I am already suffering from a 2-week skin allergy! I think this is because of eating chicken and egg seven days straight two weeks ago and that my body reacted to it. It’s so itchy that I can’t help but scratch them. Most of the rash are found in the brachial part of my arms, there are also some that are found in my hamstrings. I have taken in antihistamines for days now, but still I can’t seem to understand why this hasn’t cured yet. Maybe I’ll go check my dermatologist to help me find a cure for this. I can no longer take this anymore.
I’ll be posting some facts about allergy down below. I hope it would help you. The post will be coming from wikipedia.org. Keep on reading.
Allergy is an abnormal reaction to a substance foreign to the body that is acquired, predictable and rapid. In the strict sense of its meaning, it is the first (type 1) of five forms of hypersensitivity described by Gell and Coombs in their 1963 classification. However, by extension, the term “allergy” is often used for other abnormal reactions to substances. The term was coined by the Viennese pediatrician Clemens von Pirquet in 1906 after noting that some of his patients were hypersensitive to normally innocuous entities such as dust, pollen, or certain foods. Pirquet called this phenomenon “allergy”, from the Greek words allos meaning “other” and ergon meaning “work”.
Genetic basis
There is much evidence to support the genetic basis of allergy. Allergic parents are more likely to have allergic children, and their allergies are likely to be stronger than those from non-allergic parents. However some allergies are not consistent along genealogies with parents being allergic to peanuts, but having children allergic to ragweed, or siblings not sharing the same allergens. It seems that the likelihood of developing allergies is inherited (due to some irregularity in the way the immune system works) but the developing of an allergy to a specific allergen is not.
Ethnicity has also been shown to play a role in some allergies. Interestingly, in regard to asthma, it has been suggested that different genetic loci are responsible for asthma in people of Caucasian, Hispanic, Asian, and African origins. It has also been suggested that there are both general atopy genes and tissue-specific allergy genes that target the allergic response to specific mucosal tissues. Potential disease associated alleles include both coding region variation and SNPs. Caucasians display the greatest incidence of asthma
Relationship with parasites
Some recent research has also begun to show that some kinds of common parasites, such as intestinal worms (e.g. hookworms), secrete immunosuppressant chemicals into the gut wall and hence the bloodstream which prevent the body from attacking the parasite. This gives rise to a new slant on the “hygiene hypothesis” — that co-evolution of man and parasites has in the past led to an immune system that only functions correctly in the presence of the parasites. Without them, the immune system becomes unbalanced and oversensitive. In particular, research suggests that allergies may coincide with the delayed establishment of infant gut flora. Gutworms and similar parasites are present in untreated drinking water in undeveloped countries, and in developed countries until the routine chlorination and purification of drinking water supplies. This also coincides with the time period in which a significant rise in allergies has been observed. So far, there is only sporadic evidence to support this hypothesis — one scientist who suffered from seasonal allergic rhinitis (hayfever) infected himself with gutworms and was immediately ‘cured’ of his allergy with no other ill effects. Full clinical trials have yet to be performed however. It may be that the term ‘parasite’ could turn out to be inappropriate, and in fact a hitherto unsuspected symbiosis is at work.
Acute Response
A type I hypersensitivity reaction against an allergen via the normal humoral response against a foreign body results after plasma cells secrete IgE as opposed to other classes of immunoglobulins such as IgM (against novel antigens) or IgG (against immunized antigens). IgE binds to Fc epsilon R1 (high affinity) receptors on the surface of mast cells and basophils, both involved in the acute inflammatory response. The class switch in the plasma cell leading to IgE is tightly regulated by the immune system. CD45 plays a critical regulatory role in receptor signaling through its protein tyrosine phosphatase and Janus kinase (JAK) phosphatase activities. IL-4 is the primary interleukin which induces switch recombination. Class switch recombination to IgE can also be triggered by the TH2 cytokine IL-13. CD45 is able to function as JAK phosphatase in human B cells, and this activity is directly associated with negative regulation of the class switch recombination to IgE. IgE-bearing epidermal dendritic cells have also been found.
When IgE is first secreted it binds to the Fc receptors on a mast cell or basophil, and such an IgE-coated cell is said to be sensitized to the allergen in question. A later exposure by the same allergen causes reactivation of these IgE, which then signals for the degranulation of the sensitized mast cell or basophil. There is now strong evidence that mast cells and basophils require costimulatory signals for degranulation in vivo, derived from GPCRs such as chemokine receptors. These granules release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation and smooth muscle contraction. This results in the previously described symptoms of rhinorrhea, itchiness, dyspnea, and anaphylaxis. Depending on the individual, allergen, and mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localised to particular body systems (for example, asthma to the respiratory system; eczema to the dermis).
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Signs and Symptoms