Sex hormone changes and its relationship with cardiovascular risk factors and major adverse cardiac events in old patients with castrated prostatic cancer

Abstract

Listen

Translate article

Some literatures suggested that imbalanced sex hormones would cause an increase of cardiovascular events (MACE) [1]. As an effective treating method for prostatic cancer, castration could also lead to marked imbalance of sex hormones. The aim of this study was to explore the relationship between imbalanced sex hormones and cardiovascular risk factors and MACE in castrated old patients with early non-metastatic prostatic cancer. 247 patients in our hospital from 2000–2009 were recruited. Group I included 122 castrated prostatic cancer patients (mean[SD]age, 84.8[7.2] years), group II included 61 non-castrated prostatic cancer patients (mean[SD]age, 83.1[6.1] years), group III included 64 non-prostatic cancer patients (mean[SD]age, 83.1[6.8] years). All patients underwent comprehensive examinations to exclude advanced prostatic cancer metastasis or other malignancy, and also to rule out blood diseases, liver and kidney diseases, and infection and heart dysfunction diseases. All patients were provided verbal informed consent. Sex hormones and risk factorsweremeasured. AnyMACEwere recorded during followup for a minimum of 1 year. The chi-square test was used for count variables, one-way ANOVA test for continuous variables, and Newman–Keuls' test for comparison between any two groups. Baseline information including age, body mass index, proportions of coronary heart disease, cerebrovascular disease, diabetes, hypertension and dyslipidemia was comparable among groups. Compared to group II and group III, testosterone, estradiol, and progesterone levels were significantly lower, while luteal hormone and follicle stimulating hormone were significantly higher in group I. Also in group I, D-dimmer (DD), fibrinogen (FIB), C-reactive protein (CRP), homocysteine (Hcy), glucose, uric acid (UA), total cholesterol (TC), triglyceride (TG) and low density lipoprotein-C (LDL-C) increased significantly, blood prothrombin time, activated partial thromboplastin time shortened and international normalized ratio decreased significantly. High density lipoprotein-C, antithrombin-III levels and blood platelets counts had no significant difference among the three groups (Table 1). Platelet aggregation rates induced by arachidonic acid (PA-AA) and by adenosine diphosphate(PA-ADP) were elevated significantly and incidence of aspirin or clopidogrel resistance was also higher in group I (PA-AA ≥20% and PA-ADP N50% were respectively defined as aspirin and clopidogrel resistance) (Table 2). The incidences of MACE in three groups were 39.3% (48/122), 21.3% (13/61), 15.6% (10/64) respectively. Some studies showed that a decrease in testosterone level was an independent risk factor for cardiovascular diseases [2,3]. This study showed that sex hormones in castrated prostatic cancer patients were significantly disordered and coagulation function was activated accordingly. FIB and DD increased markedly and they were all thought to be signs of hypercoagulability and fresh thrombosis related with MACE [4,5]. PA-AA and PA-ADP increased significantly after castration, and the incidence of aspirin or clopidogrel resistance was also increased suggesting that platelets were activated. CRP, Hcy, glucose, UA, TC, TG, and LDL-C increased significantly in castrated patients concurrently and they are all independent risk factors for cardiovascular diseases, so as disorders of lipid and glucose metabolism. The study showed that MACE in castration groupwere significantly higher than that in non-castration group strongly suggesting that the decreasing of androgen might closely affect the development of cardiovascular diseases in old male patients. This study also showed that there were no significant differences about the coagulation indicators and blood parameters between noncastrated prostatic cancer patients and non-prostatic patients suggesting that therewas little likelihood that the increases in risk factors for cardiovascular diseases resulted from the prostatic tumor itself. It's more likely that there might be association between cardiovascular diseases and disorders of sex hormones. This study strongly supports the idea that disorders of sex hormones might promote the development of cardiovascular diseases, and also provides some theoretical references on the opinion regarding the reasonable application of androgen replacement therapy for castrated old patients with prostatic cancer.