[Acquired reactive perforating collagenosis following herpes zoster as isotopic response?]. / Erworbene reaktive perforierende Kollagenose nach Herpes zoster als isotopische Antwort?

Reactive perforating collagenosis is a disease whose pathogenesis is still not fully understood. Histological findings are degenerated collagen bundles which are arranged in vertical direction penetrating the epidermis into a dome-shaped crater. Usually diabetes mellitus and renal failure can be found among patients with reactive perforating collagenosis. To date, there have been five cases described where the eruption of reactive perforating collagenosis followed herpes zoster infection. This could be a form of Wolf's isotopic response, a term that is used for dermatoses which arise after the healing of a preexisting dermatosis. We report the sixth case of a herpes zoster-associated reactive perforating collagenosis and discuss the current literature.

Etanercept plus narrowband ultraviolet B phototherapy of psoriasis is more effective than etanercept monotherapy at 6 weeks.

BACKGROUND: A substantial portion of patients with psoriasis does not achieve a satisfactory response under antitumour necrosis factor (TNF)-α biological therapies. OBJECTIVES: We aimed to evaluate whether etanercept plus narrowband ultraviolet B (NB-UVB) phototherapy is superior to etanercept monotherapy in the management of psoriasis. METHODS: In this prospective study, patients with psoriasis were treated with etanercept 25 mg twice weekly. Two marker lesions were selected for determination of the modified Psoriasis Area and Severity Index (M-PASI). NB-UVB was administered thrice weekly whereby one marker lesion was covered as nonirradiated control. Skin biopsies for histology and immunohistochemistry were performed in both marker lesions after a 6-week treatment course. RESULTS: After 6 weeks of therapy, the relative M-PASI reduction (mean ± SD) in etanercept-treated sites (53·7 ± 36·9%) was significantly lower than the reduction in etanercept plus NB-UVB-treated lesions (64 ± 27·8%; P = 0·011). At the end of treatment, histology scores of etanercept-treated psoriatic plaques were significantly higher than scores of etanercept plus NB-UVB-treated sites (4·6 ± 2·7 vs. 3·7 ± 2·4; P =0·045). Epidermal immunoreactivity for CD1a, CD4 and CD8 was significantly lower in etanercept plus NB-UVB-treated lesions when compared with etanercept monotherapy. CONCLUSIONS: Etanercept combined with NB-UVB is more effective than etanercept monotherapy at 6 weeks as demonstrated at a clinical, histological and immunohistological level. However, as there is an increased risk for malignancy by treatment with TNF-α blockers alone or in combination with phototherapy, we recommend to restrict this highly effective combination to short periods of time, for instance to obtain a quicker response, and to avoid long-term treatment.

Impact of etanercept treatment on ultraviolet B-induced inflammation, cell cycle regulation and DNA damage.

BACKGROUND: Current studies indicate that treatment with tumour necrosis factor (TNF)-α blockers plus ultraviolet (UV) B phototherapy results in higher relative Psoriasis Area and Severity Index reduction as compared with TNF-α monotherapy. OBJECTIVES: This study aimed to investigate the acute impact of etanercept on UVB-induced inflammation, cell cycle regulation and DNA damage. METHODS: Eleven subjects diagnosed with psoriasis who fulfilled the indication criteria for etanercept treatment were studied. A healthy skin site on the upper back was treated with UVB at 2 minimal erythema doses (MED). After 1, 24 and 72 h punch biopsies were taken from this site. Following the 72 h biopsy etanercept 50 mg was administered subcutaneously. After 48 h, 2 MED was given on healthy skin adjacent to previously treated skin sites. Again, after 1, 24 and 72 h punch biopsies were taken from this site. UVB- as well as UVB plus etanercept-treated skin was assessed by means of colorimetry and immunohistochemical studies for caspase 3, cyclin D(1), interleukin-12, Ki-67, p16, p53, survivin, thymine dimers and TNF-α. RESULTS: Erythema formation did not differ significantly between UVB- and UVB plus etanercept-treated sites. Comparisons between UVB- and UVB plus etanercept-treated sites at a given time (1, 24, 72 h) did not result in significant differences in immunoreactivity of the markers investigated, except for cyclin D(1), p53 and survivin. Immunoreactivity of cyclin D(1) and p53 was significantly decreased in UVB plus etanercept-treated sites at 24 h. Survivin expression was significantly higher in UVB plus etanercept-treated skin as compared with UVB monotherapy. CONCLUSIONS: Our data indicate that combined treatment with broadband UVB and TNF-α blockers might increase the risk of photocarcinogenesis by influencing apoptotic as well as antiapoptotic pathways.