Prostate cancer is recognized as one of the most common cancers affecting the male population. The prostate is revealed to be a hormone-dependent tissue as testosterone and dihydrotestosterone could bind to the androgen receptor, activate it, and initiate the nuclear translocation of this receptor which is followed by subsequent signaling cascades. Regarding this androgen dependency of the prostate, it is believed that androgen deprivation therapies are able to confront aggressive prostate cancer as first-line treatment. However, prostate cancer could overcome hormone deprivation strategies through a number of cellular mechanisms, such as intratumoral androgen production and the production of ligand-independent androgen receptor splice variants, which are known clinically as castration-resistant prostate cancer. Due to the limited efficacy of first-generation antiandrogens in complete blockage of androgen receptor activity, recently, four second-generation anti-androgens, including abiraterone acetate, enzalutamide, apalutamide, and darolutamide approved by the Food and Drug Administration, and considered standard of care for patients with advanced prostate cancer. Nevertheless, prostate cancer cells may acquire drug-resistance mechanisms to overcome these novel chemotherapeutics. Furthermore, potential adverse effects on nontargeted organs such as the cardiovascular system, are possible. Hence, the current study aimed to review the efficacy and cardio-safety of these novel therapeutical strategies.
Background Coronary Artery Disease (CAD) is a common form of heart disease that is considered a serious health problem in society. Atherosclerosis is widely recognized as a chronic inflammatory disease of the vessels and can lead to CAD and myocardial infarction. The aim of the present study was to investigate serum levels of connexin-37 and stromelysin-1 as significant biomarkers of CAD and their correlation with the extent of CAD. Methods and results Sixty CAD patients with one-vessel (1VD), two-vessel (2VD), and three-vessel (3VD) disease were enrolled in this study. For comparison with the results, 20 healthy control subjects were also included in this study. Serum concentrations of connexin-37 and stromelysin-1 were determined using commercial ELISA kits. Serum connexin-37 concentrations were not significantly different between the patient and control groups (p < 0.05). The analysis showed a statistically significant difference between subjects with one-vessel disease, subjects with two-vessel disease, and subjects with three-vessel disease. Serum Stromelysin-1 concentration was significantly higher in the patients than in the control group (p < 0.05). Conclusions The results of our study indicate that serum levels of stromelysin-1, but not connexin-37, may contribute to the prediction of the occurrence and progression of CAD.
Purpose: Due to the potential benefits of allopurinol in ischemic reperfusion injury, this randomized control trial was performed to evaluate the pretreatment allopurinol effect on major adverse cardiovascular events (MACE) in patients undergoing primary percutaneous coronary intervention (pPCI). Methods: A randomized controlled trial was performed on 170 first-time STEMI patients undergoing pPCI. Before the pPCI, patients in intervention group (n=85) received 300 mg dose of allopurinol and control group (n=85) received placebo. Then, for the next 28 days, 100 mg of allopurinol was given to allopurinol group and placebo to the other group. Patients were compared regarding the baseline characteristics, clinical findings and one-year MACE. Results: Our findings showed that patients receiving allopurinol had significantly longer door-to-balloon time than the control group (60.76 ± 19.38 vs. 50.06 ± 16.38 P-value: 0.001). During one year of follow-up, HF, CVA and mortality occurred more frequently in allopurinol group but differences were not statistically significant. No significant difference was also seen between the two groups regarding MACE during follow-up or hospitalization (p-value: 0.179, 0.330 respectively). Kaplan-Meier curve could not show a significant difference between the two groups in terms of mortality and MACE (P-value: 0.317 and 0.128 respectively). Conclusion: According to findings of this trial allopurinol had no cardioprotective effect against adverse cardiovascular events or death in patients undergoing pPCI.
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