Effects of transdermal estrogen on levels of lipids, lipase activity, and inflammatory markers in men with prostate cancer.
Androgen deprivation therapy (ADT) for prostate cancer is now used in earlier disease stages and as adjuvant treatment. Recognizing and reducing the toxicity of this therapy, including worsened lipid levels and cardiovascular disease (CVD) risks, has become an important clinical concern. Oral estrogen therapy induces hypogonadism and mitigates many side effects of ADT, but has a high thrombosis risk. Transdermal estrogen therapy (TDE) has a lower thrombosis risk than oral estrogen and may improve CVD risk compared with ADT. This prospective pilot study of 18 men with androgen-independent prostate cancer receiving ADT measured effects of TDE on lipid and inflammatory CVD risk factors before and after 8 weeks of TDE (estradiol 0.6 mg/day). During treatment, estradiol levels rose 17-fold; total cholesterol, LDL cholesterol, and apolipoprotein B levels decreased. HDL2 cholesterol increased, with no changes in triglyceride or VLDL cholesterol levels. Dense LDL cholesterol decreased and LDL buoyancy increased in association with a decrease in HL activity. Highly sensitive C-reactive protein levels and other inflammatory markers did not worsen. Compared with ADT, short-term TDE therapy of prostate cancer improves lipid levels without deterioration of CVD-associated inflammatory markers and may, on longer-term follow-up, improve CVD and mortality rates.
Purnell
Jonathan Q
JQ
Department of Medicine, Division of Endocrinology, Diabetes, and Clinical Nutrition, Oregon Health and Science University, Portland, OR 97239, USA. purnellj@oshu.edu
Bland
Lisa B
LB
Garzotto
Mark
M
Lemmon
Dianne
D
Wersinger
Emily M
EM
Ryan
Christopher W
CW
Brunzell
John D
JD
Beer
Tomasz M
TM
D000279:Administration, Cutaneous; D000368:Aged; D000369:Aged, 80 and over; D001055:Apolipoproteins B / Q000097:blood; D001823:Body Composition / Q000187:drug effects; D002097:C-Reactive Protein / Q000032:analysis; D002784:Cholesterol / Q000097:blood; D004958:Estradiol / Q000097:blood; D004967:Estrogens / Q000494:pharmacology*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D020738:Leptin / Q000097:blood; D008049:Lipase / Q000097:blood*; D050356:Lipid Metabolism / Q000187:drug effects*; D008055:Lipids / Q000097:blood*; D008071:Lipoprotein Lipase / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D011471:Prostatic Neoplasms / Q000097:blood* / Q000188:drug therapy / Q000378:metabolism; D012738:Sex Hormone-Binding Globulin / Q000378:metabolism; D013739:Testosterone / Q000097:blood; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D001055:Apolipoproteins B; D004967:Estrogens; D018836:Inflammation Mediators; D015850:Interleukin-6; C504173:LIPC protein, human; D020738:Leptin; D008055:Lipids; D008074:Lipoproteins; D012738:Sex Hormone-Binding Globulin; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D013739:Testosterone; D004958:Estradiol; D002097:C-Reactive Protein; D002784:Cholesterol; D008049:Lipase; D008071:Lipoprotein Lipase