Our data reinforce the role of an altered skin barrier in the pathogenesis of AD. Our results show not only reduced expression of filaggrin and claudin 1 in lesional atopic skin but also inverse correlation of filaggrin expression and disease severity. Moreover, elevation of in situ IL-17 and of circulating interleukin levels in AD emphasize the systemic, inflammatory profile of this defective skin barrier dermatosis.
We studied 44 patients with type 1 Gaucher's disease (16 non-treated patients and 28 treated with enzyme replacement therapy). We measured serum levels of chitotriosidase (ChT), neopterin, angiotensin-converting enzyme (ACE), adenosine deaminase (ADA) and beta-hexosaminidase (Hex) and its major isoenzymes Hex A and Hex B. In the untreated group of patients, the increase in serum levels was ChT>neopterin>ACE> ADA>Hex, with all decreasing significantly in treated patients (p< 0.001). Highly significant correlations were obtained between the markers of monocyte/macrophage activation which were tested (p<0.001). However, partial correlations between serum Hex B (with Hex A constant) and ChT, ACE, neopterin and ADA did not reach statistical significance. This suggests that hepatocytes are the major cellular source of this isoenzyme. Similarly, partial correlation of ChT with neopterin, with the other variables constant, was not significant, which would suggest a different expression of these two markers in Gaucher's disease.
Serum TPS is frequently increased in alcoholics and may be a marker of alcoholic hepatitis. Specificity of this molecule as a tumor marker is limited in alcoholics.
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