling of the mucous membrane to reduce airflow.
These changes are secondary to the results of vasoactive mediators and narrowing smooth muscles, including histamine, Np-tosyl-L-arginine methyl ester esterase (TAME), leukotrienes, prostaglandin D2 (PGD2) and kinins. and mast cell kininogens and basophils. Histologically, the early response is characterized by vascular permeability, vasodilation, muscle edema, and a mild cellular infiltrate that consists primarily of granulocytes.
The sensitized late phase reaction may adhere to the early phase reaction (double reaction) or occur as an isolated event. Late phase reactions begin 2 to 4 hours after preliminary exposure to the antigen, reach maximum activity after 6 to 12 hours, and generally disappear within 12 to 24 hours. However, if the exposure is regular or continuous, the inflammatory response becomes chronic.
The late phase reaction is characterized by erythema, hardening, heat, burning and itching and microscopically by a large influx of mainly eosinophils and mononuclear tissue. Changes can also occur that relate to the reshaping of the airways and hypersensitivity of the muscles.
Mediators of the early phase reaction - with the exception of PGD2 - reappear during the late phase reaction if the antigen is not questioned. The absence of PGD2, an exclusive product of cellular discharge from the mast, in the presence of a continuous release of histamine suggests that basophils, rather than mast cells, are an important source of mediators in the late phase response.
There is an earlier accumulation of neutrophils and eosinophils, followed by an accumulation of activated T cells that synthesize TH2 cytokines. Inflammatory cells that infiltrate tissues in the late response could add sophisticated cytokines and histamine releasing elements that could continue the late-stage response, leading to persistent hyper-reactivity, mucus hypersecretion, production of IgE, eosinophilia, and tissue deficiency (e.g. bronchial membrane, nasal epithelium, or epidermal membrane) ).
There is strong evidence that eosinophils are important inflammatory tissues in the disease of sensitized neck muscles. Eosinophils are common in secretions from the nasal mucosa of patients with allergic rhinitis and in the sputum of asthmatics.
Elements of activated eosinophils, such as the major basic protein and the cationic eosinophilic protein, which destroy the respiratory epithelial muscle and predispose to persistent respiratory reactivity have also been localized in the respiratory tract of people who suffer from allergic diseases.
The recruitment of eosinophils with other inflammatory cells into the respiratory tract is largely part of activated chemokines and adhesion molecules. You will find two subfamilies of chemokines that differ in the tissue they attract and in the chromosomal region of their genes. The C-C chemokines such as RANTES, MCP-1, MCP-3 and eotaxin are located in the chromosomal segment 7q11-q21 and selectively recruit eosinophils.
Leukocytes bind to vascular endothelial cells via the receptor-ligand interaction of adhesion molecules on the cell surface of integrin, selectin and the supergenic immunoglobulin family. The interaction of these adhesion molecules with their counter-receptors mediates a sequence of events consisting of the margination of leukocytes along the walls of microvascularization, the adhesion of leukocytes to the epithelium and the transmigration of leukocytes through the walls of the vessels and migration along a chemotactic gradient, to reach the muscle compartments.
The production of each chemokine and the expression of the adhesion molecule are up-regulated by soluble inflammatory mediators. For example, the receptors for the endothelial cell adhesion molecule ICAM-1, VCAM-1 and E-selectin are up-regulated by IL-1, TNF and LPS. The clinical manifestations of sensitized respiratory disease arise from the interaction of mast cell mediators and basophils with target organs of the upper and lower respiratory tract.
Signs and symptoms of sensitized rhinitis immediately monitor coverage of certain applicable allergens (early-stage reaction), although many patients experience long-term and recurring signs and symptoms due to the late-stage inflammatory response. Serious or untreated problems with sensitized rhinitis include sinusitis, auricular dysfunction, dysosmia, sleep disorders, worsening asthma attacks, and chronic mouth breathing.
Patients with allergic rhinitis develop chronic or episodic paroxysmal sneezing; Sinus, itchy eyes or palate; and watery rhinorrhea caused by the masking of a specific allergen. Individuals may show signs of chronic itching of the upper neck muscles, including a horizontal nasal crease due to regular rubbing of the nose ("allergic greeting") and "clicking" of the palate when the itchy palate is rubbed with speech. Many mast muscle tissues are located near the terminal sensory nerve endings.
Pruritus and sneezing are caused by the histamine-mediated stimulation of these C fibers. Mucus hypersecretion results largely from the excitation of the parasympathetic-cholinergic pathways. The best way to treat signs and symptoms of the early phase is to avoid applicable allergens and oral or topical antihistamines that competitively antagonize the H1 receptor sites by focusing on the tissue.
Anti-inflammatory therapy can reduce mobile inflammation in the advanced stage and provide much more effective symptom relief than antihistamines alone. Allergen immunotherapy (hyposensitization) has been shown to effectively reduce symptoms and inflammation in the respiratory tract by inhibiting any of the early and late phase allergic reactions.
Various mechanisms of immunotherapy have been observed, such as reducing the seasonal increase in IL-4 and allergen-specific IgE, inducing allergen-specific IgG1 and IgG4 (blocking antibodies), modulating the synthesis of T cell cytokines by improving TH1 and inhibiting TH2 responses, upregulation of Treg and downregulation of eosinophilic and basophilic inflammatory responses to an allergen.
One study found that immunotherapy in patients with grass pollen allergy over a period of 3 to 4 years triggers prolonged clinical remission, which is accompanied by a persistent deterioration in immunological reactivity and associated infiltration of T lymphocytes and IL- Expression of 4 mRNAs.
The symptoms of sinus congestion can be chronic and may be due to continuous late-stage allergic mechanisms. The mucous membranes of the paranasal sinuses can appear light blue and peat-like. Children often show signs of forced mouth breathing, including long facies, narrow jawbones, flattened malar protrusions, a pronounced bite, and an arched palate (called adenoids).
These signs and symptoms are not mediated by histamine and are therefore not very sensitive to treatment with antihistamines. Oral sympathomimetics, which trigger vasoconstriction by stimulating the adrenergic receptors, are often used in combination with antihistamines to treat nasal congestion.
Topical decongestants can be used to relieve acute constipation, but are of limited value in people with long-term sensitized rhinitis, as they cause rebound vasodilation (medicinal rhinitis) when used regularly. The phenomenon of increased sensitivity of the paranasal sinuses to a decrease in the allergen concentration after an initial exposure to the allergen is called priming.
A primer can be observed clinically in people who produce strong symptoms late in the pollen season compared to the beginning of the season. In patients with long-term allergic rhinitis and asthma attacks, late-stage inflammation leads to hyperreactivity of the neck muscles towards the respective irritants and allergens.
Hypersensitivity of the respiratory tract can trigger an increased sensitivity to all environmental irritants such as tobacco smoke and harmful smells as well as to allergens such as pollen. You won't find a standardized clinical tool to accurately assess late-stage hyperreactivity in allergic rhinitis, as you will find in asthma attacks (methacholine or histamine-broncho-challenge challenge).
However, the genetic markers for hyperreactivity of the neck bronchial muscles have been identified. It also appears that late-phase cellular infiltration and eosinophilic by-products can cause epithelial damage to the neck muscles, which in turn can lead to reduced hypersensitivity of the upper airways. The accumulation of evidence supports a relationship between sensitized rhinitis and the asthma attack.
Many people with rhinitis alone show nonspecific bronchial hyperreactivity, and prospective studies recommend that sinus allergy can be a risk factor for the development of asthma. Treating people with allergic rhinitis can improve the signs and symptoms of asthma, airway size, and bronchial hypersensitivity to methacholine and exercise.
Finally, mechanistic studies of the physiology of the airways have shown that nasal diseases can affect lung function through any of the direct and indirect mechanisms. This type of mechanism could consist of the presence of the nasobronchial reflex (with stimulation of the sinuses leading to the narrowing of the bronchial tubes), a postnasal drop in inflammatory tissue and mediators of the nose in the lower airways, the absorption of cells, inflammation and mediators in the systemic Circulation and ultimately in the lungs, nasal congestion and subsequent mouth breathing, which can facilitate the entry of asthmagic triggers into the reduced neck muscles.
It is really the main tool for confirming a suspected allergy. In vivo skin tests with allergens suspected of being hypersensitive represent an indirect biological test for the presence of specific IgE allergens on mast muscle tissue or basophils. The percutaneous or intradermal administration of dilute concentrations of specific antigens causes an immediate reaction of papules and Outbreaks within a sensitized individual.
This response marks "local anaphylaxis" resulting from the controlled release of mediators from activated mast cells. Good skin control results for allergens in the air in combination with a medical history and an allergy examination make the allergen strong as the cause of the patient's symptoms. The results of harmful epidermis tests with an unconvincing allergy background strongly speak against an allergic origin.
The main advantages of skin tests are simplicity, speed and the low price. In vitro tests provide quantitative tests for specific IgE allergens in the serum. In these tests, the subject's serum initially reacts with an antigen bound to a solid phase material and is then labeled with a radioactive anti-IgE antibody or bound to an enzyme.
These immunallergosorbent tests are 70-80% correlated with pollen, mite and dandruff tests of the skin and are suitable for patients who receive long-term therapy with antihistamines and who cannot undergo skin diagnostic tests and for patients with extensive dermatitis. Serous otitis media and sinusitis are the most common comorbidities in patients with sensitized rhinitis.
Each condition occurs secondary to nasal congestion and sinuses in people with long-term allergic or non-allergic rhinitis. Long-term problems with rhinitis should be considered in patients with persistent unresponsive rhinitis, refractory asthma, or persistent bronchitis. Serous otitis media results from a blockage of the ear tube due to mucous edema and hypersecretion.
Children with serous otitis media can develop conductive hearing loss, speech delay, and recurrent otitis media associated with long-term obstruction of the sinuses. Sinusitis can be acute, subacute, or long-term, depending on the duration of the signs and symptoms. Obstruction of osteomeatal drainage in people with long-term rhinitis predisposes to bacterial infection in the sinuses.
Sufferers show signs and symptoms of persistent sinus discharge, coughing, sinus discomfort, and nasal congestion. The examination may reveal long-term otitis media, suborbital edema, inflamed sinus mucosa, and purulent discharge from the sinuses. X-ray image diagnosis using X-ray film or computer tomography shows opacification of the sinuses, thickening of the membrane or the presence of an air-liquid level.
Effective treatment of long-term infectious problems with rhinitis requires antibiotics, systemic antihistamines and decongestants, and possibly intranasal or systemic corticosteroids.
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