Patients with prostate cancer treated by ADT have significantly higher fibrinogenemia than healthy control.
OBJECTIVE
Androgen deprivation therapy (ADT) for prostate cancer (PCa) may increase peripheral insulin resistance, induce type 2 diabetes, change body composition, and alter lipoprotein profile. Some studies have reported an association between ADT and increased risk of cardiovascular events. It is known that serum level of fibrinogen (SF) is associated with coronary artery disease and increased cardiovascular risk (CVR). The aim of this study is to determine the increase in SF and C-reactive protein (CRP) of PCa patients on ADT.


METHODS
Ninety-seven patients with locally advanced PCa (study group) were analyzed [mean age 73.4 years ± 6.3 SD, mean prostate specific antigen (PSA) 15.4 ng/ml ± 7.5 SD]. They were examined with blood chemistry including serum cholesterol (CHL), high density lipoproteins (HDL), low density lipoproteins (LDL), very low density lipoproteins, triacylglycerol (TAG), serum fibrinogen (FB), CRP and serum fasting glucose (SFG), serum testosterone, free testosterone at baseline, and after 12 months of ADT.


RESULTS
Patients after 12 months of ADT (study group) had significantly higher overall serum CHL (p < 0.001), higher LDL (p = 0.01), higher FB (p < 0.001), higher serum SFG (p = 0.03) in comparison with the control group. Increase in HDL (p = 0.245) and CRP (p = 0.1) was not significant. Two patients from the study group were diagnosed with new-onset diabetes.


CONCLUSIONS
This is the first study that demonstrates the significant increase in FB in PCa patients on ADT, while CRP as inflammatory marker did not increase. Elevation of SF may contribute to increased CVR in PCa patients. Further prospective studies are warranted to confirm this association.
Department of Urology, Faculty of Medicine and University Hospital, Comenius University in Bratislava, Limbova Str. 5, 831 01, Bratislava, Slovakia. stanoziaran@gmail.com
Stanislav
S
Ziaran
Frederico Manuel
FM
Goncalves
Jan
J
Breza
D000368:Aged; D000726:Androgen Antagonists / Q000009:adverse effects*; D018931:Antineoplastic Agents, Hormonal / Q000009:adverse effects*; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D002097:C-Reactive Protein / Q000187:drug effects / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000139:chemically induced; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood / Q000187:drug effects; D008078:Cholesterol, LDL / Q000097:blood / Q000187:drug effects; D003924:Diabetes Mellitus, Type 2 / Q000139:chemically induced; D005340:Fibrinogen / Q000187:drug effects / Q000378:metabolism*; D007987:Gonadotropin-Releasing Hormone / Q000819:agonists*; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011471:Prostatic Neoplasms / Q000188:drug therapy*; D013739:Testosterone / Q000097:blood; D014280:Triglycerides / Q000097:blood
D000726:Androgen Antagonists; D018931:Antineoplastic Agents, Hormonal; D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D014280:Triglycerides; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D005340:Fibrinogen; D002097:C-Reactive Protein; D002784:Cholesterol