OBJECTIVES - To investigate the association of host metabolic factors and the metabolic syndrome on prostate cancer specific death (PCSD) and overall survival (OS) in patients treated with androgen deprivation therapy (ADT) for biochemically recurrent disease.
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PATIENTS AND METHODS - The analysis included 273 prostate cancer patients treated with ADT for rising PSA after surgery or radiotherapy. Patients were assessed for the presence of diabetes, hypertension, dyslipidaemia, and obesity prior to the commencement of ADT and using ATPIII criteria for the presence of the composite diagnosis of metabolic syndrome (MS). Competing risks regression model assessed associations of time to PCSD with the metabolic conditions, while multivariable Cox regression model assessed associations of OS with MS and metabolic conditions.
RESULTS - During a median follow-up of 11. 6 years, 157 (58%) patients died, of which 58 (21%) died of prostate cancer. At the start of ADT the median age was 74 (range=46, 92) years, the median PSA was 3. 0 ng/mL. MS were observed in 31% patients; hypertension (68%) and dyslipidaemia (47%) were the most common metabolic conditions. No association of PCSD and MS status was observed. Patients with hypertension tended to have a higher cumulative incidence of PCSD compared to those without hypertension (sub-distribution hazards ratio HR=1. 59 (95%CI 0. 89, 2. 84; p-value=0·11) though not statistically significant. Patients with MS had an increased risk of death from all causes (HR=1. 56, 95%CI: 1. 07, 2. 29; p=0. 02) when compared with patients without MS; as did patients with hypertension (HR=1·72, 95% CI: 1·18-2·49; p=0·004).
CONCLUSIONS - No association of prostate cancer specific death and metabolic syndrome was observed in this cohort of men receiving ADT for biochemically recurrent prostate cancer. Patients with MS were associated with an increased risk of death from all causes and a similar effect was also observed for prostate cancer patients with hypertension alone. This article is protected by copyright. All rights reserved.
BJU international. 2016 Jan 25 [Epub ahead of print]
S M Rudman, K P Gray, J L Batista, M J Pitt, E L Giovannucci, P G Harper, M Loda, L A Mucci, C J Sweeney
Department of Oncology, Guy's & St Thomas' NHS Foundation Trust, London, UK. , Dept of Biostatistics and Computational Biology, Dana-Farber Cancer Institute, Harvard School of Public Health, Boston, USA. , Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School Boston, USA. , Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, USA. , Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School Boston, USA. , Department of Oncology, Guy's & St Thomas' NHS Foundation Trust, London, UK. , Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, USA. , Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School Boston, USA. , Lank Center for Genitourinary Oncology, Dana Farber Cancer Institute, Boston, USA.