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311 NM UVB therapy for parapsoriasis en plaques
ESDR I JSID / SID Abstracts
1369
1372
INCREASED INFILTRATE OF CD1 lb+ CELLS AND IJLTRAVIOLET-BRESISTANT CDla+ CELLS IN SKIN OF PATIENTS WITH POLYMORPHIC LIGHT ERUPTION. W. Kiileen. H. van W&den. S. den &nest. C.L.H, Duikers. R. Kiekens. E. Knol. C.A.F.M. &u&t&-Koomen. W.A. “an VIotea and F.R. de Gruiil. Dermatology, University Hospital AZU, Utrecht, the Netherlands. After ultraviolet (UV) overexposure the Langerhans cells (epidermal CDla+ cells1 disamxar from healthv skin. and CDllb+ macroohaee-like cells appearin a matterif days, and they’are reported to produce IL-iO.‘I&e phenomena are related to the UV-induced local suppression of contact hypersensitivity reactions. A defect in this suppression might allow inadvertent
Ext’tucowotuz~~
immune reactions to develop after IN
(over)exposure; i.e., it might explain
polymorphic light eruption (PLE). In order to test this we first ex&&buttwk skin of 5 healthv volunteers to 6 MED (minimal ervthemal doses) from PhiIios TLl2 lamps, a& indeed observed a d&atic disap&rance of &la+ cells>8 and 72 hours later, at which time CDllb+ cells appeared mainly in the dermis. In 5 patients with PLE (3 with a normal MBD and 2 with a low MBD) CDla+ cells were present epidermally and dermally before exposure, and these cells were still present at 48 and 72 hours after exposure to 6 MBD. A substantial number of CDllb+ cells was already present dermally before exposure, and this number increased further after UV overexposure, and these cells then also invaded the epidermis. In a patient who underwent a UV hardening therapy, the CDla+ cells disappeared after a 6 MED exposure. This in viw test holds great promise to diagnose PLE, and to understand the early steps in its pathogen&s.
PHOTOlMMVNOTHERAPY WDUCES INCREASED ANNEXIN
V
A. Gerber’. M. B&t&. H. Stnw’. H. P. Gollnid, Institllte of Immunoloav’ and Department of Dermatolo&, _. Otto van GuAicke University. Magdetwg:-Germany. . The mechanism of extracorPoreal photoimmunotherapy (ECPI) based on the action of 8-methoxypsomlen acd UVA light on peripheral leucocytes is not tidly understood The DNA damaging e&t of WA inducing programmed cell death is assumed to be a possible mechanism of action. In the present study lymphocytes of 8 patients with cutaneous T-cell lymphoma undergoing ECPI were investigated before and a&r therapy Ann&n V known for its selective affinity to phospholipids was used to detect early phases of apoptosis when cells expose phosphatidylserine to the outer membrane Siiultar!eous staining with propidiumjodid binding 10 DNA allowed detection of late apoptotic/necrotic cells. Apoptosis of lymphocytes was obsewed 20 hours atIer each BCPI session, whereas 1,2, and 4 hours atter ECPI and in untreated lymphocytes no remarkable changes were found. The increase in apoptotic cells was more pronounced using annexin/propidiumjodid double staining (I % of cells before vs. 12 % a& treabnent) than for annexin stained cells only (17 % of cells before vs. 30 % after treatment). The decreased viabiity of the reinfused lymphocytes could be a possible mechanism of the supposed immunomodulatory therapeutic effect of ECPI. BIM)INO
IN ~yMpHo~v?‘ss.
1373
1370 EVALUATION OF PUVB (31 lnm) BATHPHOTOXICITY. Norbert J. Neumann, Kordula Schlotmann. Thomas Ruzicka and Pew Lehmann Department of Dermatology. Heinrich-Heine-University Duesseldorf.Duesseldorf..Gem&y The combination of psoralen bath and UVB (311”~) has been shown to be en effective therapy in psoriasis. However, guidelines concerning the time interval between S-MOP bath and UVB (3llnm) h-radiation end the persistence of photosensitivity ere lacking. Therefore. the aim of this study was to determine the optimal lime interval between &MOP bath and UVB (311nm) irradiation as well as the persistence of photosensitivity in normal shin after PUVB (311nm) bath treatment 10 volunteers were enrolled in the study. The volarsite of one forean was i-radiated exclusively with increasing doses of UVB (311nm). Furthermore, the opposite forearm was immersed for 20 min in a 5 mgil water solution of S-MOP. Immediately and 1 h after bath procedure UVB (311nm) were applied on lcm’ test sites. The readings were performed 24-96 h after irradiation. In test sites irradiated only with UVB (31lnm) the MED ranked from OS-l.0 J/cm’. A similar range of the ME0 (0.5-1.0 J/cm’) was observed in skin areas irradiated with UVB (3llnm) 1 h after S-MOP bath, thus showing, that the S-MOP had no phototoxic effect 1 h after bath. The combination of S-MOP bath and UVB (31 lnm) immediately after the bath led to a decreased MED (0.5 J/cm? in all volunteers. Our results demonstrate that the MED UVB (31 lnm) could be significantly decreased if the skin was irradiated with UVB (3llnm) immediately after the S-MOP bath. UVB (311nm) irradiation 1 h after the bath showed no S-MOP mediated phototoxicity. These findings indicate a rapid loss Of 8.MOP phototoxicity after 1 h having significant implications for PUVB bath therapy. First, the patients have to be inadialed immediately after the SMOP bath. Secondly. S-MOP induced photosensitivity decreases so reoidlv that the patients may pursue their da@ activities without further restrictions.
of Bath-PUVA Therapyin Pstieotr Mb Morph- by rnslyzing histologic, ultraro~ic and elinieal pwameters CM. Hager,C Cqq N. H”nMrmnn, H.A.Sohbi,CJ Hue&,T Krieg andK. ScharffetterKochanek,Department of Dermatology,Universityof Cologne,Cologne,Germany Eualudatioo
To report and evaluatebath-PU”A therapy in ptie”ts with morphea.We discussedchmcal, hirtoloSical and ultrasonographical measurements at baselineand at the end of the study (36 treatments). M&c& Evaluationof skin lesionsWBSperfomxd clbically by induration(scare O-IO), by ultrwmagraphy (skin thicknessin mm) and by histologicmorphology(mm) of lesionaland now lesiona,skina, banelineanda&r treatment. &&& 10 p&en@ with morphea(9 females,1 male) with medianageof onsetWBE34 yeamwere includedin OUTstudy.Tbe medirmdurationof their skindisorderWBSlongerthaw6 yeam.The most cmnmonsiteof skin involvement was theuppa pan of the My Substaaialclinical improvement of thewskin indurationwas seen(medianlesionalskmindurationat baselineof 5.8 with red&w to a medianof2.6 af theendof thetrearment).Ultmsonographic meawementsof lesionalskinp&ormed at baselme(medianof 3.2 mm and a&r freahnent(medianof 2.3 mm) showedreductionin both sanogmphic thickness anddensity For comparison we alsok&cd at non-involved skin(at baselinea medianof 2.1 mm and post-treatment a medianof 2.lmm) demonstmtiog that treatedlesion are comparableto non-mvolvedlesioas.Morpbolog~c measurement of the biopsy before(media 3,35 mm) andatIer (median2.86mm) thethermsshoweda siwificant diffrrmce in theskinddcknss. Conclunon:!?e treated 10 patientsw& bath-PWX therapy. All patienfs revealed clinical improvementcorrelating with uhasonagraphicand histologic tindings confuming previously publishedstudies.This clearlydemonsmttea the er?icacyof bath-PUVA as a freaementmodalityfor momhea
1371
uvBthempyiniatte._Fifteenpatients(2 females,13
Biopsies
I
1369
1372
INCREASED INFILTRATE OF CD1 lb+ CELLS AND IJLTRAVIOLET-BRESISTANT CDla+ CELLS IN SKIN OF PATIENTS WITH POLYMORPHIC LIGHT ERUPTION. W. Kiileen. H. van W&den. S. den &nest. C.L.H, Duikers. R. Kiekens. E. Knol. C.A.F.M. &u&t&-Koomen. W.A. “an VIotea and F.R. de Gruiil. Dermatology, University Hospital AZU, Utrecht, the Netherlands. After ultraviolet (UV) overexposure the Langerhans cells (epidermal CDla+ cells1 disamxar from healthv skin. and CDllb+ macroohaee-like cells appearin a matterif days, and they’are reported to produce IL-iO.‘I&e phenomena are related to the UV-induced local suppression of contact hypersensitivity reactions. A defect in this suppression might allow inadvertent
Ext’tucowotuz~~
immune reactions to develop after IN
(over)exposure; i.e., it might explain
polymorphic light eruption (PLE). In order to test this we first ex&&buttwk skin of 5 healthv volunteers to 6 MED (minimal ervthemal doses) from PhiIios TLl2 lamps, a& indeed observed a d&atic disap&rance of &la+ cells>8 and 72 hours later, at which time CDllb+ cells appeared mainly in the dermis. In 5 patients with PLE (3 with a normal MBD and 2 with a low MBD) CDla+ cells were present epidermally and dermally before exposure, and these cells were still present at 48 and 72 hours after exposure to 6 MBD. A substantial number of CDllb+ cells was already present dermally before exposure, and this number increased further after UV overexposure, and these cells then also invaded the epidermis. In a patient who underwent a UV hardening therapy, the CDla+ cells disappeared after a 6 MED exposure. This in viw test holds great promise to diagnose PLE, and to understand the early steps in its pathogen&s.
PHOTOlMMVNOTHERAPY WDUCES INCREASED ANNEXIN
V
A. Gerber’. M. B&t&. H. Stnw’. H. P. Gollnid, Institllte of Immunoloav’ and Department of Dermatolo&, _. Otto van GuAicke University. Magdetwg:-Germany. . The mechanism of extracorPoreal photoimmunotherapy (ECPI) based on the action of 8-methoxypsomlen acd UVA light on peripheral leucocytes is not tidly understood The DNA damaging e&t of WA inducing programmed cell death is assumed to be a possible mechanism of action. In the present study lymphocytes of 8 patients with cutaneous T-cell lymphoma undergoing ECPI were investigated before and a&r therapy Ann&n V known for its selective affinity to phospholipids was used to detect early phases of apoptosis when cells expose phosphatidylserine to the outer membrane Siiultar!eous staining with propidiumjodid binding 10 DNA allowed detection of late apoptotic/necrotic cells. Apoptosis of lymphocytes was obsewed 20 hours atIer each BCPI session, whereas 1,2, and 4 hours atter ECPI and in untreated lymphocytes no remarkable changes were found. The increase in apoptotic cells was more pronounced using annexin/propidiumjodid double staining (I % of cells before vs. 12 % a& treabnent) than for annexin stained cells only (17 % of cells before vs. 30 % after treatment). The decreased viabiity of the reinfused lymphocytes could be a possible mechanism of the supposed immunomodulatory therapeutic effect of ECPI. BIM)INO
IN ~yMpHo~v?‘ss.
1373
1370 EVALUATION OF PUVB (31 lnm) BATHPHOTOXICITY. Norbert J. Neumann, Kordula Schlotmann. Thomas Ruzicka and Pew Lehmann Department of Dermatology. Heinrich-Heine-University Duesseldorf.Duesseldorf..Gem&y The combination of psoralen bath and UVB (311”~) has been shown to be en effective therapy in psoriasis. However, guidelines concerning the time interval between S-MOP bath and UVB (3llnm) h-radiation end the persistence of photosensitivity ere lacking. Therefore. the aim of this study was to determine the optimal lime interval between &MOP bath and UVB (311nm) irradiation as well as the persistence of photosensitivity in normal shin after PUVB (311nm) bath treatment 10 volunteers were enrolled in the study. The volarsite of one forean was i-radiated exclusively with increasing doses of UVB (311nm). Furthermore, the opposite forearm was immersed for 20 min in a 5 mgil water solution of S-MOP. Immediately and 1 h after bath procedure UVB (311nm) were applied on lcm’ test sites. The readings were performed 24-96 h after irradiation. In test sites irradiated only with UVB (31lnm) the MED ranked from OS-l.0 J/cm’. A similar range of the ME0 (0.5-1.0 J/cm’) was observed in skin areas irradiated with UVB (3llnm) 1 h after S-MOP bath, thus showing, that the S-MOP had no phototoxic effect 1 h after bath. The combination of S-MOP bath and UVB (31 lnm) immediately after the bath led to a decreased MED (0.5 J/cm? in all volunteers. Our results demonstrate that the MED UVB (31 lnm) could be significantly decreased if the skin was irradiated with UVB (3llnm) immediately after the S-MOP bath. UVB (311nm) irradiation 1 h after the bath showed no S-MOP mediated phototoxicity. These findings indicate a rapid loss Of 8.MOP phototoxicity after 1 h having significant implications for PUVB bath therapy. First, the patients have to be inadialed immediately after the SMOP bath. Secondly. S-MOP induced photosensitivity decreases so reoidlv that the patients may pursue their da@ activities without further restrictions.
of Bath-PUVA Therapyin Pstieotr Mb Morph- by rnslyzing histologic, ultraro~ic and elinieal pwameters CM. Hager,C Cqq N. H”nMrmnn, H.A.Sohbi,CJ Hue&,T Krieg andK. ScharffetterKochanek,Department of Dermatology,Universityof Cologne,Cologne,Germany Eualudatioo
To report and evaluatebath-PU”A therapy in ptie”ts with morphea.We discussedchmcal, hirtoloSical and ultrasonographical measurements at baselineand at the end of the study (36 treatments). M&c& Evaluationof skin lesionsWBSperfomxd clbically by induration(scare O-IO), by ultrwmagraphy (skin thicknessin mm) and by histologicmorphology(mm) of lesionaland now lesiona,skina, banelineanda&r treatment. &&& 10 p&en@ with morphea(9 females,1 male) with medianageof onsetWBE34 yeamwere includedin OUTstudy.Tbe medirmdurationof their skindisorderWBSlongerthaw6 yeam.The most cmnmonsiteof skin involvement was theuppa pan of the My Substaaialclinical improvement of thewskin indurationwas seen(medianlesionalskmindurationat baselineof 5.8 with red&w to a medianof2.6 af theendof thetrearment).Ultmsonographic meawementsof lesionalskinp&ormed at baselme(medianof 3.2 mm and a&r freahnent(medianof 2.3 mm) showedreductionin both sanogmphic thickness anddensity For comparison we alsok&cd at non-involved skin(at baselinea medianof 2.1 mm and post-treatment a medianof 2.lmm) demonstmtiog that treatedlesion are comparableto non-mvolvedlesioas.Morpbolog~c measurement of the biopsy before(media 3,35 mm) andatIer (median2.86mm) thethermsshoweda siwificant diffrrmce in theskinddcknss. Conclunon:!?e treated 10 patientsw& bath-PWX therapy. All patienfs revealed clinical improvementcorrelating with uhasonagraphicand histologic tindings confuming previously publishedstudies.This clearlydemonsmttea the er?icacyof bath-PUVA as a freaementmodalityfor momhea
1371
uvBthempyiniatte._Fifteenpatients(2 females,13
Biopsies
I