Analysis of the Lipid Profile and Atherogenic Risk during Androgen Deprivation Therapy in Prostate Cancer Patients

Salvador, C.; Planas, Jacques; Agreda, F.; Placer, J.; Trilla, E.; López, Miguel; Moróte, Juan

doi:10.1159/000342814

Cited by 27 publications

(28 citation statements)

References 33 publications

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“…Thus, there may be residual confounding affecting the analysis of those on anti-androgen monotherapy. Alterations in lipid levels may be another mechanism through which systemic ADT is propagating risk of TED [26][27][28][29][30]. Our dataset does not contain information on any of these factors and thus further mechanistic studies are required to determine if these do play a role in the associations observed.…”

Section: Discussionmentioning

confidence: 99%

Risk of thromboembolic disease in men with prostate cancer undergoing androgen deprivation therapy

et al. 2015

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ObjectivesTo investigate the risk of thromboembolic disease (TED) in men with prostate cancer (PCa) on androgen deprivation therapy (ADT), while accounting for known TED risk factors. Materials and MethodsWe assessed TED risk for 42 263 men with PCa who were receiving ADT compared with a matched cohort of 190 930 without PCa. The associations between ADT and deep vein thrombosis (DVT) or pulmonary embolism (PE) were analysed using multivariate Cox proportional hazard regression models, while accounting for previous PCa-related surgeries and the following proxies for disease progression: transurethral resection of the prostate, palliative radiotherapy and nephrostomy. ResultsBetween 1997 and 2013, 11 242 men with PCa received antiandrogen monotherapy, 26 959 men received gonadotropinreleasing hormone (GnRH) agonists, 1 091 men received combined androgen blockade and 3 789 men underwent orchiectomy. When accounting for previous surgeries and proxies of disease progression, GnRH agonist users and surgically castrated men had a higher risk of TED than the comparison cohort: hazard ratios (HRs) 1.67 (95% confidence interval [CI] 1.40-1.98) and 1.61 (95% CI 1.15-2.28), respectively. Men on anti-androgen monotherapy had a lower risk: HR for DVT 0.49 (95% CI 0.33-0.74). TED risk was highest among those who switched from anti-androgen to GnRH agonists: HR for PE 2.55 (95% CI 1.76-3.70). This increased from 2.52 (95% CI 1.54-4.12) in year 1, to 4.05 (95% CI 2.51-6.55) in year 2. ConclusionThe incidence of TED among men on ADT increased with the duration of therapy and the risk was highest for those who switched regimen, suggesting that disease progression as well as ADT contribute to the propagation of TED risk. Nonetheless, these findings support the hypothesis that only men with a relevant indication should receive systemic ADT.

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Section: Discussionmentioning

confidence: 99%

Risk of thromboembolic disease in men with prostate cancer undergoing androgen deprivation therapy

et al. 2015

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“…However, the increase in cardiovascular morbidity observed in patients receiving ADT cannot be explained by the changes observed in the lipid profile [46]. Moreover, before starting ADT, it could be interesting to investigate PCa physiopathology along the pituitary-testis-prostate axis.…”

Section: Discussionmentioning

confidence: 99%

Associations of Pretreatment Serum Total Testosterone Measurements with Pathology-Detected Gleason Score Cancer

Porcaro

Petrozziello²,

Ghimenton³

et al. 2013

Urol Int

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Background and Objective: Prostate cancer is an endocrine-dependent tumor which is still under-investigated for physiopathology factors related to its natural history. The association of pretreatment total testosterone (TT) serum levels with prostate cancer is still a controversial topic. The objective of this study was to investigate potential associations and functional relationships of preoperative TT serum level and pathology-detected Gleason score (pGS). Materials and Methods: Pretreatment and pathological variables of 220 patients operated with radical prostatectomy were retrospectively reviewed. Age, prostate-specific antigen (PSA), percentage of positive biopsy cores (P+), biopsy Gleason score (bGS), pGS, TT and free testosterone were the continuous variables, while clinical stage (cT: cT1c, cT2/3), biopsy Gleason pattern (bGP: ≤3+3, 3+4, >3+4), pathology Gleason pattern (pGP: ≤3+3, 3+4, >3+4), pathology stage (pT: pT2, pT3a, pT3b), pathology nodal staging (pN: pN0, pN1, pNx) and surgical margin invasion by cancer (R-, R+) were the categorical variables. Statistical methods were computed for assessing associations of TT and pGS; moreover, simple and multiple linear regression analysis (SLRA and MLRA) were used for assessing functional relationships of TT and pGS. Results: High-grade tumors (pGS ≥8.0) were associated with bGS >6.0 (p < 0.0001), pGP ≥3+4 (p < 0.0001), P+ >0.31% (p = 0.006), cT2/3 (p = 0.01), TT >15.5 nmol/l (p = 0.0004) and, to a lesser extent, PSA >6.27 μg/l (p = 0.06). The odds ratio (OR) ranked as follows: 2.01 (PSA >6.27 μg/l), 2.88 (cT2/3), 3.23 (P+ >0.31%), 5.53 (TT >15.5 nmol/l) and 12.09 (pGP ≥3+4 and pGS ≥8.0). On SLRA, pGS variation was significantly predicted by bGS (p < 0.0001), P+ (p < 0.0001), PSA (p = 0.0005) and TT (p = 0.02); on MLRA, pGS variation was still significantly predicted by bGS (p < 0.0001), P+ (p = 0.04), PSA (p = 0.03) and TT (p = 0.002). When bGS, P+, PSA and TT were dichotomized to their median value, only bGS (p < 0.0001) and TT (p = 0.001) showed independence in predicting pGS variation. The best model for predicting pGS variations was by dichotomizing TT above its median (>15.5 nmol/l) because the predictive coefficient increased to 0.32, which means that patients with TT >15.5 have a significantly higher estimated risk for high-grade pGS than patients with TT ≤15.5 nmol/l (OR = 1.31). Conclusion: In a patient population undergoing radical prostatectomy, increased pretreatment serum measurements of TT are associated with and functionally related to high-grade pGS; moreover, baseline TT together with bGS and PSA are important factors for predicting pGS and assessing high-grade tumors. Baseline TT serum levels might have prognostic potential for assessing treatment response for continuous as well as intermittent androgen deprivation therapy.

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“…As well as weight gain, several studies showed a mean increase of 3.2–10.6% in total cholesterol and 3.8–46.6% in triglycerides, with the duration of ADT ranging from 24 weeks to 12 months (Table ) . These changes in lipid and glucose levels were noticeable in the first 3 or 6 months of ADT (Figs ) . Only one study compared the differences in lipid profile according to treatment modality .…”

Section: Metabolic Changes During Adtmentioning

confidence: 99%

Metabolic changes in patients with prostate cancer during androgen deprivation therapy

Mitsuzuka

Arai

2017

Int J of Urology

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Androgen deprivation therapy continues to be widely used for the treatment of prostate cancer despite the appearance of new-generation androgen-receptor targeting drugs after 2000. Androgen deprivation therapy can alleviate symptoms in patients with metastatic prostate cancer and might have a survival benefit in some patients, but it causes undesirable changes in lipid, glucose, muscle or bone metabolism. These metabolic changes could lead to new onset or worsening of diseases, such as obesity, metabolic syndrome, diabetes mellitus, cardiovascular disease, sarcopenia or fracture. Several studies examining the influence of androgen deprivation therapy in Japanese patients with prostate cancer also showed that metabolic changes, such as weight gain, dyslipidemia or fat accumulation, can occur as in patients in Western countries. Efforts to decrease these unfavorable changes and events are important. First, overuse of androgen deprivation therapy for localized or elderly prostate cancer patients should be reconsidered. Second, intermittent androgen deprivation therapy might be beneficial for selected patients who suffer from impaired quality of life as a result of continuous androgen deprivation therapy. Third, education and instruction, such as diet or exercise, to decrease metabolic changes before initiating androgen deprivation therapy is important, because metabolic changes are likely to occur in the early androgen deprivation therapy period. Fourth, routine monitoring of weight, laboratory data or bone mineral density during androgen deprivation therapy are required to avoid unfavorable events.

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Analysis of the Lipid Profile and Atherogenic Risk during Androgen Deprivation Therapy in Prostate Cancer Patients

Cited by 27 publications

References 33 publications

Risk of thromboembolic disease in men with prostate cancer undergoing androgen deprivation therapy

Risk of thromboembolic disease in men with prostate cancer undergoing androgen deprivation therapy

Associations of Pretreatment Serum Total Testosterone Measurements with Pathology-Detected Gleason Score Cancer

Metabolic changes in patients with prostate cancer during androgen deprivation therapy

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