Effect of chronic treatment of combined statins and aspirin on the risk of prostate cancer detection.

2012 ◽  
Vol 30 (5_suppl) ◽  
pp. 185-185
Author(s):  
Cristina Suarez ◽  
Rafael Morales ◽  
Jose Placer ◽  
Isaac Nunez ◽  
Jacques Planas ◽  
...  

185 Background: The role of chronic treatment (ChT) with statins and aspirin on prostate cancer (PC) carcinogenesis is controversial. Both drugs are frequently used in adult men who are at risk of PC, and many of them receive both drugs simultaneously. The impact of the combined treatment (CT) with statins and aspirin on PC risk has never been reported. We proposed to explore the influence of ChT with statins and aspirin in the PC risk detection and their aggressiveness. Methods: 2408 men were consecutively biopsied for cause: PSA > 4 ng/mL (64.4%), abnormal DRE (9%) or both (26.6%). ChT with statins and aspirin (>1 year) was controlled. Median age was 68 years (46–86) and median PSA 7.0 ng/mL (0.7-1279). At least 10 cores, plus 1 to 8 additional cores, were obtained. The PC detection rate was 35.2% and the Gleason score was < 7 in 20.8%, 7 in 50.9% and > 7 (HGPC) in 28.3%. Multivariate and univariate analysis were done and OR calculated to analyze the strength of the relationships. Results: 440 men (18.3%) were receiving statins alone (SA), 160 (6.6%) aspirin alone (AA), and 304 (12.6%) both drugs simultaneously. Multivariate analysis showed that CT was the only independent predictor of a reduced risk of PC detection, p=0.025, (OR 0.589, 95%CI 0.370-0-936). PC was detected in 552 of 1502 men (36.7%) not receiving statins or aspirin, 34.5% (152/440) receiving SA, 40% (64/160) receiving AA, and in 26.3% (80/304) receiving statins and aspirin simultaneously. Related to cancer aggressiveness, multivariate analysis showed that combined treatment predicted significantly an increased risk of HGPC, p=0.013, (OR 2.672, 95%CI 1.226-5.825). HGPC was detected in 136 of 552 (24.6%) PCs detected in men not receiving statins or aspirin, in 40 of 152 (26.3%) PCs detected in men receiving SA, in 24 of 64 (37.7%) PCs detected in men receiving AA, and in 40 of 80 (50%) PCs detected in men receiving statins and aspirin simultaneously. Conclusions: This study suggests that ChT with the combination of statins and aspirin reduce significantly the risk of PC detection in men subjected to prostate biopsy for cause. However, this reduction of PC detection is accompanied by a significant increase of PC aggressiveness.

2016 ◽  
Vol 34 (12) ◽  
pp. 1345-1349 ◽  
Author(s):  
Yaw A. Nyame ◽  
Adam B. Murphy ◽  
Diana K. Bowen ◽  
Gregory Jordan ◽  
Ken Batai ◽  
...  

Purpose Lower serum vitamin D levels have been associated with an increased risk of aggressive prostate cancer. Among men with localized prostate cancer, especially with low- or intermediate-risk disease, vitamin D may serve as an important biomarker of disease aggression. The aim of this study was to assess the relationship between adverse pathology at the time of radical prostatectomy and serum 25-hydroxyvitamin D (25-OH D) levels. Methods This cross-sectional study was carried out from 2009 to 2014, nested within a large epidemiologic study of 1,760 healthy controls and men undergoing prostate cancer screening. In total, 190 men underwent radical prostatectomy in the cohort. Adverse pathology was defined as the presence of primary Gleason 4 or any Gleason 5 disease, or extraprostatic extension. Descriptive and multivariate analyses were performed to assess the relationship between 25-OH D and adverse pathology at the time of prostatectomy. Results Eighty-seven men (45.8%) in this cohort demonstrated adverse pathology at radical prostatectomy. The median age in the cohort was 64.0 years (interquartile range, 59.0 to 67.0). On univariate analysis, men with adverse pathology at radical prostatectomy demonstrated lower median serum 25-OH D (22.7 v 27.0 ng/mL, P = .007) compared with their counterparts. On multivariate analysis, controlling for age, serum prostate specific antigen, and abnormal digital rectal examination, serum 25-OH D less than 30 ng/mL was associated with increased odds of adverse pathology (odds ratio, 2.64; 95% CI, 1.25 to 5.59; P = .01). Conclusion Insufficiency/deficiency of serum 25-OH D is associated with increased odds of adverse pathology in men with localized disease undergoing radical prostatectomy. Serum 25-OH D may serve as a useful biomarker in prostate cancer aggressiveness, which deserves continued study.


2015 ◽  
Vol 11 (2) ◽  
pp. 1-7
Author(s):  
Kaushal Kishore Tiwari ◽  
Alfredo Guiseppe Cerillo ◽  
Simona Storti ◽  
Stefano Bevilacqua ◽  
Aldo Clerico ◽  
...  

noBackground & Objectives: The postoperative Low T3 syndrome has been considered as a possible source of reduced myocardial contractility, resulting in increased mortality after CABG. Effect of preoperative Low T3 has not been well studied in patients undergoing CABG surgery. Aim of our study is to evaluate effect of preoperative Low T3 syndrome in patients undergoing CABG surgery.Materials & Methods: Six hundred and six patients undergoing CABG were included in this prospective study. The impact of the base-line FT3 concentration and of preoperative low T3 syndrome on the risk of postoperative low cardiac output and hospital death was analyzed.Results: Fifteen patients (2.3%) postoperatively and 159 (26.2%) developed major complications. At univariate analysis a reduced EF, the presence of peripheral vascular disease, the NYHA class, the surgical urgency, the aortic cross-clamp time, the CPB time and the FT3 concentration at admission were significantly associated with low CO and higher mortality. At multivariate analysis, the CPB time, an emergency procedure, a reduced LVEF, and the fT3 concentration were independently related to the development of low CO. However, in multivariate analysis low EF, and the fT3 concentration were the only predictors of hospital death.Conclusion: We conclude that preoperative low EF and low T3 syndrome independently causes low cardiac output and higher mortality in patients undergoing CABG. Therefore, all patients undergoing CABG should be evaluated for low T3 syndrome and patients with low T3 syndrome should be considered at increased risk. Appropriate preoperative T3 replacement therapy could decrease the postoperative complications in patients undergoing CABG.JCMS Nepal. 2015; 11(2):1-7


Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 37-37 ◽  
Author(s):  
Elena Santagostino ◽  
Angiola Rocino ◽  
Maria E. Mancuso ◽  
Maria G. Mazzucconi ◽  
Giacomo Mancuso ◽  
...  

Abstract In a multicenter case-control study we investigated the impact of prenatal/perinatal events and early FVIII exposure on the inhibitor risk in hemophiliacs. Patients: 102 children (age:13–196 months) with hemophilia A (FVIII≤2%) exclusively treated with recombinant FVIII and evaluated for inhibitors every 3 months were included. Forty-seven patients who developed inhibitors at the median age of 26 months (4–80) after a median of 16 exposure days (ED, 5–150), 37 high-responders (6–500 BU/mL) and 10 low-responders (<5 BU/mL), were compared with 55 children who did not develop inhibitors after at least 20 ED (5<50, 4<100, 10<200 and 36>200 ED). Results: by univariate analysis, family history of inhibitors, intron 22 inversion and prophylaxis started after the first 20 ED were significantly associated with an increased risk of inhibitor development (OR 9.5, 95%CI 1.1–79.9; OR 2.7, 95%CI 1.1–6.6; OR 3.7, 95%CI 1.1–12.1, respectively). No statistically significant differences were found for variables such as villocentesis/amniocentesis, premature/caesarian birth, breast-feeding, surgery, central venous devices and FVIII infusions associated with infections/vaccinations. By multivariate analysis, the inhibitor risk was 2.8-folds (95%CI 1.1–7.3) in children with intron 22 inversion and 4.5-folds (95%CI 1.1–17.5) in patients who started prophylaxis after the first 20 ED. By univariate and multivariate analysis, there was not a linear trend in the inhibitor development according to the age at first FVIII exposure (≤6, 7–12, 13–18, 19–24, >24 months). Conclusions: this study showed that starting prophylaxis within the first 20 ED had a favourable impact on the inhibitor risk independently from the age at first FVIII exposure.


2004 ◽  
Vol 22 (3) ◽  
pp. 446-453 ◽  
Author(s):  
Stephen J. Freedland ◽  
William J. Aronson ◽  
Christopher J. Kane ◽  
Joseph C. Presti ◽  
Christopher L. Amling ◽  
...  

Purpose Given the limited information regarding the impact of obesity on treatment outcomes for prostate cancer, we sought to examine the relationship between body mass index (BMI) and cancer control after radical prostatectomy (RP). Patients and Methods We compared clinicopathologic and biochemical outcome information across BMI groups from 1,106 men treated with RP between 1988 and 2002. Multivariate analysis was used to determine if BMI significantly predicted adverse pathology or biochemical recurrence. Results Obesity was related to year of surgery (P < .001) and race (P < .001), with black men having the highest obesity rates. Obese patients had higher biopsy and pathologic grade tumors (P < .001). On multivariate analysis, BMI ≥ 35 kg/m2 was associated with a trend for higher rates of positive surgical margins (P = .008). Overweight patients (BMI, 25 to 30 kg/m2) had a significantly decreased risk of seminal vesicle invasion (P = .039). After controlling for all preoperative clinical variables including year of surgery, BMI ≥ 35 kg/m2 significantly predicted biochemical failure after RP (P = .002). After controlling for surgical margin status, BMI ≥ 35 kg/m2 remained a significant predictor of biochemical failure (P = .012). There was a trend for BMI ≥ 35 kg/m2 to be associated with higher failure rates than BMI between 30 and 35 kg/m2 (P = .053). Conclusion The percentage of obese men undergoing RP in our data set doubled in the last 10 years. Obesity was associated with higher-grade tumors, a trend toward increased risk of positive surgical margins, and higher biochemical failure rates among men treated with RP. A BMI ≥ 35 kg/m2 was associated with a higher risk of failure than a BMI between 30 and 35 kg/m2.


Author(s):  
Naomi Morka ◽  
Joseph M. Norris ◽  
Mark Emberton ◽  
Daniel Kelly

AbstractProstate cancer affects a significant proportion of men worldwide. Evidence from genetic and clinical studies suggests that there may be a causal association between prostate cancer and the human papilloma virus (HPV). As HPV is a vaccine-preventable pathogen, the possibility of a role in prostate cancer causation may reinforce the importance of effective HPV vaccination campaigns. This is of particular relevance in light of the COVID-19 pandemic, which may have considerable effects on HPV vaccine uptake and distribution.


2021 ◽  
Vol 22 (10) ◽  
pp. 5100
Author(s):  
Paulina Kozakiewicz ◽  
Ludmiła Grzybowska-Szatkowska ◽  
Marzanna Ciesielka ◽  
Jolanta Rzymowska

The mitochondria are essential for normal cell functioning. Changes in mitochondrial DNA (mtDNA) may affect the occurrence of some chronic diseases and cancer. This process is complex and not entirely understood. The assignment to a particular mitochondrial haplogroup may be a factor that either contributes to cancer development or reduces its likelihood. Mutations in mtDNA occurring via an increase in reactive oxygen species may favour the occurrence of further changes both in mitochondrial and nuclear DNA. Mitochondrial DNA mutations in postmitotic cells are not inherited, but may play a role both in initiation and progression of cancer. One of the first discovered polymorphisms associated with cancer was in the gene NADH-ubiquinone oxidoreductase chain 3 (mt-ND3) and it was typical of haplogroup N. In prostate cancer, these mutations and polymorphisms involve a gene encoding subunit I of respiratory complex IV cytochrome c oxidase subunit 1 gene (COI). At present, a growing number of studies also address the impact of mtDNA polymorphisms on prognosis in cancer patients. Some of the mitochondrial DNA polymorphisms occur in both chronic disease and cancer, for instance polymorphism G5913A characteristic of prostate cancer and hypertension.


2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Victoria Hale ◽  
Maren Weischer ◽  
Jong Y. Park

Although the causes of prostate cancer are largely unknown, previous studies support the role of genetic factors in the development of prostate cancer.CHEK2plays a critical role in DNA replication by responding to double-stranded breaks. In this review, we provide an overview of the current knowledge of the role of a genetic variant, 1100delC, ofCHEK2on prostate cancer risk and discuss the implication for potential translation of this knowledge into clinical practice. Currently, twelve articles that discussedCHEK2∗1100delC and its association with prostate cancer were identified. Of the twelve prostate cancer studies, five studies had independent data to draw conclusive evidence from. The pooled results of OR and 95% CI were 1.98 (1.23–3.18) for unselected cases and 3.39 (1.78–6.47) for familial cases, indicating thatCHEK2∗1100delC mutation is associated with increased risk of prostate cancer. Screening for CHEK2∗1100delC should be considered in men with a familial history of prostate cancer.


2022 ◽  
Vol 23 (2) ◽  
pp. 870
Author(s):  
Anna Kawalec ◽  
Danuta Zwolińska

The microbiome of the urinary tract plays a significant role in maintaining health through the impact on bladder homeostasis. Urobiome is of great importance in maintaining the urothelial integrity and preventing urinary tract infection (UTI), as well as promoting local immune function. Dysbiosis in this area has been linked to an increased risk of UTIs, nephrolithiasis, and dysfunction of the lower urinary tract. However, the number of studies in the pediatric population is limited, thus the characteristic of the urobiome in children, its role in a child’s health, and pediatric urologic diseases are not completely understood. This review aims to characterize the healthy urobiome in children, the role of dysbiosis in urinary tract infection, and to summarize the strategies to modification and reshape disease-prone microbiomes in pediatric patients with recurrent urinary tract infections.


2014 ◽  
Vol 2014 ◽  
pp. 1-23 ◽  
Author(s):  
Flavio Barchetti ◽  
Valeria Panebianco

The clinical suspicion of local recurrence of prostate cancer (PCa) after radical prostatectomy (RP) and after radiation therapy (RT) is based on the onset of biochemical failure. The aim of this paper was to review the current role of multiparametric-MRI (mp-MRI) in the detection of locoregional recurrence. A systematic literature search using the Medline and Cochrane Library databases was performed from January 1995 up to November 2013. Bibliographies of retrieved and review articles were also examined. Only those articles reporting complete data with clinical relevance for the present review were selected. This review article is divided into two major parts: the first one considers the role of mp-MRI in the detection of PCa local recurrence after RP; the second part provides an insight about the impact of mp-MRI in the depiction of locoregional recurrence after RT (interstitial or external beam). Published data indicate an emerging role for mp-MRI in the detection and localization of locally recurrent PCa both after RP and RT which represents an information of paramount importance to perform focal salvage treatments.


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