The recent prescription of incretin therapy is associated with an increased risk of pancreatic cancer. The reason for such an increase is likely the consequence of an occult pancreatic cancer that provokes or aggravates diabetes. Studies are warranted for assessing the risk of pancreatic cancer associated with long-term use of incretin drugs.
Background Cancer-related fatigue (CRF) is the most common side effect of cancer and cancer treatment. CRF prevalence is up to 50% in breast cancer patients and can continue several years after cancer remission. This persistent subjective sense of exhaustion is multifactorial. Numerous parameters have been evidenced to be related to CRF across biological, physical, psychological, social and/or behavioral dimensions. Although CRF has been studied for many years, the majority of previous studies focused on only one dimension, i.e., physical function. Moreover, few studies investigated CRF longitudinally with repeated measures. These are the two main obstacles that limit the understanding of CRF mechanisms. The purpose of this study is to create a biopsychosocial model of CRF with simultaneous and longitudinal anthropometric, clinical, biological, physical, psychological and sociological parameters. Methods BIOCARE FActory is a multicentric prospective study that will consist of an 18-month follow-up of 200 women diagnosed with breast cancer. Four visits will be scheduled at diagnosis, after treatments, and 12 and 18 months after diagnosis. The same procedure will be followed for each visit. Each session will be composed of anthropometric data collection, a semi-structured interview, cognitive tests, postural control tests, neuromuscular fatigability tests and a cardiorespiratory fitness test. Clinical and biological data will be collected during medical follow-ups. Participants will also complete questionnaires to assess psychological aspects and quality of life and wear an actigraphy device. Using a structural equation modeling analysis (SEM), collected data will build a biopsychosocial model of CRF, including the physiological, biological, psychological, behavioral and social dimensions of CRF. Discussion This study aims to highlight the dynamics of CRF and its correlates from diagnosis to post treatment. SEM analysis could examine some relations between potential mechanisms and CRF. Thus, the biopsychosocial model will contribute to a better understanding of CRF and its underlying mechanisms from diagnosis to the aftermaths of cancer and its treatments. Trial registration This study is registered at ClinicalTrials.gov (NCT04391543), May 2020.
4126 Background: Concerns have been raised on the risk of pancreatic cancer associated with specific anti-diabetic therapies. We have examined the risk of pancreatic cancer among patients with diabetes prescribed with an oral anti-diabetic drug (OAD) or an incretin drug (DPP4i and GLP-1 RA) or insulin. Methods: The public health insurance databases of Belgium and of Lombardy Region, Italy include nearly 100% of the population living in these countries. We created within these databases two cohorts that included adult patients who were first prescribed an incretin drug or another noninsulin antidiabetic drug (NIAD) during 01/07/2008-31/12/2013 in Belgium and during 01/01/2008-31/12/2012 in Lombardy Region. The risk of pancreatic cancer after prescription of an anti-diabetic drug was evaluated using multivariate adjusted Cox models including time-dependent variables. Adjusted hazard ratios (aHRs) from Belgium and Italy were pooled using fixed effects meta-analyses. Results: Results in both cohorts were similar. Among those patients prescribed an OAD, 45% of pancreatic cancers occurred within the 6 months following first prescription, 20% in months 7 to 12 after first prescription and proportions decreased progressively during follow-up. The aHR of pancreatic cancer among subjects prescribed an incretin compared to an OAD was 2.14 [95% CI, 1.71 to 2.67]. The aHR decreased from 3.35 [CI, 2.32 to 4.84] in the first 3 months after first incretin prescription, 2.12 [CI, 1.22 to 3.66] in months 3 to 5.9, 1.95 [CI, 1.20 to 3.16] in months 6 to 11.9, to 1.69 [CI, 1.12 to 2.55] after 12 months. The risk of pancreatic cancer among subjects who were subsequently prescribed insulin was 6.89 [CI, 6.05 to 7.85]. The time from OAD prescription to a shift to incretins or to insulin was significantly lower in patients who were subsequently diagnosed with a pancreatic cancer. Conclusions: The increased risk of pancreatic cancer associated with anti-diabetic therapies could be the consequence of an occult pancreatic cancer that provokes diabetes (reverse causation bias). The search for an occult pancreatic cancer in subjects with newly diagnosed diabetes or patients shifting to more potent anti-diabetic therapy may lead to earlier detection of this cancer.
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