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22 results on '"Sardy, Miklos"'

1. Identification of two novel bullous pemphigoid- associated alleles, HLA-DQA1*05:05 and-DRB1*07:01, in Germans

Author

Schwarm, Christian, Gola, Damian, Holtsche, Maike M., Dieterich, Anabelle, Bhandari, Anita, Freitag, Miriam, Nuernberg, Peter, Toliat, Mohammad, Lieb, Wolfgang, Wittig, Michael, Franke, Andre, Worm, Margitta, Sticherling, Michael, Ehrchen, Jan, Guenther, Claudia, Glaeser, Regine, Peitsch, Wiebke K., Sardy, Miklos, Eming, Ruediger, Hertl, Michael, Benoit, Sandrine, Goebeler, Matthias, Pfoehler, Claudia, Kunz, Manfred, Kreuter, Alexander, van Beek, Nina, Erdmann, Jeanette, Busch, Hauke, Zillikens, Detlef, Sadik, Christian D., Hirose, Misa, Koenig, Inke R., Schmidt, Enno, Ibrahim, Saleh M., Schwarm, Christian, Gola, Damian, Holtsche, Maike M., Dieterich, Anabelle, Bhandari, Anita, Freitag, Miriam, Nuernberg, Peter, Toliat, Mohammad, Lieb, Wolfgang, Wittig, Michael, Franke, Andre, Worm, Margitta, Sticherling, Michael, Ehrchen, Jan, Guenther, Claudia, Glaeser, Regine, Peitsch, Wiebke K., Sardy, Miklos, Eming, Ruediger, Hertl, Michael, Benoit, Sandrine, Goebeler, Matthias, Pfoehler, Claudia, Kunz, Manfred, Kreuter, Alexander, van Beek, Nina, Erdmann, Jeanette, Busch, Hauke, Zillikens, Detlef, Sadik, Christian D., Hirose, Misa, Koenig, Inke R., Schmidt, Enno, and Ibrahim, Saleh M.

Abstract

Bullous pemphigoid (BP) is the most common autoimmune skin blistering disease characterized by autoimmunity against the hemidesmosomal proteins BP180, type XVII collagen, and BP230. To elucidate the genetic basis of susceptibility to BP, we performed the first genome-wide association study (GWAS) in Germans. This GWAS was combined with HLA locus targeted sequencing in an additional independent BP cohort. The strongest association with BP in Germans tested in this study was observed in the two HLA loci, HLA-DQA1*05:05 and HLA-DRB1*07:01. Further studies with increased sample sizes and complex studies integrating multiple pathogenic drivers will be conducted.

Published
2021

2. Identification of two novel bullous pemphigoid- associated alleles, HLA-DQA1*05:05 and-DRB1*07:01, in Germans

Author

Schwarm, Christian, Gola, Damian, Holtsche, Maike M., Dieterich, Anabelle, Bhandari, Anita, Freitag, Miriam, Nuernberg, Peter, Toliat, Mohammad, Lieb, Wolfgang, Wittig, Michael, Franke, Andre, Worm, Margitta, Sticherling, Michael, Ehrchen, Jan, Guenther, Claudia, Glaeser, Regine, Peitsch, Wiebke K., Sardy, Miklos, Eming, Ruediger, Hertl, Michael, Benoit, Sandrine, Goebeler, Matthias, Pfoehler, Claudia, Kunz, Manfred, Kreuter, Alexander, van Beek, Nina, Erdmann, Jeanette, Busch, Hauke, Zillikens, Detlef, Sadik, Christian D., Hirose, Misa, Koenig, Inke R., Schmidt, Enno, Ibrahim, Saleh M., Schwarm, Christian, Gola, Damian, Holtsche, Maike M., Dieterich, Anabelle, Bhandari, Anita, Freitag, Miriam, Nuernberg, Peter, Toliat, Mohammad, Lieb, Wolfgang, Wittig, Michael, Franke, Andre, Worm, Margitta, Sticherling, Michael, Ehrchen, Jan, Guenther, Claudia, Glaeser, Regine, Peitsch, Wiebke K., Sardy, Miklos, Eming, Ruediger, Hertl, Michael, Benoit, Sandrine, Goebeler, Matthias, Pfoehler, Claudia, Kunz, Manfred, Kreuter, Alexander, van Beek, Nina, Erdmann, Jeanette, Busch, Hauke, Zillikens, Detlef, Sadik, Christian D., Hirose, Misa, Koenig, Inke R., Schmidt, Enno, and Ibrahim, Saleh M.

Abstract

Bullous pemphigoid (BP) is the most common autoimmune skin blistering disease characterized by autoimmunity against the hemidesmosomal proteins BP180, type XVII collagen, and BP230. To elucidate the genetic basis of susceptibility to BP, we performed the first genome-wide association study (GWAS) in Germans. This GWAS was combined with HLA locus targeted sequencing in an additional independent BP cohort. The strongest association with BP in Germans tested in this study was observed in the two HLA loci, HLA-DQA1*05:05 and HLA-DRB1*07:01. Further studies with increased sample sizes and complex studies integrating multiple pathogenic drivers will be conducted.

Published
2021

3. Scleroderma Renal Crisis: Risk Factors for an Increasingly Rare Organ Complication

Author

Moinzadeh, Pia, Kuhr, Kathrin, Siegert, Elise, Blank, Norbert, Sunderkoetter, Cord, Henes, Joerg, Krusche, Martin, Schmalzing, Marc, Worm, Margitta, Schmeiser, Tim, Guenther, Claudia, Aberer, Elisabeth, Susok, Laura, Riemekasten, Gabriela, Kreuter, Alexander, Zeidler, Gabriele, Juche, Aaron, Hadjiski, Denitsa, Mueller-Ladner, Ulf, Gaebelein-Wissing, Noemi, Distler, Joerg H. W., Sardy, Miklos, Krieg, Thomas, Hunzelmann, Nicolas, Moinzadeh, Pia, Kuhr, Kathrin, Siegert, Elise, Blank, Norbert, Sunderkoetter, Cord, Henes, Joerg, Krusche, Martin, Schmalzing, Marc, Worm, Margitta, Schmeiser, Tim, Guenther, Claudia, Aberer, Elisabeth, Susok, Laura, Riemekasten, Gabriela, Kreuter, Alexander, Zeidler, Gabriele, Juche, Aaron, Hadjiski, Denitsa, Mueller-Ladner, Ulf, Gaebelein-Wissing, Noemi, Distler, Joerg H. W., Sardy, Miklos, Krieg, Thomas, and Hunzelmann, Nicolas

Abstract

Objective. Scleroderma renal crisis (SRC) is a severe life-threatening manifestation in patients with systemic sclerosis (SSc). However, the knowledge about risk factors for SRC is limited. We determined here the frequency of SRC and identified risk factors for the prediction of SRC. Methods. Based on regular followup data from the German Network for Systemic Scleroderma, we used univariate and multivariate generalized estimating equations to analyze the association between clinical variables, SSc subsets, therapy [i.e., angiotensin-converting enzyme inhibitors (ACEi), corticosteroids], and the occurrence of SRC. Results. Data of 2873 patients with 10,425 visits were available for analysis with a mean number of registry visits of 3.6 +/- 2.8 and a mean time of followup of 3.6 +/- 3.8 years. In total, 70 patients developed SRC (70/ 2873, 2.4%). Of these patients, 57.1% (40/70) were diagnosed with diffuse cutaneous SSc, 31.4% (22/70) with limited cutaneous SSc, and 11.4% (8/70) with SSc- overlap syndromes. Predictive independent factors with the highest probability for SRC were positive anti-RNA polymerase antibodies (RNAP), a history of proteinuria prior to SRC onset, diminished DLCO, and a history of hypertension. Interestingly, positive antitopoisomerase autoantibodies did not predict a higher risk for SRC. Further, patients with SRC were significantly more frequently treated with ACEi and corticosteroids without being independently associated with SRC. Conclusion. In this cohort, SRC has become a rare complication. By far the highest risk for SRC was associated with the detection of anti-RNAP and proteinuria.

Published
2020

4. S2k guidelines for the treatment of pemphigus vulgaris/foliaceus and bullous pemphigoid: 2019 update

Author

Schmidt, Enno, Sticherling, Michael, Sardy, Miklos, Eming, Ruediger, Goebeler, Matthias, Hertl, Michael, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Nast, Alexander, Orzechowski, Hans-Dieter, Pfeiffer, Christiane, Schuster, Volker, Sitaru, Cassian, Zidane, Miriam, Zillikens, Detlef, Worm, Margitta, Schmidt, Enno, Sticherling, Michael, Sardy, Miklos, Eming, Ruediger, Goebeler, Matthias, Hertl, Michael, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Nast, Alexander, Orzechowski, Hans-Dieter, Pfeiffer, Christiane, Schuster, Volker, Sitaru, Cassian, Zidane, Miriam, Zillikens, Detlef, and Worm, Margitta

Published
2020

5. Scleroderma Renal Crisis: Risk Factors for an Increasingly Rare Organ Complication

Author

Moinzadeh, Pia, Kuhr, Kathrin, Siegert, Elise, Blank, Norbert, Sunderkoetter, Cord, Henes, Joerg, Krusche, Martin, Schmalzing, Marc, Worm, Margitta, Schmeiser, Tim, Guenther, Claudia, Aberer, Elisabeth, Susok, Laura, Riemekasten, Gabriela, Kreuter, Alexander, Zeidler, Gabriele, Juche, Aaron, Hadjiski, Denitsa, Mueller-Ladner, Ulf, Gaebelein-Wissing, Noemi, Distler, Joerg H. W., Sardy, Miklos, Krieg, Thomas, Hunzelmann, Nicolas, Moinzadeh, Pia, Kuhr, Kathrin, Siegert, Elise, Blank, Norbert, Sunderkoetter, Cord, Henes, Joerg, Krusche, Martin, Schmalzing, Marc, Worm, Margitta, Schmeiser, Tim, Guenther, Claudia, Aberer, Elisabeth, Susok, Laura, Riemekasten, Gabriela, Kreuter, Alexander, Zeidler, Gabriele, Juche, Aaron, Hadjiski, Denitsa, Mueller-Ladner, Ulf, Gaebelein-Wissing, Noemi, Distler, Joerg H. W., Sardy, Miklos, Krieg, Thomas, and Hunzelmann, Nicolas

Abstract

Objective. Scleroderma renal crisis (SRC) is a severe life-threatening manifestation in patients with systemic sclerosis (SSc). However, the knowledge about risk factors for SRC is limited. We determined here the frequency of SRC and identified risk factors for the prediction of SRC. Methods. Based on regular followup data from the German Network for Systemic Scleroderma, we used univariate and multivariate generalized estimating equations to analyze the association between clinical variables, SSc subsets, therapy [i.e., angiotensin-converting enzyme inhibitors (ACEi), corticosteroids], and the occurrence of SRC. Results. Data of 2873 patients with 10,425 visits were available for analysis with a mean number of registry visits of 3.6 +/- 2.8 and a mean time of followup of 3.6 +/- 3.8 years. In total, 70 patients developed SRC (70/ 2873, 2.4%). Of these patients, 57.1% (40/70) were diagnosed with diffuse cutaneous SSc, 31.4% (22/70) with limited cutaneous SSc, and 11.4% (8/70) with SSc- overlap syndromes. Predictive independent factors with the highest probability for SRC were positive anti-RNA polymerase antibodies (RNAP), a history of proteinuria prior to SRC onset, diminished DLCO, and a history of hypertension. Interestingly, positive antitopoisomerase autoantibodies did not predict a higher risk for SRC. Further, patients with SRC were significantly more frequently treated with ACEi and corticosteroids without being independently associated with SRC. Conclusion. In this cohort, SRC has become a rare complication. By far the highest risk for SRC was associated with the detection of anti-RNAP and proteinuria.

Published
2020

6. S2k guidelines for the treatment of pemphigus vulgaris/foliaceus and bullous pemphigoid: 2019 update

Author

Schmidt, Enno, Sticherling, Michael, Sardy, Miklos, Eming, Ruediger, Goebeler, Matthias, Hertl, Michael, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Nast, Alexander, Orzechowski, Hans-Dieter, Pfeiffer, Christiane, Schuster, Volker, Sitaru, Cassian, Zidane, Miriam, Zillikens, Detlef, Worm, Margitta, Schmidt, Enno, Sticherling, Michael, Sardy, Miklos, Eming, Ruediger, Goebeler, Matthias, Hertl, Michael, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Nast, Alexander, Orzechowski, Hans-Dieter, Pfeiffer, Christiane, Schuster, Volker, Sitaru, Cassian, Zidane, Miriam, Zillikens, Detlef, and Worm, Margitta

Published
2020

7. Significance of pulmonary involvement in systemic sclerosis (SSc)- data from the German SSc-network

Author

Kreuter, Michael, Bonella, Francesco, Blank, Nobert, Siegert, Elise, Henes, Joerg, Worm, Margitta, Sunderkoetter, Cord, Schmalzing, Marc, Kreuter, Alexander, Guenther, Claudia, Susok, Laura, Zeidler, Gabriele, Koetter, Ina, Mueller-Ladner, Ulf, Krieg, Thomas, Juche, Aaron, Schmeiser, Tim, Riemekasten, Gabriele, Aberer, Elisabeth, Gaebelein-Wissing, Noemi, Distler, Joerg H. W., Sardy, Miklos, Pfeiffer, Christiane, Kuhr, Kathrin, Lorenz, Hanns-Martin, Moinzadeh, Pia, Hunzelmann, Nicolas, Kreuter, Michael, Bonella, Francesco, Blank, Nobert, Siegert, Elise, Henes, Joerg, Worm, Margitta, Sunderkoetter, Cord, Schmalzing, Marc, Kreuter, Alexander, Guenther, Claudia, Susok, Laura, Zeidler, Gabriele, Koetter, Ina, Mueller-Ladner, Ulf, Krieg, Thomas, Juche, Aaron, Schmeiser, Tim, Riemekasten, Gabriele, Aberer, Elisabeth, Gaebelein-Wissing, Noemi, Distler, Joerg H. W., Sardy, Miklos, Pfeiffer, Christiane, Kuhr, Kathrin, Lorenz, Hanns-Martin, Moinzadeh, Pia, and Hunzelmann, Nicolas

Published
2018

8. Transglutaminases in autoimmune and inherited skin diseases: The phenomena of epitope spreading and functional compensation

Author

Karpati, Sarolta, Sardy, Miklos, Nemeth, Krisztian, Mayer, Balazs, Smyth, Neil, Paulsson, Mats, Traupe, Heiko, Karpati, Sarolta, Sardy, Miklos, Nemeth, Krisztian, Mayer, Balazs, Smyth, Neil, Paulsson, Mats, and Traupe, Heiko

Abstract

Transglutaminases (TGs) are structurally and functionally related enzymes that modify the post-translational structure and activity of proteins or peptides, and thus are able to turn on or switch off their function. Depending on location and activities, TGs are able to modify the signalling, the function and the fate of cells and extracellular connective tissues. Besides mouse models, human diseases enable us to appreciate the function of various TGs. In this study, skin diseases induced by genetic damages or autoimmune targeting of these enzymes will be discussed. TG1, TG3 and TG5 contribute to the cutaneous barrier and thus to the integrity and function of epidermis. TGM1 mutations related to autosomal recessive ichthyosis subtypes, TGM5 mutations to a mild epidermolysis bullosa phenotype and as novelty TGM3 mutation to uncombable hair syndrome will be discussed. Autoimmunity to TG2, TG3 and TG6 may develop in a few of those genetically determined individuals who lost tolerance to gluten, and manifest as coeliac disease, dermatitis herpetiformis or gluten-dependent neurological symptoms, respectively. These gluten responder diseases commonly occur in combination. In autoimmune diseases, the epitope spreading is remarkable, while in some inherited pathologies, a unique compensation of the lost enzyme function is noted.

Published
2018

9. Transglutaminases in autoimmune and inherited skin diseases: The phenomena of epitope spreading and functional compensation

Author

Karpati, Sarolta, Sardy, Miklos, Nemeth, Krisztian, Mayer, Balazs, Smyth, Neil, Paulsson, Mats, Traupe, Heiko, Karpati, Sarolta, Sardy, Miklos, Nemeth, Krisztian, Mayer, Balazs, Smyth, Neil, Paulsson, Mats, and Traupe, Heiko

Abstract

Transglutaminases (TGs) are structurally and functionally related enzymes that modify the post-translational structure and activity of proteins or peptides, and thus are able to turn on or switch off their function. Depending on location and activities, TGs are able to modify the signalling, the function and the fate of cells and extracellular connective tissues. Besides mouse models, human diseases enable us to appreciate the function of various TGs. In this study, skin diseases induced by genetic damages or autoimmune targeting of these enzymes will be discussed. TG1, TG3 and TG5 contribute to the cutaneous barrier and thus to the integrity and function of epidermis. TGM1 mutations related to autosomal recessive ichthyosis subtypes, TGM5 mutations to a mild epidermolysis bullosa phenotype and as novelty TGM3 mutation to uncombable hair syndrome will be discussed. Autoimmunity to TG2, TG3 and TG6 may develop in a few of those genetically determined individuals who lost tolerance to gluten, and manifest as coeliac disease, dermatitis herpetiformis or gluten-dependent neurological symptoms, respectively. These gluten responder diseases commonly occur in combination. In autoimmune diseases, the epitope spreading is remarkable, while in some inherited pathologies, a unique compensation of the lost enzyme function is noted.

Published
2018

10. Significance of pulmonary involvement in systemic sclerosis (SSc)- data from the German SSc-network

Author

Kreuter, Michael, Bonella, Francesco, Blank, Nobert, Siegert, Elise, Henes, Joerg, Worm, Margitta, Sunderkoetter, Cord, Schmalzing, Marc, Kreuter, Alexander, Guenther, Claudia, Susok, Laura, Zeidler, Gabriele, Koetter, Ina, Mueller-Ladner, Ulf, Krieg, Thomas, Juche, Aaron, Schmeiser, Tim, Riemekasten, Gabriele, Aberer, Elisabeth, Gaebelein-Wissing, Noemi, Distler, Joerg H. W., Sardy, Miklos, Pfeiffer, Christiane, Kuhr, Kathrin, Lorenz, Hanns-Martin, Moinzadeh, Pia, Hunzelmann, Nicolas, Kreuter, Michael, Bonella, Francesco, Blank, Nobert, Siegert, Elise, Henes, Joerg, Worm, Margitta, Sunderkoetter, Cord, Schmalzing, Marc, Kreuter, Alexander, Guenther, Claudia, Susok, Laura, Zeidler, Gabriele, Koetter, Ina, Mueller-Ladner, Ulf, Krieg, Thomas, Juche, Aaron, Schmeiser, Tim, Riemekasten, Gabriele, Aberer, Elisabeth, Gaebelein-Wissing, Noemi, Distler, Joerg H. W., Sardy, Miklos, Pfeiffer, Christiane, Kuhr, Kathrin, Lorenz, Hanns-Martin, Moinzadeh, Pia, and Hunzelmann, Nicolas

Published
2018

11. Vasoactive Therapy in Systemic Sclerosis: Real-life Therapeutic Practice in More Than 3000 Patients

Author

Moinzadeh, Pia, Riemekasten, Gabriela, Siegert, Elise, Fierlbeck, Gerhard, Henes, Joerg, Blank, Norbert, Melchers, Inga, Mueller-Ladner, Ulf, Frerix, Marc, Kreuter, Alexander, Tigges, Christian, Lahner, Nina, Susok, Laura, Guenther, Claudia, Zeidler, Gabriele, Pfeiffer, Christiane, Worm, Margitta, Karrer, Sigrid, Aberer, Elisabeth, Bretterklieber, Agnes, Genth, Ekkehard, Simon, Jan C., Distler, Joerg H. W., Hein, Ruediger, Schneider, Matthias, Seitz, Cornelia S., Herink, Claudia, Steinbrink, Kerstin, Sardy, Miklos, Varga, Rita, Mensing, Hartwig, Mensing, Christian, Lehmann, Percy, Neeck, Gunther, Fiehn, Christoph, Weber, Manfred, Goebeler, Matthias, Burkhardt, Harald, Buslau, Michael, Ahmadi-Simab, Keihan, Himsel, Andrea, Juche, Aaron, Koetter, Ina, Kuhn, Annegret, Sticherling, Michael, Hellmich, Martin, Kuhr, Kathrin, Krieg, Thomas, Ehrchen, Jan, Sunderkoetter, Cord, Hunzelmann, Nicolas, Moinzadeh, Pia, Riemekasten, Gabriela, Siegert, Elise, Fierlbeck, Gerhard, Henes, Joerg, Blank, Norbert, Melchers, Inga, Mueller-Ladner, Ulf, Frerix, Marc, Kreuter, Alexander, Tigges, Christian, Lahner, Nina, Susok, Laura, Guenther, Claudia, Zeidler, Gabriele, Pfeiffer, Christiane, Worm, Margitta, Karrer, Sigrid, Aberer, Elisabeth, Bretterklieber, Agnes, Genth, Ekkehard, Simon, Jan C., Distler, Joerg H. W., Hein, Ruediger, Schneider, Matthias, Seitz, Cornelia S., Herink, Claudia, Steinbrink, Kerstin, Sardy, Miklos, Varga, Rita, Mensing, Hartwig, Mensing, Christian, Lehmann, Percy, Neeck, Gunther, Fiehn, Christoph, Weber, Manfred, Goebeler, Matthias, Burkhardt, Harald, Buslau, Michael, Ahmadi-Simab, Keihan, Himsel, Andrea, Juche, Aaron, Koetter, Ina, Kuhn, Annegret, Sticherling, Michael, Hellmich, Martin, Kuhr, Kathrin, Krieg, Thomas, Ehrchen, Jan, Sunderkoetter, Cord, and Hunzelmann, Nicolas

Abstract

Objective. Vasculopathy is a key factor in the pathophysiology of systemic sclerosis (SSc) and the main cause for Raynaud phenomenon (RP), digital ulcers (DU), and/or pulmonary arterial hypertension (PAH). It is so far unknown how patients with SSc are treated with vasoactive agents in daily practice. To determine to which extent patients with SSc were treated with different vasoactive agents, we used data from the German Network for Systemic Scleroderma registry. Methods. The data of 3248 patients with SSc were analyzed. Results. Patients were treated with vasoactive drugs in 61.1% of cases (1984/3248). Of these, 47.6% received calcium channel inhibitors, followed by 34.2% treated with angiotensin-converting enzyme (ACE) inhibitors, 21.1% treated with intravenous (IV) prostanoids, 10.1% with pentoxifylline, 8.8% with angiotensin 1 receptor antagonists (AT1RA), 8.7% with endothelin 1 receptor antagonists (ET1RA), 4.1% with phosphodiesterase type 5 (PDE5) inhibitors, and 5.3% with others. Patients with RP received vasoactive therapy in 63.3% of cases, with DU in 70.1%, and with PAH in 78.2% of cases. Logistic regression analysis revealed that patients with PAH were significantly more often treated with PDE5 inhibitors and ET1RA, and those with DU with ET1RA and IV prostanoids. In addition, 41.8% of patients were treated with ACE inhibitors and/or AT1RA. Patients registered after 2009 received significantly more often ET1RA, AT1RA, and IV prostanoids compared with patients registered prior to 2005. Conclusion. These data clearly indicate that many patients with SSc do not yet receive sufficient vasoactive therapy. Further, in recent years, a marked change of treatment regimens can be observed.

Published
2016

12. The Predict Study: low risk for digital ulcer development in patients with systemic sclerosis with increasing disease duration and lack of topoisomerase‐1 antibodies

Author

Hunzelmann, Nicolas, Riemekasten, G., Becker, M.O., Moinzadeh, Pia, Kreuter, Alexander, Melchers, I., Müller‐Ladner, Ulf, Meier, Friedegund, Worm, Margitta, Lee, H., Herrgott, I., Pfeiffer, C., Fierlbeck, G., Henes, J., Juche, A., Zeidler, G., Mensing, H., Günther, C., Sardy, Miklos, Burkhardt, H., Koehm, M., Kuhr, K., Krieg, Thomas M., Sunderkötter, C., Hunzelmann, Nicolas, Riemekasten, G., Becker, M.O., Moinzadeh, Pia, Kreuter, Alexander, Melchers, I., Müller‐Ladner, Ulf, Meier, Friedegund, Worm, Margitta, Lee, H., Herrgott, I., Pfeiffer, C., Fierlbeck, G., Henes, J., Juche, A., Zeidler, G., Mensing, H., Günther, C., Sardy, Miklos, Burkhardt, H., Koehm, M., Kuhr, K., Krieg, Thomas M., and Sunderkötter, C.

Published
2016

13. Vasoactive Therapy in Systemic Sclerosis: Real-life Therapeutic Practice in More Than 3000 Patients

Author

Moinzadeh, Pia, Riemekasten, Gabriela, Siegert, Elise, Fierlbeck, Gerhard, Henes, Joerg, Blank, Norbert, Melchers, Inga, Mueller-Ladner, Ulf, Frerix, Marc, Kreuter, Alexander, Tigges, Christian, Lahner, Nina, Susok, Laura, Guenther, Claudia, Zeidler, Gabriele, Pfeiffer, Christiane, Worm, Margitta, Karrer, Sigrid, Aberer, Elisabeth, Bretterklieber, Agnes, Genth, Ekkehard, Simon, Jan C., Distler, Joerg H. W., Hein, Ruediger, Schneider, Matthias, Seitz, Cornelia S., Herink, Claudia, Steinbrink, Kerstin, Sardy, Miklos, Varga, Rita, Mensing, Hartwig, Mensing, Christian, Lehmann, Percy, Neeck, Gunther, Fiehn, Christoph, Weber, Manfred, Goebeler, Matthias, Burkhardt, Harald, Buslau, Michael, Ahmadi-Simab, Keihan, Himsel, Andrea, Juche, Aaron, Koetter, Ina, Kuhn, Annegret, Sticherling, Michael, Hellmich, Martin, Kuhr, Kathrin, Krieg, Thomas, Ehrchen, Jan, Sunderkoetter, Cord, Hunzelmann, Nicolas, Moinzadeh, Pia, Riemekasten, Gabriela, Siegert, Elise, Fierlbeck, Gerhard, Henes, Joerg, Blank, Norbert, Melchers, Inga, Mueller-Ladner, Ulf, Frerix, Marc, Kreuter, Alexander, Tigges, Christian, Lahner, Nina, Susok, Laura, Guenther, Claudia, Zeidler, Gabriele, Pfeiffer, Christiane, Worm, Margitta, Karrer, Sigrid, Aberer, Elisabeth, Bretterklieber, Agnes, Genth, Ekkehard, Simon, Jan C., Distler, Joerg H. W., Hein, Ruediger, Schneider, Matthias, Seitz, Cornelia S., Herink, Claudia, Steinbrink, Kerstin, Sardy, Miklos, Varga, Rita, Mensing, Hartwig, Mensing, Christian, Lehmann, Percy, Neeck, Gunther, Fiehn, Christoph, Weber, Manfred, Goebeler, Matthias, Burkhardt, Harald, Buslau, Michael, Ahmadi-Simab, Keihan, Himsel, Andrea, Juche, Aaron, Koetter, Ina, Kuhn, Annegret, Sticherling, Michael, Hellmich, Martin, Kuhr, Kathrin, Krieg, Thomas, Ehrchen, Jan, Sunderkoetter, Cord, and Hunzelmann, Nicolas

Abstract

Objective. Vasculopathy is a key factor in the pathophysiology of systemic sclerosis (SSc) and the main cause for Raynaud phenomenon (RP), digital ulcers (DU), and/or pulmonary arterial hypertension (PAH). It is so far unknown how patients with SSc are treated with vasoactive agents in daily practice. To determine to which extent patients with SSc were treated with different vasoactive agents, we used data from the German Network for Systemic Scleroderma registry. Methods. The data of 3248 patients with SSc were analyzed. Results. Patients were treated with vasoactive drugs in 61.1% of cases (1984/3248). Of these, 47.6% received calcium channel inhibitors, followed by 34.2% treated with angiotensin-converting enzyme (ACE) inhibitors, 21.1% treated with intravenous (IV) prostanoids, 10.1% with pentoxifylline, 8.8% with angiotensin 1 receptor antagonists (AT1RA), 8.7% with endothelin 1 receptor antagonists (ET1RA), 4.1% with phosphodiesterase type 5 (PDE5) inhibitors, and 5.3% with others. Patients with RP received vasoactive therapy in 63.3% of cases, with DU in 70.1%, and with PAH in 78.2% of cases. Logistic regression analysis revealed that patients with PAH were significantly more often treated with PDE5 inhibitors and ET1RA, and those with DU with ET1RA and IV prostanoids. In addition, 41.8% of patients were treated with ACE inhibitors and/or AT1RA. Patients registered after 2009 received significantly more often ET1RA, AT1RA, and IV prostanoids compared with patients registered prior to 2005. Conclusion. These data clearly indicate that many patients with SSc do not yet receive sufficient vasoactive therapy. Further, in recent years, a marked change of treatment regimens can be observed.

Published
2016

14. Disease progression in systemic sclerosis-overlap syndrome is significantly different from limited and diffuse cutaneous systemic sclerosis

Author

Moinzadeh, Pia, Aberer, Elisabeth, Ahmadi-Simab, Keihan, Blank, Norbert, Distler, Joerg H. W., Fierlbeck, Gerhard, Genth, Ekkehard, Guenther, Claudia, Hein, Ruediger, Henes, Joerg, Herich, Lena, Herrgott, Ilka, Koetter, Ina, Kreuter, Alexander, Krieg, Thomas, Kuhr, Kathrin, Lorenz, Hanns-Martin, Meier, Florian, Melchers, Inga, Mensing, Hartwig, Mueller-Ladner, Ulf, Pfeiffer, Christiane, Riemekasten, Gabriela, Sardy, Miklos, Schmalzing, Marc, Sunderkoetter, Cord, Susok, Laura, Tarner, Ingo H., Vaith, Peter, Worm, Margitta, Wozel, Gottfried, Zeidler, Gabriele, Hunzelmann, Nicolas, Moinzadeh, Pia, Aberer, Elisabeth, Ahmadi-Simab, Keihan, Blank, Norbert, Distler, Joerg H. W., Fierlbeck, Gerhard, Genth, Ekkehard, Guenther, Claudia, Hein, Ruediger, Henes, Joerg, Herich, Lena, Herrgott, Ilka, Koetter, Ina, Kreuter, Alexander, Krieg, Thomas, Kuhr, Kathrin, Lorenz, Hanns-Martin, Meier, Florian, Melchers, Inga, Mensing, Hartwig, Mueller-Ladner, Ulf, Pfeiffer, Christiane, Riemekasten, Gabriela, Sardy, Miklos, Schmalzing, Marc, Sunderkoetter, Cord, Susok, Laura, Tarner, Ingo H., Vaith, Peter, Worm, Margitta, Wozel, Gottfried, Zeidler, Gabriele, and Hunzelmann, Nicolas

Abstract

Background Systemic sclerosis (SSc)-overlap syndromes are a very heterogeneous and remarkable subgroup of SSc-patients, who present at least two connective tissue diseases (CTD) at the same time, usually with a specific autoantibody status. Objectives To determine whether patients, classified as overlap syndromes, show a disease course different from patients with limited SSc (lcSSc) or diffuse cutaneous SSc (dcSSc). Methods The data of 3240 prospectively included patients, registered in the database of the German Network for Systemic Scleroderma and followed between 2003 and 2013, were analysed. Results Among 3240 registered patients, 10% were diagnosed as SSc-overlap syndrome. Of these, 82.5% were female. SSc-overlap patients had a mean age of 48 +/- 1.2 years and carried significantly more often 'other antibodies' (68.0%; p<0.0001), including anti-U1RNP, -PmScl, -Ro, -La, as well as anti-Jo-1 and -Ku antibodies. These patients developed musculoskeletal involvement earlier and more frequently (62.5%) than patients diagnosed as lcSSc (32.2%) or dcSSc (43.3%) (p<0.0001). The onset of lung fibrosis and heart involvement in SSc-overlap patients was significantly earlier than in patients with lcSSc and occurred later than in patients with dcSSc. Oesophagus, kidney and PH progression was similar to lcSSc patients, whereas dcSSc patients had a significantly earlier onset. Conclusions These data support the concept that SSc-overlap syndromes should be regarded as a separate SSc subset, distinct from lcSSc and dcSSc, due to a different progression of the disease, different proportional distribution of specific autoantibodies, and of different organ involvement.

Published
2015

15. Disease progression in systemic sclerosis-overlap syndrome is significantly different from limited and diffuse cutaneous systemic sclerosis

Author

Moinzadeh, Pia, Aberer, Elisabeth, Ahmadi-Simab, Keihan, Blank, Norbert, Distler, Joerg H. W., Fierlbeck, Gerhard, Genth, Ekkehard, Guenther, Claudia, Hein, Ruediger, Henes, Joerg, Herich, Lena, Herrgott, Ilka, Koetter, Ina, Kreuter, Alexander, Krieg, Thomas, Kuhr, Kathrin, Lorenz, Hanns-Martin, Meier, Florian, Melchers, Inga, Mensing, Hartwig, Mueller-Ladner, Ulf, Pfeiffer, Christiane, Riemekasten, Gabriela, Sardy, Miklos, Schmalzing, Marc, Sunderkoetter, Cord, Susok, Laura, Tarner, Ingo H., Vaith, Peter, Worm, Margitta, Wozel, Gottfried, Zeidler, Gabriele, Hunzelmann, Nicolas, Moinzadeh, Pia, Aberer, Elisabeth, Ahmadi-Simab, Keihan, Blank, Norbert, Distler, Joerg H. W., Fierlbeck, Gerhard, Genth, Ekkehard, Guenther, Claudia, Hein, Ruediger, Henes, Joerg, Herich, Lena, Herrgott, Ilka, Koetter, Ina, Kreuter, Alexander, Krieg, Thomas, Kuhr, Kathrin, Lorenz, Hanns-Martin, Meier, Florian, Melchers, Inga, Mensing, Hartwig, Mueller-Ladner, Ulf, Pfeiffer, Christiane, Riemekasten, Gabriela, Sardy, Miklos, Schmalzing, Marc, Sunderkoetter, Cord, Susok, Laura, Tarner, Ingo H., Vaith, Peter, Worm, Margitta, Wozel, Gottfried, Zeidler, Gabriele, and Hunzelmann, Nicolas

Abstract

Background Systemic sclerosis (SSc)-overlap syndromes are a very heterogeneous and remarkable subgroup of SSc-patients, who present at least two connective tissue diseases (CTD) at the same time, usually with a specific autoantibody status. Objectives To determine whether patients, classified as overlap syndromes, show a disease course different from patients with limited SSc (lcSSc) or diffuse cutaneous SSc (dcSSc). Methods The data of 3240 prospectively included patients, registered in the database of the German Network for Systemic Scleroderma and followed between 2003 and 2013, were analysed. Results Among 3240 registered patients, 10% were diagnosed as SSc-overlap syndrome. Of these, 82.5% were female. SSc-overlap patients had a mean age of 48 +/- 1.2 years and carried significantly more often 'other antibodies' (68.0%; p<0.0001), including anti-U1RNP, -PmScl, -Ro, -La, as well as anti-Jo-1 and -Ku antibodies. These patients developed musculoskeletal involvement earlier and more frequently (62.5%) than patients diagnosed as lcSSc (32.2%) or dcSSc (43.3%) (p<0.0001). The onset of lung fibrosis and heart involvement in SSc-overlap patients was significantly earlier than in patients with lcSSc and occurred later than in patients with dcSSc. Oesophagus, kidney and PH progression was similar to lcSSc patients, whereas dcSSc patients had a significantly earlier onset. Conclusions These data support the concept that SSc-overlap syndromes should be regarded as a separate SSc subset, distinct from lcSSc and dcSSc, due to a different progression of the disease, different proportional distribution of specific autoantibodies, and of different organ involvement.

Published
2015

16. S2k guideline for the diagnosis of pemphigus vulgaris/foliaceus and bullous pemphigoid

Author

Schmidt, Enno, Goebeler, Matthias, Hertl, Michael, Sardy, Miklos, Sitaru, Cassian, Eming, Ruediger, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Orzechowski, Hans-Dieter, Pfeiffer, Christiane, Schuster, Volker, Sporbeck, Birte, Sticherling, Michael, Worm, Margitta, Zillikens, Detlef, Nast, Alexander, Schmidt, Enno, Goebeler, Matthias, Hertl, Michael, Sardy, Miklos, Sitaru, Cassian, Eming, Ruediger, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Orzechowski, Hans-Dieter, Pfeiffer, Christiane, Schuster, Volker, Sporbeck, Birte, Sticherling, Michael, Worm, Margitta, Zillikens, Detlef, and Nast, Alexander

Published
2015

17. S2k Guidelines for the treatment of pemphigus vulgaris/foliaceus and bullous pemphigoid

Author

Eming, Ruediger, Sticherling, Michael, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Pfeiffer, Christiane, Schuster, Volker, Zillikens, Detlef, Goebeler, Matthias, Hertl, Michael, Nast, Alexander, Orzechowski, Hans-Dieter, Sardy, Miklos, Schmidt, Enno, Sitaru, Cassian, Sporbeck, Birte, Worm, Margitta, Eming, Ruediger, Sticherling, Michael, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Pfeiffer, Christiane, Schuster, Volker, Zillikens, Detlef, Goebeler, Matthias, Hertl, Michael, Nast, Alexander, Orzechowski, Hans-Dieter, Sardy, Miklos, Schmidt, Enno, Sitaru, Cassian, Sporbeck, Birte, and Worm, Margitta

Published
2015

18. Vasoactive Therapy in Systemic Sclerosis: Real-life Therapeutic Practice in More Than 3000 Patients

Author

Moinzadeh, Pia, Riemekasten, Gabriela, Siegert, Elise, Fierlbeck, Gerhard, Henes, Joerg, Blank, Norbert, Melchers, Inga, Müller-Ladner, Ulf, Frerix, Marc, Kreuter, Alexander, Tigges, Christian, Lahner, Nina, Susok, Laura, Guenther, Claudia, Zeidler, Gabriele, Pfeiffer, Christiane, Worm, Margitta, Karrer, Sigrid, Aberer, Elisabeth, Bretterklieber, Agnes, Genth, Ekkehard, Simon, Jan C., Distler, Joerg H.W., Hein, Ruediger, Schneider, Matthias, Seitz, Cornelia S., Herink, Claudia, Steinbrink, Kerstin, Sardy, Miklos, Varga, Rita, Mensing, Hartwig, Mensing, Christian, Lehmann, Percy, Neeck, Gunther, Fiehn, Christoph, Weber, Manfred, Goebeler, Matthias, Burkhardt, Harald, Buslau, Michael, Ahmadi-Simab, Keihan, Himsel, Andrea, Juche, Aaron, Koetter, Ina, Kuhn, Annegret, Sticherling, Michael, Hellmich, Martin, Kuhr, Kathrin, Krieg, Thomas M., Ehrchen, Jan, Sunderkoetter, Cord, Hunzelmann, Nicolas, Moinzadeh, Pia, Riemekasten, Gabriela, Siegert, Elise, Fierlbeck, Gerhard, Henes, Joerg, Blank, Norbert, Melchers, Inga, Müller-Ladner, Ulf, Frerix, Marc, Kreuter, Alexander, Tigges, Christian, Lahner, Nina, Susok, Laura, Guenther, Claudia, Zeidler, Gabriele, Pfeiffer, Christiane, Worm, Margitta, Karrer, Sigrid, Aberer, Elisabeth, Bretterklieber, Agnes, Genth, Ekkehard, Simon, Jan C., Distler, Joerg H.W., Hein, Ruediger, Schneider, Matthias, Seitz, Cornelia S., Herink, Claudia, Steinbrink, Kerstin, Sardy, Miklos, Varga, Rita, Mensing, Hartwig, Mensing, Christian, Lehmann, Percy, Neeck, Gunther, Fiehn, Christoph, Weber, Manfred, Goebeler, Matthias, Burkhardt, Harald, Buslau, Michael, Ahmadi-Simab, Keihan, Himsel, Andrea, Juche, Aaron, Koetter, Ina, Kuhn, Annegret, Sticherling, Michael, Hellmich, Martin, Kuhr, Kathrin, Krieg, Thomas M., Ehrchen, Jan, Sunderkoetter, Cord, and Hunzelmann, Nicolas

Published
2015

19. Disease progression in systemic sclerosis-overlap syndrome is significantly different from limited and diffuse cutaneous systemic sclerosis

Author

Moinzadeh, Pia, Aberer, Elisabeth, Ahmadi-Simab, Keihan, Blank, Norbert, Distler, Joerg H. W., Fierlbeck, Gerhard, Genth, Ekkehard, Guenther, Claudia, Hein, Ruediger, Henes, Joerg, Herich, Lena, Herrgott, Ilka, Koetter, Ina, Kreuter, Alexander, Krieg, Thomas, Kuhr, Kathrin, Lorenz, Hanns-Martin, Meier, Florian, Melchers, Inga, Mensing, Hartwig, Mueller-Ladner, Ulf, Pfeiffer, Christiane, Riemekasten, Gabriela, Sardy, Miklos, Schmalzing, Marc, Sunderkoetter, Cord, Susok, Laura, Tarner, Ingo H., Vaith, Peter, Worm, Margitta, Wozel, Gottfried, Zeidler, Gabriele, Hunzelmann, Nicolas, Moinzadeh, Pia, Aberer, Elisabeth, Ahmadi-Simab, Keihan, Blank, Norbert, Distler, Joerg H. W., Fierlbeck, Gerhard, Genth, Ekkehard, Guenther, Claudia, Hein, Ruediger, Henes, Joerg, Herich, Lena, Herrgott, Ilka, Koetter, Ina, Kreuter, Alexander, Krieg, Thomas, Kuhr, Kathrin, Lorenz, Hanns-Martin, Meier, Florian, Melchers, Inga, Mensing, Hartwig, Mueller-Ladner, Ulf, Pfeiffer, Christiane, Riemekasten, Gabriela, Sardy, Miklos, Schmalzing, Marc, Sunderkoetter, Cord, Susok, Laura, Tarner, Ingo H., Vaith, Peter, Worm, Margitta, Wozel, Gottfried, Zeidler, Gabriele, and Hunzelmann, Nicolas

Abstract

Background Systemic sclerosis (SSc)-overlap syndromes are a very heterogeneous and remarkable subgroup of SSc-patients, who present at least two connective tissue diseases (CTD) at the same time, usually with a specific autoantibody status. Objectives To determine whether patients, classified as overlap syndromes, show a disease course different from patients with limited SSc (lcSSc) or diffuse cutaneous SSc (dcSSc). Methods The data of 3240 prospectively included patients, registered in the database of the German Network for Systemic Scleroderma and followed between 2003 and 2013, were analysed. Results Among 3240 registered patients, 10% were diagnosed as SSc-overlap syndrome. Of these, 82.5% were female. SSc-overlap patients had a mean age of 48 +/- 1.2 years and carried significantly more often 'other antibodies' (68.0%; p<0.0001), including anti-U1RNP, -PmScl, -Ro, -La, as well as anti-Jo-1 and -Ku antibodies. These patients developed musculoskeletal involvement earlier and more frequently (62.5%) than patients diagnosed as lcSSc (32.2%) or dcSSc (43.3%) (p<0.0001). The onset of lung fibrosis and heart involvement in SSc-overlap patients was significantly earlier than in patients with lcSSc and occurred later than in patients with dcSSc. Oesophagus, kidney and PH progression was similar to lcSSc patients, whereas dcSSc patients had a significantly earlier onset. Conclusions These data support the concept that SSc-overlap syndromes should be regarded as a separate SSc subset, distinct from lcSSc and dcSSc, due to a different progression of the disease, different proportional distribution of specific autoantibodies, and of different organ involvement.

Published
2015

20. Disease progression in systemic sclerosis-overlap syndrome is significantly different from limited and diffuse cutaneous systemic sclerosis

Author

Moinzadeh, Pia, Aberer, Elisabeth, Ahmadi-Simab, Keihan, Blank, Norbert, Distler, Joerg H. W., Fierlbeck, Gerhard, Genth, Ekkehard, Guenther, Claudia, Hein, Ruediger, Henes, Joerg, Herich, Lena, Herrgott, Ilka, Koetter, Ina, Kreuter, Alexander, Krieg, Thomas, Kuhr, Kathrin, Lorenz, Hanns-Martin, Meier, Florian, Melchers, Inga, Mensing, Hartwig, Mueller-Ladner, Ulf, Pfeiffer, Christiane, Riemekasten, Gabriela, Sardy, Miklos, Schmalzing, Marc, Sunderkoetter, Cord, Susok, Laura, Tarner, Ingo H., Vaith, Peter, Worm, Margitta, Wozel, Gottfried, Zeidler, Gabriele, Hunzelmann, Nicolas, Moinzadeh, Pia, Aberer, Elisabeth, Ahmadi-Simab, Keihan, Blank, Norbert, Distler, Joerg H. W., Fierlbeck, Gerhard, Genth, Ekkehard, Guenther, Claudia, Hein, Ruediger, Henes, Joerg, Herich, Lena, Herrgott, Ilka, Koetter, Ina, Kreuter, Alexander, Krieg, Thomas, Kuhr, Kathrin, Lorenz, Hanns-Martin, Meier, Florian, Melchers, Inga, Mensing, Hartwig, Mueller-Ladner, Ulf, Pfeiffer, Christiane, Riemekasten, Gabriela, Sardy, Miklos, Schmalzing, Marc, Sunderkoetter, Cord, Susok, Laura, Tarner, Ingo H., Vaith, Peter, Worm, Margitta, Wozel, Gottfried, Zeidler, Gabriele, and Hunzelmann, Nicolas

Abstract

Background Systemic sclerosis (SSc)-overlap syndromes are a very heterogeneous and remarkable subgroup of SSc-patients, who present at least two connective tissue diseases (CTD) at the same time, usually with a specific autoantibody status. Objectives To determine whether patients, classified as overlap syndromes, show a disease course different from patients with limited SSc (lcSSc) or diffuse cutaneous SSc (dcSSc). Methods The data of 3240 prospectively included patients, registered in the database of the German Network for Systemic Scleroderma and followed between 2003 and 2013, were analysed. Results Among 3240 registered patients, 10% were diagnosed as SSc-overlap syndrome. Of these, 82.5% were female. SSc-overlap patients had a mean age of 48 +/- 1.2 years and carried significantly more often 'other antibodies' (68.0%; p<0.0001), including anti-U1RNP, -PmScl, -Ro, -La, as well as anti-Jo-1 and -Ku antibodies. These patients developed musculoskeletal involvement earlier and more frequently (62.5%) than patients diagnosed as lcSSc (32.2%) or dcSSc (43.3%) (p<0.0001). The onset of lung fibrosis and heart involvement in SSc-overlap patients was significantly earlier than in patients with lcSSc and occurred later than in patients with dcSSc. Oesophagus, kidney and PH progression was similar to lcSSc patients, whereas dcSSc patients had a significantly earlier onset. Conclusions These data support the concept that SSc-overlap syndromes should be regarded as a separate SSc subset, distinct from lcSSc and dcSSc, due to a different progression of the disease, different proportional distribution of specific autoantibodies, and of different organ involvement.

Published
2015

21. S2k Guidelines for the treatment of pemphigus vulgaris/foliaceus and bullous pemphigoid

Author

Eming, Ruediger, Sticherling, Michael, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Pfeiffer, Christiane, Schuster, Volker, Zillikens, Detlef, Goebeler, Matthias, Hertl, Michael, Nast, Alexander, Orzechowski, Hans-Dieter, Sardy, Miklos, Schmidt, Enno, Sitaru, Cassian, Sporbeck, Birte, Worm, Margitta, Eming, Ruediger, Sticherling, Michael, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Pfeiffer, Christiane, Schuster, Volker, Zillikens, Detlef, Goebeler, Matthias, Hertl, Michael, Nast, Alexander, Orzechowski, Hans-Dieter, Sardy, Miklos, Schmidt, Enno, Sitaru, Cassian, Sporbeck, Birte, and Worm, Margitta

Published
2015

22. S2k guideline for the diagnosis of pemphigus vulgaris/foliaceus and bullous pemphigoid

Author

Schmidt, Enno, Goebeler, Matthias, Hertl, Michael, Sardy, Miklos, Sitaru, Cassian, Eming, Ruediger, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Orzechowski, Hans-Dieter, Pfeiffer, Christiane, Schuster, Volker, Sporbeck, Birte, Sticherling, Michael, Worm, Margitta, Zillikens, Detlef, Nast, Alexander, Schmidt, Enno, Goebeler, Matthias, Hertl, Michael, Sardy, Miklos, Sitaru, Cassian, Eming, Ruediger, Hofmann, Silke C., Hunzelmann, Nicolas, Kern, Johannes S., Kramer, Harald, Orzechowski, Hans-Dieter, Pfeiffer, Christiane, Schuster, Volker, Sporbeck, Birte, Sticherling, Michael, Worm, Margitta, Zillikens, Detlef, and Nast, Alexander

Published
2015

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