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7. Platin-related Hearing Loss: Further Results from PanCareLIFE

Author

Parfitt, R, Matulat, P, Byrne, J, Langer, T, Deuster, D, Hesping, A, Clemens, E, Kaatsch, P, Grabow, D, O'Brien, K, Kaiser, M, Spix, C, Kremer, LC, van Dulmen-den Broeder, E, Calaminus, G, Baust, K, Kuehni, C, Weiss, A, Strebel, S, Kuonen, R, Elsner, S, Haupt, R, Garré, ML, Kepak, T, Kapakova, K, Falck Winther, J, Kenborg, L, Rechnitzer, C, Hasle, H, Kruseova, J, Luks, A, Lackner, H, Beilack, S, Hecker-Nolting, S, Beck, JD, van den Heuvel-Eibrink, M, Zolk, O, am Zehnhoff-Dinnesen, A, PanCareLIFE Consortium, Parfitt, R, Matulat, P, Byrne, J, Langer, T, Deuster, D, Hesping, A, Clemens, E, Kaatsch, P, Grabow, D, O'Brien, K, Kaiser, M, Spix, C, Kremer, LC, van Dulmen-den Broeder, E, Calaminus, G, Baust, K, Kuehni, C, Weiss, A, Strebel, S, Kuonen, R, Elsner, S, Haupt, R, Garré, ML, Kepak, T, Kapakova, K, Falck Winther, J, Kenborg, L, Rechnitzer, C, Hasle, H, Kruseova, J, Luks, A, Lackner, H, Beilack, S, Hecker-Nolting, S, Beck, JD, van den Heuvel-Eibrink, M, Zolk, O, am Zehnhoff-Dinnesen, A, and PanCareLIFE Consortium

Abstract

Background: Cisplatin and Carboplatin are widely-used in paediatric cancer treatment. Sensorineural hearing loss (SNHL) is one long-term side-effect. This study utilises a larger sample than previous research in order to investigate risk-factors for platin-related ototoxicity.Material and methods: Retrospective audiological and treatment data of 997 children and adolescents were gathered with the involvement of 18 pan-European institutions in 7 different countries as part of the PanCareLIFE consortium. Prior hearing loss was excluded. Conductive hearing losses were excluded where identified.Results: Prevalence rates of clinically-significant hearing loss (=> 2b Münster Classification) after treatment were 49 % (Cisplatin) and 15 % (Carboplatin). Where Cisplatin was administered prior to Carboplatin, prevalence rose to 76 %. Frequencies in the high and extended high-frequency range were predominantly affected, with mean threholds between 25-35 dB HL. Mean thresholds at frequencies below 3 kHz remained lower than 20 dB HL. No significant air-bone gap was apparent.50 % of clinically-significant hearing losses began within 3 years of start of treatment (Kaplan-Meier analysis). No significant difference in time-to-onset at different frequencies within the standard range was found. Further analyses, including multifactorial analysis to account for platin doses, presence of cranial radiotherapy, age and date of diagnosis will be conducted.Discussion: Analysis of this large sample was able to confirm the significant risk of SNHL posed by platin-based chemotherapeutics. Some quantitative and qualitative variation were present in this multi-centre retrospective dataset.Conclusion: This large sample confirms that platin-based chemotherapeutics, especially cisplatin, pose a significant risk of SNHL and underlines the necessity of audiological monitoring during and after end of chemotherapy.Acknowledgement: This work was supported by the PanCareLIFE consortium that has received

Published
2023

10. TCERG1L allelic variation is associated with cisplatin-induced hearing loss in childhood cancer, a PanCareLIFE study

Author

Meijer, A, Diepstraten, FA, Langer, T, Broer, L, Domingo, IK, Clemens, E, Uitterlinden, AG, de Vries, ACH, van Grotel, M, Vermeij, WP, Ozinga, RA, Binder, H, Byrne, J, van Dulmen-den Broeder, E, Garrè, ML, Grabow, D, Kaatsch, P, Kaiser, M, Kenborg, L, Falck-Winther, J, Rechnitzer, C, Hasle, H, Kepak, T, Kepakova, K, Tissing, WJE, van der Kooi, ALF, Kremer, LC, Kruseova, J, Pluijm, SMF, Kuehni, CF, van der Pal, H, Parfitt, R, Spix, C, Hesping, A, Deuster, D, Matulat, P, Calaminus, G, Hoetink, AE, Elsner, S, Gebauer, J, Haupt, R, Lackner, H, Blattmann, C, Neggers, SJCMM, Rassekh, SR, Wright, GEB, Brooks, B, Nagtegaal, AP, Drögemöller, BI, Ross, CJD, Bhavsar, AP, am Zehnhoff-Dinnesen, A, Carleton, BC, Zolk, O, van den Heuvel-Eibrink, M, Meijer, A, Diepstraten, FA, Langer, T, Broer, L, Domingo, IK, Clemens, E, Uitterlinden, AG, de Vries, ACH, van Grotel, M, Vermeij, WP, Ozinga, RA, Binder, H, Byrne, J, van Dulmen-den Broeder, E, Garrè, ML, Grabow, D, Kaatsch, P, Kaiser, M, Kenborg, L, Falck-Winther, J, Rechnitzer, C, Hasle, H, Kepak, T, Kepakova, K, Tissing, WJE, van der Kooi, ALF, Kremer, LC, Kruseova, J, Pluijm, SMF, Kuehni, CF, van der Pal, H, Parfitt, R, Spix, C, Hesping, A, Deuster, D, Matulat, P, Calaminus, G, Hoetink, AE, Elsner, S, Gebauer, J, Haupt, R, Lackner, H, Blattmann, C, Neggers, SJCMM, Rassekh, SR, Wright, GEB, Brooks, B, Nagtegaal, AP, Drögemöller, BI, Ross, CJD, Bhavsar, AP, am Zehnhoff-Dinnesen, A, Carleton, BC, Zolk, O, and van den Heuvel-Eibrink, M

Abstract

Background: Ototoxicity (hearing loss, tinnitus and/or vertigo) is a serious adverse event of cisplatin treatment in children with cancer. The heterogeneity in ototoxicity occurrence after similar treatment suggests a role for genetic susceptibility. This study investigated the association between carriership of novel single nucleotide polymorphisms (SNPs) and cisplatin-induced hearing loss (CIHL) in childhood cancer patients.Material and methods: The discovery cohort included cisplatin treated, non-cranial irradiated pediatric cancer patients within the European PanCareLIFE (PCL) study (N=390). CIHL at end of cancer treatment was defined as Muenster grade >=2b, assessed by pure tone audiometry. DNA was genotyped using the Infinium© Global Screening Array. Logistic regression models were applied including age at diagnosis, sex, cisplatin total cumulative dose and principal components 1-4, assuming an additive effect of the minor allele. Replication of the findings was performed in two independent, similarly treated cohorts (N=192 and N=188). Functional validation experiments in cultured human HeLa cell lines were performed to determine the effect of knockdown of the SNPs nearest identified gene on cisplatin-induced toxicity.Results: In the PCL discovery cohort, 8 SNPs reached a suggestive significance of P<1.0x10-5. One variant (rs893507) within the TCERG1L gene showed evidence of replication (P=0.01) in the Canadian first replication cohort. Analysis in the PCL second replication cohort confirmed this finding (P=1.0x10-4). The combined analysis showed that carriership of the C-allele of this newly discovered variant increases the odds of CIHL with 3.11-fold (P=5.3x10-10, 95% CI 2.2-4.5). Modulating TCERG1L expression significantly altered cell viability in response to cisplatin treatment, where TCERG1L overexpression and silencing protected and sensitized cells to cisplatin toxicity, respectively.Discussion: Children with cancer who carry a variant in the TCERG1L g

Published
2021

11. TCERG1L allelic variation is associated with cisplatin-induced hearing loss in childhood cancer, a PanCareLIFE study

Author

Meijer, A. J.M., Diepstraten, F. A., Langer, T., Broer, L., Domingo, I. K., Clemens, E., Uitterlinden, A. G., de Vries, A. C.H., van Grotel, M., Vermeij, W. P., Ozinga, R. A., Binder, H., Byrne, J., van Dulmen-den Broeder, E., Garrè, M. L., Grabow, D., Kaatsch, P., Kaiser, M., Kenborg, L., Winther, J. F., Rechnitzer, C., Hasle, H., Kepak, T., Kepakova, K., Tissing, W. J.E., van der Kooi, A. L.F., Kremer, L. C.M., Kruseova, J., Pluijm, S. M.F., Kuehni, C. E., van der Pal, H. J.H., Parfitt, R., Spix, C., Tillmanns, A., Deuster, D., Matulat, P., Calaminus, G., Hoetink, A. E., Elsner, S., Gebauer, J., Haupt, R., Lackner, H., Blattmann, C., Neggers, S. J.C.M.M., Rassekh, S. R., Wright, G. E.B., Brooks, B., Nagtegaal, A. P., Drögemöller, B. I., Ross, C. J.D., Meijer, A. J.M., Diepstraten, F. A., Langer, T., Broer, L., Domingo, I. K., Clemens, E., Uitterlinden, A. G., de Vries, A. C.H., van Grotel, M., Vermeij, W. P., Ozinga, R. A., Binder, H., Byrne, J., van Dulmen-den Broeder, E., Garrè, M. L., Grabow, D., Kaatsch, P., Kaiser, M., Kenborg, L., Winther, J. F., Rechnitzer, C., Hasle, H., Kepak, T., Kepakova, K., Tissing, W. J.E., van der Kooi, A. L.F., Kremer, L. C.M., Kruseova, J., Pluijm, S. M.F., Kuehni, C. E., van der Pal, H. J.H., Parfitt, R., Spix, C., Tillmanns, A., Deuster, D., Matulat, P., Calaminus, G., Hoetink, A. E., Elsner, S., Gebauer, J., Haupt, R., Lackner, H., Blattmann, C., Neggers, S. J.C.M.M., Rassekh, S. R., Wright, G. E.B., Brooks, B., Nagtegaal, A. P., Drögemöller, B. I., and Ross, C. J.D.

Abstract

In children with cancer, the heterogeneity in ototoxicity occurrence after similar treatment suggests a role for genetic susceptibility. Using a genome-wide association study (GWAS) approach, we identified a genetic variant in TCERG1L (rs893507) to be associated with hearing loss in 390 non-cranial irradiated, cisplatin-treated children with cancer. These results were replicated in two independent, similarly treated cohorts (n = 192 and 188, respectively) (combined cohort: P = 5.3 × 10−10, OR 3.11, 95% CI 2.2–4.5). Modulating TCERG1L expression in cultured human cells revealed significantly altered cellular responses to cisplatin-induced cytokine secretion and toxicity. These results contribute to insights into the genetic and pathophysiological basis of cisplatin-induced ototoxicity.

Published
2021

12. Association of candidate pharmacogenetic markers with platinum-induced ototoxicity: PanCareLIFE dataset

Author

Langer, T. (Thomas), Clemens, E. (Eva), Broer, L. (Linda), Maier, L. (Lara), Uitterlinden, A.G. (André), Vries, A.C.H. (Andrica) de, Grotel, M. (Martine) van, Pluijm, S.F.M. (Saskia F.M.), Binder, H. (Harald), Mayer, B. (Benjamin), von dem Knesebeck, A. (Annika), Byrne, J. (Julianne), Dulmen-den Broeder, E. (Eline) van, Crocco, M. (Marco), Grabow, D. (Desiree), Kaatsch, P. (Peter), Kaiser, M. (Melanie), Spix, C. (Claudia), Kenborg, L. (Line), Winther, J.F. (Jeanette F.), Rechnitzer, C. (Catherine), Hasle, H. (Henrik), Kepak, T. (Tomas), Kooi, A.L.F. (Anne-Lotte) van der, Kremer, L.C.M. (Leontien), Kruseova, J. (Jarmila), Bielack, S. (Stefan), Sorg, B. (Benjamin), Hecker-Nolting, S. (Stefanie), Kuehni, C. (Claudia), Ansari, M. (Marc), Kompis, M. (Martin), van der Pal, H.J. (Heleen J.), Parfitt, R. (Ross), Deuster, D. (Dirk), Matulat, P. (Peter), Tillmanns, A. (Amelie), Tissing, W.J.E. (Wim), Beck, J.D. (Jörn D.), Elsner, S. (Susanne), am Zehnhoff-Dinnesen, A. (Antoinette), Heuvel-Eibrink, M.M. (Marry) van den, Zolk, O. (Oliver), Langer, T. (Thomas), Clemens, E. (Eva), Broer, L. (Linda), Maier, L. (Lara), Uitterlinden, A.G. (André), Vries, A.C.H. (Andrica) de, Grotel, M. (Martine) van, Pluijm, S.F.M. (Saskia F.M.), Binder, H. (Harald), Mayer, B. (Benjamin), von dem Knesebeck, A. (Annika), Byrne, J. (Julianne), Dulmen-den Broeder, E. (Eline) van, Crocco, M. (Marco), Grabow, D. (Desiree), Kaatsch, P. (Peter), Kaiser, M. (Melanie), Spix, C. (Claudia), Kenborg, L. (Line), Winther, J.F. (Jeanette F.), Rechnitzer, C. (Catherine), Hasle, H. (Henrik), Kepak, T. (Tomas), Kooi, A.L.F. (Anne-Lotte) van der, Kremer, L.C.M. (Leontien), Kruseova, J. (Jarmila), Bielack, S. (Stefan), Sorg, B. (Benjamin), Hecker-Nolting, S. (Stefanie), Kuehni, C. (Claudia), Ansari, M. (Marc), Kompis, M. (Martin), van der Pal, H.J. (Heleen J.), Parfitt, R. (Ross), Deuster, D. (Dirk), Matulat, P. (Peter), Tillmanns, A. (Amelie), Tissing, W.J.E. (Wim), Beck, J.D. (Jörn D.), Elsner, S. (Susanne), am Zehnhoff-Dinnesen, A. (Antoinette), Heuvel-Eibrink, M.M. (Marry) van den, and Zolk, O. (Oliver)

Abstract

Genetic association studies suggest a genetic predisposition for cisplatin-induced ototoxicity. Among other candidate genes, thiopurine methyltransferase (TPMT) is considered a critical gene for susceptibility to cisplatin-induced hearing loss in a pharmacogenetic guideline. The PanCareLIFE cross-sectional cohort study evaluated the genetic associations in a large pan-European population and assessed the diagnostic accuracy of the genetic markers. 1,112 pediatric cancer survivors who had provided biomaterial for genotyping were screened for participation in the pharmacogenetic association study. 900 participants qualified for inclusion. Based on the assessment of original audiograms, patients were assigned to three phenotype categories: no, minor, and clinically relevant hearing loss. Fourteen variants in eleven candidate genes (ABCC3, OTOS, TPMT, SLC22A2, NFE2L2, SLC16A5, LRP2, GSTP1, SOD2, WFS1, and ACYP2) were genotyped. The genotype and phenotype data represent a resource for conducting meta-analyses to derive a more precise pooled estimate of the effects of genes on the risk of hearing loss due to platinum treatment.

Published
2020
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13. Association of candidate pharmacogenetic markers with platinum-induced ototoxicity: PanCareLIFE dataset

Author

Langer, T, Clemens, Eva, Broer, Linda, Maier, L, Uitterlinden, André, Vries, ACH, van Grotel, Martine, Pluijm, Saskia F.M., Binder, H, Mayer, Benjamin, von dem Knesebeck, A, Byrne, J, van Dulmen-den Broeder, E, Crocco, M, Grabow, D, Kaatsch, P, Kaiser, M, Spix, C, Kenborg, L, Winther, JF, Rechnitzer, C, Hasle, H, Kepak, T, Kooi, Anne-Lotte, Kremer, LC, Kruseova, J, Bielack, S, Sorg, B, Hecker-Nolting, S, Kuehni, CE, Ansari, M, Kompis, M, van der Pal, HJ, Parfitt, R, Deuster, D, Matulat, P, Tillmanns, A, Tissing, WJ, Beck, JD, Elsner, S, am Zehnhoff-Dinnesen, A, Eibrink, Marry, Zolk, O, Langer, T, Clemens, Eva, Broer, Linda, Maier, L, Uitterlinden, André, Vries, ACH, van Grotel, Martine, Pluijm, Saskia F.M., Binder, H, Mayer, Benjamin, von dem Knesebeck, A, Byrne, J, van Dulmen-den Broeder, E, Crocco, M, Grabow, D, Kaatsch, P, Kaiser, M, Spix, C, Kenborg, L, Winther, JF, Rechnitzer, C, Hasle, H, Kepak, T, Kooi, Anne-Lotte, Kremer, LC, Kruseova, J, Bielack, S, Sorg, B, Hecker-Nolting, S, Kuehni, CE, Ansari, M, Kompis, M, van der Pal, HJ, Parfitt, R, Deuster, D, Matulat, P, Tillmanns, A, Tissing, WJ, Beck, JD, Elsner, S, am Zehnhoff-Dinnesen, A, Eibrink, Marry, and Zolk, O

Published
2020

16. Confirmation of genetic risk markers of platinum-induced ototoxicity

Author

Tillmanns, A, Parfitt, R, Matulat, P, Abdel-Kahaar, E, Maier, L, Zolk, O, Elsner, S, Wolschon, EM, Kuehni, CE, Kuonen, R, Weiss, A, Garré, ML, Kepak, T, Kepakova, K, Kruseova, J, Luks, A, Falck Winther, J, Kenborg, L, Lackner, H, Bielack, S, van den Heuvel-Eibrink, M, Calaminus, G, Baust, K, Beck, J, Kremer, L, Clemens, E, Langer, T, am Zehnhoff-Dinnesen, A, and PanCareLIFE consortium

Subjects
ddc: 610
Abstract

Background: Platinum compounds such as cisplatin or carboplatin are potent antineoplastic agents widely used for a variety of cancer types. Unfortunately, their use leads to dose-limiting side effects such as ototoxicity. Our study aimed at investigating the predictive value of 11 candidate genetic markers in a large non-selected pediatric population of cancer survivors who had been treated with cisplatin and/or carboplatin.Materials and Methods: As a part of the PanCareLIFE study, the ototoxicity study included 2,696 survivors from 7 European countries treated with cisplatin and/or carboplatin for childhood cancer, resulting in the largest clinical European cohort assembled for this late-effect study. Hearing loss was audiologically classified using the Münster Classification. Three groups were defined, i.e., no hearing loss, minor hearing loss, and clinically relevant hearing loss. Patients were genotyped for single nucleotide polymorphisms (SNPs) in 7 candidate genes. Genetic association analyses were performed considering non-genetic covariates.Results: 900 patients were included in the final genetic analysis. Multinomial logistic regression was performed to model the relationship between the predictors and membership in the hearing loss group. The model explained 25% of the variance in hearing loss and correctly classified 58% of cases. Significant unique contributions were made by SLC22A2 rs316019 (P=0.017), age at the start of platinum treatment (P=1.46x10-17), cranial radiation (P=5.42x10-6), and the cumulative dose of cisplatin (P=5.86x10-19). Addition of the rs316019 genetic marker to the non-genetic risk factors (age, dose, cranial radiation) improved the area under the ROC curve only marginally (0.731 vs. 0.730).Discussion: Our study confirmed one potential genetic marker, rs316019 in SLC22A2. Its predictive value, however, is low.Conclusion: Due to the heterogeneity of results from genetic association studies performed so far, the evidence seems not yet sufficient to recommend screening for specific markers. Advances in the understanding of the pathophysiologic mechanisms of cisplatin-induced ototoxicity, as well as future genome-wide association studies, may help identify suitable genetic markers.Acknowledgement: This work was supported by the PanCareLIFE project that has received funding from the European Union's Seventh Framework Programme for research, technological development and demonstration under grant agreement no. 602030.

Published
2019

17. Platin treatment and hearing loss: initial audiological results from PanCareLIFE

Author

Parfitt, R, Tillmanns, A, Matulat, P, Deuster, D, Elsner, S, Wolschon, EM, Kuehni, CE, Kuonen, R, Weiss, A, Garré, ML, Kepak, T, Kepakova, K, Kruseova, J, Luks, A, Falck Winther, J, Kenborg, L, Lackner, H, Bielack, S, van den Heuvel-Eibrink, M, Calaminus, G, Baust, K, Beck, J, Kremer, L, Clemens, E, Langer, T, Zolk, O, and am Zehnhoff-Dinnesen, A

Subjects
ddc: 610
Abstract

Background: Cisplatin and carboplatin are widely used in paediatric cancer treatment. Cisplatin especially can have long-term side effects, including sensorineural hearing loss. The aim of this study is to define the risk factors for platin-related ototoxicity.Materials and Methods: As part of the PanCareLIFE consortium, we gathered audiological data from 13 pan-European clinics. Eligible patients were 20 dB HL at any frequency).A total of 2,696 patients with 10,320 audiograms from various stages of cancer treatment were obtained. Audiometric data were quality-checked and classified (Münster and SIOP classifications) and 736 patients with sufficient data were phenotyped. A logistic regression investigated the likelihood of developing a hearing loss >=Münster 2b (thresholds >40 dB HL at >=4 kHz) after treatment given age, gender, cisplatin dose and cranial irradiation.Results: 48.2% of 1,385 patients with a post-treatment audiogram had clinically-relevant hearing loss (defined as >=Münster 2b) after platin treatment.Children 15 years (odds ratio 2.7, 95% CI 1.5-4.9, p=0.0006). Patients with a cumulative cisplatin dose >450 mg/m2 were more likely to develop hearing loss than those treated with carboplatin alone (OR 12.5, 95% CI 6.8-23.0, p=3.7x10-16). Treatment with cranial irradiation was more likely to lead to hearing loss than without (OR 4.5, 95% CI 3.0-6.7, p=7.2x10-13).Discussion: This is the first study of platin ototoxicity with such a large sample size. The results support tendencies found in previous studies with smaller groups. The high risk groups identified here must be monitored regularly for ototoxicity. Further detailed analyses into audiological changes and possible pharmacogenetic confounders are planned.Conclusion: 48% of patients treated with cisplatin develop clinically-relevant hearing loss. Age

Published
2019

18. Kardiovaskuläre und endokrine Parameter bei Jugendlichen aus künstlicher Zeugung (ICSI)

Author

Eisemann, N, Elsner, S, Sonntag, B, Ludwig, AK, Ludwig, M, and Katalinic, A

Subjects
ddc: 610, Intrazytoplasmatische Spermieninjektion, Kardiovaskuläre Krankheiten, 610 Medical sciences, Medicine, Hormone
Abstract

Einleitung: Bei unerfülltem Kinderwunsch ist die häufigste Methode der künstlichen Befruchtung die Intrazytoplasmatische Spermieninjektion (ICSI). Bei durch ICSI gezeugten Kindern ist das Risiko für Fehlbildungen und Schwangerschaftskomplikationen erhöht. Mögliche Ursachen[zum vollständigen Text gelangen Sie über die oben angegebene URL], 64. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie e.V. (GMDS)

Published
2019
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19. Abszess im Adduktorenkanal nach TUR-Prostata

Author

Linges, M., Milovanovic, L., Elsner, S., and Kleinschmidt, K.

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Einleitung: Wir berichten über eine seltene Komplikation nach TUR-Prostata. Fallbericht: Zwei Wochen postoperativ berichtete der Patient über suprapubische Schmerzen mit Ausstrahlung in den rechten Oberschenkel. Das CRP war mit 16 mg/dl erhöht, Urinstatus und Urinkultur unauffällig.[zum vollständigen Text gelangen Sie über die oben angegebene URL], 60. Jahrestagung der Südwestdeutschen Gesellschaft für Urologie e.V.

Published
2019
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20. Fallbericht: Die emphysematöse Pyelonephritis, eine seltene lebensbedrohliche Erkrankung

Author

Linges, M., Elsner, S., and Kleinschmidt, K.

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Einleitung: Die emphysematöse Pyelonephritis ist eine seltene Erkrankung mit einer hohen Mortalität von 8,7-40%. Der häufigste prädisponierende Faktor ist ein unzureichend eingestellter Diabetes mellitus. Die häufigsten ursächlichen Erreger sind E. coli und Klebsiella,[zum vollständigen Text gelangen Sie über die oben angegebene URL], 60. Jahrestagung der Südwestdeutschen Gesellschaft für Urologie e.V.

Published
2019
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27. P4386Sleep disordered breathing (SDB) increases the risk of heart failure decompensation: clinical factors and bioelectrical impedance analysis

Author

Bekfani, T., primary, Schoebel, C.H., additional, Pietrock, C.H., additional, Valentova, M., additional, Ebner, N., additional, Elsner, S., additional, Sandek, A., additional, Doehner, W., additional, Noutsias, M., additional, Schulze, P.C., additional, Anker, S.D., additional, and Von Haehling, S., additional

Published
2017
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28. Harninkontinenz bei Frauen - (k)ein Thema für Hausärztinnen/Hausärzte?

Author

Elsner, S., Jürgensen, M., Faust, E., Kold, M.L., Schreiber Pedersen, L., Lückert, J., Niesel, A., Rudnicki, P.M., and Waldmann, A.

Subjects
ddc: 610, Unterversorgung, 610 Medical sciences, Medicine, Gesprächsbarrieren, Harninkontinenz
Abstract

Hintergrund: Viele Frauen sind zeitweise oder dauerhaft von Harninkontinenz betroffen und fühlen sich dadurch in ihrer Lebensqualität beeinträchtigt. Die Vermutung liegt nahe, dass dieses Thema in Hausarztpraxen alltäglich ist. Studienergebnisse zeigen, dass dem nicht so ist. [zum vollständigen Text gelangen Sie über die oben angegebene URL], 49. Kongress für Allgemeinmedizin und Familienmedizin

Published
2015

29. Harninkontinenz bei Frauen – weit verbreitet und doch oft totgeschwiegen?

Author

Elsner, S, Jürgensen, M, Faust, E, Kold, ML, Schreiber Pedersen, L, Rudnicki, PM, and Waldmann, A

Subjects
ddc: 610, Arzt-Patienten Kommunikation, Tabuthema, 610 Medical sciences, Medicine, Harninkontinenz
Abstract

Hintergrund: Obwohl Harninkontinenz viele Frauen aller Altersklassen betrifft, weisen quantitative Studien darauf hin, dass dieses Thema in Hausarztpraxen eher selten angesprochen wird. Eine Behandlung von Harninkontinenzsymptomen kann sowohl im hausärztlichen, gynäkologischen oder urologischen[zum vollständigen Text gelangen Sie über die oben angegebene URL], 49. Kongress für Allgemeinmedizin und Familienmedizin

Published
2015
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31. Retest-Reliabilität eines Fragebogens für Hausärzte zur Harninkontinenz

Author

Faust, E, Juergensen, M, Elsner, S, Niesel, A, and Waldmann, A

Subjects
ddc: 610, Retestvalidität, validierter Fragebogen, 610 Medical sciences, Medicine, Harninkontinenz
Abstract

Hintergrund: In einer derzeit durchgeführten Querschnittstudie (Lower Urinary Tract Symptoms, LUTS) werden 929 niedergelassene Hausärzte und Allgemeinmediziner der Fehmarnbeltregion in Deutschland und Dänemark zum Thema Urininkontinenz (UI) befragt. Der eingesetzte Fragebogen wurde auf[for full text, please go to the a.m. URL], 48. Kongress für Allgemeinmedizin und Familienmedizin

Published
2014
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34. Alterations in the expression patterns of Akt and p-Akt in the cochlea of the guinea pig after intratympanic application of gentamicin

Author

Heinrich, UR, Brieger, J, Elsner, S, Schmidtmann, I, Mann, WJ, and Helling, K

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Objective: The therapeutic application of gentamicin generally induces numerous different, partly contrary, biochemical processes. Besides apoptosis and resulting cell death, there is some evidence for the induction of cell protecting mechanisms in which proteine kinase B (Akt) is involved. The aim [for full text, please go to the a.m. URL], 84th Annual Meeting of the German Society of Oto-Rhino-Laryngology, Head and Neck Surgery

Published
2013
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36. Gentamicin verändert das Expressionsmuster der endothelialen und induzierbaren Stickstoffmonoxidsynthase in der Kochlea des Meerschweinchens

Author

Fischer, I, Heinrich, UR, Bastian, A, Grether, B, Elsner, S, Brieger, J, Mann, W, and Helling, K

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Einleitung: Die intratympanale Applikation von Gentamicin wird zur Behandlung beim Morbus Ménière eingesetzt. Neben der gezielten Schädigung vestibulärer Strukturen kommt es zu ungewollten pathophysiologischen Prozessen in der Kochlea, die u.a. auf einem Anstieg von Stickstoffmonoxid[for full text, please go to the a.m. URL], 81. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie

Published
2010
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44. Effect of combination therapy with all-trans-retinoic acid and recombinant human granulocyte colony-stimulating factor in patients with myelodysplastic syndromes

Author

Ganser A, Seipelt G, Verbeek W, Oliver Ottmann, Maurer A, Kolbe K, Hess U, Elsner S, Reutzel R, and Wörmann B

Subjects
Adult, Aged, 80 and over, Male, Neutrophils, Platelet Count, Anemia, Refractory, Pilot Projects, Tretinoin, Middle Aged, Drug Administration Schedule, Leukocyte Count, Bone Marrow, Granulocyte Colony-Stimulating Factor, Cytokines, Humans, Drug Therapy, Combination, Female, Aged
Abstract

Since all-trans retinoic acid (ATRA) and granulocyte colony-stimulating factor (G-CSF) not only enhance proliferation and differentiation of normal myeloid cells but also synergistically promote the differentiation of myeloid leukemic blast cells in vitro, we have started a pilot study of combined treatment with ATRA and G-CSF in patients with myelodysplastic syndrome, to analyze the effect of these drugs on hematopoietic differentiation. ATRA was given at 45 mg/m2/day p.o. from week 1-12 and G-CSF at 5 micrograms/kg/day s.c. from week 5-12 with dose modifications according to the absolute neutrophil counts (ANC). A total of 15 patients, predominantly with refractory anemia, were treated. During initial ATRA therapy, a bilineage response with increases of both ANC and platelet counts occurred in three patients. During combined ATRA/G-CSF therapy, ANC increased in all patients, and platelets increased in three out of 14 evaluable patients. An increase in hemoglobin concentration and a decrease in transfusion requirements occurred in one patient each. In the bone marrow, the myeloid-to-erythroid ratio increased during ATRA treatment and remained increased during concomitant G-CSF administration, while the maturation index of myeloid cells increased only in response to ATRA therapy, but returned to baseline during ATRA/G-CSF treatment. Cytogenetic analysis demonstrated persistence of the abnormal clones in all patients. The number of circulating progenitor cells CFU-GM increased in all patients studied. Serum concentrations of the soluble TNF receptor and IL-2 receptor both increased, while TNF-alpha--already elevated prior to therapy--and soluble ICAM-1 concentrations did not significantly change. Adverse effects included dermatitis and cheilosis in most patients, and a drop in platelet counts related to G-CSF in one patient. The pilot study demonstrates that the combination treatment with ATRA/G-CSF is well tolerated, leading to normalization of ANC in most, and improvement of platelets and red blood cells in a subgroup of patients.

Published
1994

46. Evidenzbasierte Qualitätsindikatoren für die Schlaganfallbehandlung in Deutschland

Author

Heuschmann, P.U., primary, Biegler, M., additional, Busse, O., additional, Elsner, S., additional, Grau, A., additional, Hasenbein, U., additional, Hermanek, P., additional, Janzen, R.W.C., additional, Kolominsky-Rabas, P., additional, Kraywinkel, K., additional, Lowitzsch, K., additional, Misselwitz, B., additional, Nabavi, D.G., additional, Otten, K., additional, von Reutern, G., additional, Ringelstein, E.B., additional, Sander, D., additional, Pientka, L., additional, Wagner, M., additional, and Berger, K., additional

Published
2006
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48. Reply

Author

Stefan, N., primary, Elsner, S., additional, Schnaidt, M., additional, Wernet, D., additional, and Stumvoll, M., additional

Published
1999
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