This report describes 9 patients who developed allergic contact dermatitis to methyl aminolevulinate used for photodynamic therapy (PDT). The risk of developing contact allergy to methyl aminolevulinate in PDT treated patients was calculated to 1% after an average of 7 treatments (range 2-21).

Based on this case report we recommend treatment with alemtuzumab to severe cases of PNP in CLL. However, further follow-up of this case is needed in order to assess the long-term effect of alemtuzumab treatment in PNP.

Thymus- and activation-regulated chemokine (TARC)/CCL17 and cutaneous T cell-attracting chemokine (CTACK)/CCL27 are both pivotal mediators of the inflammatory reaction of atopic dermatitis (AD). TARC attracts CCR4 positive T cells known to be mainly of Th2 subtype whereas CTACK attracts skin-homing T cells of both Th1 and Th2 subtype that express CCR10. We found that CTACK can be induced in cultured human keratinocytes by tumor necrosis factor-alpha (TNF-alpha), but not by TARC alone. However, if the keratinocytes were preincubated with TNF-a for 6 h, TARC was able to augment the CTACK-inducing effect of TNF-a. Performing immunohistochemical stainings, reverse-transcription polymerase chain reaction (RT-PCR), and Western blotting, we found that TNF-a-induced CCR4 mRNA production, but that stimulated as well as non-stimulated keratinocytes expressed CCR4. In order to see if these results had any clinical relevance, we investigated the plasma concentrations of TARC and CTACK from 48 patients suffering from AD. This revealed that TARC and CTACK concentrations in plasma correlate with each other. Surprisingly, p-CTACK correlated inversely with SCORAD scores of the patients, which most likely is due to the treatment the patients received. Our results suggest that the primary Th2-dominated inflammatory reaction in AD induced by TARC leads to an augmented skin-specific inflammatory reaction through CTACK.

The collectin surfactant protein-D (SP-D) shows antimicrobial and immuno-regulatory properties and has recently been detected in the basal layers of normal human skin. This molecule potentially plays an important role in inflammatory skin diseases and therefore SP-D content and location was examined using immunohistochemistry on skin biopsies from patients with the two major dermatologic diseases, psoriasis and atopic dermatitis. SP-D was located in the stratum basale of all biopsies with similar intense staining in both diseased and normal skin. Differences were detected in stratum spinosum where involved psoriatic skin showed intense staining through the entire region significantly different from uninvolved and normal skin. Lesional atopic skin showed moderate staining extending through the basal three-fourths of stratum spinosum. Using real time polymerase chain reaction analysis, no substantial up-regulation of SP-D mRNA was detected in lesional psoriatic skin, and a comparison of serum levels of SP-D between patients with atopic dermatitis or psoriasis and a group of age matched healthy controls did not show significant differences. In conclusion SP-D was significantly more abundant in the stratum spinosum of lesional psoriatic and atopic skin due to more cells producing the molecule rather than up-regulation of production in single cells of diseased skin. Further studies are needed to show if SP-D plays a role in the protection against skin infections or modulation of the inflammatory process in these common skin diseases.