Many mental health disorders and states, such as obsessive-compulsive disorder, anxiety, stress, and other psychological conditions can cause skin diseases as the nature of the skin is an easy target accessible for patients with such a delicate situation. It is also evident that, conversely, skin diseases can cause psychosocial distress due to their unfavorable cosmetic and/or symptomatic effects. What has remained unclear is the etiological role of psychological stress in the onset and worsening of skin diseases. The probability of a causal effect of emotional stress, especially stressful life events, on the course of various skin diseases has long been postulated. Clinical knowledge and experience, as well as the number of observations and uncontrolled case series, support this statement. In this essay I will review the available evidence on the role of stressful life events in triggering or exacerbating skin diseases. The role of stressful events in vitiligo, lichen planus, acne, pemphigus, and seborrheic dermatitis has been little explored or controversial. The role of stressful life events in psoriasis, alopecia areata, atopic dermatitis and urticaria was evidently clearer. Few studies take into account potential common confounding factors (e.g. age, disease duration, genetic factors) and almost no studies adequately consider the influence of other critical factors (e.g. treatment discontinuation, smoking, seasonal effects). So far it can be said with certainty that only preliminary evidence has been published on the role of stressful life events in the initiation or worsening of any dermatological disease. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an Original EssayThe skin plays a vital role as a tactile organ in socialization processes from early childhood and through the entire life cycle, having focal significance as an organ of communication, being affected by an assortment of emotional stimuli, and significantly influencing a person's self-perception and confidence. It is very important to remember that the skin and the central nervous system are embryologically related, since the epidermis and the neural plate both derive from the embryonic ectoderm1. It is therefore not surprising that the presence of a connection between mental state and dermatological disease has long been seen and portrayed. Some possible connections between mental state or conditions and skin diseases have been proposed. First, patients with a diagnosed psychological illness may come to the dermatologist's attention due to hypochondriasis, self-mutilation, or skin-related delusions. Second, systemic diseases, such as systemic lupus erythematosus or porphyria, might present as both skin diseases and mental side effects. Thirdly, drugs used to treat dermatological diseases (for example, corticosteroids, antihistamines) can cause mental disorders, and on the other hand, psychotropic drugs such as lithium or some antipsychotics can affect the skin. Fourth, psychological side effects may occur. in patients with primary skin diseases in response to reaction to disfigurement or perceived social stigma2. In this essay, I will review the available evidence on the role of stressful life events in relation to the triggering or exacerbation of skin diseases. I will try to answer the following question: what, if any, is the relationship between psychological conditions and skin diseases? Although the association seems almost clear, and is often taken for grantedgranted, it is a very difficult task to explain the relationship between these two large entities, as research data is systematically reviewed or subjected to meta-analysis. This complex chronic skin disease has gained the highest consideration from a psychological perspective. For more than a century there have been many hypotheses writing about the link between psychological stress and psoriasis, and the trend continues to this day. Psychological stress has been found to be invoked as a causal factor in psoriasis, both by dermatologists and patients. In a sample of 62 French dermatologists who responded to a small questionnaire, 100% agreed that stress has an essential impact on psoriasis3. Similarly, the number of patients who think that psychological stress is an independent causal factor or occurs as an aggravating element of psoriasis is very high, with studies reporting a percentage ranging from 37 to 78%4. Numerous uncontrolled investigations support the thesis that emotional stress, most commonly in the form of stressful life events, plays an important role in the onset or exacerbation of psoriasis in high percentages of cases. Susskind and McGuire found that 40% of 20 hospitalized patients mentioned anxiety and unexpressed resentment induced by upsetting life events before the onset of the illness; with relapses the percentage rises to 70%5. Similarly, de la Brassinne and Nays examined the medical records of more than 200 patients and reported that a major psychological event was a precipitating factor in 40% of new cases and 80% of relapses6. In summary, most of the studies reviewed implicate a role for stressful life events in the onset, exacerbation, or worsening of psoriasis. However, no conclusive evidence appears to exist yet because widely accepted methodological standards for life event research have been met by only a small number of studies, and no studies have controlled for the influence of possible confounding factors such as discontinuation of medical treatment , alcohol use, smoking, exposure to sunlight, or seasonal effects, as noted above. It can be concluded that preliminary evidence has been gathered for now and that further research is needed. Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with skin hyperreactivity to environmental factors and is often the first step in the atopic march leading to the onset of asthma and allergic rhinitis [1]. Clinically, AD is characterized by itchy, eczematous, ill-defined, and erythematous patches with a predilection for skin folds. Typically, AD presents during infancy and early childhood; 85% of affected children show symptoms before the age of 5 [2]. With an estimated prevalence of 17% among US schoolchildren, AD is the most common chronic childhood disease; its prevalence appears to be increasing [3]. The cause of AD is poorly understood, but is believed to involve a complex interaction between genetic predisposition, environment, altered immunological function, and psychological influences. New information on its etiology includes filaggrin and Toll-like receptor 2 (TLR2) mutations. Filaggrin is involved in the cornified cell envelope of epidermal cells and is critical for maintaining epidermal barrier function. TLR2 is involved in the innate immune system's ability to recognize and warn of the presence of external pathogens. New genes and chromosomal candidates include chromosome 1q21 (contains the gene encoding filaggrin); Kazal serine protease inhibitor type 5 (SPINK5, a protease inhibitor); signal transducer and activator of transcription 6 (STAT-6, an important transcription factor in.
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