20 Of note, changes in the plasticity and receptor density, as well as neuronal sensitization, may also be involved in AD pruritus. 6 Cutaneous inductors of itch include histamine, 10 proteases, 11– 13 neuropeptides (eg, SP), 14, 15 acetylcholine (in atopic patients), 16 cytokines, 17 neurotrophin-4, 18 platelet-activating factor, 19 endothelin, and certain leukotrienes. 8, 9 The receptor for substance P (SP), the neurokinin-1 receptor, is also highly expressed by lamina 1 neurons, which appears to be crucial for the transmission of itch to the brain. For example, in lamina 1 of the dorsal horn, the gastrin-releasing peptide receptor plays a role in mediating itch sensation in the spinal cord. Various mediators of pruritus in AD interact with the pruritoception pathway at different levels. 6, 7 Thus, the central nervous system modulates the perception of “itch” and triggers the desire to scratch. ![]() Other cortical and subcortical regions can modulate the itch response, leading to “sensitized skin” and itch-associated mood changes, for example. In the cortex, the scratching reflex is initialized in the motor-cortex and associated motor-cortex. The pruritogenic stimulus is then signaled along the dorsal root ganglion (which harbors the RNA and generates the proteins expressed by or released from the cell surface of nerve-endings) via the spinal cord before it crosses the contralateral spinothalamic tract, reaching different areas of the cortex. The sensation of pruritus can be triggered by endogenous and exogenous stimuli, which activate specific peripheral un-myelinated C-fiber nerve endings in the epidermis and dermis. This review highlights various topical, systemic, and complementary and alternative therapies, as well as provide a therapeutic ladder for optimized long-term control of itch in atopic dermatitis. In addition, patient education and a therapeutic regimen to help the patient cope with the itch and eczema are important adjuvant strategies for optimized long-term management. Mild forms of atopic dermatitis may be controlled with topical therapies, but moderate-to-severe forms often require a combination of systemic treatments consisting of antipruritic and immunosuppressive drugs, phototherapy, and topical compounds. Modern management consists of anti-inflammatory, occasionally antiseptic, as well as antipruritic therapies to address the epidermal barrier as well as immunomodulation or infection. ![]() The threshold for itch and alloknesis is markedly reduced in these patients, and infections can promote exacerbation and thereby increase the itch. Chronic, localized, or even generalized pruritus is the diagnostic hallmark of atopic dermatitis, and its management remains a challenge for physicians. ![]() Atopic dermatitis is a common, pruritic, inflammatory skin disorder.
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