Allergic diseases, are a number of conditions caused by hypersensitivity of the immune system to something in the environment that usually causes little or no problem in most people.

Allergic diseases include hay fever, food allergies, atopic dermatitis, allergic asthma, and anaphylaxis.

Allergic symptoms may include red eyes, an itchy rash, runny nose, shortness of breath, or swelling.

Food intolerances and food poisoning are separate conditions.

Common allergens include pollen and certain foods.

Metals and other substances may also cause problems, as may foods, insect stings, and medications are common causes of severe reactions.

Their development is due to both genetic and environmental factors.

The underlying mechanism involves immunoglobulin E antibodies (IgE).

IgE antibodies bind to an allergen and then to a receptor on mast cells or basophils where it triggers the release of inflammatory chemicals such as histamine.

In allergy, mast cells release inflammatory substances such as histamine, neutral proteases, arachidonic acid derivatives, platelet activating factor and a variety of cytokines and chemokines. 

Diagnosis is typically based on a person’s medical history.

Further testing of the skin or blood may be useful in certain cases.

Positive tests, however, may not mean there is a significant allergy to the substance in question.

Early exposure to potential allergens may be protective to the development of allergy.

Treatments for allergies include avoiding known allergens and the use of medications such as steroids and antihistamines.

In severe reactions injectable epinephrine is recommended.

Allergen immunotherapy, which gradually exposes people to larger and larger amounts of allergen, is useful for some types of allergies such as hay fever and reactions to insect bites.

Allergen immunotherapy use in food allergies is unclear.

About 20% of people are affected by allergic rhinitis.

About 6% of people have at least one food allergy.

About 20% have atopic dermatitis at some point in time.

Depending on the country about 1–18% of people have asthma.

Anaphylaxis occurs in between 0.05–2% of people.

Rates of many allergic diseases appear to be increasing.

Common allergic symptoms in the nose includes swelling of the nasal mucosa runny nose, and sneezing.

Allergic symptoms of the eyes include: Redness and itching of the conjunctiva and watery discharge.

Airway symptoms include sneezing, coughing, bronchoconstriction, wheezing and dyspnea, asthma, in severe cases the airway constricts due to swelling known as laryngeal edema.

Ear symptoms include fullness, pain, and impaired hearing due to the lack of eustachian tube drainage.

Skin changes include rashes, such as eczema and hives.

Gastrointestinal tract manifestations include abdominal pain, bloating, vomiting, and diarrhea.

Many allergens such as dust or pollen are airborne particles.

With airborne particles symptoms arise in areas in contact with air, such as eyes, nose, and lungs.

Allergic rhinitis causes irritation of the nose, sneezing, itching, and redness of the eyes.

Inhaled allergens can also lead to increased production of mucus in the lungs, shortness of breath, coughing, and wheezing.

Allergic reactions can result from foods, insect stings, and reactions to medications like aspirin and antibiotics such as penicillin.

Food allergy symptoms include: abdominal pain, bloating, vomiting, diarrhea, itchy skin, and swelling of the skin during hives.

Food allergies rarely cause respiratory symptoms, or rhinitis.

Insect stings, and antibiotics produce a systemic allergic response, known as anaphylaxis.

With anaphylaxis, multiple organ systems including the digestive system, the respiratory system, and the circulatory system can be affected.

Anaphylaxis can cause a skin reactions, bronchoconstriction, swelling, low blood pressure, coma, and death.

Anaphylaxis reaction can be triggered suddenly, or the onset can be delayed.

Substances like latex, that come in contact with the skin are commonly cause allergic reactions, known as contact dermatitis or eczema.

Skin allergies frequently cause hives and angioedema.

Risk factors include host and environmental factors.

Host factors include heredity, sex, race, and age.

Heredity is the most significant host factor.

Four major environmental factors include: exposure to infectious diseases during early childhood, environmental pollution, allergen levels, and dietary changes.

90% of allergic responses to foods are caused by cow’s milk, soy, eggs, wheat, peanuts, tree nuts, fish, and shellfish.

Other food allergies, affecting less than 1 person per 10,000 population, are rare.

The use of hydrolysed milk baby formula does not change the risk of food allergy.

Most common food allergy in the US is a sensitivity to crustacea.

Peanut allergies are noted for their severity.

Peanut allergies are not the most common food allergy.

Severe or life-threatening reactions may be triggered by other allergens, and are more common when combined with asthma.

Peanut allergies can sometimes be outgrown by children.

Egg allergies affect one to two percent of children but are outgrown by about two-thirds of children by the age of 5.

Egg allergy sensitivity is usually to proteins in the white, rather than the yolk.

Milk-protein allergies are most common in children.

Approximately 60% of milk-protein reactions are immunoglobulin E-mediated, with the remaining usually attributable to inflammation of the colon.

Some people are unable to tolerate milk from goats or sheep as well as from cows, and many are also unable to tolerate dairy products such as cheese.

Roughly 10% of children with a milk allergy will have a reaction to beef.

Beef contains a small amount of protein that is present in cow’s milk.

With tree nut allergies one may be allergic to one or to many tree nuts, including pecans, pistachios, pine nuts, and walnuts.

Seeds, including sesame seeds and poppy seeds, contain oils in which protein is present, which may elicit an allergic reaction.

Latex can trigger an IgE-mediated cutaneous, respiratory, and systemic reaction.

Prevalence of latex allergy in the general population is believed to be less than one percent, although the sensitivity among healthcare workers is higher, between seven and ten percent.

The higher level to the exposure of healthcare workers to areas with significant airborne latex allergens, such as operating rooms, intensive-care units, and dental suites.

Latex-rich environments may sensitize healthcare workers who regularly inhale allergenic proteins.

The most prevalent response to latex is an allergic

Contact dermatitis is the most common response to latex and manifests as an allergic delayed hypersensitive reaction, appearing as dry, crusted lesions.

The contact dermatitis reaction usually lasts 48–96 hours.

Anaphylactic reactions can occur most in sensitive patients who exposed to a surgeon’s latex gloves during abdominal surgery, but other mucosal exposures, can also produce systemic reactions.

Latex and banana sensitivity may cross-react, and individuals with latex allergy may also have sensitivities to avocado, kiwifruit, and chestnuts manifesting with perioral itching and local urticaria.

Cross-reactivity of latex with banana, avocado, kiwifruit, and chestnut occurs because latex proteins are structurally homologous with other plant proteins.

About 10% of people report that they are allergic to penicillin.

Serious penicillin allergies only occur in about 0.03%, while 90% reporting such allergy are not.

Urushiol-induced contact dermatitis, originates after contact with poison ivy, eastern poison oak, western poison oak, or poison sumac.

Urushiol, is not a protein.

Urushiol acts as a hapten and chemically reacts with, binds to, and changes the shape of integral membrane proteins on exposed skin cells, causing a T-cell-mediated immune response.

Sumac is the most virulent of the poisonous plants resulting in dermatological response to the reaction between urushiol and membrane proteins including redness, swelling, papules, vesicles, blisters, and streaking.

It is estimated 25 percent of the population have a strong allergic response to urushiol.

Approximately 80-90 percent of adults develop a rash exposed to .0050 milligrams (7.7×10−5 gr) of purified urushiol.

In sensitive patients it takes only a molecular trace on the skin to initiate an allergic reaction.

Allergic diseases are strongly familial.

Identical twins are likely to have the same allergic diseases about 70% of the time.

The same allergy occurs about 40% of the time in non-identical twins.

Allergic parents are more likely to have allergic children.

Children’s allergies are likely to be more severe than those in children of non-allergic parents.

The likelihood of developing allergies is inherited and related to an irregularity in the immune system, but the specific allergen is not.

Young children are most at risk for allergic sensitization and the development of allergies varies with age.

IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years.

The peak prevalence of hay fever is highest in children and young adults.

The incidence of asthma is highest in children under 10.

Boys have a higher risk of developing allergies than girls.

Asthma, however in young adults, females are more likely to be affected.

Differences between the genders tend to decrease in adulthood.

Ethnicity may play a role in some allergies.

Allergic diseases are caused by inappropriate immunological responses to harmless antigens driven by a TH2-mediated immune response.

Many bacteria and viruses elicit a TH1-mediated immune response, which down-regulates TH2 responses.

It is proposed mechanism of action that insufficient stimulation of the TH1 arm of the immune system leads to an overactive TH2 arm, which in turn leads to allergic disease.

Supposedly, individuals living in too sterile an environment are not exposed to enough pathogens to keep the immune system busy, and when they are not exposed to this level, the immune system will attack harmless antigens like pollen, will trigger an immune response.

Hay fever and eczema, both allergic diseases, are less common in children from larger families, which were, it is presumed, exposed to more infectious agents through their siblings, than in children from families with only one child.

Higher incidence of allergic diseases is seen in more developed countries.

Exposure to symbiotic bacteria and parasites are important modulators of immune system development, along with infectious agents.

Immigrants to the industrialized world from the developing world increasingly develop immunological disorders in relation to the length of time since arrival in the industrialized world.

Studies demonstrate an increase in immunological disorders as a country grows more affluent and, it is presumed, cleaner.

The use of antibiotics in the first year of life has been linked to asthma and other allergic diseases.

The use of antibacterial cleaning products has also been associated with higher incidence of asthma.

Birth by Caesarean section rather than vaginal birth is associated with higher incidence of asthma.

Chronic stress can increase allergic conditions, attributed to a T helper 2 (TH2)-predominant response driven by suppression of interleukin 12 by both the autonomic nervous system and the hypothalamic–pituitary–adrenal axis.

Controlling stress in highly susceptible individuals may improve symptoms.

Allergic diseases are more common in industrialized countries than in countries that are more traditional or agricultural.

There is a higher rate of allergic disease in urban populations versus rural populations.

Alterations in exposure to microorganisms is another explanation, for the increase in atopic allergy.

Research suggests that allergies may coincide with the delayed establishment of gut flora in infants.

In early allergy, a type I hypersensitivity reaction against an allergen encountered for the first time and presented by a professional antigen-presenting cell causes a response in a type of immune cell called a TH2 lymphocyte, which belongs to a subset of T cells that produce a cytokine called interleukin-4 (IL-4).

TH2 cells interact with B cell lymphocytes whose role is production of antibodies.

IL-4 provides signals to TH2 cells and B cells for the latter to begin production of a large amount of a particular type of antibody known as IgE.

The secreted IgE circulates in the blood and binds to an IgE-specific receptor, a kind of Fc receptor called FcεRI, on the surface of immune cells called mast cells and basophils, which are both involved in the acute inflammatory response.

Cells coated with IgE are sensitized to the allergen.

In subsequent exposure to the same allergen, the allergen can bind to the IgE molecules held on the surface of the mast cells or basophils.

Cross-linking of the IgE and Fc receptors can occur when more than one IgE-receptor complex interacts with the same allergenic molecule, and can activate the sensitized cell.

Activated mast cells and basophils undergo degranulation, during which they release histamine and other inflammatory chemical mediators which include cytokines, interleukins, leukotrienes, and prostaglandins.

These released granules into the surrounding tissue causing vasodilation, mucous secretion, nerve stimulation, and smooth muscle contraction.

Released granules result in rhinorrhea, itchiness, dyspnea, and anaphylaxis.

Symptoms can be system-wide as in anaphylaxis, or localized to particular body systems, as with asthma localized to the respiratory system and eczema is localized to the dermis.

When the acute response of chemical mediators subsides late responses usually seen 2–24 hours after the original reaction. are due to migration of other leukocytes such as neutrophils, lymphocytes, eosinophils and macrophages can occur at the initial site.

Mast cell release of cytokines are probably associated with the persistence of long-term effects.

Late-phase responses seen in asthma are caused by release of mediators from eosinophils.

Allergic contact dermatitis is referred to as a type I hypersensitivity

In type IV hypersensitivity, T cells (CD8+) destroy target cells on contact, as well as activated macrophages that produce hydrolytic enzymes.

To assess the presence of allergen-specific IgE antibodies, a skin prick test, or an allergy blood test are used.

Skin prick tests, or allergy blood test have similar diagnostic value.

As allergy undergoes dynamic changes over time, regular allergy testing of relevant allergens provides information if management can be changed.

Annual testing is often performed to determine whether allergy to milk, egg, soy, and wheat have been outgrown.

Testing interval may be extended to 2–3 years for allergy to peanut, tree nuts, fish, and crustacean shellfish.

With skin testing a series of tiny punctures or pricks made into the patient’s skin with small amounts of allergens and/or their extracts

These pollen, grass, mite proteins, peanut extract, etc.,

are introduced to sites on the skin marked with pen or dye.

Sometimes, the allergens are injected intradermally into the patient’s skin.

Common sites for testing include the inside forearm and the back.

If the patient is allergic to the injected substance, a visible inflammatory reaction will usually occur within 30 minutes.

Skin responses range from slight reddening of the skin to a full-blown hive.

Interpretation of the results of the skin prick test on a scale of severity, with +/− meaning borderline reactivity, and 4+ being a large reaction.

If a patient had a life-threatening anaphylactic reaction some allergists will prefer an initial blood test prior to performing the skin prick test.

Skin tests may not be an adequate option with widespread skin disease, or have taken antihistamines in the last several days.

Patch testing is used to determine if a specific substance causes allergic inflammation of the skin.

Patch testing, tests for delayed reactions.

Patch testing is used to help ascertain the cause of skin contact allergy, or contact dermatitis.

Adhesive patches, treated common allergic chemicals or skin sensitizers, are applied to the back.

The skin is then examined for local reactions at least twice, usually at 48 hours after application and again two or three days later.

An allergy blood test is quick and simple, and can be performed irrespective of age, skin condition, medication, symptom, disease activity, and pregnancy.

Adults and children of any age can take an allergy blood test.

Multiple allergens can be detected with a single blood sample.

Allergy blood tests measure the concentration of specific IgE antibodies in the blood, and quantification results increase the possibility of ranking how different substances may affect symptoms.

Higher the IgE antibody value, the greater the likelihood of symptoms.

IGE allergens found at low levels that today do not result in symptoms can help predict future symptom development.

The quantitative allergy blood tests can help determine what a patient is allergic to, help predict and follow the disease development, and estimate the risk of a severe reaction, and explain cross-reactivity.

Low IgE levels do not rule out sensitization to commonly inhaled allergens.

Patients with a high total IgE have a high probability of allergic sensitization.

Measuring IgE specific antibodies can be achieved by enzyme-linked immunosorbent assay (ELISA), radioallergosorbent test (RAST) and fluorescent enzyme immunoassay (FEIA).

Rarely challenge testing with a small amounts of a suspected allergen introduced orally, or through inhalation, or other routes.

Elimination/Challenge tests are used most often with foods or medicines.

A suspected allergen is instructed to modify their diet to totally avoid that allergen for a set time, and if the patient experiences significant improvement, he may then be challenged by reintroducing the allergen, to see if symptoms are reproduced.

Vasomotor rhinitis, shares symptoms with allergic rhinitis.

The consumption of various foods during pregnancy has been linked to eczema; these include celery, citrus fruit, raw pepper, margarine, and vegetable oil.

A high intake of antioxidants, zinc, and selenium during pregnancy may help prevent allergies, and reduce risk for childhood-onset asthma, wheezing, and eczema.

Probiotic supplements during pregnancy or infancy may help to prevent atopic dermatitis.

An early introduction of solid food and high diversity before week 17 could increase a child’s risk for allergies.

Studies suggest introduction of solid food and avoidance of highly allergenic food such as peanuts during the first year does not help in allergy prevention.

Management of allergies involves avoiding what triggers the allergy and medications to improve symptoms.

Allergen immunotherapy may be useful for some types of allergies.

Medications may be used to block the action of allergic mediators, or to prevent activation of cells and degranulation processes.

Medications utilized include:

antihistamines, steroids, epinephrine, mast cell stabilizers, and antileukotriene agents.

Other agents like anti-cholinergics, decongestants that impair eosinophil chemotaxis, are also commonly used.

Allergen immunotherapy is used treatment of environmental, and insect bite allergies and asthma.

Allergen immunotherapy for food allergies questionably beneficial.

Immunotherapy involves exposing people to allergen to change the immune system’s response.

Intradermal injections of allergens are effective in the treatment in allergic rhinitis in children, and in asthma.

Intradermal injections of allergens is safe and effective for allergic rhinitis and conjunctivitis, allergic forms of asthma, and stinging insects.

Sublingual immunotherapy for rhinitis and asthma is available but it is less effective than intradermal immunotherapy.

Sublingual immunotherapy benefit

for seasonal allergies is small.

The allergic diseases of hay fever and asthma have increased over the past 2–3 decades.

Allergic rhinitis 35.9 million, or about 11% of the population.

About 10 million have allergic asthma, about 3% of the population.

Asthma prevalence is 39% higher in African Americans than in Europeans.

Atopic eczema occurs in about 9% of the population.

Anaphylaxis accounts for about 40 deaths per year due to insect venom.

Anaphylaxis accounts for about 400 deaths due to penicillin anaphylaxis.

About 220 cases of anaphylaxis and 3 deaths per year are related to latex allergy.

Around 15% of adults have mild, localized allergic reactions to insect venom, with systemic reactions occur in 3% of adults and less than 1% of children.

About 6% of US children under age 3 and 3.5–4% of the overall US population have food allergy.

Genetic factors govern susceptibility to atopic disease.

But increases in atopy have occurred within a time frame that is too short to be explained by a genetic change in the population, suggesting environmental or lifestyle changes.

Attempts to explain this increased rate of allergy include: increased exposure to perennial allergens due to housing changes, increasing time spent indoors, changes in cleanliness or hygiene that have resulted in the decreased activation of a common immune control mechanism, coupled with dietary changes, obesity and decline in physical exercise.

High living standards and hygienic conditions exposes children to fewer infections, and reduces bacterial and viral infections early in life directing the maturing immune system away from TH1 type responses, leading to unrestrained TH2 responses that allow for an increase in allergy.

Exposure to food and fecal-oral pathogens, such as hepatitis A, Toxoplasma gondii, and Helicobacter pylori can reduce the overall risk of atopy by more than 60%.

An increased rate of parasitic infections has been associated with a decreased prevalence of asthma.

There are four types of hypersensitivity reactions, known as Type I to Type IV hypersensitivity.

Allergy is restricted to type I hypersensitivities, also called immediate hypersensitivity, characterized as rapidly developing reactions.

Radiometric assays include the radioallergosorbent test (RAST test) method, which uses IgE-binding (anti-IgE) antibodies labeled with radioactive isotopes for quantifying the levels of IgE antibody in the blood.

A superior test named the ImmunoCAP Specific IgE blood test, which uses the newer fluorescence-labeled technology.

The RAST terminology has been abandoned.

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