Significant advances in our understanding of the pathogenesis of atopic dermatitis (AD) have led to improvements in therapy. Nevertheless, assessment of the condition and therapeutic efficacy is often based on crude ‘eyeballing’, which is neither scientific nor reliable. The problems with not utilizing validated objective assessment tools and methodology will continue to adversely affect the merits of clinical research in AD. Th2 chemokines, especially CCL27 (CTACK), are involved in the inflammatory process. CCL27, being a skin-specific immune marker, correlates with the objective features (extent and intensity) but not the subjective features (pruritus and sleep loss). Correlations with disease severity are also demonstrated in other CC chemokines (such as CCL17, CCL18 and CCL22), interleukins (such as IL-17 and IL-31) and neuropeptides (such as BDNF and substance P). As the inflammatory process in AD is complex, it may be impossible to characterize the disease with a single clinical score or marker. Quantifying the various markers and correlating their levels with clinical scores may lead to a better understanding of AD and improve research in its management.
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Hon et al. (2010) studied this question.
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