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Claire Good Group

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Atopy may have a hereditary component, although contact with the allergen or irritant must occur before the hypersensitivity reaction can develop (characteristically after re-exposure).[3] Maternal psychological trauma in utero may also be a strong indicator for development of atopy.[4]


Atopic reactions are caused by localized hypersensitivity reactions to an allergen. Atopy appears to show a strong hereditary component. One study concludes that the risk of developing atopic dermatitis (3%) or atopy in general (7%) "increases by a factor of two with each first-degree family member already suffering from atopy".[14] As well, maternal stress and perinatal programming is increasingly understood as a root cause of atopy, finding that "...trauma may be a particularly robust potentiator of the cascade of biological events that increase vulnerability to atopy and may help explain the increased risk found in low-income urban populations."[4]

Environmental factors are also thought to play a role in the development of atopy, and the 'hygiene hypothesis' is one of the models that may explain the steep rise in the incidence of atopic diseases, though this hypothesis is incomplete and in some cases, contradictory to findings.[4] This hypothesis proposes that excess 'cleanliness' in an infant's or child's environment can lead to a decline in the number of infectious stimuli that are necessary for the proper development of the immune system. The decrease in exposure to infectious stimuli may result in an imbalance between the infectious-response ("protective") elements and the allergic-response ("false alarm") elements within the immune system.[15]

A Swedish research study titled "Atopy In Children Of Families With An Anthroposophic Lifestyle" comparing the rate of bronchial asthma, allergies, dermatitis, and other atopic diseases among Steiner school pupils and pupils in public schools originally appeared in the May 1, 1999, edition of the British medical journal The Lancet. The findings indicated that Steiner school pupils were "at a significantly lower risk of atopy" than children attending public schools. The researchers investigated a variety of factors in the lives of the Steiner school pupils that might have contributed to this lower rate of atopy, which included breastfeeding, reduced immunization, avoidance of antibiotics and medications that reduce fevers, consumption of bio-dynamic and organic foods, and other physical aspects of the children's lives.[16]

There is a strong genetic predisposition toward atopic allergies, especially on the maternal side. Because of the strong familial evidence, investigators have tried to map susceptibility genes for atopy.[18][19] Genes for atopy (C11orf30, STAT6, SLC25A46, HLA-DQB1, IL1RL1/IL18R1, TLR1/TLR6/TLR10, LPP, MYC/PVT1, IL2/ADAD1, HLA-B/MICA)[20] tend to be involved in allergic responses or other components of the immune system. The gene C11orf30 seems to be the most relevant for atopy as it may increase susceptibility to poly-sensitization.[21]

Atopy is a predisposition to an immune response against diverse antigens and allergens leading to CD4+ Th2 differentiation and overproduction of immunoglobulin E (IgE). The clinical consequence is an increased propensity to hypersensitivity reactions. Allergic bronchial asthma and allergic rhinitis are the most frequent manifestations of atopy, followed by atopic dermatitis and food allergy. Other diseases described as atopic include allergic conjunctivitis, IgE-mediated drug allergy, urticaria and angioedema, and anaphylactic shock. This activity describes the evaluation and management of patients with the most common manifestations of atopy and highlights the role of the interprofessional team in improving care for these patients.

Objectives:Describe the pathophysiology of atopy.List the signs and symptoms of an anaphylactic reaction.Identify treatment options for people with food allergies.Outline the importance of improving care coordination amongst interprofessional team members to improve outcomes for patients affected by atopy.Access free multiple choice questions on this topic.

Atopy is a predisposition to respond immunologically to diverse antigens/allergens, leading to CD4+ Th2 differentiation and overproduction of immunoglobulin E (IgE). The clinical consequence of this is the propensity to develop hypersensitivity reactions to allergens. Allergic bronchial asthma and allergic rhinitis are the most common manifestations of atopy followed by atopic dermatitis and food allergy. Two or more clinical diseases can coexist in an individual at the same time or at different times.

The etiology of atopy is unknown. Twin and epidemiological studies, as well as family and animal experiments, provide striking evidence that the genetic factors play a crucial role in the propensity for atopy, regulating the total IgE synthesis, and in the production of IgE antibodies to specific epitopes. The inheritance of several genes influences the tendency to overproduce IgE, and this runs in families as shown clearly in the autosomal transmission of allergy, but the full inheritance pattern is believed to be multigenic.[5]

A theory that explains the genesis of atopy suggests that it may arise through abnormal regulation by T helper cells and suppressor T lymphocytes that should help in the production of IgE by plasma cells.[6][7]

Examples of chromosomal locations and genes associated with atopy are 5q associated with cytokine gene cluster (IL-3, IL-4, IL-5, IL-13, CD14, beta-2-adrenergic receptor, and GM-CSF). IL-4 and IL-13 promote IgE switching, and IL-5 stimulates eosinophil growth and activation. Beta-2-adrenergic receptors regulate contraction of bronchial smooth muscles. The chromosome 6p houses MHC class II, and some of the alleles regulate T cell responses to environmental antigens or allergens. The chromosome 11q gene (high-affinity IgE receptor beta-subunit) that mediates mast cell activation. Chromosome 12q houses genes for stem cell factor (intervene in mast cell growth and differentiation), IFN-gamma (inhibits IL-4 synthesis) and STAT6 (mediates IL-4 signal transduction). Other genes associated with atopy are IL-4 receptor alpha chain, DPP10 (a protein that regulates chemokine and cytokine activity), ADAM33 metalloproteinase, which is involved in airway remodeling, and CD80/CD86 located in 3q and RANTES in 17q are genes thought to be involved in atopy. Finally, PHF11 in 13q encodes for a transcriptional regulator involved in the clonal expansion of B cells and immunoglobulin expression.[8][9][10][11]

The pathophysiology of atopy characteristically demonstrates by mast cell activation. Antigen binding to IgE cross-links Fc epsilon RI proteins on mast cells. It activates protein tyrosine kinases (Lyn and Syk) that in turn cause activation of a MAP kinase cascade and a phosphatidylinositol-specific phospholipase C, which catalyzes the release of the following molecules: IP3 and DAG from membrane PIP2. Inositol trisphosphate (IP3) causes the release of intracellular calcium from the endoplasmic reticulum. DAG and calcium activate PKC that phosphorylates substrates such as myosin light chain molecule and thus leads to degradation and release of preformed mediators. MAP kinases and calcium react to activate the enzyme cytosolic phospholipase A2, which stimulates the synthesis of lipid mediators including PGD2, LTC4, LTD4, and LTE4. Ras/MAP kinases in the presence of calcium and PKC cause cytokine gene expression, which releases TNF and other cytokines (IL-4, IL-5, IL-6, IL-13 among others). Lipid mediators, cytokines and histamine cause an inflammatory response.[16][17][18]

It is a manifestation of atopy localized in the bronchus. There is a release of critical mediators including histamine, leukotrienes, and cytokines including IL-4, IL-5, IL-13, TNF and eosinophil chemotactic factor. The aim of symptomatic asthma is controlling the hyperirritable bronchial mucosa using environmental measures, drugs, and other therapies.

Atopic individuals have a lifelong tendency for the development of allergic reactions as it is incurable. Nevertheless, the manifestations of atopy often change over some time. Atopic dermatitis has a better prognosis and is treatable with some success with immunotherapy. Allergic asthma has a prognosis that varies according to the persistence of the causative environmental allergen, the IgE levels in blood or tissues, and the genetic makeup.

When you have atopy and an allergen enters your body -- through your skin, airways, or mouth -- your immune system overreacts. It treats allergens like dangerous germs and makes germ-fighting antibodies called immunoglobulin E (IgE). These proteins make certain cells release chemicals that cause allergy symptoms in your nose, throat, and lungs, or on your skin.

With atopic dermatitis (atopy), the dog's immune system overreacts to an airborne allergen that gains entry to the skin due to a defective skin barrier. Other causes of allergies include fleas, certain dietary ingredients, skin contact with certain substances, and hypersensitivity to skin bacteria or yeast.

Affected dogs chew, lick, and scratch all over, especially on the feet, face, axillae (armpits), and groin. There may be reddish-brown saliva staining of overly itchy areas. The skin will be red and chronic infection of the ears or skin, secondary to atopy, can lead to dark, thickened elephant-like skin. Clinical signs of atopy may recur or worsen in certain seasons if they are allergic to certain outdoor pollens or molds.

Seasonal allergy and atopy are terms used to describe the same type of allergic skin disease. The majority of dogs with atopy experience itching during certain seasons, when flowers or trees are blooming and producing pollens. Other affected dogs will have problems year-round, which means that the allergen is constantly present or that the dog has developed multiple allergies. A common cause of non-seasonal atopy is the house dust mite. 041b061a72


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