![]() Pruritus induced by sweating is the most common trigger of itching in patients with AD ( 12– 16). In a survey of 100 Chinese patients with AD, daily life activities that increased the severity of itch were sweat in 96% of the patients’ dryness in 71%, stress in 71%, physical effort in 73%, specific fabrics in 64% and hot water in 48% ( 12). In general, the most commonly described provocative agents are heat, sweating, hot water, dust, irritants, xerosis, wool fibers, harsh soaps and emotional stress. Modified from Ständer S: Experimental Dermatology 2002 (11):12–24. Their results support the importance of developing and using objective measurements of itch, and suggest that the relation between subjective and objective measures of disease severity may not be straightforward ( 8). Increased actigraphy scores, independent of subjective pruritus scores, correlated with poor sleep quality. They demonstrated discrepancies between subjective measures of itch and objectively recorded actigraphy activity ( 9, 10). Using scratch monitors placed on a patient’s wrist (actigraphy) overnight, this group brought to light the inherent error in using subjective measurements of pruritus. Work from Rees and colleagues, however, has shown these subjective measures of itch do not correlate with objective measures of itch such as nocturnal scratching ( 8). More recently, measurement tools have been developed to measure the impact of pruritic skin conditions on a patient’s quality of life, such as the Dermatology Quality of Life Index ( 7). The measurement of a patient’s itch level has traditionally been assessed using a 10 cm visual analogue scale (VAS), similar to pain scales. One barrier to studying itch and the effect of therapy on itch is our inability to accurately measure it. ![]() While significant progress has been made in understanding the itch of AD, these advances have not yet led to effective targeted therapies. Histamine-independent cholinergic mechanisms of itch have also been postulated to play a role in AD itch. These neurophysiogical and neuroimmune itch pathways have been recently reviewed in detail elsewhere ( 5, 6). The roles of opioid receptors, other cytokines and proteinase-activated receptors have also been explored, but no one molecule or pathway has emerged as the predominant mediator of itch in AD. Newly identified itch mediators include the histamine 4 receptor and interleukin-31. Recent human studies in AD identify roles for neuropeptides such as calcitonin, gene-related peptide, substance P, as well as neutrophophins such as nerve growth factor. More modern concepts of itch pathophysiology in AD involve understanding the close relationship between the nervous system and the skin two organ systems derived from the same embryological origin (ectoderm). Unfortunately, clinical studies revealed that histamine receptor (H1, H2) blockade does not lead to significant improvement in itch or inflammation in AD ( 4). Early research attempting to understand the pruritus of AD focused on the role of histamine. ![]() Nocturnal itch leads to intense scratching, leading to skin damage and poor sleep quality. The pathophysiology of AD is complex and not fully understood, but the so-called itch/scratch cycle perpetuates the disease.
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