Antiandrogenic therapy can cause coronary arterial disease

Abstract

Aim : To study the change of lipid metabolism by antiandrogen therapy in patients with prostate cancer. Materials and methods : We studied with a 2.5 years follow-up the changes in plasma cholesterols (C), triglycerides (TG), lipoproteins (LP), and apolipoproteins (Apo) B-100, A-I, and A-II profiles in 24 patients of mean age 60 years with low risk prostate cancer (stage: T1cN 0 M 0 , Gleason score: 2-5) during treatment with cyproterone acetate (CPA) without surgical management or radiation therapy.Results : Significant decreases of HDL-C, Apo A-I and Apo A-II and an increase of triglyceride levels in VLDL were induced by CPA. After a period of 2.5 years on CPA treatment, four patients out of twenty-four were found to be affected by coronary heart disease. Conclusions : Ischaemic coronary arteriosclerosis with an incidence rate of 16.6% as caused by prolonged CPA therapy is mediated through changes in HDL cholesterol, Apo A-I and Apo A-II profiles, other than the well-known hyperglyceridemic effect caused by estrogen.

Cardiovascular Disease Risk Factors: How Relevant in African Men With Prostate Cancer Receiving Androgen-Deprivation Therapy?

“…Similar findings were observed by Smith et al 21 and Nishiyama et al 22 Smith et al 23 reported that ADT for CaP using GnRH agonist treatment of a period of months resulted in significantly increased triglyceride levels. Chen et al 24 reported that ADT for 2.5 years resulted in significantly increased triglyceride and decreased HDL cholesterol values; however, only HDLC3 was affected. Another prospective study of 40 men who received ADT for a year showed a 9% increase in total cholesterol, 7.3% in LDL cholesterol, and 26.5% in triglyceride levels.…”

Metabolic Complications and Increased Cardiovascular Risks as a Result of Androgen Deprivation Therapy in Men with Prostate Cancer

“…Chen et al studied changes in plasma cholesterols, lipoproteins, and apolipoproteins (Apo) B-100, A-I, and A-II profiles over 2.5 years. They found significant decreases of HDL-C, Apo A-I and Apo A-II and an increase of triglyceride levels and VLDL associated with ADT [55]. In the same study, Apo B-100 levels were not statistically different between ADT and control group.…”

“…It has been shown consistently in various studies that ADT increase total cholesterol level. Some studies also showed increases in triglyceride level [28, 54, 55] versus others, which did not show significant elevations in triglyceride level in the ADT group [25, 26, 53]. Although total cholesterol was often increased during ADT therapy, HDL-C also found to increase in some studies, which might decrease the adverse consequence of increased total cholesterol.…”

“…After adjusting for potential confounders, including baseline Hb level, a decline in Hb after 3 months of ADT was associated independently with shorter survival (hazards ratio [HR], 1.10 per 1 g/dL decline; P = 0.0035) and shorter progression-free survival (HR, 1.08 per 1 g/dL decline; P = 0.013) [67] In another study, after a period of 2.5 years on ADT, four patients out of twenty-four were found to be affected by coronary heart disease. In that study, ischemic coronary arteriosclerosis with an incidence rate of 16.6% as caused by prolonged ADT is mediated through changes in HDL cholesterol, Apo A-I and Apo A-II profiles [55]. …”

The Effect of Androgen Deprivation Therapy in Arterial Stiffness of the Aorta and the Endothelial Function of Peripheral Arteries

“…Moreover, studies have demonstrated that ADT is associated with dyslipidemias, lower levels of high density lipoprotein and higher levels of triglycerides, total cholesterol and low density lipoprotein concentrations. Furthermore, Chen et al [19] revealed that long-term ADT (mean duration: 2.5 years) significantly decreased the levels of apolipoproteins I and II. Lastly, Nishiyama et al [20] demonstrated that after 6 months of ADT, body weight, levels of fasting blood sugar, serum total cholesterol, blood urea nitrogen, compensated calcium, inorganic phosphorus, bone-specific alkaline phosphatase, and compensated urinary deoxypyridinoline increased significantly.…”