trelstar and Atherosclerosis

This study has aimed to analyze the changes observed in the lipid profile and atherogenic risk in prostate cancer patients subjected to androgen deprivation.. 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).. 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.. 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.

Topics: Adenocarcinoma; Androgen Antagonists; Anilides; Antineoplastic Agents, Hormonal; Atherosclerosis; Biopsy; Cholesterol; Cholesterol, HDL; Cholesterol, LDL; Combined Modality Therapy; Gonadotropin-Releasing Hormone; Humans; Lipoproteins; Male; Nitriles; Prostate; Prostatectomy; Prostatic Neoplasms; Retrospective Studies; Risk; Tosyl Compounds; Triglycerides; Triptorelin Pamoate

The very high carrier frequency of 21-hydroxylase deficiency worldwide has been postulated as indicating a survival advantage. The 'mediators' of such an effect remain speculative.. To look for possible differences in the metabolic and atherogenic risk profile of carriers and noncarriers of CYP21A2 gene mutations at puberty in order to identify possible mediators of the presumed survival advantage for the carriers. It is anticipated that by studying atherogenic risk factors at such an early developmental stage, age-related alterations in these factors may be minimized.. The study group included 45 adolescent girls diagnosed in our center with premature pubarche, 29 of whom were noncarriers and 16 carriers of CYP21A2 mutations. The two groups did not differ in chronological age, age at pubarche or menarche, pubertal stage, body mass index and waist-to-hip ratio. Biochemical and hormonal profile markers as well as markers of endothelial dysfunction were determined by appropriate methodology. Additionally, in each subject, an oral glucose tolerance test and a gonadotrophin-releasing hormone GnRH analogue stimulation test were carried out.. Endothelin-1 values were lower in the carriers compared to the noncarriers (p = 0.031). Higher tissue plasminogen activator and lower plasminogen activator inhibitor-1 values were found in carriers compared to noncarriers (p = 0.02 and <0.001, respectively). The ratio of the insulinogenic index/homeostasis model assessment for insulin resistance, which reflects beta-cell function, was higher in carriers (p = 0.048), indicating a more favorable beta-cell function in the carriers.. Our findings that carriers of CYP21A2 gene mutations have a more favorable internal milieu with regard to the metabolic syndrome and atherogenesis support the theory that heterozygous CYP21A2 mutations provide a survival advantage. The mechanisms involved may be related to the insulin secretion-action pathway, hypothalamic-pituitary-adrenal axis responsiveness or other still unrecognized factors.

Topics: Adolescent; Atherosclerosis; Case-Control Studies; Child; Endothelin-1; Female; Glucose Tolerance Test; Heterozygote; Humans; Hypothalamo-Hypophyseal System; Insulin; Insulin Resistance; Insulin Secretion; Metabolic Syndrome; Mutation; Pituitary-Adrenal System; Plasminogen Activator Inhibitor 1; Risk Factors; Steroid 21-Hydroxylase; Triptorelin Pamoate