News Release

Inflammation from ADT may cause fatigue in prostate cancer patients

Moffitt Cancer Center study suggests elevation in inflammation marker IL-6 linked to higher levels of fatigue

Peer-Reviewed Publication

H. Lee Moffitt Cancer Center & Research Institute

TAMPA, Fla. -- Prostate cancer is one of the most common cancers among men in the U.S. For many patients, hormone therapy is a treatment option. This type of therapy, also called androgen deprivation therapy (ADT), reduces the level of testosterone and other androgens in the body. Lowering androgen levels can make prostate cancer cells grow more slowly or shrink tumors over time. However, patients receiving ADT often experience higher levels of fatigue, depression and cognitive impairment.

Moffitt Cancer Center researchers are investigating whether inflammation in the body, a side effect of ADT, contributes to these symptoms in prostate cancer patients. In a new study published in the journal Cancer, they pinpoint a specific inflammation marker that is associated with increased fatigue in this group of patients.

"This is the first study that we know of that examines the association between inflammation and symptoms of fatigue, depression or cognitive impairment in prostate cancer patients receiving ADT," said Heather Jim, Ph.D., corresponding author and co-leader of the Health Outcomes & Behavior Program at Moffitt. "Because the blocking of testosterone can increase inflammation in the body, we believe that inflammation may also be contributing to these symptoms."

For the study, the research team evaluated two groups of men: prostate cancer patients beginning ADT and a control group of healthy men the same age. The men were assessed at the start of the study and again at six and 12 months. Assessments included fatigue, depression and other neuropsychological tests and a blood draw. The bloodwork was to check for circulating markers of inflammation, specifically interleukin-1 receptor antagonist (IL-1RA), interleukin-6 (IL-6), soluble tumor necrosis factor receptor-2 (sTNF-R2) and C-reactive protein (CRP).

While the groups did not differ at baseline, researchers noticed a significant increase in fatigue and depressive symptoms in the ADT patients over the 12-month period. They also saw an increase in one inflammation marker, IL-6, in this group of patients.

"Interleukin-6 is a pro-inflammatory cytokine that is often associated with disruption of sleep and therefore fatigue," said Aasha Hoogland, Ph.D., lead study author and an applied research scientist in the Health Outcomes & Behavior Program at Moffitt. "Studies have shown testosterone can suppress the effects of IL-6, but ADT limits testosterone production in the body, which is why we may be seeing increased levels in this patient group."

The researchers say additional studies are needed to see if interventions, such as anti-inflammatory medications and exercise, can help alleviate fatigue and depressive symptoms in ADT patients.

###

This study was supported by the National Institutes of Health (R01 CA132803 and P30 CA076292) and a Miles for Moffitt Milestone Award.

About Moffitt Cancer Center

Moffitt is dedicated to one lifesaving mission: to contribute to the prevention and cure of cancer. The Tampa-based facility is one of only 51 National Cancer Institute-designated Comprehensive Cancer Centers, a distinction that recognizes Moffitt's scientific excellence, multidisciplinary research, and robust training and education. Moffitt is the No. 11 cancer hospital and has been nationally ranked by U.S. News & World Report since 1999. Moffitt's expert nursing staff is recognized by the American Nurses Credentialing Center with Magnet® status, its highest distinction. With more than 7,000 team members, Moffitt has an economic impact in the state of $2.4 billion. For more information, call 1-888-MOFFITT (1-888-663-3488), visit MOFFITT.org, and follow the momentum on Facebook, Twitter, Instagram and YouTube.


Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.