- Email: [email protected]
Effects of bath PUVA therapy on the expression of interstitial collagenase (MMP-1) in morphea
S316
Posters - Photodermatology Day
We present our experiences with this modified PUVA-bath therapy in treating 5 potients with severe, rapidly progressing alopecia areata which had been resistent to prior local and systemic therapy. The cumulative UVA doses given over treatment periods of up to 16 weeks were 60.9-82.4 J/cm2 with single doses ranging from 0.3 to 5.0 J/cm*. After 4-6 weeks of treatment hair was visible in the hair follicles of all the patients and after 16 weeks this had grown to approximately one centimeter in length. PUVA-turban-therapy as a variant of PUVA-bath-therapy can therefore be considered an extremely useful method of administering dilute psoralen solution selectively to the head of patients, and has shown itself to be an efficient and well tolerated therapeutic alternative in the treatment of alopecia areata. I P555 REM syndrome reproduced in UVA cabin H. Adamski, J. Chevrant-Breton, F. Le Gall, E. Desrues. HGpital Pontchaillou, Rennes, France A 67-year-old woman, was seen with one year history of REM syndrome (reticular erythematous mucinosis plaque) located on the upper-chest. Biopsy confirmed the dermal presence of mucin by Alcian blue staining. Direct immunofluorescence of lesional skin was negative. Antinuclear antibodies were absent. An aggravation was noted in summer after sun exposure. UVA irradiation in the cabin (2 x 10 J/cm*) reproduced typical lesions at the 8”’ day. UVB (3 x 3 MED) and UVA (3 x 10 J/cm*) phototests were negative. Comment: Described by Steigleder in 1974, REM is a rare entity and belongs to dermal mucinosis group. This cutaneous disease, which often affects women, principally involves the prestemal and back areas (I). Despite the frequent reports of sun exacerbation, it has been difficult to trigger the eruption by phototesting. Biopsy proved lesions were reproduced by UVB phototest (2.5 x MED) after one month in one case (2). In our case, UVA radiation performed in the cabin induced REM syndrome as it has previously been reported (3). The mechanism of the triggering is actually unclear. It is supposed that UV, heat and perspiration are necessary to reveal this affection. References [l] Steigleder GK et al. Br J Dermntol 1974; 91: 191-199. [2] Morison WL et al. Arch Dennotol 1979; 115: 1340-1342. [3] Adarnski H et al. Nouv Dermatol 1996; 15: 402-404. I P556 Effects of bath PUVA therapy on the
expression of interstitial collagenase (MMP-1) in morphea
C. Gruss’, J.A. Reed*, S. Behrens3. R. Pete?, M. Kersche?. ‘Department of Dermatology, University of Regensburg, Regensburg; 3Departntent of Dermatology, University of Ubn, Ultn, Germany; 2Department of Derntatopathology, Cornell University Medical Center New York, USA Bath PUVA photochemotherapy as well as ultraviolet light A-l phototherapy have been increasingly used in the successful treatment of morphea within the last three years. Recently, UVA-1 phototherapy was shown to act by induction of inter-
stitial collagenase (matrix metalloproteinase I, MMP-1). However, if bath PUVA treatment also acts by induction of MMP-1 is unknown. Therefore, we initiated this study in which we examined specimens of morphea plaques before and after bath PUVA therapy using nucleic acid in situ hybridisation (ISH) to detect interstitial collagenase-specific mRNA transcripts and immunohistochemistry (IHC) to detect translated interstitial collagenase protein. Five female and one male patients with severe localised scleroderma were admitted and treated with 28-42 treatment sessions of bath PUVA photochemotherapy. ISH was performed on formalin-fixed and paraffin-embedded tissue specimens taken before therapy and 18 hours after the last treatment course using human interstitial collagenase-specific mRNA transcript. For IHC a monoclonal mouse serum specific for human MMP-l-protein was used. Both assays produced calorimetric reactions of variable intensity. After bath PUVA treatment an increase of signal intensity was identified either by ISH and/or IHC in the keratinocytes of all tissue specimens. For fibroblastic cells an increased labelling for interstitial collagenase protein was detected in scattered cells of the upper papillary dermis in four patients. These results are evidence that induction of interstitial collagenase is also involved in the improvement of morphea by bath PUVA therapy. Comparative studies are needed to exactly determine the optimal therapeutic modality for treatment of morphea and possible positive effects of bath PUVA and/or UVA-1 irradiation on other conditions characterised by excessive collagen production. I P557 All clinical stages of morphea improve after
ultraviolet A-l phototherapy
C. Gruss’, J.A. Reed*, S. Behrens3, N.S. McNutt*, P. A1tmeyer4, R. Pete?, M. Kersche?. ‘Department of Dermatology, University of Regensburg, Regensburg; 3Departnrent of Dermatology, University of Ubn, Ubn; 4Departntent of Dermatology, University of Bochunt, Germany; 2Departntent of Derntatopathology, New York Hospital, Cornell University Medical CenteG New York, USA The effects of low dose ultraviolet A-l (UVA-1) phototherapy on clinical stages of morphea (localised scleroderma) were analysed in this study on a histopathological basis. Three patients with severe morphea of the plaque type in different stages were enrolled: One patient with late-stage lesions having stable sclerotic plaques; another patient with acute plaque-stage inflammatory lesions; and the last patient with late-stage lesions associated with overlying lichen sclerosus et atrophicus. The treatment given was low dose UVA-1 phototherapy, with doses of 20 J/cm* administered four times a week for 6 weeks, and once a week for another six weeks. Additional therapy was restricted to the use of emollients. The patients were examined clinically before, after six weeks, and at the end of the phototherapy treatment. For histopathological analysis skin biopsies were obtained from the centres of markedly indurated sclerotic areas before and after UVA-I treatment. Following UVA-1 phototherapy, the sclerotic plaques resolved leaving smooth and soft skin with normal consistency and folding abilities. The histologic features of morphea disappeared, and the findings in the posttreatment biopsy sections resembled the histology of normal skin. However, mild changes of oberlying
Posters - Photodermatology Day
We present our experiences with this modified PUVA-bath therapy in treating 5 potients with severe, rapidly progressing alopecia areata which had been resistent to prior local and systemic therapy. The cumulative UVA doses given over treatment periods of up to 16 weeks were 60.9-82.4 J/cm2 with single doses ranging from 0.3 to 5.0 J/cm*. After 4-6 weeks of treatment hair was visible in the hair follicles of all the patients and after 16 weeks this had grown to approximately one centimeter in length. PUVA-turban-therapy as a variant of PUVA-bath-therapy can therefore be considered an extremely useful method of administering dilute psoralen solution selectively to the head of patients, and has shown itself to be an efficient and well tolerated therapeutic alternative in the treatment of alopecia areata. I P555 REM syndrome reproduced in UVA cabin H. Adamski, J. Chevrant-Breton, F. Le Gall, E. Desrues. HGpital Pontchaillou, Rennes, France A 67-year-old woman, was seen with one year history of REM syndrome (reticular erythematous mucinosis plaque) located on the upper-chest. Biopsy confirmed the dermal presence of mucin by Alcian blue staining. Direct immunofluorescence of lesional skin was negative. Antinuclear antibodies were absent. An aggravation was noted in summer after sun exposure. UVA irradiation in the cabin (2 x 10 J/cm*) reproduced typical lesions at the 8”’ day. UVB (3 x 3 MED) and UVA (3 x 10 J/cm*) phototests were negative. Comment: Described by Steigleder in 1974, REM is a rare entity and belongs to dermal mucinosis group. This cutaneous disease, which often affects women, principally involves the prestemal and back areas (I). Despite the frequent reports of sun exacerbation, it has been difficult to trigger the eruption by phototesting. Biopsy proved lesions were reproduced by UVB phototest (2.5 x MED) after one month in one case (2). In our case, UVA radiation performed in the cabin induced REM syndrome as it has previously been reported (3). The mechanism of the triggering is actually unclear. It is supposed that UV, heat and perspiration are necessary to reveal this affection. References [l] Steigleder GK et al. Br J Dermntol 1974; 91: 191-199. [2] Morison WL et al. Arch Dennotol 1979; 115: 1340-1342. [3] Adarnski H et al. Nouv Dermatol 1996; 15: 402-404. I P556 Effects of bath PUVA therapy on the
expression of interstitial collagenase (MMP-1) in morphea
C. Gruss’, J.A. Reed*, S. Behrens3. R. Pete?, M. Kersche?. ‘Department of Dermatology, University of Regensburg, Regensburg; 3Departntent of Dermatology, University of Ubn, Ultn, Germany; 2Department of Derntatopathology, Cornell University Medical Center New York, USA Bath PUVA photochemotherapy as well as ultraviolet light A-l phototherapy have been increasingly used in the successful treatment of morphea within the last three years. Recently, UVA-1 phototherapy was shown to act by induction of inter-
stitial collagenase (matrix metalloproteinase I, MMP-1). However, if bath PUVA treatment also acts by induction of MMP-1 is unknown. Therefore, we initiated this study in which we examined specimens of morphea plaques before and after bath PUVA therapy using nucleic acid in situ hybridisation (ISH) to detect interstitial collagenase-specific mRNA transcripts and immunohistochemistry (IHC) to detect translated interstitial collagenase protein. Five female and one male patients with severe localised scleroderma were admitted and treated with 28-42 treatment sessions of bath PUVA photochemotherapy. ISH was performed on formalin-fixed and paraffin-embedded tissue specimens taken before therapy and 18 hours after the last treatment course using human interstitial collagenase-specific mRNA transcript. For IHC a monoclonal mouse serum specific for human MMP-l-protein was used. Both assays produced calorimetric reactions of variable intensity. After bath PUVA treatment an increase of signal intensity was identified either by ISH and/or IHC in the keratinocytes of all tissue specimens. For fibroblastic cells an increased labelling for interstitial collagenase protein was detected in scattered cells of the upper papillary dermis in four patients. These results are evidence that induction of interstitial collagenase is also involved in the improvement of morphea by bath PUVA therapy. Comparative studies are needed to exactly determine the optimal therapeutic modality for treatment of morphea and possible positive effects of bath PUVA and/or UVA-1 irradiation on other conditions characterised by excessive collagen production. I P557 All clinical stages of morphea improve after
ultraviolet A-l phototherapy
C. Gruss’, J.A. Reed*, S. Behrens3, N.S. McNutt*, P. A1tmeyer4, R. Pete?, M. Kersche?. ‘Department of Dermatology, University of Regensburg, Regensburg; 3Departnrent of Dermatology, University of Ubn, Ubn; 4Departntent of Dermatology, University of Bochunt, Germany; 2Departntent of Derntatopathology, New York Hospital, Cornell University Medical CenteG New York, USA The effects of low dose ultraviolet A-l (UVA-1) phototherapy on clinical stages of morphea (localised scleroderma) were analysed in this study on a histopathological basis. Three patients with severe morphea of the plaque type in different stages were enrolled: One patient with late-stage lesions having stable sclerotic plaques; another patient with acute plaque-stage inflammatory lesions; and the last patient with late-stage lesions associated with overlying lichen sclerosus et atrophicus. The treatment given was low dose UVA-1 phototherapy, with doses of 20 J/cm* administered four times a week for 6 weeks, and once a week for another six weeks. Additional therapy was restricted to the use of emollients. The patients were examined clinically before, after six weeks, and at the end of the phototherapy treatment. For histopathological analysis skin biopsies were obtained from the centres of markedly indurated sclerotic areas before and after UVA-I treatment. Following UVA-1 phototherapy, the sclerotic plaques resolved leaving smooth and soft skin with normal consistency and folding abilities. The histologic features of morphea disappeared, and the findings in the posttreatment biopsy sections resembled the histology of normal skin. However, mild changes of oberlying