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1. Association of Hospital Volume with Perioperative Mortality of Endovascular Repair of Complex Aortic Aneurysms: A Nationwide Cohort Study

Author

Alberga, Anna J., von Meijenfeldt, Gerdine C. I., Rastogi, Vinamr, de Bruin, Jorg L., Wever, Jan J., van Herwaarden, Joost A., Hamming, Jaap F., Hazenberg, Constantijn E. V. B., van Schaik, Jan, Mees, Barend M. E., van der Laan, Maarten J., Zeebregts, Clark J., Schurink, Geert W. H., Verhagen, Hence J. M., van den Akker, P. J., Akkersdijk, G. P., Akkersdijk, W. L., van Andringa de Kempenaer, M. G., Arts, C. H. P., Avontuur, A. M., Bakker, O. J., Balm, R., Barendregt, W. B., Bekken, J. A., Bender, M. H. M., Bendermacher, B. L. W., van den Berg, M., Beuk, R. J., Blankensteijn, J. D., Bode, A. S., Bodegom, M. E., van der Bogt, K. E. A., Boll, A. P. M., Booster, M. H., Borger van der Burg, B. L. S., de Borst, G. J., Bos-van Rossum, W. T. G. J., Bosma, J., Botman, J. M. J., Bouwman, L. H., Brehm, V., de Bruijn, M. T., de Bruin, J. L., Brummel, P., van Brussel, J. P., Buijk, S. E., Buimer, M. G., Buscher, H. C. J. L., Cancrinus, E., Castenmiller, P. H., Cazander, G., Cuypers, P. W. M., Daemen, J. H. C., Dawson, I., Dierikx, J. E., Dijkstra, M. L., Diks, J., Dinkelman, M. K., Dirven, M., Dolmans, D. E. J. G. J., van Dortmont, L. M. C., Drouven, J. W., van der Eb, M. M., Eefting, D., van Eijck, G. J. W. M., Elshof, J. W. M., Elsman, A. H. P., van der Elst, A., van Engeland, M. I. A., van Eps, G. S., Faber, M. J., de Fijter, W. M., Fioole, B., Fritschy, W. M., Fung Kon Jin, P. H. P., Geelkerken, R. H., van Gent, W. B., Glade, G. J., Govaert, B., Groenendijk, R. P. R., de Groot, H. G. W., van den Haak, R. F. F., de Haan, E. F. A., Hajer, G. F., Hamming, J. F., van Hattum, E. S., Hazenberg, C. E. V. B., Hedeman Joosten, P. P. A., Helleman, J. N., van der Hem, L. G., Hendriks, J. M., van Herwaarden, J. A., Heyligers, J. M. M., Hinnen, J. W., Hissink, R. J., Ho, G. H., den Hoed, P. T., Hoedt, M. T. C., van Hoek, F., Hoencamp, R., Hoffmann, W. H., Hoksbergen, A. W. J., Hollander, E. J. F., Huisman, L. C., Hulsebos, R. G., Huntjens, K. M. B., Idu, M. M., Jacobs, M. J. H. M., van der Jagt, M. F. P., Jansbeken, J. R. H., Janssen, R. J. L., Jiang, H. H. L., de Jong, S. C., Jongbloed-Winkel, T. A., Jongkind, V., Kapma, M. R., Keller, B. P. J. A., Jahrome, A. Khodadade, Kievit, J. K., Klemm, P. L., Klinkert, P., Koedam, N. A., Koelemaij, M. J. W., Kolkert, J. L. P., Koning, G. G., Koning, O. H. J., Konings, R., Krasznai, A. G., Kropman, R. H. J., Kruse, R. R., van der Laan, L., van der Laan, M. J., van Laanen, J. H. H., van Lammeren, G. W., Lamprou, D. A. A., Lardenoije, J. H. P., Lauret, G. J., Leenders, B. J. M., Legemate, D. A., Leij-Dekkers, V. J., Lemson, M. S., Lensvelt, M. M. A., Lijkwan, M. A., van der Linden, F. T. P. M., Lung, P. F. L., Loos, M. J. A., Loubert, M. C., van de Luijtgaarden, K. M., Mahmoud, D. E. A. K., Manshanden, C. G., Mat-Tens, E. C. J. L., Meerwaldt, R., Mees, B. M. E., Menting, T. P., Metz, R., de Mol van Otterloo, J. C. A., Molegraaf, M. J., Montauban van Swijn-Dregt, Y. C. A., Morak, M. J. M., van de Mortel, R. H. W., Mulder, W., Nagesser, S. K., Naves, C. C. L. M., Nederhoed, J. H., Nevenzel, A. M., de Nie, A. J., Nieuwenhuis, D. H., van Nieuwenhuizen, R. C., Nieuwenhui-Zen, J., Nio, D., Oomen, A. P. A., Oranen, B. I., Oskam, J., Palamba, H. W., Peppelenbosch, A. G., van Petersen, A. S., Petri, B. J., Pierie, M. E. N., Ploeg, A. J., Pol, R. A., Ponfoort, E. D., Poyck, P. P. C., Prent, A., ten Raa, S., Raymakers, J. T. F. J., Reichmann, B. L., Reijnen, M. M. P. J., de Ridder, J. A. M., Rijbroek, A., van Rijn, M. J. E., de Roo, R. A., Rouwet, E. V., Saleem, B. R., van Sambeek, M. R. H. M., Samyn, M. G., van't Sant, H. P., van Schaik, J., van Schaik, P. M., Scharn, D. M., Scheltinga, M. R. M., Schepers, A., Schlejen, P. M., Schlösser, F. J. V., Schol, F. P. G., Scholtes, V. P. W., Schouten, O., Schreve, M. A., Schurink, G. W. H., Sikkink, C. J. J. M., te Slaa, A., Smeets, H. J., Smeets, L., Smeets, R. R., de Smet, A. A. E. A., Smit, P. C., Smits, T. M., Snoeijs, M. G. J., Sondakh, A. O., Speijers, M. J., van der Steenhoven, T. J., van Sterkenburg, S. M. M., Stigter, D. A. A., Stokmans, R. A., Strating, R. P., Stultiëns, G. N. M., Sybrandy, J. E. M., Teijink, J. A. W., Telgenkamp, B. J., Testroote, M. J. G., Tha-in, T., The, R. M., Thijsse, W. J., Thomassen, I., Tielliu, I. F. J., van Tongeren, R. B. M., Toorop, R. J., Tournoij, E., Truijers, M., Türkcan, K., Nolthenius, R. P. Tutein, Ünlü, C., Vaes, R. H. D., Vahl, A. C., Veen, E. J., Veger, H. T. C., Veldman, M. G., Verhagen, H. J. M., Verhoeven, B. A. N., Vermeulen, C. F. W., Vermeulen, E. G. J., Vierhout, B. P., van der Vijver-Coppen, R. J., Visser, M. J. T., van der Vliet, J. A., van Vlijmen-van Keulen, C. J., van der Vorst, J. R., Vos, A. W. F., Vos, C. G., Vos, G. A., de Vos, B., Voûte, M. T., Vriens, B. H. R., Vriens, P. W. H. E., de Vries, D. K., de Vries, J. P. P. M., de Vries, M., de Vries, A. C., van der Waal, C., Waasdorp, E. J., de Vries, B. M. Wallis, van Walraven, L. A., van Wanroi, J. L., Warlé, M. C., van Weel, V., van Well, A. M. E., Welten, G. M. J. M., Wever, J. J., Wiersema, A. M., Wikkeling, O. R. M., Willaert, W. I. M., Wille, J., Willems, M. C. M., Willigendael, E. M., Wilschut, E. D., Wisselink, W., Witte, M. E., Wittens, C. H. A., Wong, C. Y., Yazar, O., Yeung, K. K., Zeebregts, C. J. A. M., van Zeeland, M. L. P., Physiology, ACS - Pulmonary hypertension & thrombosis, Surgery, ACS - Atherosclerosis & ischemic syndromes, ACS - Microcirculation, VU University medical center, AII - Inflammatory diseases, APH - Digital Health, Medical Biochemistry, ACS - Diabetes & metabolism, AII - Infectious diseases, and AGEM - Amsterdam Gastroenterology Endocrinology Metabolism

Subjects
volume-outcome, complex AAA, endovascular, mortality
Abstract

Objective: We evaluate nationwide perioperative outcomes of complex EVAR and assess the volume-outcome association of complex EVAR. Summary of Background Data: Endovascular treatment with fenestrated (FEVAR) or branched (BEVAR) endografts is progressively used for excluding complex aortic aneurysms (complex AAs). It is unclear if a volumeoutcome association exists in endovascular treatment of complex AAs (complex EVAR). Methods: All patients prospectively registered in the Dutch Surgical Aneurysm Audit who underwent complex EVAR (FEVAR or BEVAR) between January 2016 and January 2020 were included. The effect of annual hospital volume on perioperative mortality was examined using multivariable logistic regression analyses. Patients were stratified into quartiles based on annual hospital volume to determine hospital volume categories. Results: We included 694 patients (539 FEVAR patients, 155 BEVAR patients). Perioperative mortality following FEVAR was 4.5% and 5.2% following BEVAR. Postoperative complication rates were 30.1% and 48.7%, respectively. The first quartile hospitals performed

Published
2023
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2. Treatment Outcome Trends for Non-Ruptured Abdominal Aortic Aneurysms: A Nationwide Prospective Cohort Study

Author

Alberga, Anna J., Karthaus, Eleonora G., Wilschut, Janneke A., de Bruin, Jorg L., Akkersdijk, George P., Geelkerken, Robert H., Hamming, Jaap F., Wever, Jan J., Verhagen, Hence J. M., van den Akker, P. J., Akkersdijk, G. P., Akkersdijk, W. L., van Andringa de Kempenaer, M. G., Arts, C. H. P., Avontuur, A. M., Bakker, O. J., Balm, R., Barendregt, W. B., Bekken, J. A., Bender, M. H. M., Bendermacher, B. L. W., van den Berg, M., Beuk, R. J., Blankensteijn, J. D., Bode, A. S., Bodegom, M. E., van der Bogt, K. E. A., Boll, A. P. M., Booster, M. H., Borger van der Burg, B. L. S., de Borst, G. J., Bos-van Rossum, W. T. G. J., Bosma, J., Botman, J. M. J., Bouwman, L. H., Brehm, V., de Bruijn, M. T., de Bruin, J. L., Brummel, P., van Brussel, J. P., Buijk, S. E., Buimer, M. G., Buscher, H. C. J. L., Cancrinus, E., Castenmiller, P. H., Cazander, G., Cuypers, P. H. W. M., Daemen, J. H. C., Dawson, I., Dierikx, J. E., Dijkstra, M. L., Diks, J., Dinkelman, M. K., Dirven, M., Dolmans, D. E. J. G. J., van Dortmont, L. M. C., Drouven, J. W., van der Eb, M. M., Eefting, D., van Eijck, G. J. W. M., Elshof, J. W. M., Elsman, B. H. P., van der Elst, A., van Engeland, M. I. A., van Eps, G. S., Faber, M. J., de Fijter, W. M., Fioole, B., Fritschy, W. M., Jin, P. H. P. F. K., Geelkerken, R. H., van Gent, W. B., Glade, G. J., Govaert, B., Groenendijk, R. P. R., de Groot, H. G. W., van den Haak, R. F. F., de Haan, E. F. A., Hajer, G. F., Hamming, J. F., van Hattum, E. S., Hazenberg, C. E. V. B., Hedeman Joosten, P. P. H. A., Helleman, J. N., van der Hem, L. G., Hendriks, J. M., van Herwaarden, J. A., Heyligers, J. M. M., Hinnen, J. W., Hissink, R. J., Ho, G. H., den Hoed, P. T., Hoedt, M. T. C., van Hoek, F., Hoencamp, R., Hoffmann, W. H., Hoksbergen, A. W. J., Hollander, E. J. F., Huisman, L. C., Hulsebos, R. G., Huntjens, K. M. B., Idu, M. M., Jacobs, M. J. H. M., van der Jagt, M. F. P., Jansbeken, J. R. H., Janssen, R. J. L., Jiang, H. H. L., de Jong, S. C., Jongbloed-Winkel, T. A., Jongkind, V., Kapma, M. R., Keller, B. P. J. A., Jahrome, A. K., Kievit, J. K., Klemm, P. L., Klinkert, P., Koedam, N. A., Koelemaij, M. J. W., Kolkert, J. L. P., Koning, G. G., Koning, O. H. J., Konings, R., Krasznai, A. G., Kropman, R. H. J., Kruse, R. R., van der Laan, L., van der Laan, M. J., van Laanen, J. H. H., van Lammeren, G. W., Lamprou, D. A. A., Lardenoije, J. H. P., Lauret, G. J., Leenders, B. J. M., Legemate, D. A., Leijdekkers, V. J., Lemson, M. S., Lensvelt, M. M. A., Lijkwan, M. A., van der Linden, F. T. H. P. M., Lung, P. F. Liqui, Loos, M. J. A., Loubert, M. C., van de Luijtgaarden, K. M., Mahmoud, D. E. A. K., Manshanden, C. G., Mattens, E. C. J. L., Meerwaldt, R., Mees, B. M. E., Menting, T. P., Metz, R., de Mol van Otterloo, J. C. A., Molegraaf, M. J., Montauban van Swijndregt, Y. C. A., Morak, M. J. M., van de Mortel, R. H. W., Mulder, W., Nagesser, S. K., Naves, C. C. L. M., Nederhoed, J. H., Nevenzel, A. M., de Nie, A. J., Nieuwenhuis, D. H., van Nieuwenhuizen, R. C., Nieuwenhuizen, J., Nio, D., Oomen, A. P. A., Oranen, B. I., Oskam, J., Palamba, H. W., Peppelenbosch, A. G., van Petersen, A. S., Petri, B. J., Pierie, M. E. N., Ploeg, A. J., Pol, R. A., Ponfoort, E. D., Poyck, P. P. C., Prent, A., Raa, S. ten, Raymakers, J. T. F. J., Reichmann, B. L., Reijnen, M. M. P. J., de Ridder, J. A. M., Rijbroek, A., van Rijn, M. J. E., de Roo, R. A., Rouwet, E. V., Saleem, B. R., van Sambeek, M. R. H. M., Samyn, M. G., van ’t Sant, H. P., van Schaik, J., van Schaik, P. M., Scharn, D. M., Scheltinga, M. R. M., Schepers, A., Schlejen, P. M., Schlösser, F. J. V., Schol, F. P. G., Scholtes, V. P. W., Schouten, O., Schreve, M. A., Schurink, G. W. H., Sikkink, C. J. J. M., Slaa, A. te, Smeets, H. J., Smeets, L., Smeets, R. R., de Smet, A. A. E. A., Smit, P. C., Smits, T. M., Snoeijs, M. G. J., Sondakh, A. O., Speijers, M. J., van der Steenhoven, T. J., van Sterkenburg, S. M. M., Stigter, D. A. A., Stokmans, R. A., Strating, R. P., Stultiëns, G. N. M., Sybrandy, J. E. M., Teijink, J. A. W., Telgenkamp, B. J., Testroote, M. J. G., Tha-in, T., The, R. M., Thijsse, W. J., Thomassen, I., Tielliu, I. F. J., van Tongeren, R. B. M., Toorop, R. J., Tournoij, E., Truijers, M., Türkcan, K., Tutein Nolthenius, R. P., Ünlü, C., Vaes, R. H. D., Vahl, A. C., Veen, E. J., Veger, H. T. C., Veldman, M. G., Verhagen, H. J. M., Verhoeven, B. A. N., Vermeulen, C. F. W., Vermeulen, E. G. J., Vierhout, B. P., van der Vijver-Coppen, R. J., Visser, M. J. T., van der Vliet, J. A., van Vlijmen - van Keulen, C. J., van der Vorst, J. R., Vos, A. W. F., Vos, C. G., Vos, G. A., de Vos, B., Voûte, M. T., Vriens, B. H. R., Vriens, P. W. H. E., de Vries, D. K., de Vries, J. P. P. M., de Vries, M., de Vries, A. C., van der Waal, C., Waasdorp, E. J., Wallis de Vries, B. M., van Walraven, L. A., van Wanroi, J. L., Warlé, M. C., van Weel, V., van Well, A. M. E., Welten, G. M. J. M., Wever, J. J., Wiersema, A. M., Wikkeling, O. R. M., Willaert, W. I. M., Wille, J., Willems, M. C. M., Willigendael, E. M., Wilschut, E. D., Wisselink, W., Witte, M. E., Wittens, C. H. A., Wong, C. Y., Yazar, O., Yeung, K. K., Zeebregts, C. J. A. M., van Zeeland, M. L. P., ACS - Microcirculation, Anesthesiology, Physiology, ACS - Pulmonary hypertension & thrombosis, Surgery, ACS - Atherosclerosis & ischemic syndromes, VU University medical center, ACS - Diabetes & metabolism, TechMed Centre, Multi-Modality Medical Imaging, Medical Biochemistry, and AGEM - Amsterdam Gastroenterology Endocrinology Metabolism

Subjects
Male, Time Factors, Operative procedure, Vascular damage Radboud Institute for Health Sciences [Radboudumc 16], Risk Assessment, Blood Vessel Prosthesis Implantation, Postoperative Complications, Risk Factors, Humans, Hospital Mortality, Prospective Studies, Registries, Treatment outcome, Aged, Netherlands, Retrospective Studies, Aged, 80 and over, Endovascular Procedures, Quality of care, Middle Aged, Endovascular procedure, Abdominal aortic aneurysm, Surgery, Female, Trends, Cardiology and Cardiovascular Medicine, Aortic Aneurysm, Abdominal
Abstract

Contains fulltext : 251573.pdf (Publisher’s version ) (Open Access) OBJECTIVE: The Dutch Surgical Aneurysm Audit (DSAA) initiative was established in 2013 to monitor and improve nationwide outcomes of aortic aneurysm surgery. The objective of this study was to examine whether outcomes of surgery for intact abdominal aortic aneurysms (iAAA) have improved over time. METHODS: Patients who underwent primary repair of an iAAA by standard endovascular (EVAR) or open surgical repair (OSR) between 2014 and 2019 were selected from the DSAA for inclusion. The primary outcome was peri-operative mortality trend per year, stratified by OSR and EVAR. Secondary outcomes were trends per year in major complications, textbook outcome (TbO), and characteristics of treated patients. The trends per year were evaluated and reported in odds ratios per year. RESULTS: In this study, 11 624 patients (74.8%) underwent EVAR and 3 908 patients (25.2%) underwent OSR. For EVAR, after adjustment for confounding factors, there was no improvement in peri-operative mortality (aOR [adjusted odds ratio] 1.06, 95% CI 0.94 - 1.20), while major complications decreased (2014: 10.1%, 2019: 7.0%; aOR 0.91, 95% CI 0.88 - 0.95) and the TbO rate increased (2014: 68.1%, 2019: 80.9%; aOR 1.13, 95% CI 1.10 - 1.16). For OSR, the peri-operative mortality decreased (2014: 6.1%, 2019: 4.6%; aOR 0.89, 95% CI 0.82 - 0.98), as well as major complications (2014: 28.6%, 2019: 23.3%; aOR 0.95, 95% CI 0.91 - 0.99). Furthermore, the proportion of TbO increased (2014: 49.1%, 2019: 58.3%; aOR 1.05, 95% CI 1.01 - 1.10). In both the EVAR and OSR group, the proportion of patients with cardiac comorbidity increased. CONCLUSION: Since the establishment of this nationwide quality improvement initiative (DSAA), all outcomes of iAAA repair following EVAR and OSR have improved, except for peri-operative mortality following EVAR which remained unchanged.

Published
2022
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8. A phase II study of temozolomide in hormone-refractory prostate cancer.

Author

van Brussel, Jérôme P., Busstra, Martijn B., Lang, Margreet S., Catsburg, Tilly, Schröder, Fritz H., Mickisch, Gerald H., van Brussel, J P, Busstra, M B, Lang, M S, Catsburg, T, Schröder, F H, and Mickisch, G H

Subjects
PROSTATE cancer, PROSTATE diseases, CANCER treatment, CANCER patients, PROSTATE, CANCER pain, THERAPEUTICS
Abstract

Introduction: Hormone-refractory disseminated prostate cancer is a major oncological problem. Preclinical studies with temozolomide, an oral alkylating agent, in prostate cancer have shown encouraging results. In phase I studies the safety of temozolomide in non-prostate cancer patients has been demonstrated. Based on these results, a phase II study of temozolomide in patients with metastatic disease who had developed progressive symptomatic disease while on antiandrogen therapy, was initiated.Methods: A group of 18 patients started a 5-day temozolomide regimen, with a 28-day treatment cycle. Response parameters (prostate-specific antigen, bone scan, quality of life questionnaire) and toxicity (common toxicity criteria for international studies) were recorded at regular intervals.Results: Of the 18 patients, 16 were evaluable by completing two or three cycles. All patients developed progressive disease within two cycles, except one who had progressive disease at the end of cycle 3. Of the 16 evaluable patients, 11 developed new bone metastases (bone scan), 1 developed lung metastases, 4 had progressive disease as reflected by a 25% increase in serum PSA together with subjective progression, and 7 and 5 had progressive disease as reflected by decreased quality of life and increased pain score, respectively. Toxicity was limited to nausea and vomiting, which was effectively treated with antiemetic medication, and anemia and thrombocytopenia, which returned to normal values within 1 week.Discussion: Treatment with temozolomide was generally well tolerated, with occasionally moderate toxicity. As all patients developed progressive disease the results are rather discouraging. Temozolomide is ineffective for the treatment of patients with symptomatic progressive hormone-refractory prostate cancer. [ABSTRACT FROM AUTHOR]

Published
2000
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10. Editor's Choice - Nationwide Analysis of Patients Undergoing Iliac Artery Aneurysm Repair in the Netherlands.

Author

Jalalzadeh H, Indrakusuma R, Koelemay MJW, Balm R, Van den Akker LH, Van den Akker PJ, Akkersdijk GJ, Akkersdijk GP, Akkersdijk WL, van Andringa de Kempenaer MG, Arts CH, Avontuur JA, Baal JG, Bakker OJ, Balm R, Barendregt WB, Bender MH, Bendermacher BL, van den Berg M, Berger P, Beuk RJ, Blankensteijn JD, Bleker RJ, Bockel JH, Bodegom ME, Bogt KE, Boll AP, Booster MH, Borger van der Burg BL, de Borst GJ, Bos-van Rossum WT, Bosma J, Botman JM, Bouwman LH, Breek JC, Brehm V, Brinckman MJ, van den Broek TH, Brom HL, de Bruijn MT, de Bruin JL, Brummel P, van Brussel JP, Buijk SE, Buimer MG, Burger DH, Buscher HC, den Butter G, Cancrinus E, Castenmiller PH, Cazander G, Coveliers HM, Cuypers PH, Daemen JH, Dawson I, Derom AF, Dijkema AR, Diks J, Dinkelman MK, Dirven M, Dolmans DE, van Doorn RC, van Dortmont LM, van der Eb MM, Eefting D, van Eijck GJ, Elshof JW, Elsman BH, van der Elst A, van Engeland MI, van Eps RG, Faber MJ, de Fijter WM, Fioole B, Fritschy WM, Geelkerken RH, van Gent WB, Glade GJ, Govaert B, Groenendijk RP, de Groot HG, van den Haak RF, de Haan EF, Hajer GF, Hamming JF, van Hattum ES, Hazenberg CE, Hedeman Joosten PP, Helleman JN, van der Hem LG, Hendriks JM, van Herwaarden JA, Heyligers JM, Hinnen JW, Hissink RJ, Ho GH, den Hoed PT, Hoedt MT, van Hoek F, Hoencamp R, Hoffmann WH, Hoksbergen AW, Hollander EJ, Huisman LC, Hulsebos RG, Huntjens KM, Idu MM, Jacobs MJ, van der Jagt MF, Jansbeken JR, Janssen RJ, Jiang HH, de Jong SC, Jongkind V, Kapma MR, Keller BP, Khodadade Jahrome A, Kievit JK, Klemm PL, Klinkert P, Knippenberg B, Koedam NA, Koelemay MJ, Kolkert JL, Koning GG, Koning OH, Krasznai AG, Krol RM, Kropman RH, Kruse RR, van der Laan L, van der Laan MJ, van Laanen JH, Lardenoye JH, Lawson JA, Legemate DA, Leijdekkers VJ, Lemson MS, Lensvelt MM, Lijkwan MA, Lind RC, van der Linden FT, Liqui Lung PF, Loos MJ, Loubert MC, Mahmoud DE, Manshanden CG, Mattens EC, Meerwaldt R, Mees BM, Metz R, Minnee RC, de Mol van Otterloo JC, Moll FL, Montauban van Swijndregt YC, Morak MJ, van de Mortel RH, Mulder W, Nagesser SK, Naves CC, Nederhoed JH, Nevenzel-Putters AM, de Nie AJ, Nieuwenhuis DH, Nieuwenhuizen J, van Nieuwenhuizen RC, Nio D, Oomen AP, Oranen BI, Oskam J, Palamba HW, Peppelenbosch AG, van Petersen AS, Peterson TF, Petri BJ, Pierie ME, Ploeg AJ, Pol RA, Ponfoort ED, Poyck PP, Prent A, Ten Raa S, Raymakers JT, Reichart M, Reichmann BL, Reijnen MM, Rijbroek A, van Rijn MJ, de Roo RA, Rouwet EV, Rupert CG, Saleem BR, van Sambeek MR, Samyn MG, van 't Sant HP, van Schaik J, van Schaik PM, Scharn DM, Scheltinga MR, Schepers A, Schlejen PM, Schlosser FJ, Schol FP, Schouten O, Schreinemacher MH, Schreve MA, Schurink GW, Sikkink CJ, Siroen MP, Te Slaa A, Smeets HJ, Smeets L, de Smet AA, de Smit P, Smit PC, Smits TM, Snoeijs MG, Sondakh AO, van der Steenhoven TJ, van Sterkenburg SM, Stigter DA, Stigter H, Strating RP, Stultiëns GN, Sybrandy JE, Teijink JA, Telgenkamp BJ, Testroote MJ, The RM, Thijsse WJ, Tielliu IF, van Tongeren RB, Toorop RJ, Tordoir JH, Tournoij E, Truijers M, Türkcan K, Tutein Nolthenius RP, Ünlü Ç, Vafi AA, Vahl AC, Veen EJ, Veger HT, Veldman MG, Verhagen HJ, Verhoeven BA, Vermeulen CF, Vermeulen EG, Vierhout BP, Visser MJ, van der Vliet JA, Vlijmen-van Keulen CJ, Voesten HG, Voorhoeve R, Vos AW, de Vos B, Vos GA, Vriens BH, Vriens PW, de Vries AC, de Vries JP, de Vries M, van der Waal C, Waasdorp EJ, Wallis de Vries BM, van Walraven LA, van Wanroij JL, Warlé MC, van Weel V, van Well AM, Welten GM, Welten RJ, Wever JJ, Wiersema AM, Wikkeling OR, Willaert WI, Wille J, Willems MC, Willigendael EM, Wisselink W, Witte ME, Wittens CH, Wolf-de Jonge IC, Yazar O, Zeebregts CJ, and van Zeeland ML

Subjects
Aged, Aged, 80 and over, Endovascular Procedures methods, Endovascular Procedures mortality, Endovascular Procedures statistics & numerical data, Female, Guideline Adherence statistics & numerical data, Humans, Iliac Aneurysm epidemiology, Iliac Aneurysm mortality, Iliac Aneurysm pathology, Iliac Artery pathology, Iliac Artery surgery, Male, Netherlands epidemiology, Registries, Retrospective Studies, Sex Factors, Treatment Outcome, Iliac Aneurysm surgery
Abstract

Objective: The new 2019 guideline of the European Society for Vascular Surgery (ESVS) recommends consideration for elective iliac artery aneurysm (eIAA) repair when the iliac diameter exceeds 3.5 cm, as opposed to 3.0 cm previously. The current study assessed diameters at time of eIAA repair and ruptured IAA (rIAA) repair and compared clinical outcomes after open surgical repair (OSR) and endovascular aneurysm repair (EVAR)., Methods: This retrospective observational study used the nationwide Dutch Surgical Aneurysm Audit (DSAA) registry that includes all patients who undergo aorto-iliac aneurysm repair in the Netherlands. All patients who underwent primary IAA repair between 1 January 2014 and 1 January 2018 were included. Diameters at time of eIAA and rIAA repair were compared in a descriptive fashion. The anatomical location of the IAA was not registered in the registry. Patient characteristics and outcomes of OSR and EVAR were compared with appropriate statistical tests., Results: The DSAA registry comprised 974 patients who underwent IAA repair. A total of 851 patients were included after exclusion of patients undergoing revision surgery and patients with missing essential variables. eIAA repair was carried out in 713 patients, rIAA repair in 102, and symptomatic IAA repair in 36. OSR was performed in 205, EVAR in 618, and hybrid repairs and conversions in 28. The median maximum IAA diameter at the time of eIAA and rIAA repair was 43 (IQR 38-50) mm and 68 (IQR 58-85) mm, respectively. Mortality was 1.3% (95% CI 0.7-2.4) after eIAA repair and 25.5% (95% CI 18.0-34.7) after rIAA repair. Mortality was not significantly different between the OSR and EVAR subgroups. Elective OSR was associated with significantly more complications than EVAR (intra-operative: 9.8% vs. 3.6%, post-operative: 34.0% vs. 13.8%, respectively)., Conclusion: In the Netherlands, most eIAA repairs are performed at diameters larger than recommended by the ESVS guideline. These findings appear to support the recent increase in the threshold diameter for eIAA repair., (Copyright © 2020 European Society for Vascular Surgery. Published by Elsevier B.V. All rights reserved.)

Published
2020
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12. Expression of multidrug resistance related proteins and proliferative activity is increased in advanced clinical prostate cancer.

Author

Van Brussel JP, Jan Van Steenbrugge G, Van Krimpen C, Bogdanowicz JF, Van Der Kwast TH, Schröder FH, and Mickisch GH

Subjects
Aged, Case-Control Studies, Cell Division, Drug Resistance, Multiple, Humans, Immunohistochemistry, Male, Middle Aged, Multidrug Resistance-Associated Proteins, Prostatic Neoplasms drug therapy, Prostatic Neoplasms pathology, Up-Regulation, ATP-Binding Cassette Transporters metabolism, Neoplasm Proteins metabolism, Prostatic Neoplasms metabolism
Abstract

Purpose: Advanced disseminated prostate cancer is highly resistant to cytotoxic chemotherapy. We identified proteins that may be involved in multidrug resistance in clinical prostate cancer. Expression of these proteins was examined in the context of tumor progression., Materials and Methods: Paraffin embedded, formalin fixed prostate cancer specimens from archival sources of 3 distinct patient groups were examined. These groups were clearly distinct with regard to pathological stage and responsiveness to antihormonal therapy. Group 1 consisted of patients with organ confined prostate cancer treated with radical prostatectomy (early pathological stage T2N0M0). Group 2 patients had disseminated, early advanced prostate cancer and were treated with transurethral prostatic resection for urinary obstruction before receiving antihormonal therapy. Group 3 patients had disseminated prostate cancer with relapse despite antihormonal treatment (late advanced prostate cancer) and they underwent transurethral prostatic resection to relieve the symptoms of urinary obstruction. Immunohistochemical study was done to detect P-glycoprotein, multidrug resistance associated protein, lung resistance protein, glutathione-S-transferase pi, p53, Bcl-2, Bax, topoisomerase I, IIalpha and IIbeta, and Ki-67., Results: Advanced tumors were distinguished from locally confined tumors because they exhibited significantly higher histological grade and proliferative activity. The expression of multidrug resistance associated protein, p53, topoisomerase IIalpha, Ki-67 and topoisomerase IIbeta was significantly related to a higher Gleason sum score. The number of cases expressing multidrug resistance associated protein, lung resistance protein, glutathione-S-transferase pi, p53, Bcl-2, topoisomerase IIalpha and Ki-67 was significantly increased in the group with advanced disseminated prostate cancer. Topoisomerase I and IIbeta were homogeneously and highly expressed at all stages of prostate cancer progression, while P-glycoprotein was not expressed in any tumors regardless of the patient group., Conclusions: Up-regulation of the expression of the drug transporters multidrug resistance associated protein and lung resistance protein, detoxifying enzyme glutathione-S-transferase pi, and apoptosis inhibiting proteins Bcl-2 and p53 may be an explanation of the resistance of disseminated progressive prostate cancer to chemotherapy. As shown by the up-regulation of Ki-67 and topoisomerase IIalpha, increased proliferation reflects the aggressiveness of metastatic prostate cancer. Research on agents that counteract multidrug resistance mechanisms and may sensitize prostate carcinoma to cytotoxic chemotherapy may possibly lead to more effective treatment of progressive disseminated prostate cancer.

Published
2001
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13. [Luxatio cordis in blunt-trauma thoraco-abdominal injuries].

Author

van Brussel JP, Vles WJ, and Leenen LP

Subjects
Diagnosis, Differential, Female, Heart Injuries diagnostic imaging, Heart Injuries etiology, Hernia, Diaphragmatic, Traumatic diagnosis, Hernia, Diaphragmatic, Traumatic diagnostic imaging, Hernia, Diaphragmatic, Traumatic surgery, Humans, Laparotomy, Middle Aged, Radiography, Thoracic, Rupture diagnosis, Rupture surgery, Thoracic Surgical Procedures methods, Treatment Outcome, Wounds, Nonpenetrating diagnostic imaging, Accidents, Traffic, Heart Injuries diagnosis, Heart Injuries surgery, Hernia, Diaphragmatic, Traumatic complications, Pericardium injuries, Wounds, Nonpenetrating diagnosis, Wounds, Nonpenetrating surgery
Abstract

A 56-year old woman was admitted to the emergency ward after suffering a blunt thoraco-abdominal high-velocity trauma as she hit the wheel when her car drove into a tree. A laparotomy was performed because of haemodynamic instability and radiographic suspicion of a diaphragmatic rupture. Besides haemorrhage from liver and spleen injuries, an abdominal herniation of the heart through a ruptured pericardium and diaphragm was found. Haemostasis of liver, splenectomy and suturing of defects in pericardium and diaphragm resulted in a haemodynamically stable situation. A high index of suspicion of rupture of pericardium and diaphragm with luxation of the heart in the trauma patient is important to reduce morbidity and mortality due to delay of surgical intervention.

Published
2000

14. Chemosensitivity of prostate cancer cell lines and expression of multidrug resistance-related proteins.

Author

van Brussel JP, van Steenbrugge GJ, Romijn JC, Schröder FH, and Mickisch GH

Subjects
ATP Binding Cassette Transporter, Subfamily B, Member 1 metabolism, Blotting, Western, DNA Topoisomerases, Type I metabolism, Drug Resistance, Multiple, Drug Resistance, Neoplasm, Glutathione Transferase metabolism, Humans, Immunohistochemistry, Male, Proto-Oncogene Proteins metabolism, Proto-Oncogene Proteins c-bcl-2 metabolism, Tumor Cells, Cultured, bcl-2-Associated X Protein, Neoplasm Proteins metabolism, Prostatic Neoplasms drug therapy, Prostatic Neoplasms metabolism
Abstract

The aim of this study was to obtain insight into the role of the multidrug resistance (MDR) phenomenon in hormone-independent progressive prostate cancer. Using immunocytochemistry and Western blotting we determined the expression of P-glycoprotein (Pgp), multidrug resistance-associated protein (MRP), glutathione-S-transferase-pi (GST-pi), Bcl-2, Bax, topoisomerase (Topo) I, II alpha and II beta in the human prostate cancer cell lines PC3, TSU-Pr1, DU145 and LNCaP derivatives LNCaP-R, LNCaP-LNO and LNCaP-FGC. Proliferative activity was assessed by immunocytochemistry. MTT assays were used to determine the sensitivity to etoposide, doxorubicin and vinblastin. Pgp was not expressed in any of the cell lines. MRP was variably expressed. GST-pi was expressed in TSU-Pr1, PC3 and DU145. The expression of Bcl-2 was restricted to TSU-Pr1, whereas Bax was found in all cell lines. Topo II alpha was expressed at the highest level in the rapidly proliferating cell lines TSU-Pr1 and DU145. Topo I and II beta were equally expressed. Resistance profiles varied among the cell lines, with TSU-Pr1 being the most sensitive and LNCaP-LNO relatively resistant. Multiple MDR proteins were expressed in prostate cancer cell lines and may well influence response to chemotherapy. Future functional studies, using chemo-selected MDR models, may further help to determine the mechanism or combination of mechanisms underlying the resistance of prostate cancer to chemotherapy.

Published
1999
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15. Circumvention of multidrug resistance in genitourinary tumors.

Author

van Brussel JP and Mickisch GH

Subjects
Carcinoma, Renal Cell drug therapy, Carcinoma, Renal Cell physiopathology, Humans, Kidney Neoplasms drug therapy, Kidney Neoplasms physiopathology, Male, Prostatic Neoplasms drug therapy, Prostatic Neoplasms physiopathology, Testicular Neoplasms drug therapy, Testicular Neoplasms physiopathology, Urinary Bladder Neoplasms drug therapy, Urinary Bladder Neoplasms physiopathology, Drug Resistance, Multiple physiology, Urogenital Neoplasms drug therapy, Urogenital Neoplasms physiopathology
Abstract

Chemotherapy is the principal strategy to systemically challenge metastasized cancers of genitourinary origin. Unfortunately, the efficacy of chemotherapy is often hampered by multidrug resistance, the resistance to a variety of structurally and functionally distinct cytotoxic agents. Multidrug resistance can be either intrinsic or acquired, and can be caused by several mechanisms. The so-called classical multidrug resistance, mediated by the MDR1 gene product P-glycoprotein, has been held mainly responsible for inferring the multidrug resistance phenotype on urologic malignancies. However, several other multidrug resistance pathways have been identified. Multidrug resistance can be caused by the membrane-bound multidrug-resistance-associated protein, the detoxifying glutathione metabolism, the antiapoptotic protein BCL2, and changes in levels or activity of the topoisomerase enzymes. Strategies to overcome multidrug resistance of genitourinary tumors have arisen from the better understanding of the biologic and molecular mechanisms of multidrug resistance, and have been studied in experimental and clinical settings. However, attempts to modulate multidrug resistance in clinical renal cell, bladder, prostate, and testicular cancer have not been very rewarding so far, despite the optimism that had arisen from experimental data. Nevertheless, application of novel therapies to reverse multidrug resistance and to increase efficacy of chemotherapy for urologic cancers should be further pursued, within the setting of controlled clinical trials, to improve on current strategies.

Published
1998
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16. Wilkie's syndrome, a rare cause of vomiting and weight loss: diagnosis and therapy.

Author

Van Brussel JP, Dijkema WP, Adhin SK, and Jonkers GJ

Subjects
Adolescent, Duodenoscopy, Enterostomy, Humans, Male, Superior Mesenteric Artery Syndrome complications, Superior Mesenteric Artery Syndrome therapy, Superior Mesenteric Artery Syndrome diagnosis, Vomiting etiology, Weight Loss
Abstract

Wilkie's syndrome is a rare disease that should be considered in the differential diagnosis of upper abdominal discomfort and weight loss. Compression of the inferior part of the horizontal duodenum by the superior mesenteric artery may result in high intestinal obstruction with postprandial or positional discomfort, vomiting and weight loss. The diagnosis is based on clinical presentation and confirmed by radiographic studies during a symptomatic period. Therapy of first choice is conservative. Nevertheless, surgical intervention with duodenojejunostomy is often required.

Published
1997
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