94 Background: Chemotherapy-associated steatosis (CAS) is poorly understood in context of colorectal cancer (CRC). It has been anecdotally observed that CRC patients undergoing chemotherapy appeared to develop steatosis at a higher rate than expected, and that statin therapy may have protective effects against CAS. Here, we sought to evaluate 1) the frequency of CAS in Stage II-III CRC patients; and 2) whether patients on statins throughout adjuvant chemotherapy develop CAS at a lower frequency. Methods: This study retrospectively examined medical records of 267 Stage II-III CRC patients who received adjuvant chemotherapy and were followed up at St. Michael’s Hospital, Toronto, Canada between January 1, 2006 and January 1, 2017. Patient information, relevant co-morbid conditions, statin use, and adjuvant chemotherapy were collected. Baseline and incident steatosis for up to one year from chemotherapy start date was assessed based on imaging reports (CT, ultrasound, MR). Results: Of 267 patients, 78 (29.2%) had steatosis at baseline radiology, prior to treatment with adjuvant chemotherapy. Of the remaining 189 cases, the incidence of steatosis within one year of adjuvant chemotherapy start date was significantly greater in patients who received adjuvant treatment (n = 132) compared to those who did not (n = 57), (39% vs. 23%, p = 0.03). Among patients who underwent chemotherapy, statin use for preexisting hyperlipidemia, a known risk factor for steatosis (n = 39), was associated with a lower incidence of steatosis compared to no statin administration (n = 93), although this result was not significant (31% vs. 42%, p = 0.243). Among statin users, 42.9% of patients treated using oxaliplatin-containing FOLFOX regimen (n = 21) developed steatosis, compared to 20% in patients on a capecitabine regimen (n = 15). There was a trend towards significance, with p = 0.151. Conclusions: Chemotherapeutic treatment of Stage II-III CRC is associated with an increased incidence of steatosis. Statins may protect against acute development of CAS within one year following chemotherapy, particularly with single agent capecitabine. Prospective clinical trials should be considered to assess protective use of statin in this curative patient population.
Mendelian randomization analysis rules out disylipidaemia as colorectal cancer cause