Response of serum cholesterol and triglycerides to hormone treatment and the relation of pretreatment values to mortality in patients with prostatic cancer

Abstract

Cholesterol and triglycerides were measured in plasma samples from patient with cancer of the prostate before and after 3 months treatment with either Premarin, Provera, Provera and diethylstilbestrol, or diethylstilbestrol alone. Cholesterol was also measured before and after one of three doses of diethylstilbestrol or placebo. Pretreatment cholesterol levels at 196 +/- 1.3 mg per 100 ml (X +/- SE, N = 1093) were significantly lower than these reported for similar age group noncancer controls. Significant increases occurred with some of the estrogen treatments. Pretreatment cholesterol levels showed a significant negative correlation with age in Stage III and IV patients of both studies and a positive correlation with hemoglobin in Stage III patients of both studies. Pretreatment triglyceride levels at 120 +/- 1.9 mg per 100 ml (X +/- SE, N = 1089) were similar to levels reported for noncancer controls of similar age. Estrogen treatment produced a significant increase in triglyceride levels. Serum triglycerides were significantly correlated with hemoglobin, weight, and cholesterol and negatively correlated with age, Analysis of covariance for both cholesterol and triglycerides showed highly significant treatment effects, but no stage effects and no stage-treatment interactions. It showed that the pretreatment value is of extreme importance for predicting or explaining the 3-month value. Death rates were calculated by level of pretreatment cholesterol or pretreatment triglycerides for all Stage II and IV patients, all treatments combined, and for Study 2 and Study 3 separately. No consistent trends were evident for cholesterol. Spearman correlation coefficients between category of initial triglyceride value and rank of death rate were computed to test for a quadratic effect. When the absolute values of the initial triglyceride values minus the overall mean were correlated with the death rate, a significant negative correlation was found for all causes of death and for deaths due to cardiovascular disease and prostatic cancer. These results indicate that the death rate is highest near the overal mean for initial triglyceride values and decreases as the initial values deviate above or below the mean. Initial triglyceride levels appear to have potential as indicators of risk of death in patients with prostatic cancer. The percentage of patients dead at 1 year by initial triglyceride levels, measured only in Study 3, revealed a pattern similar to that observed for the death rate, that is, the highest percentages were associated with values near the overall mean.

Effects of transdermal estrogen on levels of lipids, lipase activity, and inflammatory markers in men with prostate cancer

“…This absence of an increase in triglyceride levels by transdermal estrogen in this study may be of prognostic relevance. Elevated triglyceride levels were a consistent finding in previous treatment studies of men with prostate cancer receiving oral estrogen (19,(44)(45)(46), and in one study, mortality rates were worse in those who experienced a rise in triglyceride levels with therapy (19). Results are median (range).…”

“…Oral estrogen therapy has been used to suppress testosterone levels and improve some lipid levels in men with prostate cancer (16)(17)(18), but in early studies, oral formulations were associated with an unacceptably high risk of thromboembolic disease and CVD (19,20). Subsequent studies have shown that oral estrogen significantly increases the risk of thromboembolic complications, increases triglyceride levels, and raises levels of inflammatory markers in both women and men.…”

Decrease in malonyl-CoA and its background metabolic alterations in murine model of cancer cachexia

“…In fact, several experiments have shown that blood triglyceride levels increased significantly in animal models of cancer cachexia. However, this is not common in cancer patients or always the case, even in animal models of typical cancer cachexia (8)(9)(10).…”

“…Clone 20 tumors provoke a severe loss of body weight and storage fat accompanied by a decrease in food intake in syngeneic mice with normal immune function, while clone 5 tumors do not elicit this response (8). In addition, as observed in cancer patients (9,10), the serum triglyceride levels in cachectic mice bearing the clone 20 tumor are not elevated (8). The study of this animal model will provide useful information for understanding the metabolic backgroud of human cancer cachexia.…”