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A higher prediagnostic insulin level is a prospective risk factor for incident prostate cancer.

Artikel i vetenskaplig tidskrift
Författare J Hammarsten
Jan-Erik Damber
Ralph Peeker
Dan Mellström
B Högstedt
Publicerad i Cancer epidemiology
Volym 34
Nummer/häfte 5
Sidor 574-9
ISSN 1877-783x
Publiceringsår 2010
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för urologi
Institutionen för medicin, avdelningen för invärtesmedicin
Sidor 574-9
Språk en
Länkar dx.doi.org/10.1016/j.canep.2010.06....
Ämnesord Aged, Diabetes Mellitus, Type 2, blood, epidemiology, Humans, Hypertension, blood, epidemiology, Insulin, blood, Male, Neoplasm Staging, Prospective Studies, Prostatic Neoplasms, blood, diagnosis, epidemiology, pathology, Sweden, epidemiology
Ämneskategorier Urologi och andrologi

Sammanfattning

A higher insulin level has been linked to the risk of prostate cancer promotion. However, several reports claim that there is no association between a higher insulin level and the risk of incident prostate cancer. In the present report, the insulin hypothesis was tested once more prospectively in men with a benign prostatic disorder. Three hundred and eighty-nine consecutive patients referred with lower urinary tract symptoms without clinical prostate cancer were included during 1994-2002. Follow-up was performed in 2006. Data were obtained from the Swedish National Cancer Register and the Regional Cancer Register, Oncological Centre, Göteborg, Sweden. At this follow-up, 44 of the patients included had developed prostate cancer. Men with prostate cancer diagnosis had a higher systolic (P<0.001) and diastolic blood pressure (P<0.000), were more obese as measured by BMI (P=0.010), waist (P=0.007) and hip measurements (P=0.041) than men who did not have prostate cancer diagnosis at follow-up. These men also had a higher uric acid level (P=0.040), and a higher fasting serum insulin level (P=0.023) than men who did not have prostate cancer diagnosis at follow-up. Following exclusion of T1a/b prostate cancer cases, the difference of the fasting serum insulin level between the groups was still significant (P=0.038). Our data support the hypothesis that a higher insulin level is a promoter of prostate cancer. Moreover, our data suggest that the insulin level could be used as a marker of the risk of developing prostate cancer. The present findings also seem to confirm that prostate cancer is a component of the metabolic syndrome. Finally, our data generate the hypothesis that the metabolic syndrome conceals early prostate cancer.

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