scholarly journals Does a prostate cancer diagnosis affect management of pre-existing diabetes? Results from PCBaSe Sweden: a nationwide cohort study

BMJ Open ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. e020787 ◽  
Author(s):  
Danielle Crawley ◽  
Hans Garmo ◽  
Sarah Rudman ◽  
Pär Stattin ◽  
Björn Zethelius ◽  
...  

ObjectivesBoth prostate cancer (PCa) and type 2 diabetes mellitus (T2DM) are increasingly prevalent conditions, which frequently coexist in men. Here, we set out to specifically examine the impact of a PCa diagnosis and its treatment on T2DM treatment.SettingThis study uses observational data from Prostate Cancer database Sweden Traject.ParticipantsThe study was undertaken in a cohort of 16 778 men with T2DM, of whom 962 were diagnosed with PCa during mean follow-up of 2.5 years.Primary and secondary outcome measuresWe investigated the association between PCa diagnosis and escalation in T2DM treatment in this cohort. A treatment escalation was defined as a new or change in anti-T2DM prescription, as recorded in the prescribed drug register (ie, change from diet to metformin or sulphonylurea or insulin). We also investigated how PCa diagnosis was associated with two treatment escalations. Multivariate Cox proportional hazards regression with age as a time scale was used while adjusting for educational level and initial T2DM treatment.ResultsWe found no association between PCa diagnosis and risk of a single treatment escalation (HR 0.99, 95% CI 0.87 to 1.13). However, PCa diagnosis was associated with an increased risk of receiving two consecutive T2DM treatment escalations (HR 1.75, 95% CI 1.38 to 2.22). This increase was strongest for men on gonadotropin-releasing hormone (GnRH) agonists (HR 3.08, 95% CI 2.14 to 4.40). The corresponding HR for men with PCa not on hormonal treatment was 1.40 (95% CI 1.03 to 1.92) and for men with PCa on antiandrogens 0.91 (95% CI 0.29 to 2.82).ConclusionsMen with T2DM who are diagnosed with PCa, particularly those treated with GnRH agonists, were more likely to have two consecutive escalations in T2DM treatment. This suggests a need for closer monitoring of men with both PCa and T2DM, as coexistence of PCa and its subsequent treatments could potentially worsen T2DM control.

2015 ◽  
Vol 33 (11) ◽  
pp. 1243-1251 ◽  
Author(s):  
Sean O'Farrell ◽  
Hans Garmo ◽  
Lars Holmberg ◽  
Jan Adolfsson ◽  
Pär Stattin ◽  
...  

Purpose Findings on the association between risk of cardiovascular disease (CVD) and the duration and type of androgen-deprivation therapy (ADT) in men with prostate cancer (PCa) are inconsistent. Methods By using data on filled drug prescriptions in Swedish national health care registers, we investigated the risk of CVD in a cohort of 41,362 men with PCa on ADT compared with an age-matched, PCa-free comparison cohort (n = 187,785) by use of multivariable Cox proportional hazards regression models. Results From 2006 to 2012, 10,656 men were on antiandrogens (AA), 26,959 were on gonadotropin-releasing hormone (GnRH) agonists, and 3,747 underwent surgical orchiectomy. CVD risk was increased in men on GnRH agonists compared with the comparison cohort (hazard ratio [HR] of incident CVD, 1.21; 95% CI, 1.18 to 1.25; and orchiectomy: HR, 1.16; 95% CI, 1.08 to 1.25). Men with PCa on AA were at decreased risk (HR of incident CVD, 0.87; 95% CI, 0.82 to 0.91). CVD risk was highest during the first 6 months of ADT in men who experienced two or more cardiovascular events before therapy, with an HR of CVD during the first 6 months of GnRH agonist therapy of 1.91 (95% CI, 1.66 to 2.20), an HR of CVD with AA of 1.60 (95% CI, 1.24 to 2.06), and an HR of CVD with orchiectomy of 1.79 (95% CI, 1.16 to 2.76) versus the comparison cohort. Conclusion Our results support that there should be a solid indication for ADT in men with PCa so that benefit outweighs potential harm; this is of particular importance among men with a recent history of CVD.


2013 ◽  
Vol 7 (5-6) ◽  
pp. 299 ◽  
Author(s):  
Julie M. DeGroot ◽  
Michael D. Brundage ◽  
Miu Lam ◽  
Susan L. Rohland ◽  
Jeremy Heaton ◽  
...  

Objective: We compared the cause-specific survival of patientswho received radiotherapy to those who received surgery for cureof their prostate cancer using a number of design and analytic stepsto mitigate confounding by indication.Methods: This was a case-cohort study of 2213 patients in theOntario Cancer Registry diagnosed between 1990 and 1998 whowere either treatment candidates or received curative radiotherapyor surgery. Cases included patients who died of prostate cancerwithin 10 years. The study population was restricted to those whowere candidates for either treatment (radiotherapy or surgery)based on disease severity (low and intermediate risk using theGenitourinary Radiation Oncologists of Canada risk groups). Themedian follow-up was 51 months. Cause-specific survival wasanalyzed using Cox-proportional hazards regression with casecohortvariance adjustment.Results from intent-to-treat analyseswere compared to results by treatment received.Results: Adjusted hazard ratios for risk of prostate cancer death forradiotherapy compared to surgery for the entire study populationwere 1.62 (95%CI 1.00-2.61) and 2.02 (1.19-3.43) analyzing byintent-to-treat and treatment received, respectively. Intent-to-treathazard ratios for the low- and intermediate-risk groups were 0.87(0.28-2.76) and 1.57 (0.95-2.61), respectively.Conclusion: Overall results were driven by the finding in the intermediate-risk group, which indicated that radiotherapy was not aseffective as surgery in this group. Confirmation was needed withspecial attention paid to risk stratification and the impact of morecontemporary delivery of these treatment options.


2019 ◽  
Vol 37 (15_suppl) ◽  
pp. 10051-10051
Author(s):  
Danielle Novetsky Friedman ◽  
Pamela J Goodman ◽  
Wendy Leisenring ◽  
Lisa Diller ◽  
Susan Lerner Cohn ◽  
...  

10051 Background: Infants with neuroblastoma typically have low-risk disease with excellent survival. Therapy has been de-intensified over time to minimize late effects, however the impact on survivors’ risk of late mortality, subsequent malignant neoplasms (SMN), and chronic health conditions (CHC) is unclear. Methods: We evaluated late mortality, SMNs and CHCs (graded according to CTCAE v4.03), overall and by diagnosis era, among 990 5-year neuroblastoma survivors diagnosed at < 1 year of age between 1970-1999. Cumulative mortality, standardized mortality ratios (SMR), and standardized incidence ratios (SIR) of SMNs were estimated using the National Death Index and SEER rates, respectively. Cox proportional hazards estimated hazard ratios (HR) and 95% confidence intervals (CI) for CHC, compared to 5,051 CCSS siblings. Results: Among survivors (48% female; median attained age: 24 years, range 6-46), there was increased treatment with surgery alone across the 1970s, 1980s and 1990s (21.5%, 35.3%, 41.1%, respectively), but decreased treatment with combination surgery + radiation (22.5%, 5.3%, 0.3%, respectively) and surgery + radiation + chemotherapy (28.7%, 14.7%, 9.3%, respectively). The 20-year cumulative mortality was 2.3% (95% CI, 1.4-3.8), primarily due to SMNs (SMRSMN= 10.0, 95% CI, 4.5-22.3). The 20-year cumulative incidence of SMN was 1.2% (95% CI, 0.3-3.2), 2.5% (95% CI, 1.3-4.4), and zero for those diagnosed in the 1970s, 1980s, and 1990s, respectively. SIR was highest for renal SMNs (SIR 12.5, 95% CI, 1.7-89.4). Compared to siblings, survivors were at increased risk for grade 1-5 CHC (HR 2.1, 95% CI, 1.9-2.3) with similar HR across eras (HR1970s= 1.9, 95% CI, 1.6-2.2; HR1980s= 2.2, 95% CI, 1.9-2.6; HR1990s= 2.0, 95% CI, 1.7-2.4). The HR of severe, disabling, life-threatening and fatal CHC (grades 3-5) decreased in more recent eras (HR1970s= 4.7, 95% CI, 3.4-6.6; HR1980s= 4.4, 95% CI, 3.2-6.2; HR1990s= 2.9, 95% CI, 2.0-4.3). Conclusions: Survivors of infant neuroblastoma remain at increased risk for late mortality, SMN, and CHCs many years after diagnosis. However, the risk of grade 3-5 CHCs has declined in more recent eras, likely reflecting de-intensification of therapy.


2018 ◽  
Vol 36 (6_suppl) ◽  
pp. 41-41
Author(s):  
Daniel Canter ◽  
Julia E. Reid ◽  
Maria Latsis ◽  
Margaret Variano ◽  
Shams Halat ◽  
...  

41 Background: Prostate cancer (PC) is the most common male malignancy. Prior data has suggested that African American (AA) men present with more aggressive disease relative to men of other ancestries. Here, we examined the effects of ancestry on clinical and molecular measures of disease aggressiveness as well as pathologic outcomes in men treated with radical prostatectomy (RP) for localized PC. Methods: Data was collected from patients undergoing RP at the Ochsner Clinic from 2006 to 2011. Formalin−fixed paraffin embedded biopsy tissue was analyzed for the RNA expression of 31 cell cycle progression (CCP) genes and 15 housekeeping genes to obtain a CCP score (a validated molecular measure of PC aggressiveness). Cancer of the Prostate Risk Assessment (CAPRA) scores were also determined based on clinicopathologic features at the time of diagnosis. Clinical (Gleason score, tumor stage, CAPRA score) and molecular (CCP score) measures of disease aggressiveness were compared based on ancestry (AA versus non−AA). Cox proportional hazards models were used to test association of ancestry to biochemical recurrence (BCR) and progression to metastatic disease. Fisher’s exact and Wilcoxon rank sum tests were used to compare ancestries. Results: A total of 384 patients were treated with RP, including 133 (34.8%) AA men. At the time of diagnosis, the median age was 62 years (interquartile range (IQR) 56, 66) and PSA was 5.4 ng/mL (IQR 4.2, 7.6). When compared by ancestry, there were no significant differences in biopsy Gleason score (p = 0.26), clinical stage (p = 0.27), CAPRA score (p = 0.58), or CCP score (p = 0.87). In addition, there was no significant difference in the risk of BCR between ancestries (p = 0.55). Only non−AA men progressed to metastatic disease within the ten years of follow−up. Conclusions: Contrary to prior reports, these data appears to indicate that men of AA ancestry do not necessarily present with or develop a more biologically aggressive form of PC. Although these data represents only one institution’s experience, it contains a highly robust AA population compared to prior reports. Further research is required to account for the discrepancy in the previously published literature.


2013 ◽  
Vol 141 (12) ◽  
pp. 2663-2670 ◽  
Author(s):  
S. D. CHUNG ◽  
Y. K. LIN ◽  
C. C. HUANG ◽  
H. C. LIN

SUMMARYThe relationship between sexually transmitted infections (STIs) and prostate cancer (PC) remains inconclusive. Moreover, all such studies to date have been conducted in Western populations. This study aimed to investigate the risk of PC following STI using a population-based matched-cohort design in Taiwan. The study cohort comprised 1055 patients with STIs, and 10 550 randomly selected subjects were used as a comparison cohort. Cox proportional hazards regression analysis revealed that the hazard ratio for PC during the 5-year follow-up period for patients with a STI was 1·95 (95% confidence interval 1·18–3·23), that of comparison subjects after adjusting for urbanization level, geographical region, monthly income, hypertension, diabetes, hyperlipidaemia, obesity, chronic prostatitis, history of vasectomy, tobacco use disorder, and alcohol abuse. We concluded that the risk of PC was higher for men who were diagnosed with a STI in an Asian population.


2020 ◽  
Author(s):  
Hayley Martin ◽  
Kelly Thevenet-Morrison ◽  
Ann Dozier

Abstract Background: It is well established that mothers with above-normal pre-pregnancy BMI are at increased risk of breastfeeding cessation; however, the impact of pregnancy weight-gain (PWG) is less well-defined. Excess PWG may alter the hormonal preparation of breast tissue for lactation, increase the risk of complications that negatively impact breastfeeding (e.g. Cesarean-section, gestational diabetes), and may make effective latch more difficult to achieve. Methods: Our objective was to determine the impact of PWG and pre-pregnancy BMI on the risk of breastfeeding cessation utilizing the Institute of Medicine’s 2009 recommendations. Cox proportional hazards models were utilized to estimate the risk of cessation of exclusive breastfeeding, and cessation of any breastfeeding among women who initiated exclusive and any breastfeeding, respectively, in a cross sectional sample of survey respondents from a New York county (N=1207). PWG category was interacted with pre-pregnancy BMI (3 levels of pre-pregnancy BMI, 3 levels of PWG). Confounders of the relationship of interest were evaluated using directed acyclic graphs and bivariate analyses; variables not on the proposed causal pathway and associated with the exposure and outcome were included in multivariate models. Results: After adjustment, women of normal and obese pre-pregnancy BMI with greater-than-recommended PWG had 1.39 (1.03-1.86) and 1.48 (1.06-2.07) times the risk of any breastfeeding cessation within the first 3 months postpartum compared to women with normal pre-pregnancy BMI who gained within PWG recommendations. Overweight women with greater-than-recommended PWG were at increased risk of cessation, although not significantly (aHR[95% CI]: 1.29 [0.95 – 1.75]). No significant relationship was observed for exclusive breastfeeding cessation. Conclusions: Pre-pregnancy BMI and PWG may be modifiable risk factors for early breastfeeding cessation. Understanding the mechanism behind this risk should be ascertained by additional studies aimed at understanding the physiological, social, logistical (positioning) and other issues that may lead to early breastfeeding cessation.


2020 ◽  
Author(s):  
Hayley Martin ◽  
Kelly Thevenet-Morrison ◽  
Ann Dozier

Abstract Background: It is well established that mothers with above-normal pre-pregnancy BMI are at increased risk of breastfeeding cessation; however, the impact of pregnancy weight-gain (PWG) is less well-defined. Excess PWG may alter the hormonal preparation of breast tissue for lactation, increase the risk of complications that negatively impact breastfeeding (e.g. Cesarean-section, gestational diabetes), and may make effective latch more difficult to achieve. Methods: Our objective was to determine the impact of PWG and pre-pregnancy BMI on the risk of breastfeeding cessation utilizing the Institute of Medicine’s 2009 recommendations. Cox proportional hazards models were utilized to estimate the risk of cessation of exclusive breastfeeding, and cessation of any breastfeeding among women who initiated exclusive and any breastfeeding, respectively, in a cross sectional sample of survey respondents from a New York county (N=1207). PWG category was interacted with pre-pregnancy BMI (3 levels of pre-pregnancy BMI, 3 levels of PWG). Confounders of the relationship of interest were evaluated using directed acyclic graphs and bivariate analyses; variables not on the proposed causal pathway and associated with the exposure and outcome were included in multivariate models. Results: After adjustment, women of normal and obese pre-pregnancy BMI with greater-than-recommended PWG had 1.39 (1.03-1.86) and 1.48 (1.06-2.07) times the risk of any breastfeeding cessation within the first 3 months postpartum compared to women with normal pre-pregnancy BMI who gained within PWG recommendations. Overweight women with greater-than-recommended PWG were at increased risk of cessation, although not significantly (aHR[95% CI]: 1.29 [0.95 – 1.75]). No significant relationship was observed for exclusive breastfeeding cessation. Conclusions: Pre-pregnancy BMI and PWG may be modifiable risk factors for early breastfeeding cessation. Understanding the mechanism behind this risk should be ascertained by additional studies aimed at understanding the physiological, social, logistical (positioning) and other issues that may lead to early breastfeeding cessation.


2017 ◽  
Vol 35 (5_suppl) ◽  
pp. 168-168
Author(s):  
David Tat ◽  
Erin Van Blarigan ◽  
Stacey A. Kenfield ◽  
Jenny Broering ◽  
Janet E. Cowan ◽  
...  

168 Background: Recent research suggests a positive relationship between intake of high-fat dairy, particularly whole milk, and prostate cancer (PC) mortality. However, data are limited in men after PC diagnosis. Methods: We conducted a prospective cohort study among 1336 men with non-metastatic PC in CaPSURE. The men answered a food frequency questionnaire (FFQ) in 2004-2005 (median time from diagnosis to the FFQ: 2 y) and were followed for PC progression until April 2016. PC progression was defined as: prostate cancer death, bone metastasis from PC, biochemical recurrence, or secondary treatment. Multivariate Cox Proportional Hazards regression was used to calculate hazards ratios (HR) and 95% confidence intervals (CI) for associations between total, whole fat, and low-fat milk; total, high-fat, and low-fat dairy; and specific dairy items and PC progression. We adjusted for time from diagnosis to FFQ, calories, age at diagnosis, CAPRA score, smoking, BMI, walking pace, and primary PC treatment. Results: 314 events were observed (mean follow-up: 7.2 y). Whole milk was associated with an increased risk of PC progression when adjusting for age, calories, and time since diagnosis (HR ≥1 vs. <1 serving/wk: 1.37; 95% CI: 1.03, 1.84; p-value: 0.03). This association was slightly attenuated, and not statistically significant, when adjusting for clinical and other lifestyle factors (HR: 1.27; 95% CI: 0.91, 1.77; p-value: 0.15). High-fat dairy intake also appeared associated with an increased risk of PC progression, but the association was not statistically significant (adjusted HR ≥4 vs. <1 servings/day: 1.40; 95% CI: 0.92, 2.13; p-trend: 0.18). Post-diagnostic intakes of low-fat milk and other dairy foods were not associated with PC progression. Conclusions: Post-diagnostic intake of milk and other dairy foods was not associated with PC progression. Research in populations with greater intake of whole milk is warranted to further investigate whether post-diagnostic whole milk intake increases risk of PC progression. Funding: This work was funded by the DOD Prostate Cancer Research Program (W81XWH-13-2-0074) and the NIH (K07CA197077).


2017 ◽  
Vol 177 (4) ◽  
pp. 297-308 ◽  
Author(s):  
Yi X Chan ◽  
Matthew W Knuiman ◽  
Mark L Divitini ◽  
Suzanne J Brown ◽  
John Walsh ◽  
...  

Context Thyroid hormones modulate proliferative, metabolic and angiogenic pathways. However few studies have examined associations of thyroid hormones with cancer risk. Objectives To explore associations of thyrotropin (TSH), free thyroxine (FT4) and anti-thyroperoxidase antibodies (TPOAb) with the incidence of all (non-skin) cancers and specific common cancers. Design and setting A prospective cohort study of a community-dwelling population aged 25–84 years in Western Australia. Main outcome measures Archived sera from 3649 participants in the 1994/1995 Busselton Health Survey were assayed for TSH, FT4 and TPOAb. Cancer outcomes until 30 June 2014 were ascertained using data linkage. Longitudinal analyses were performed using Cox proportional hazards regression. Results During 20-year follow-up, 600 participants were diagnosed with non-skin cancer, including 126, 100, 103 and 41 prostate, breast, colorectal and lung cancers respectively. Higher TSH was associated with a lower risk of prostate cancer after adjusting for potential confounders, with a 30% lower risk for every 1 mIU/L increase in TSH (adjusted hazard ratio (HR): 0.70, 95% confidence interval (CI): 0.55–0.90, P = 0.005). Similarly, higher FT4 was associated with an increased risk of prostate cancer (adjusted HR: 1.11 per 1 pmol/L increase, 95% CI: 1.03–1.19, P = 0.009). There were no associations of TSH, FT4 or TPOAb with all non-skin cancer events combined, or with breast, colorectal or lung cancer. Conclusion In a community-dwelling population, lower TSH and higher FT4 were associated with an increased risk of prostate cancer. Further studies are required to assess if thyroid function is a biomarker or risk factor for prostate cancer.


Author(s):  
Salome Weiss ◽  
Indrani Sen ◽  
Ying Huang ◽  
Jill M Killian ◽  
W. Scott Harmsen ◽  
...  

Background: Acute aortic syndrome (AAS) includes aortic dissection (AD), intramural hematoma (IMH) and penetrating aortic ulcer (PAU) and confers high rates of aortic related events. However, the risk of cardiovascular (CV) events in this patient group is unknown. The aim of this study was to define the rates of CV events in an incident cohort of AAS patients. Methods: Medical records and death certificates of all Olmsted County, MN residents with a diagnosis of AAS from 1995-2015 were reviewed and compared to age- and sex- matched population controls. Primary outcome was non-aortic CV mortality. Secondary outcome was overall mortality and first time non-fatal CV event (myocardial infarction (MI), heart failure (HF) or stroke). Events were analyzed using Cox proportional hazards regression adjusting for comorbidities. Results: Of 133 patients with AAS (77 AD, 21 IMH, 35 PAU) 57% were male, median age was 72 (SD 14) and median follow-up was 10 years. Overall survival in AAS cases and controls was 62% versus 83% at 5 years and 44% versus 60% at 10 years (adj HR 1.8, p<.001, 95% CI 1.3-2.4). CV death occurred in 21 (29%) of 73 AAS decedents due to HF (9), MI (5), other cardiac causes (5), stroke (1) and peripheral vascular disease (1). CV-related survival at 5 and 10 years after AAS diagnosis (91% and 81%) was not significantly different from controls (95% and 86%) after adjustment for comorbidities (adj HR 1.8, p=.1, 95% CI 0.9-3.6). AAS was associated with an increased risk of any first time CV event (adj HR 2.6, p<.001, 95% CI 1.6-4.4; Figure), first time diagnosis of MI (adj HR 2.8, p<.001, 95% CI 1.7-4.7) and HF (adj HR 3.2, p<.001, 95% CI 1.6-6.2) but not stroke. When excluding acute events within 14 days of diagnosis, AAS was still associated with a significantly higher mortality (adj HR 1.6, p=.011, 95% CI 1.1-2.4) and an increased risk of any first time CV event (adj HR 2.2, p=.018, 95% CI 1.1-4.1), first time MI (adj HR 2.2, p=.012, 95% CI 1.2-4.1) and HF (adj HR 2.9, p=.006, 95% CI 1.4-6.2) but not stroke. Conclusions: AAS is associated with a higher overall mortality and an increased risk of any first time CV event, first time MI and HF that persists beyond the acute phase. These data highlight the risk of CV events among those with AAS and implicate the need for long-term cardiovascular management in these patients.


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