|
|
|
 |
What are skin allergies?
|
|
Skin allergies represent a group of skin diseases the appearance of which is directly connected to allergic mechanisms. The activity of mediators (substances released from the mastocyte cells participating in an allergic reaction) and lymphokines (biologically active substances produced by simulated lymphocytes) damages the tissue which is manifested as an allergic inflammation. Allergic skin manifestation can be divided into the ones in which the prevalent mechanisms are of early or humoral type (causing increased production of immunoglobuline; e.g. urticaria), and the ones in which the prevalent mechanisms are of late or cell-mediated type (specifically sensitive lymphocyes react with the antigen; e.g. contact allergic dermatitis).
|
|
|
 |
|
What is urticaria?
|
|
Urticaria comes from the Latin word urtica meaning nettle and uro meaning to roast or to burn up. Acute urticaria is a skin disease manifested by eruption of wheals called urticas (changes on the skin correspond to those caused by nettle leaves, hence the name urtica). Urticas are elevated, reddish or pale changes of various scales and forms. Eruption of urtica is usually accompanied by a strong itch. Urticas erupt and disappear abruptly, usually within 24 hours. Mastocyte (subcutaneous cell) plays the key role for the development of urtica because it releases histamine and other inflammation mediators such as prostaglandins, leukotrienes, etc. According to the medical data, 15-25% of the total population can develop urticaria once in a lifetime. Urticas can erupt daily or intermittently (with shorter or longer period without eruption of urticas) within 6 weeks which is diagnosed as acute urticaria. If eruption of urtica occures within the period exceeding 6 weeks, it is diagnosed as chronic urticaria.
|
|
|
|
|
What causes urticaria?
|
|
Since urticaria is defined as a skin reaction to various stimuli its etiology can be very different. Causes of acute urticaria are food content, fish, clams, strawberries and other fruits, cheeses, eggs, preservatives, additives and dyes in food, drugs (medicamentous antigens, especially penicillin), analgetics, acetylsalicylic acid, insulin, anti-tetanus serum, insects venom, etc.
|
|
|
|
|
What are the symptoms of acute urticaria?
|
Urticaria is generally localized on the skin, but there is a risk of systematic (general) reaction (anaphylactic shock).
The following manifestations are also possible: tongue swelling, larynx edema, bronchial asthma attack, digestive tract disorders (vomiting, diarrhea), swelling of joints..
|
|
|
|
|
Contact urticaria
|
|
Urticas appear on the parts directly exposed to the toxins of plants (e.g. nettle), sea fauna (jellyfish, sea anemone), insects, drugs, etc. Urticas are localized to the contact spot. In case of immunologically caused urticarias, hypersensitivity is developed only if there has been some previous contact with the allergen causing the disorder whereas in case of the non-immunological contact urticarias, even the first contact can lead to development of urtica.
|
|
|
|
|
Physical urticaria
|
|
In case of physical urticaria, immunological mechanism do not participate in releasing of inflammation mediators and development of urticas. This group of urticarias includes urticarias caused by various physical stimuli: urticaria caused by pressure, urticaria caused by cold sensitivity, urticaria caused by warm sensitivity, urticaria caused by the sun rays, urticaria triggered by a rise in temperature and hard labor, and urticaria caused by acetylcholine sensitivity. Urticas appear only on the parts exposed to physical factor and can rarely erupt on other parts (reflexive urticaria). Changes are usually localized and not accompanied by general symptoms. However, urticaria caused by cold sensitivity can trigger generalized changes and anaphylactic shock if the patient takes a cold bath or swims in a cold water.
|
|
|
|
|
Non-immunological drug urticaria
|
|
Urticaria can be caused by non-immunological factors - idiosyncratic mechanisms (direct non-immunological releasing of inflammation mediators from the matocyte cells): drugs (morphine, codeine, nonsteroid antirheumatics, (NSAR), acetylsalicylic acid), preservatives, neorupeptides (e.g. substance P which explains deterioration of urticaria in stress condition), radiocontrast agents and hormones (estrogene, corticotropin). In case of non-immunological urticarias, prior sensitization (development of hypersensitivity) is not necessary and allergic reaction can occur during the first contact with the drug.
|
|
|
|
|
What is chronic urticaria?
|
Chronic urticaria is diagnosed when urticas erupt during the period exceeding 6 weeks. Chronic recidivistic urticaria is diagnosed if remission periods are present. In case of remission periods, acute urticaria is more frequent in children and younger population, whereas chronic urticaria is more frequent in adults, usually in middle-aged women. Chronic urticaria is problematic from the point of view of diagnosis and therapy.
0.1 to 3% of the overall population develop chronic urticaria. 25% of patients with acute urticaria develop a chronic form of the disease. The average duration of the disease is from 3 to 5 years whereas in 20% of patients with chronic urticaria, the disease can persist for 20 years. Angioedema (swelling) is present in 50% patients with chronic urticaria. The cause of the disease is identified in 20 to 30% of cases: drugs (acetylsalicylic acid, nonsteroid antirheumatics, angiotensin converting inhibitors), food (approx. 2%), preservatives and additives (approx. 10%), infections (2-5%) (hepatitis B and C, Helicobacter pylori, parasites, chronic sinusitis, etc.), malignancies of internal organs, physical agents (heat, cold, sunlight, pressure, vibration, water). A specific cause is not found in 70-80% of cases of chronic urticaria.
|
|
|
|
|
What is chronic idiopathic urticaria?
|
A specific cause of chronic urticaria can be found in only 20 to 30% of cases. Thus, in the majority of cases (70-80%) one talks about chronic idiopathic urticaria.
However, today there is a growing amount of evidence that the blood of the patients with chronic idiopathic urticaria contains autoantibodies against the receptor for the IgE antibody on the matocyte cell which further supports the standpoint that this disease has autoimmune basis. Autologus skin test by application of serum on the patient's skin is used for proving the existence of functional autoantibodies (that trigger releasing of histamine from the mastocyte).
|
|
|
|
|
Treatment of chronic idiopathic urticaria
|
Chronic idiopathic therapy is based on avoiding the factors that might cause deterioration of the disease such as: additives, alcohol, drugs (acetylsalicylic acid, NSAR, angiotensin converting inhibitors, codeine, morphine) and psychological stress.
Antihistamines represent the first drug in amelioration of symptoms in patient with chronic idiopathic urticaria. Due to the possible relapses and chronic nature of the disease, it is recommended to take nonsedative antihistamines (second generation: loratadine, fexofenadine, cetirizine).
|
|
|
|
|
What is angioedema (symptoms and causes)?
|
Synonyms: Quincke's disease, Quincke's edema (Oedema Quincke), angioneurotic edema (Oedema angioneuroticum)
Angioedema is eruption of acute skin or mucous membrane edema most frequently caused by food, humoral hypersensitivity reaction (type I reaction) often accompanying urticaria. It is a very frequent disease usually detected in younger women. Hypersensitivity reaction is most often triggered by food antigens (egg protein), preservatives (Na-benzoate, tatrazine, etc.), drugs, (acetylsalicylic acid, NSAR, angiotensin converting inhibitors, etc.) and inhalant allergens.
Clinical symptoms include sudden eruption of a more diffuse swelling that most frequently affects: lips, joints area, genitalia, larynx, pharynx and the tongue. After several hours or during 2 to 3 days, edema subsides. Lifelong diagnosis is usually good. Relapses of swelling are sometimes possible. Larynx and pharynx swelling can produce respiratory distress (obstruction, blocking of respiratory tracts) and possible suffocation which sometimes calls for intubation (or tracheotomy).
|
|
|
|
|
What is anaphylactic shock?
|
|
Anaphylaxis is an acute life threatening syndrome with multisystemic manifestations. It represents the most severe form of an early allergy reaction (type I reaction) with acute systemic symptoms and possible fatal outcome in the peak stage of the shock. It is triggered in a hypersensitive patient (when the patient has already been in contact with a corresponding allergen that has lead to hypersensitivity) via consumption of the allergen (usually parenterally - via injection, infusion), insect sting or, less frequently, via peroral consumption (food products, drugs). The causes can be: drugs (antibiotics, sulfonamides, local anesthetics), serums (gamma globulin), insect venom (bees, wasps, hornets, ants), hyposensitized solutions (e.g. pollen allergens during immunotherapy), hormones (insulin, estradiol, methylprednisolone), enzymes (streptokinase, trypsin) and food product (nuts, flour, milk, shellfish, egg-white, kiwi). The most frequent causes of anaphylactic shock are the following: application of penicillin (1 reaction to 5000 expositions), insect venoms and application of radiocontrast agents. Notwithstanding, less than 10% of such reactions have fatal outcome.
|
|
|
|
|
How to identify anaphylactic shock
|
Clinical syndromes start immediately upon consumption of an allergen (parenteral intake) or can be delayed (peroral intake).
Majority of reactions occur within one hour from allergen exposure. Initial symptoms can occur, such as itching of the skin and numbness of the mucous membrane in the mouth cavity. Changes on the skin are also frequent: itching, redness, urticaria, andioedema. Mucous membrane swelling, itching of the eyes and the nose are also frequent symptoms as well as mouth and tongue swelling that might lead to obstructed respiration and swallowing. Severe signs of anaphylactic reactions are manifested as the upper respiratory tract obstruction which have been triggered by edema of larynx, epiglottis and of the surrounding tissue, and bronchoconstriction of the lower respiratory tract with the development of hypoxia. Development of cardiovascular collapse is accompanied by hypotension, tachycardia (rapid heart action) that might lead to severe arrhythmia. Nausea, vomiting, cramps and diarrhea can also occur since the shock affects gastrointestinal tract. Due to cerebral hypovolemia and a direct toxic effect of the released mediators, dizziness, unrest and loss of consciousness can also be manifested.
The most important symptoms of anaphylaxis:
•itching and redness of the skin, urticaria, angioedema;
•dyspnea (difficult respiration), cough;
•rhinorrhea (excessive mucous secretion from the nose), wheezing;
•difficult swallowing;
•nausea, vomiting, diarrhea, stomach pains, flatulence;
•tachycardia (rapid heart beat), hypotension (low pressure), arrhythmia (irregular heart beat), shock;
•malaise, chill sensation;
•mydriasis (dilatation of the pupil of the eye);
•anxiety (unrest, fear), tremor (shivering), conscious disorder, syncope (unconsciousness), coma.
|
|
|
|
|
What to do - ask for medical help!
|
Development of anaphylaxis is extremely rapid and unexpected. In such situations it is crucial to detect anaphylactic event rapidly because it might soon turn into anaphylactic shock that might have fatal outcome. It is crucial to cease applying a specific drug (if that drug is the cause of anaphylactic reaction), prevent further absorption of the drug, monitor vital function: frequency and rhythm of heart beat, measure pressure and pulse, pulmonary functions, monitor rhythm and depth of respiration, ensure appropriate oxygenation of the patient and organize fast transport of the patient to the nearest hospital.
Regarding the patients with higher risk of anaphylactic reaction relapse (e.g. patients that have experienced anaphylactic reaction to insect venom or food), it is necessary to instruct them to always carry with them self-aid set (e.g. EPI-PEN, ANA-KIT). EPI-PEN consists of a syringe with a needle and adrenaline for singular intramuscular application. ANA-KIT contains two doses of adrenaline and chlorpheniramine (antihistamine) chewing tablets. Patients with anaphylactic reaction to insect venom must undergo hyposensitization.
|
|
|
|
|
Anaphylactic shock treatment
|
Patient should be put in a comfortable laying position with elevated legs and undergo oxygen therapy via nasal probe or mask. In laryngeal edema, it is necessary to establish ventilation of respiratory tracts by endotracheal intubation or tracheotomy. It is necessary to stop with consumption of antigens (if possible) and ensure vein access (infusion of physiological solution). The most important drug in treating a severe anaphylactic reaction is adrenalin. In laryngeal edema, adrenalin can be administered also via inhalation. Antihistamines influence on itch, urticaria and angioedema. It is important to be very careful during intravenous application because of the possible hypotension. Corticosteroids delay late anaphylactic reaction, but during the acute event, they are not particularly effective. They become effective several hours following intravenous application.
It is important to remember that all patients with anaphylactic reaction must be taken to the hospital and be monitored at least 24 hours in the intensive care units.
|
|
|
|
|
What are atopic skin diseases (atopic dermatitis, neurodermatitis)?
|
Atopic dermatitis is a chronic, relapsing inflammation dermatosis characterized by strong itch and manifested in atopic patients (The term atopy denotes hereditary increased production of immunoglobuline E). Changes on the skin can be manifested at any age, but most typically between the 3rd and 4th month (30% of children) of life. The disease tends to withdraw with age, but there is no available method to foretell a possible development of the disease in children. 50% of children suffering from the disease in their early childhood get well by the 4th or 8th year of life and 80% get well by the time they reach 12 years of age.
Changes on the skin can be localized on antecubital and poplietal fossae, or disseminated. 80% of patients have a higher value of the total immunoglobuline E in blood and positive results of intradermal test for specific allergens (e.g. dust, dust mites, feathers, animal fur, cow milk protein, egg-white, pollen).
Allergic diseases such as allergic rhinitis, asthma and atopic skin diseases represent systemic diseases with localized immunological reaction on numerous organs. Combination of atopic dermatitis and allergic rhinitis and bronchial asthma is very frequent. Interestingly enough, bronchial asthma attacks and neurodermatitis attacks do not occur simultaneously.
|
|
|
|
|
Treatment of atopic dermatitis
|
Adequate rehydration of the skin is important: oil bath: 20-30 min, with application of oil, 10% of urea, alpha-hydroxy acid within 3 minutes after the bath.
Topical anti-inflammatory preparations and antiallergic preparations (corticosteroid creams and ointments) are applied locally on the skin and recently immunomodulatory preparations (tacrolimus) have been introduced. Antihistamines can also be applied in the stage of deterioration of skin condition. For children antihistamine (first generation: dyphenhidramine) can also be used as a sedative at bedtime because it diminished itching and soothes the child before sleep.
Reduced diet
In case of atopic dermatitis it is important to avoid nutritive allergens the patient is hypersensitive to. This particularly applies to mothers breastfeeding their children. In patient with acute urticaria it is important to administer a very strict diet regime at the initial stage of the disease and to avoid preservatives and food additives that might be allergens that trigger allergic reactions.
|
|
|
|
|
What is photodermatosis and photoallergic dermatosis?
|
|
Photodermatosis implies skin lesions caused by exposure to UV light and is divided into two groups: primary and secondary photodermatoses. In primary photodermatoses (e.g. solar dermatitis), skin lesions are caused directly by UV light whereas in secondary photodermatoses (phototoxic dermatoses), beside light, other photosensitizer agents contained in cosmetic preparations or plants must also be active. Photoallergic dermatoses imply skin lesions the appearance of which is equally attributable to photosensitizers, UV light and immunological mechanisms. Photoallergic reactions are more rare than phototoxic ones. Light activates photosensitizer which has directly penetrated the skin, from gastrointestinal tract or parenterally. Under the influence of light, photosensitizer is activated and amalgamates with skin proteins followed by activation of immunological mechanisms and development of lesions on the skin. Here are some of the photosensitiers used locally: tetrachlorsalycilamide, para-amiobenzoic acid, hexachlorophene, bitionol, musk (contained in soaps, cosmetic products, sun lotions and perfumes). Among drugs applied perorally, strong photosensitizes are the following: tetracyclines, sulfonamides, sulfonylurea (antidiabetic drug), phenothiazine (psychopharmaceutical), triprolidine (antihistaminic), chlorothiazide (diuretic) and cyclamate (sweetener).
|
|
|
|
|
|
 |
|
|
How schools handle food allergy?
A survey of nurses in elementary and middle schools in the U.S. found that food allergy action plans for students with food allergies are used inconsistently.
|
|
|
|
|
|
|
|
|
|
