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Volume 96, Issue 1, Pages 25-29 (July 2010)


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Prostate-specific antigen kinetics following external-beam radiotherapy and temporary (Ir-192) or permanent (I-125) brachytherapy for prostate cancer

Michael PinkawaaCorresponding Author Informationemail address, Marc D. Pirotha, Richard Holya, Karin Fischedicka, Sandra Schaara, Holger Borchersb, Axel Heidenreichb, Michael J. Eblea

Received 19 August 2009; received in revised form 21 December 2009; accepted 14 February 2010. published online 15 March 2010.

Abstract 

Background and purpose

The aim of the study was the evaluation of PSA kinetics after different radiotherapy methods.

Materials and methods

Two-hundred and ninety five patients received external-beam radiotherapy (EBRT; 70.2Gy; n=135), Ir-192 brachytherapy as a boost to EBRT (HDR-BT; 18Gy+50.4Gy; n=66) or I-125 brachytherapy (LDR-BT; 145Gy; n=94) as monotherapy. “PSA bounce” was defined as a PSA rise of ⩾0.2ng/ml followed by spontaneous return to prebounce level or lower, biochemical failure as “nadir+2ng/ml”.

Results

Patients without biochemical failure reached a lower nadir after brachytherapy (median ⩽0.05ng/ml after LDR- and HDR-BT without NHT) in comparison to EBRT (0.55ng/ml without NHT; p<0.01). Not a single patient without NHT and a nadir <0.1ng/ml failed biochemically (0% vs. 45% with a nadir ⩾0.1ng/ml; p<0.01). PSA bounces were found predominantly in the LDR-BT group (42% vs. 23%/20% after HDR-BT/EBRT; p<0.01). In a multivariate Cox regression analysis, LDR-BT and HDR-BT were associated with a significantly lower biochemical failure rate in comparison to EBRT.

Conclusions

PSA kinetics differ significantly following different radiotherapy methods. A lower nadir and a higher biochemical control rate suggest a higher radiobiological efficiency of brachytherapy in comparison to EBRT (with a dose of 70.2Gy).

a Department of Radiation Oncology; and

b Department of Urology, RWTH Aachen University, Aachen, Germany

Corresponding Author InformationCorresponding author. Address: Department of Radiation Oncology, RWTH Aachen University, Aachen, Germany.

PII: S0167-8140(10)00103-9

doi:10.1016/j.radonc.2010.02.010


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