Factors That Exacerbate Itching in Patients with Atopic Dermatitis

Factors that Exacerbate itching in Patients with Atopic dermatitis

Factors that Exacerbate itching in Patients with Atopic dermatitis

Abstract

Itching in Patients with Atopic Dermatitis, Patients with atopic dermatitis (AD) exhibit different clinical symptoms, progression, and treatment responses during childhood and adulthood. In adults, itching of the skin is followed by the formation of well-circumscribed plaques or polymorphous dermatoses at the site of itching and is often accompanied by dryness.

AD patients show hypersensitivity exhibited by AD patients may arise from abnormal nerves. Itching can worsen when excess sweat is left on the skin or when insufficient sweating results in heat retention.Endogenous factor such as cytokine and chemical messengers can also induce itch by stimulating nerve fibers in the skin.

Itching can be caused not only by stimulation of the skin surface but also by visual and auditory stimulation, with psychologically induced “contagious itch” being stronger in AD patients than in healthy individuals. Furthermore, itch often increase in the evening when sympathetic nerve activity decreases. This chapter discusses factors that exacerbate itching in AD and guidance for the proper management of the disease.

Keyword: Atopic Dermatitis, Itch, Exacerbate, Dry skin, Temperature, Sweat, psychological Factors

Clinical Characteristics of Itching in patients with Atopic Dermatitis (AD)

Itching in Patients with Atopic Dermatitis
Clinical manifestation: eczema/exudative papules / Clinical manifestation: Chronic dermatitis/neurodermatitis, Itching in Patients with Atopic Dermatitis.

Patients with AD exhibit different clinical features depending on their age and duration of disease. The primary characteristics of AD at different development stages have been described by Sulzberger, who was responsible for naming AD.

In childhood, AD present as eczema changes and serous papules that procedure intense itching, which may lead to excoriation and the formation of new papules induced by scratching. In adulthood, the clinical manifestations of AD are move varied. Over 100 years ago, Brocq and jacquet described AD as a chronic “disseminated neurodermatitis” characterized by mental nervousness, persistent itching before the visible appearance of skin lesions similar to neurodermatoses, skin dryness, skin pigmentation, and hypertrophied skin papillae.

the same time, “Besnier’s prurigo” was described as a type of “diathetic prurigo” characterized by ithcing followed by nonspecific skin lesions in infants and “paroxystic and chronic polymorphous and pruriginous dermatoses, Herba’s prurigo type,” in young adults. Such historical description of the clinical practice.

Today, AD is characterized by itching before the appearances of dermatitis, and AD-associated itching is known to be aggravated by a variety of factor such as heat, perspiration, psychological stress, specific foods and alcohol, wool fibers, and the common cold; therefore, the active avoidance with AD show different symptoms and responses to treatment, additional research is required to elucidate the distinct mechanisms underlying AD-related itching at each developmental stage.

Neural Transmission and processing of AD-related itching

Electrical impulses traveling through peripheral nerve fibers transmit itching-related signals to the brain, which produces a bodily reaction. Recent studies using animal models of AD indicated that astrogliosis in the dorsal horn of the spinal cord contributed to chronic itching and that the itching sensation is processed in the central nervous system. Although the transmission and processing of AD-related itching in humans requires further clarification, the general process of the neural transmission of itch is summarized here.

Thermal and mechanical stimuli activate receptors on free nerve ending in the skin, which leads to the opening of ion channels and the transmission of electrical current to the spinal cord. Several different itching-related ligands and receptors have been described in the literature. In particular, itch ligands (i.e.,pruritogens) can induce an itching sensation by activating the histaminergic transient receptors potential cation channel subfamily V member 1 (TRPVI) and the non-histaminergic transient receptor potential cation channel member A1 (TRPVI) [7-10], and inhibition of TRPVI or TRPAI or reduces itching in AD-like animal models.

Thus, TRPVI and TRPAI have recently received much attention as possible targets for drug development. After itching-related electrical impulses are sent to the spinal cord, they are modulated by interneurons in the spinal cord that release inhibitory neurotransmiters such as gamma-aminobutyric acid, glycine, and dynorphins, which reduce the intensity of itch-related signals. Therefore, the control of inhibitory interneurons is another strong candidate approach for treating chronic itching.

After processing in the spinal cord, itch-related signals are sent through ascending tracts to the amygdala via the thalamus or medulla oblongata, where they are analyzed the brain circuitry underlying itching is not completely understood, activation of sympathetic neurons in the medulla or midbrain induces the release of noradrenaline, which suppresses itch-related signal through the adrenoceptor., Itching in Patients with Atopic Dermatitis.

Hence, ithcing is attenuated under conditions of significant sympathetic nervous system activity, such as during the daytime or when individuals concentrate on stimulati other than the itch. However, the central processing of itch-related signals differes between AD patients and healthy individuals. Thus, a greater understanding of the antipruritic nervous system will help advance approaches to treating AD-relating itching.

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