Atopic March Research Paper

Like we learned in chapter 1 the job of the integumentary system is to cover and protect the body but what happens if your skin develops a disease like eczema? Eczema is a chronic, common, non-infective inflammatory condition characterized by intense pruritus, redness, and scaling (Eczema, p.1). This condition can appear at any age, but it usually occurs during infancy or early childhood (Eczema, p.1). Eczema or any skin disease are the most common group of occupational health problems leading to absence from work (Eczema, p.1). Several factors play a big role in eczema, both internally and externally, depending on your genetic makeup you may be prone to getting eczema in as early as a few months after you were born or by allergens as a young

Atopic eczema is a skin condition that can be in remission and can flare up because of different factors. The skin condition is known for its distinct characteristics, such as red, itchy skin. Although it is mostly common in children, it can occur at any age. Over the years, there has been growing interest in different strategies to prevent and manage atopic eczema. Each person is different in the way their condition flares, and most of the time has been treated with topical calcineurin inhibitors and topical corticosteroids.

The function of the epidermis to prevent entry of pathogens is disturbed, which leads in dry skin. The dermatopathological signs associated with Atopic dermatitis include spongiosis, hyperkeratosis, exocytosis, parakeratosis, eosinophilis and lymphocytic infiltrates (Williams, 2005). People with the Atopic dermatitis condition produce immunoglobin E even with just trigger from low amounts of allergens. Rhinoconjunctivitis and asthma are some of the symptoms associated with Atopic dermatitis. In infancy, an individual may develop a desquamation that is yellow in color on the scalp (Darsow et al., 2010). The rashes spread to the face of the individual and later to the

Atopy is defined as an inherited tendency to produce immunoglobulin E antibodies in response to common environmental proteins such as pollen, house dust mites, and food allergens. Atopic dermatitis affects about one-fifth of all individuals during their lifetime, but the prevalence varies throughout the world. Around 50 percent of patients with atopic dermatitis will develop symptoms within their first year of life, and probably 95 percent experience an onset below five years of age. A child with moderate to severe atopic dermatitis have 50 percent of risk of developing asthma and 75 percent of risk of developing hay fever. A typical patient with atopic dermatitis will present with an early onset of itchy eczema localized at sites such as the flexures of the elbows and knees. The skin lesion in atopic dermatitis is not differ from other eczemas such as contact eczema. In its acute form, eczema is characterized by a lively red infiltrate with edema, vesicles, oozing, and crusting. Whereas in the subacute and chronic form, lichenification, excoriations, papules, and nodules are noted (Thomsen,

In the present study, the epidermal and dermal H-score of LXR-α and its epidermal nucleocytoplasmic expression in lesional skin were higher than in non lesional skin which was higher than in control skin. This goes with Kumar et al. (2010) demonstrated the expression of LXR-α was significantly higher in perilesional skin as compared to the normal skin of vitiligo patients [10].While the cytoplasmic expression of LXR-α was higher in the control skin in comparison with lesional and non lesional skin. This can be explained by the suggestion of Hu et al. who supposed that the cytoplasmic fraction of LXRα is in inactive form [19].

The majority of the diagnosed AD cases (>95%) fall under the late-onset form of AD (LOAD), with the age of onset >65 years. In contrast to the genetics of EO-FAD caused by autosomal dominant pathogenic variants showing a Mendelian inheritance mode, LOAD is attributed to genetically complex and heterogeneous variants that modify disease susceptibility depending on the environmental factors and life style of the individuals. The e4 allele in the Apolipoprotein E (APOE) (19q13.32) gene remains the most established genetic risk factor in LOAD. The risk effect of APOE-e4 (~4 to 15 fold) has been consistently replicated in a large number of study cohorts from different ethnic groups. There are at least three major alleles in the APOE gene corresponding to combinations of two amino acid changes at residues 112 (rs429358) and 158 (rs7412), which determine the three alleles: e2 (Cys112/ Cys158), e3 (Cys112/Arg158) and e4 (Arg112/Arg158). The most commonly occurring e3 allele is present in more than half of the general population (up to 70%).

Although it is not known what reinforces the formation of IgG autoantibodies in PV, the debt of tolerance for autoimmune target molecules may perform a vital role (Hindawi, 2015). A few triggering agents capable of activating pemphigus in genetically predisposed individuals include; various environmental factors, medications, and dietary components (Perm J, 2015). During a Histological examination, a key hallmark of PV is the presence of suprabasal acantholysis and is essential for diagnosis. In addition to the acantholysis seen, necrosis of individual keratinocytes is highly common in pemphigus (Perm J, 2015). The preferred biopsy sight for diagnosis is considered the oral mucosa, and the ulcerated tissue should be avoided because it will not show the root of the vesicle (Kluwer, 2016). It is key to identify (PV) as early as possible. Since it is a potentially fatal disease, it is required that there is early diagnosis and treatment involving corticosteroids, to prevent future complications (Kuriachan,

Atopic dermatitis has limited treatment options. Dupixent therapy is indicated for the treatment of adult patients with moderate-to-severe atopic dermatitis whose disease is not adequately controlled with topical

Dermographism is reported to occur in 25% -50% of healthy population among which 5% are symptomatic. Histamine is most likely a mediator, other mast cells such as prostaglandins, leukotrienes, platelet activating factor, serotonin , chemotactic factors are not directly related. It has been hypothesized that the IgE-sensitized mast cells can react to unknown antigen which is induced by skin stroking. H.Pylori have an etiologic role in dermographism.

The epidermis of the skin has the functions of immune nonspecific defense and water retention due to barrier qualities. Nonspecific defense is innate and defined by the fact that it does not differentiate between foreign matters; it protects against all external materials rapidly (Stanfield, 2013, p. 675). The stratum corneum is the tough superficial layer of the skin, which is bound by non-nucleated cells called corneocytes. Corneocytes are keratin bundles bound by proteins and lipids. Lipids are necessary for the skin to function as a barrier in order to maintain moisture levels in the skin (WHO, 2009). Chronic atopic dermatitis (AD) is an inherited genetic skin disease which typically begins in childhood and is characterized by dry, itchy, and inflamed skin. Genetic defects in the production of filaggrin are the basis of dry skin and a risk factor for developing AD. Histamines produce1 the sensation of itch and are released into the skin as an immune response, triggered by inflammation. AD creates inflammation in the skin by autoimmune abnormalities, even without the presence of a bacteria, virus, or irritant. This chronic disease may be controlled through medical treatment

The most characteristic features of AD are intense itch and recurrent eczematous skin lesions, which typically show an age-related morphology and distribution. The majority of patients display generalized skin dryness and a personal or familial history of atopy. Other associated features are a hyperlinearity of the palms and soles, Dennie-Morgan infraorbital folds, and Hertoghe’s sign.

“Acne is a polymorphic and multifactorial inflammatory disease of the pilosebaceous follicles in the skin of the face and trunk” (Layton, 2016). There are three factors involve in acne (1) the hormone

[Adapted from Pan M, Liu X, Zheng J. The pathogenic role of autoantibodies in pemphigus vulgaris. Clin Ex. Dermatol 2011;36(7):703-07.]

The causes of atopy are multifactorial with genetic and environmental factors (Purvis et al, 2005). There is a genetic component to atopic diseases but so far there have been no specific atopy genes that have been identified. A child is thought to inherit a predisposition to sensitisation against environmental allergens. Maternal history of atopy is a significant risk factor for children developing AD (Bohme et al, 2003). There are also many environmental factors which are as important, for example regional differences, allergen exposure, parental smoking, use of antibiotics and mode of delivery. Caesarean section (CS) may be a risk factor for allergic manifestations due to a delayed microbial colonisation (Salam et al, 2006). This may delay

(Hughes, 2013) This is simply a proposed idea as it is unknown how psoriatic lesions actually occur. Another hypothesis is that T cells become activated by an unknown activator; this causes the release of cytokines. This release is due to activated T cells, inflammatory cells and keratinocytes; keratinocytes are thought to be the cause of the psoriatic lesions on the skin. (Das, 2009)