Allergies (including atopic) and other hypersensitivity reactions are inappropriate or exaggerated immune responses to foreign antigens. Inappropriate immune reactions include those that are misdirected against intrinsic body components, resulting in autoimmune diseases. Classification of hypersensitivity reactions hypersensitivity reactions are divided with the Gell and Coombs Classification into 4 types of. Usually more than just one type is involved in hypersensitivity reactions. Type I Type I reactions (immediate type) are IgE-mediated responses. The antigen (Ag) adheres to IgE (this is bound to mast cells in tissues and basophils in the blood), whereby the release of preformed mediators (z. B. histamine, proteases, chemotactic factors), and the synthesis of other mediators (e.g. . as prostaglandins, leukotrienes, platelet-activating factor, cytokines) are triggered. These mediators cause vasodilation, increased capillary permeability, excessive mucus secretion, spasms of the smooth muscle and the infiltration of the tissue with eosinophil cells, type 2 T-helper cells (TH2) and other inflammatory cells. Type I reactions develop <1 h after exposure to the antigen. Type I hypersensitivity reactions include all atopic disorders (eg. As allergic asthma, rhinitis, conjunctivitis) and many allergic diseases (eg., Anaphylaxis, some cases of angioedema, urticaria, a sensitivity to latex and some food allergies). The terms atopy and allergies are often used interchangeably, but they are different: atopy is an exaggerated IgE-mediated immune response; all atopic diseases are type I hypersensitivity disorders. An allergy is, each caused by a foreign antigen exaggerated response of the immune system, regardless of mechanism. Consequently all atopic diseases are considered as allergic disorders, whereas many allergic diseases (eg. As hypersensitivity pneumonitis) are not atopic. Allergic diseases are the most common diseases in humans. Atopic diseases affect ordinary nose, eyes, skin and lungs. These diseases extrinsic atopic dermatitis, immune-mediated urticaria, immune-mediated angioedema, acute latex allergy, some allergic diseases of the lung include (z. B. some cases of asthma, IgE-mediated components of allergic bronchopulmonary aspergillosis), allergic rhinitis and allergic reactions to toxic Stacheln.Typ II type II reactions (antibody-dependent cytotoxic hypersensitivity) occur when antibodies bind to the cell surface antigens or to a molecule that is coupled to a cell surface receptor. The antigen-antibody complex activates cells in antibody-dependent cellular cytotoxicity (z. B. natural killer cells, eosinophils, macrophages) are involved in the complement, or both. This results in a cell and tissue damage. Among the disorders of type II hyperacute rejection of an organ transplant, the Coombs-positive hemolytic anemia, Hashimoto's thyroiditis and antiglomerular basement membrane disease (z. B. Goodpasture syndrome) .typ include III Type III reactions (immune complex disease) cause in response to circulating antigen-antibody complexes which are deposited in blood vessels or tissue inflammation. These complexes can activate the complement system or binding to specific immune cells and activate them, resulting in the release of inflammatory mediators. The consequences of immune complex formation depend in part on the relative relationship between antigen and antibody in the immune complex. First, an excessive proportion of antigen associated with low Ag-Ab complexes that do not lead to complement activation. Later, when antigens (Ag) and antibodies present in a balanced ratio, the immune complexes are larger and tend to deposit in various tissues (eg. B. glomeruli, blood vessels) and thereby cause systemic reactions. The isotype of the induced changes in the antibody, and glycosylation, the size and the charge of the complex components contribute to the clinical response. To the Type-III disorders include serum sickness, systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), leukocytoclastic vasculitis, cryoglobulinemia, acute hypersensitivity pneumonitis, and various forms of glomerulonephritis. Type III reactions develop 4 to 10 days after exposure to the antigen, and can become chronic if exposure andauert.Typ IV Type IV reactions (delayed type) are T-cell mediated. T cells are sensitized upon contact with a specific antigen and activated by repeated exposure with the antigen. They destroy tissue through direct toxic effect or by release of cytokines, eosinophils, monocytes, macrophages, neutrophils or natural killer cells activate. To the Type IV reactions are contact dermatitis (z. B. nickel allergy, drug, poison ivy), subacute and chronic hypersensitivity pneumonitis, allograft rejection, immune response to tuberculosis, and many of the drug hypersensitivity. Latex sensitivity latex sensitivity is an exaggerated immune response to water-soluble proteins in latex products (eg. As gloves, "dental dams", condoms, tubing for respiratory equipment, catheters, Klistierspitzen with inflatable latex cuff). Beginning in the late 1980s, the incidence increased among health workers, as a result of the general precautions routinely latex gloves were used. The reactions to latex can be acute (IgE-mediated) Delayed (cell-mediated) reactions cause acute urticaria and anaphylaxis; Delayed reactions have dermatitis. After wearing latex gloves, the skin is often irritated and crusty. However, this reaction is generally a chemical irritation, no latex allergy. The diagnosis of latex sensitivity is primarily based on the history. Skin tests and assays for the detection of IgE anti-latex antibodies are available. The therapy is to avoid latex. Health facilities should have available latex-free gloves and equipment. Etiology Complex genetic, environmental and site-specific factors contribute to the development of allergies. The frequent occurrence of diseases in families, suggesting that genetic factors are involved and a connection between atopy and specific HLA loci and polymorphisms of several genes, including those for the high-affinity IgE receptor beta chain, IL-4 receptor alpha chain, IL-4 , IL-13, CD14, dipeptidyl peptidase 10 (DPP10) and a disintegrin and metalloproteinase domain 33 (ADAM33) consists. Environmental factors interact with genetic factors to produce a type 2 T helper (Th2) -Immunantwort is obtained. TH2 cells activate eosinophils, promote IgE production and proallergisch. Early childhood exposure to bacterial and viral infections and endotoxins (z. B. lipopolysaccharides) can normally move -cell reactions, which in turn suppress the TH2 cells and hence allergic native TH2-cell responses to Type 1 T helper (TH1) prevent reactions. Regulatory T (CD4 + CD25 + Foxp3 +; Treg) cells (which are capable of TH2-cell responses to suppress) and IL-12-producing dendritic cells (TH1 cell responses abut) are probably also involved. But the trend in developed countries towards smaller families with fewer children, a more hygienic home environment and the early use of antibiotics limits the exposure of children to infectious substances that stimulate a Th1 cell response in the first place; Such behavioral changes may explain the increasing prevalence of some allergic diseases. Other factors that are believed to contribute to the development of allergies are a chronic allergen exposure and awareness, nutrition and pollution. Site-specific factors include adhesion molecules in the bronchial epithelium and in the skin as well as molecules in the gastrointestinal tract, direct the TH2 cells to the target tissue. By definition, allergens induces an allergen IgE-mediated or Type IV T cell-mediated immune responses. Allergy Inducing are almost always low-molecular proteins, many of which attach to airborne particles. Allergens that trigger most common acute and chronic allergic reactions house dust mite animal hair pollens (tree, grass, weed) molds pathophysiology When allergens attach to IgE-sensitized mast cells and basophils, released from their intracellular granules histamine. Mast cells are widely used, most concentrated but they are in the skin, lungs, and in the lining of the gastrointestinal tract; Histamine enables inflammation and is the primary mediator of the clinical atopy. The histamine release can, regardless of IgE, by physical tissue destruction and a variety of substances (eg., Tissue-irritants, opiates, surfactants, complement components C3a and C5a) are triggered directly. Histamine following causes: Local vasodilatation (flare) Increased capillary permeability and edema (wheal) vasodilation of the surrounding arterioles by neural reflex mechanisms (causing a flare - the redness around a wheal) The stimulation of the sensory nerves (itching) contraction of smooth muscle in (increase increased gastrointestinal motility) the airways (bronchoconstriction) and in the gastrointestinal tract increased nasal, saliva and bronchial secretion in the cardiovascular system histamine is considered strong dilator of arterioles, which may lead to considerable accumulation of blood in the periphery and hypotension; cerebral vasodilation may play a role in migraine. Histamine increased capillary permeability; the resulting loss of plasma and plasma proteins from the vascular space may result in the aggravation of circulatory shock. This loss stimulates a compensatory Katecholaminschub from adrenal, chromaffin cells. Symptoms and complaints Common symptoms of allergic diseases include rhinorrhea, sneezing and stuffy nose (upper respiratory tract) wheezing and shortness of breath (lower respiratory tract) Itching (eyes, nose, skin) Other signs are Nasenmuschelödem, on palpation painful sinuses, wheezing, conjunctival hyperemia, Konjunktivalödem , urticaria, angioedema, dermatitis and lichenification of the skin. Stridor, wheezing, and hypotension are life-threatening signs of anaphylaxis. Diagnosis Clinical Investigation Sometimes blood count and occasionally serum IgE levels (non-specific tests) Often skin testing and allergen-specific serum IgE tests (specific tests) Rare provocative testing A thorough history is generally more reliable than tests or screening. The history should if identifiable to seasonal comprise questions about frequency and duration of attacks and changes over time Triggering factors relationship or situational settings (eg predictable during pollen seasons;. After exposure to animals, hay or dust; during the training or at certain locations) family history of similar symptoms or atopic diseases reactions to attempts at treatment suffering from asthma can be an important key age at onset in childhood, the disease is more atopic than after 30 years. Health professionals are possibly unaware that exposure to latex products may be the cause of their allergic reaction. Non-specific tests Specific test procedures may provide clues, but give no confirmation of the allergic origin of the symptoms. For the detection of eosinophilia complete blood counts in patients should be placed not receiving corticosteroids as these can lower the eosinophil. A blood count, however, is of limited value, since eosinophils may be increased when atopy or other conditions (eg. As drug hypersensitivity, cancer, some autoimmune diseases, parasitic infection) and a normal eosinophil count does not necessarily rule out an allergy. The absolute number of leukocytes in the complete blood count is usually normal. Anemia and thrombocytosis are not typical of allergic reactions and it should be a systemic inflammatory disease should be considered. Leukocytes can be determined in conjunctival and nasal discharge or sputum. The presence of eosinophils is an indication of a TH2vermittelte inflammatory response. Atopic diseases increased IgE levels found. For diagnosing this is not very helpful since IgE levels (hyper-IgE syndrome and Wiskott-Aldrich syndrome) and some forms of multiple myeloma are elevated in parasitic infections, infectious mononucleosis, autoimmune diseases, drug reactions, immune defects. Most useful to determine the IgE levels is likely to control the course of therapy in allergic Lungenaspergillose.Spezifische tests use skin tests standardized antigen concentrations that are introduced directly into the skin. They are indicated when cause and trigger factors of prolonged and severe symptoms through a detailed history and physical examination can not be identified. Skin tests have a higher positive predictive value for the diagnosis of allergic rhinitis and conjunctivitis than for allergic asthma or food allergy; the negative predictive value for a food allergy is high. The most commonly used antigens are pollen (tree, grass, weeds), mold, dust mites droppings, animal sheds and serums, insecticides, food and beta-lactam antibiotics. The choice of the test antigens depends on the history and geographic prevalence. Two types of skin tests can be used: percutaneous (Prick) Intradermal With the prick test, the häufgisten allergies can be detected. The intradermal test, although more sensitive, but less specific; with it, the sensitivity can be assessed against antigens that brought negative or inconclusive results in the prick test. When prick test, a drop of antigen extract is applied to the skin. Then the skin is pierced, or with a 27-gauge needle or a commercially available test stamp by the extract punctured. When the intradermal test just as much extract is injected intradermally (typically 0.02 ml) such that a 1 or 2 mm large bubbles formed with a 0.5 or 1 ml syringe and a 27 gauge short beveled needle. In each of these tests, the diluent alone or histamine (mg / ml for the skin prick test or 0.01 ml of a 1 10: 1000 solution for intradermal test) as negative control are applied as positive control. If patients have only recent (<1 year) generalized response to a test antigen demonstrated the test series initially starts with a 100-fold diluted standard reagent, then is tested with a 10-fold diluted solution and finally with the standard concentration. A skin test is to be regarded as positive if after 15-20 minutes, a wheal and erythema and wheal arise in diameter is 3-5 mm greater than the negative control. False positive reactions occur at dermographism on (wheals and erythema by brushing or scraping of the skin). False-negative reactions there when allergen extracts have been improperly stored or are outdated. Certain medications can affect the results and should a few days up to a week to be sold before the test. These drugs include non-prescription and prescription antihistamines, antidepressants and monoamine oxidase inhibitors. Some clinicians suggest to avoid the testing in patients taking beta-blockers, because in these patients risk factors are given more frequently, which can cause a severe reaction. These risk factors indicate limited cardiopulmonary reserves. These include coronary heart disease, heart rhythm disturbances and a higher age. Beta-blockers can also influence the treatment of severe reactions by blocking the response to ?-adrenergic agonists such as epinephrine. Allergen-specific IgE testing using an enzyme-labeled anti-IgE antibody to detect the binding of serum IgE to a known allergen. They are done when skin tests could-z ineffective or risky. For example, when drugs that distort the test results can not be temporarily discontinued prior to the test or if a skin disorder such as eczema or psoriasis would make the skin tests difficult. In allergen-specific IgE tests, the allergen is immobilized on a synthetic surface. After incubation with patient serum and enzymbenanntem anti-IgE antibody, a substrate for the enzyme is added; the substrate provides a colorimetric or chemiluminescent detection on a fluorescent binding. Allergen-specific IgE tests have radioallergosorbente tests replaced (RAST), inserting the 125I-labeled anti-IgE antibody. Although the allergen-specific IgE tests are not radioactive, they are still sometimes called a RAST. When provocation test mucous membranes are brought into direct contact with the allergen. The implementation of this test is indicated for people who need to document their reactions (eg. As for the detection of an occupational disease or disability). Sometimes it is also used in the diagnosis of food allergies. For example, patients are asked to train in order to diagnose a triggered by exercise or asthma it is given for 4 minutes on the skin, in order to determine a cold-induced urticaria an ice cube. The Ophthalmotest brings no advantage over the skin tests and is rarely applied. Nasal and bronchial challenge primarily serve research purposes, but the bronchial provocation is sometimes used when the clinical significance of a positive skin test is unclear or antigen extracts are not available (eg. As in occupational asthma). Therapy emergency treatment to remove or avoid allergic triggers H1 blockers mast cell stabilizers, anti-inflammatory corticosteroids, and leukotriene inhibitors immunotherapy (desensitization) emergency treatment requires a severe allergic reaction (eg., Anaphylaxis) an immediate emergency treatment. When the airways are affected (eg. As in a angioedema keeping open the respiratory system is extremely important. Treatment may include epinephrine and / or include intubation. Patients who have severe allergic reactions should be advised to always have a pre-filled syringe of adrenaline to carry for self-injection and oral antihistamines with you and if a severe reaction occurs, use it as soon as possible and then go to the emergency room. There the patients are closely monitored and the treatment can be repeated or adjusted as needed werden.Kontrolle Near removal or avoidance of allergic triggers is the primary treatment of allergy, as well as the primary Präventionsstrategie.H 1 blocker antihistamines block receptors, they have no effect on histamine production or metabolism. a mainstay in the treatment of allergic diseases are H1 blockers. H2 blockers are used primarily for the suppression of gastric acid and are of limited use for the treatment of allergic reactions; but they can be indicated in certain atopic diseases as an adjunctive treatment, especially in chronic urticaria. Oral H1-blockers (see Table: Oral H1 blockers) alleviate the symptoms of various atopic and allergic disorders (e.g. seasonal hay fever, allergic rhinitis, conjunctivitis, urticaria, other skin diseases, lighter reactions to blood incompatibilities under transfusions.); they are less effective in allergic bronchoconstriction and vasodilation. The effect usually occurs within 15 to 30 minutes and reached the summit within an hour; the effect of time is usually 3-6 hours. Products containing an oral H1-blocker and a sympathomimetic (eg., Pseudoephedrine), ? 12 years of age are widely available over the counter for use in adults and children. These products are particularly useful when both an antihistamine and a nasal decongestant are needed; However, they are sometimes contraindicated (z. B. when patients are taking an MAOI). Oral H1 blockers are classified as sedative Nichtsedierend (better: less sedating) antihistamines with sedative effects are widely available without a prescription. All have significant sedative and anticholinergic properties; special problems they represent for the elderly and patients suffering from glaucoma, benign prostatic hyperplasia, constipation, orthostatic hypotension, delirium or dementia. Nonsedating (non-anticholinergic) antihistamines are preferred, unless the sedative effect is of therapeutic benefit (eg. As improving sleep in allergy, short-term treatment of insomnia in adults or nausea in younger patients). Because of their anticholinergic effect the application sedating antihistamines is also justified for the relief of rhinorrhea in infections of the upper respiratory tract. Antihistaminikalösungen may be intranasal (azelastine or olopatadine for the treatment of rhinitis) eyepiece (azelastine, emedastine, ketotifen, levocabastine, olopatadine or Pemirolast to treat conjunctivitis) Topically applicable diphenhydramine is available, but should not be used because its effectiveness has not been established; there may be a drug sensitization (d. h. allergy) and in small children, take the same oral H1-blocker, an anticholinergic toxicity can develop. Oral H1 blocker drug Usual adult dosage Usual dosage for children Available preparations sedating * brompheniramine 4 mg every 4-6 hours or 8 mg every 8-12 h <2 years: contraindicated 2-6 years: 0.125 mg / kg every 6 h ( maximum dose 6-8 mg / day) 6-11: 2-4 mg every 6-8 h (maximum dose 12-16 mg / day) ? 12 years: adult dose 4 - 8 - and 12-mg tablets 2 mg / 5 ml elixir 8 - and 12-mg tablets (sustained free reduction) chlorpheniramine 2-4 mg every 4-6 h <2 years: Contraindicated 2-6 years: Not recommended 6-11 years: 2 mg every 4-6 h (maximum dose 12 mg / day) ? 12 years: adult dose 2 -Mg chewable 4 - 8 - and 12-mg tablets 2 mg / 5 ml syrup 8 - and 12-mg tablets or capsules (time-controlled release) clemastine 1.34 mg (1.0 mg of base) of 2- twice daily to 2.68 mg three times a day <1: Contraindicated 1-3 years: 0.33 to 0.67 mg every 12 h 3-5 years: 0.67 mg q12h 6-11 years: 0 , from 67 to 1.34 mg every 12 hours ? 12 years: adult dose 1,34- and 2,68 -mg tablets 0.67 mg / 5 ml syrup Cyproheptadine 4 mg 3 times a day, or 4 times daily (maximum of 0.5 mg / kg / day) <2 years of age: 2-6 years contraindicated: 2 mg 2 times to 3 times a day (maximum 12 mg / day) 7-14: 4 mg 2 times a day to 3 times (up to 16 mg / day) 4 mg tablets † 2 mg / 5 ml syrup dexchlorpheniramine 2 mg every 4-6 h <2 years: contraindicated 2-5 years: 0.5 mg every 4-6 h (maximum dose 3 mg / day) 6-11: 1 mg every 4-6 h (maximum dose 6 mg / day) ? 12 years: adult dose 2 mg tablet 2 mg / 5 ml syrup 4 - (and 6 mg tablets prolonged Release of active substance) diphenhydramine 25-50 mg every 4-6 h <2 years: contraindicated 2-11 years: 1.25 mg / kg every 6 hours (maximum dose 300 mg / day) ? 12 years: adult dose 25 - and 50-mg capsules or tablets 12.5 mg / ml syrup 12.5 mg / 5 ml elixir hydroxyzine 25-50 mg 3 times a day, or 4 times daily <2 years: Not recommended 2-11: 0.7 mg / kg 3 times daily ?12 years: adult dose 25 -, 50 - and 100 mg capsules 10 -, 25 -, 50 - and 100 mg tablets 10 mg / 5 ml syrup 25 mg / 5 ml oral suspension Promethazine from 12.5 to 25 mg twice daily <2 years: Contraindicated ?2 years: 6.25 to 12.5 mg 2 times or 3 times a day 12.5, 25 - and 50-mg tablets † 6.25 mg / 5 ml and 25 mg / 5 ml syrup sedating acrivastine / pseudoephedrine 8/60 mg 2 times or 3 times a day <12 years: Not recommended ?12 years: adult dose 8 mg acrivastine plus 60 mg pseudoephedrine capsules cetirizine 5 -10 mg 1 time a day 6-11 months: 2.5 mg of 1-times daily 12-23 months: 2.5 mg twice daily 2-5 years: 5 mg of 1-times daily ?6 years: adult dose 5 - and 10-mg tablets 1 mg / ml syrup desloratadine 5 mg of 1-times daily 6-11 months: 1 mg / day 1-5 years: 1.25 mg / day 6-11: 2.5 mg of 1-times daily ?12 years: adult dose 5- mg tablets 0.5 mg / ml syrup fexofenadine 60 mg2 times daily or 180 mg of 1-times daily 6-23 months: 15 mg twice a day 2-11 years: 30 mg twice daily ?12 years: adult dose 30 -, 60 - and 180-mg tablets 6 mg / ml oral suspension levocetirizine 5 mg of 1-times daily <6 years: contraindicated 6-11: 2.5 mg of 1-times daily ?12 years: adult dose of 5-mg tablets 0,5 mg/ml Suspension zum Einnehmen Loratadin 10 mg 1-mal täglich 2–5 Jahre: 5 mg 1-mal täglich ?6 Jahre: Erwachsenendosis 10-mg-Tabletten 1 mg/ml Sirup Mizolastin 10 mg 1-mal täglich < 12 Jahre: Nicht empfehlenswert ?12 Jahre: Erwachsenendosis 10-mg-Tabletten * Alle sedierende Antihistaminika haben starke anticholinerge Eigenschaften. Generell sollten sie nicht bei älteren Menschen oder bei Patienten mit Glaukom, benigner Prostatahyperplasie, Verstopfung, Delirium, Demenz oder orthostatischer Hypotonie verwendet werden. Diese Medikamente verursachen häufig Mundtrockenheit, Sehstörungen, Harnverhaltung, Verstopfung und orthostatische Hypotonie. †Anwendungshäufigkeit sollte bei Kindern nicht erhöht werden. Mastzellstabilisatoren Diese Medikamente blockieren die Freisetzung von Mediatoren aus Mastzellen. Mastzellenstabilisatoren kommen zur Anwendung, wenn andere Arzneimittel

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