Síndrome metabólico en pacientes con cáncer de próstata sometidos a supresión androgénica / Metabolic syndrome in patients with prostate cancer undergoing androgen suppression

Objetivos: La mortalidad cardiovascular es la primera causa de muerte en pacientes con cáncer de próstata (CP) y el síndrome metabólico (SM) está relacionado con ella. El objetivo principal de este estudio fue conocer la prevalencia del SM en pacientes con CP sometidos a supresión androgénica (SA). Material y métodos: Se realizó un estudio retrospectivo de casos y controles que incluyó 159 pacientes. Cincuenta y tres pacientes con CP sometidos a SA durante un periodo superior a 12 meses formaron el grupo de casos; 53 pacientes con CP en el momento de su diagnóstico y 53 pacientes con biopsia prostática negativa formaron el grupo control. En todos los pacientes se evaluó la existencia de SM según los criterios del NCEP-ATPIII. Resultados: La prevalencia de SM en pacientes sin CP fue del 32,1% y en pacientes con CP no tratados fue del 35,8%; p = 0,324. En pacientes con CP sometidos a SA la prevalencia de SM fue del 50,9%; p < 0,001. Cuando la SA fue inferior a 36 meses se observó una prevalencia del 44,0% y cuando fue superior o igual a 36 meses del 57,1%; p < 0,001. El perímetro abdominal (> 102 cm) y la hiperglucemia (> 110 mg/dl) fueron los 2 componentes del SM que se incrementaron significativamente. La SA y su duración fueron factores predictores independientes del desarrollo de SM. Conclusiones: La SA continuada incrementa la prevalencia de SM y especialmente el perímetro abdominal y la hiperglucemia. Su desarrollo aumenta con la duración de la SA

Objectives: Cardiovascular mortality is the leading cause of death in patients with prostate cancer (PC), metabolic syndrome (MS) being related to it. The main objective of this study was to determine the prevalence of MS in patients with CP undergoing androgen suppression (AS). Materials and methods: We performed a retrospective study of cases and controls that included 159 patients. The study group was made up of 53 patients with PC undergoing SA for a period exceeding 12 months. The control group had 53 patients with PC at the time of diagnosis and 53 patients with negative prostate biopsy. All the patients were evaluated for presence of MS according to NCEP-ATPIII criteria. Results: Prevalence of MS in patients without PC was 32.1% and in those with non-treated PC 35.8%, P = 0.324. In patients with PC undergoing AS, prevalence of MS was 50.9%, P < 0.001. When AS duration was less than 36 months, prevalence of MS was 44.0% and when greater than 36 months 57.1%, P < 0.001. Waist circumference and hyperglycemia were the two MS components that significantly increased. AS and its duration were independent predictors factors for the development of MS. Conclusions: Continuous AS therapy increases the prevalence of MS and especially waist circumference and hyperglycemia. Development of MS increases according to AS duration

Metabolic syndrome in patients with prostate cancer undergoing androgen suppression.

OBJECTIVES: Cardiovascular mortality is the leading cause of death in patients with prostate cancer (PC), metabolic syndrome (MS) being related to it. The main objective of this study was to determine the prevalence of MS in patients with CP undergoing androgen suppression (AS). MATERIAL AND METHODS: We performed a retrospective study of cases and controls that included 159 patients. The study group was made up of 53 patients with PC undergoing SA for a period exceeding 12 months. The control group was formed by 53 patients with PC at the time of diagnosis and 53 patients with negative prostate biopsy. All patients were evaluated for presence of MS according to NCEP-ATPIII criteria. RESULTS: Prevalence of MS in patients without PC was 32.1% and in those with non-treated PC 35.8%, P = .324. In patients with PC undergoing AS, prevalence of MS was 50.9%, P < .001. When AS duration was less than 36 months, prevalence of MS was 44.0% and when greater than 36 months 57.1%, P < .001. Waist circumference and hyperglycemia were the two MS components that significantly increased. AS and its duration were independent predictors factors for the development of MS. CONCLUSIONS: Continuous AS therapy increases the prevalence of MS and especially waist circumference and hyperglycemia. Development of MS increases according to AS duration.

Impacto de la supresión androgénica sobre el perfil lipídico y el riesgo aterogénico en pacientes con cáncer de próstata / Impact of Androgen Deprivation on the Lipid Profile and Atherogenic Risk in Prostate Cancer Patients

Objetivo: Analizar los cambios observados en el perfil lipídico y el riesgo aterogénico en pacientes con cáncer de próstata sometidos a supresión androgénica. Material y métodos: Los niveles séricos de lipoproteínas (colesterol total, colesterol HDL, colesterol LDL y triglicéridos) fueron determinados en 636 pacientes entre 2001 y 2008. De estos, 120 fueron tratados con bloqueo androgénico máximo y 177 fueron tratados únicamente con análogo de LHRH. El grupo control estaba formado por 339 pacientes sometidos a biopsia prostática (212 con cáncer de próstata y 127 sin cáncer de próstata). El riesgo aterogénico fue calculado según la fórmula de Castelli (colesterol total/HDL). Resultados: El riesgo aterogénico medio en el grupo control fue de 4,2 y de 4 en el grupo sometido a supresión androgénica (p>0,05). El riesgo aterogénico medio en los pacientes sometidos a monoterapia con análogos de LHRH fue de 4,1, mientras que en los pacientes en tratamiento con bloqueo androgénico máximo fue de 3,9 (p=0,02). No se observaron diferencias significativas del valor del riesgo aterogénico en función de la duración del tratamiento. El análisis multivariante confirmó que la modalidad de tratamiento fue la única variable significativa respecto al riesgo aterogénico. Conclusiones: Este estudio demuestra que la supresión androgénica no incrementa el riesgo aterogénico en pacientes con cáncer de próstata. Este riesgo tampoco se incrementa a lo largo del tratamiento. La asociación de la bicalutamida al análogo de LHRH parece ejercer un efecto protector sobre el riesgo aterogénico (AU)

Objective: This study has aimed to analyze the changes observed in the lipid profile and atherogenic risk in prostate cancer patients subjected to androgen deprivation. Material and methods: Between 2001 and 2008, serum lipoproteins (total cholesterol, HDL, LDL and triglycerides) were determined in 636 patients. Of these, 129 were treated with maximum androgen blockade and 177 patients were only treated with LHRH analogue. The control group was formed by 339 subjected to prostate biopsy (212 with prostate cancer and 127 without prostate cancer). The atherogenic risk was calculated using the Castelli formula (total cholesterol/HDL). Results: Mean atherogenic risk was 4.2 in the control group and 4 in the group of patients subjected to androgenic deprivation, p>0.05. The mean atherogenic risk in those subjected to monotherapy with LHRH analogues was 4.1 while it was 3.9 in patients subjected to maximal androgen blockade, p=0.02. We did not found significant differences for atherogenic risk according to length of treatment, p>0.05. The multivariate analysis confirmed that the treatment modality was the only significant variable influencing atherogenic risk. Conclusions: This study demonstrates that continuous androgen deprivation does not increase atherogenic risk in patients with prostate cancer. This risk also did not increase during the treatment. The association of bicalutamide to the LHRH analogue seems to have a protective effect on atherogenic risk (AU)

[Impact of androgen deprivation on the lipid profile and atherogenic risk in prostate cancer patients]. / Impacto de la supresión androgénica sobre el perfil lipídico y el riesgo aterogénico en pacientes con cáncer de próstata.

OBJECTIVE: This study has aimed to analyze the changes observed in the lipid profile and atherogenic risk in prostate cancer patients subjected to androgen deprivation. MATERIAL AND METHODS: Between 2001 and 2008, serum lipoproteins (total cholesterol, HDL, LDL and triglycerides) were determined in 636 patients. Of these, 129 were treated with maximum androgen blockade and 177 patients were only treated with LHRH analogue. The control group was formed by 339 subjected to prostate biopsy (212 with prostate cancer and 127 without prostate cancer). The atherogenic risk was calculated using the Castelli formula (total cholesterol/HDL). RESULTS: Mean atherogenic risk was 4.2 in the control group and 4 in the group of patients subjected to androgenic deprivation, p>0.05. The mean atherogenic risk in those subjected to monotherapy with LHRH analogues was 4.1 while it was 3.9 in patients subjected to maximal androgen blockade, p=0.02. We did not found significant differences for atherogenic risk according to length of treatment, p>0.05. The multivariate analysis confirmed that the treatment modality was the only significant variable influencing atherogenic risk. CONCLUSIONS: This study demonstrates that continuous androgen deprivation does not increase atherogenic risk in patients with prostate cancer. This risk also did not increase during the treatment. The association of bicalutamide to the LHRH analogue seems to have a protective effect on atherogenic risk.