Inflammatory bowel disease may raise prostate Ca risk

Inflammatory bowel disease (IBD) increases the risk of any and clinically significant prostate cancer, according to an examination of data from a large, single medical network.

On adjusted analyses, IBD was associated with four- to five-fold increased risk of any and clinically significant prostate cancer over 10 years, Shilajit Kundu, MD, reported at the Genitourinary Cancers Symposium in San Francisco.

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“It has long been thought that chronic gut inflammation and cancer are related,” said Dr. Kundu, chief of urologic oncology, Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago. “Gut inflammation increases the risk of colon cancer, liver cancer, and cholangiocarcinoma, but the link between gut inflammation and prostate cancer is not well established. Data linking IBD and prostate cancer are limited and come mostly from the era before PSA screening was widely practiced.”

Dr. Kundu and colleagues examined a cohort of 1,033 men with IBD and prospectively matched them on the basis of race and age to 9,306 men without IBD. All men had at least one screening PSA test between 1996 and 2017 and none had a history of prostate cancer. The median age at first PSA test was 53 years in both cohorts, and 74% in each cohort were Caucasian. The median number of PSA tests per man over 5 years was two.

The median follow-up was 4.7 years for the controls and 6.5 years for the men with IBD. At 5 years of follow-up, there were 30 cases of prostate cancer and 16 cases of clinically significant prostate cancer (Gleason grade group >1) among the men with IBD and 29 cases of prostate cancer and 17 cases of clinically significant prostate cancer among the controls.

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The 10-year incidence of any prostate cancer was 0.65% among controls and 4.4% among men with IBD. When adjusted for age, race, number of PSA tests, baseline PSA level, and history of abnormal rectal examination, the hazard ratio (HR) for any prostate cancer among men with IBD compared with controls was 4.84 (p<.001).

The 10-year incidence of clinically significant prostate cancer was 0.42% among controls and 2.4% among men with IBD. The adjusted HR for clinically significant prostate cancer among men with IBD compared with controls was 4.04 (p<.001).

At 10 years of follow-up, the incidence of metastatic prostate cancer was 0.03% for controls and 0.19% for men with IBD (p=.61).

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When assessing IBD characteristics and prostate cancer incidence among the men with IBD, use of biologic medications, duration of IBD, history of bowel resection, and ulcerative colitis versus Crohn’s disease did not affect prostate cancer incidence. Prednisone treatment for IBD was protective of any prostate cancer (adjusted HR=0.22; p=.019), but not of clinically significant prostate cancer (p=.5).

After age 60 years, PSA values were higher among patients with IBD compared with controls (p=.004), and the difference widened with increasing age.

The findings need to be further validated to consider IBD as a risk factor for prostate cancer and to optimize screening for this population, said Dr. Kundu.

“My main message would be to consider prostate cancer screening in men with IBD, and we may want to consider them potentially as a higher risk group for developing prostate cancer than men without IBD,” he said. “Second, from a practical standpoint, if a man comes in with an elevated PSA and he has a history of IBD, don’t assume that the elevated PSA is from inflammation. It may be truly prostate cancer. I would pursue it a bit more rigorously, with a consideration for imaging or having a discussion about biopsy, as their risk may be increased.”