So here we know about some factor about atopic dermatitis and What happen when skin become dry in atopic eczema.
In skin condition such as eczema and dryness, molecules that cause itching (i.e., pruritogens), including cytokines and chemical messenger, are released from the affected area and act on nerve ending in the skin.
The itching caused by pruritogens triggers scratching of the affected area, which aggravates the dermatitis, resulting in a vicious “itch-scratch cycle.” Dryness and inflammation, such as that which occurs in AD, induce elongation of sensory nerves in the epidermis under the stratum corneum, which causes skin hyperesthesia. This aberrant nerve elongation in AD involves nerve growth factor, artemin, interleukin (IL)-31, and semaphor in 3A. Histamines derived from the degranulation of mast cells and substance P released from nerve ending can act directly or indirectly on elongated nerves, causing itching.
The inflammatory mediators thymic stromal lymphopoietin and IL-31, which are derived from epidermal keratinocytes and infiltrated lymphocytes, respectively, cause itching through direct actions on nerve fibers. Furthermore, elevated levels of autotaxins (e.g., lysophospholipase) due to cholestasis induce itching in hepatic disorders and blood autotaxin concentration is correlated with itch intensity in AD patients.
Temperatures and itching in Atopic dermatitis
Healthy individuals can experience relief from histamine-evoked itching by exposure to extreme temperature, such as taking a very hot shower or using ice to cool the itchy area.
However, although AD-related itching can be suppressed by painful cold stimulation, it is worsened by painful heat stimulation. Moreover, AD patients often report that their itchiness increases in warner conditions as an itching sensation. Unfortunately, this heat-provoked itching responds poorly to treatment, and although it is thought to result from the sensitization of peripheral or central nerves, its underlying mechanism is still uncertain.
Peripheral nerve fibres are distributed across the dermis and are affected by factors secreted by surrounding fibroblasts. To identify molecules that contribute to skin nerve fiber hypersensitization, we comprehensively analyzed the expression of genes in dermal fibroblasts that were stimulated by allergic inflammation and itch related factors. We found that substance P induced thee expression of artemin, a neurotrophic factor that is important for the development of sympathetic innervation, in dermal fibroblasts.
Whereas no artemin expression was detected in normal human skin, we found its accumulation in dermal lesions associated with AD and numular eczema. Furthermore, we observe that mice treated with artemin on their back exhibited increased sensory innervation of the skin and abnormal behavior such as rubbing their skin across their entire body when exposed to a warm temprature (38’C), which was not observe in artemin receptor knockout mice. This finding suggests that the abnormal local accumulation of artemin inn the skin causes systemic thermally provoked itching, although the underlying mechanism is unnclear. However, we found that capsazepine, a selective antagonist of TRPV1, did not suppress the artemin-induced abnormal behavior, indicating that the systemic response occurs independently of TRPV1.
In clinical practice, we have encountered AD patients who developed itching immediately after taking a hot bath or removing their clothes, which we assume arises from a rapid changes in the temperature of the skin surface.
This phenomenon has been confirmed by experimental studies. for instance, pfab and colleagues observed increased itching when histamine treated skin was exposed to rapidly alternating cool and warn temperatures (between 25 and 32’C). Therefore, even within temperatures ranges typically encountered in daily life, rapid changes in temperatures in their daily life, such as hot bathwater or cold air conditioning. japanese guidelines for AD recommend that the temperature of bathwater should be set between 38 and 40’C.
Perspiration and itching
Mammals are homeothermic organism that maintain stable body temperature through thermal control mechanism such as perspiration, expiration and heat transfer. In humans, perspiration through eccrine sweat glands distributed throughout the body is an important physiological function tha regulates body temperature.
Sweat contains several molecules that are beneficial for the skin, such as natural moisture retaining factors (eg., urea, sodium lactate), bacterial peptides (e.g., dermcidin, cathelicidin, bita-defension), and secretory IgA to defend against infection. Sweat also inhibits cysteine and serine protease activity, helps prevent inflammatory responses to allergens, and aids in the formation of mature stratum corneum. Although sweat can reduce the intensify of experience mentally induced itching in healthy individuals, many patients with AD report that sweating aggravates itching.
In one study, basophils derived from AD patients showed positive reactions in a histamine release test to semipurified antigens extracted from the sweat of healthy subjects, suggesting the existence of a “sweat allergy”. However, another study failed to detect positive reaction.
Interestingly, an antigen derived from malassezia globosa, a fungus indigenous to the skin, was identified in the sweat of AD patients and may be involved in this “sweat allergy”. In addition, reduce levels of antimicrobial components in sweat are associated with a weaker ability to defend against infection in AD patients.
Smptoms of AD can be aggravated by leaving excess sweat on the skin. One cause of this aggravation is that excess sweat increase the pH level of the skin surface. Under normal conditions]’, the pH of sweat remains low because sodium bicarbonate (HCO3) and alkaline ions in sweat are reduced via reabsorption by sweat ducts. However, excess sweat on the skin leads to a failure of HCO3 reabsorption, which increases the pH of the skin and thereby promotes detachment of the horny cell layer and increase susceptibility to inflammation. In addition to increasing pH, various molecules contained in sweat (e.g., malassezia-derived antigens) can cause itching. Moreover, the beneficial effects of sweat, such as proteinase inhibition, may be lost when excess sweat is left on the skin. Hence, AD patients are advised to wash or wipe off excess sweat with a wet towel inn case of itching accompanying perspiration.
Atopic dermatitis patients show less ability to perspire, either due to abnormalities in the production of sweat or the obstruction of its released to the skin surface. One possible mechanism by which the release of sweat is obstructed is the formation of horny plugs in sweat pores, although it is not clear whether this might be due to inflammation related keratosis or dryness resulting from reduced sweating. Also, Shiohara and colleagues detected the presence of dermcidin, an antimicrobial peptide produced by sweat glands, surrounding sweat ducts, which might reduce the amount of sweat discharge to the skin surface and increase heat retention.
Perspiration tests using acetylcholine or temperature loading have confirmed that sweat secretion is reduced in AD patients, which is related to dysautonomia and a tendency toward an anxiogenic by affecting sweat glands, suggesting that allergic inflammation is a cause of reduced sweating in AD patients.
Because sweat aggravates AD, patients may be told to avoid sweating, although there is no evidence that this improves skin symptoms. Rather, as proper treatment of skin symptoms in AD also restores perspiration function, increased sweating to facilitate heat transfer should be considered an important goal in the management of AD.
Daily Rhythms and itching
Atopic dermatitis patients often complain that their itching increase at night. One potential explanation is that body temperature declines overnights and fluctuate during sleep. The drops in body temperatures are accompanied by dilation of peripheral vessels, which elevates skin temperature and may increase itching. Another possible explanation is that transepidermal water loss increase at night, making the skin susceptible to itching, Nighttime is also associated with decreased cortisol and increased IL-2 production, which are related to inflammation. Furthermore, staying up late reduces melatonin production by the pineal gland, which inhibits normal decline in body temperature and circadian dysregulation can cause an imbalance in agonists of U-opioid and k-opioid receptors, which may increase the severity of itching. Therefore, AD patients are advised to practice good sleep habits and maintain regular sleep schedule.
Psychological Factor and itching
Itching can arise not only from stimulation of the skin but also from visual or auditory information. For example, a person may have an urge to scratch himself or herself upon seeing an image suggestive of itching, such as being bitten by a mosquito, or hearing the sound of another person scratching their skin. This phenomenon, known as “contagious itch”, is stronger in AD patients than in healthy individuals. The onset and worsening of itching can also be caused by psychological facotor and related conditions such as insomnia.
Conclusion what happen when skin become dry in atopic eczema
The management of AD is continuing to improve through advances in our understanding of factor that exacerbate itching, their mechanisms and their countermeasures because AD can be aggravated by commonplace features of our environment within a normal physiological range, it can be difficult to provide sound guidance for minimizing the symptoms of AD. As some questions remain unresolved, we hope that evidence accumulating from recent and future studies can be applied to improved the health and quality of life of patients with AD.
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