236 research outputs found
Interstitiaalisen virtsarakkotulehduksen eli virtsarakon kipuoireyhtymän hoito
Kansainvälinen urologityöryhmä on ehdottanut, että termi virtsarakon kipuoireyhtymä korvaisi aiemman interstitiaalinen kystiitti -termin laajan merkityksen. Interstitiaalinen kystiitti tarkoittaisi tällöin yhtä Âkipuoireyhtymän alatyyppiä, jossa on histologisesti varmennettu inflammaatio. Virtsarakon kipuoireyhtymän diagnoosi perustuu kliiniseen oirekuvaan ja muiden samantapaisia oireita Âaiheuttavien tunnettujen sairauksien poissulkemiseen. Koska sairauden etiologiaa ei tunnetta, kaikki virtsarakon kipuoireyhtymän hoitomenetelmätkin ovat Âkokemusperäisiä. Virtsarakon kipuoireyhtymä on krooninen kiputila, jonka ei oleteta paranevan. Oirelääkkeistä ja kokeilevista hoidoista on kuitenkin hyötyä.Peer reviewe
Costs of screening for prostate cancer : Evidence from the Finnish Randomised Study of Screening for Prostate Cancer after 20-year follow-up using register data
Objectives: Few empirical analyses of the impact of organised prostate cancer (PCa) screening on healthcare costs exist, despite cost-related information often being considered as a prerequisite to informed screening decisions. Therefore, we estimate the differences in register-based costs of publicly funded healthcare in the two arms of the Finnish Randomised Study of Screening for Prostate Cancer (FinRSPC) after 20 years. Methods: We obtained individual-level register data on prescription medications, as well as inpatient and outpatient care, to estimate healthcare costs for 80,149 men during the first 20 years of the FinRSPC. We compared healthcare costs for the men in each trial arm and performed statistical analysis. Results: For all men diagnosed with PCa during the 20-year observation period, mean PCa-related costs appeared to be around 10% lower in the screening arm (SA). Mean all-cause healthcare costs for these men were also lower in the SA, but differences were smaller than for PCa-related costs alone, and no longer statistically significant. For men dying from PCa, although the difference was not statistically significant, mean all-cause healthcare costs were around 10% higher. When analysis included all observations, cumulative costs were slightly higher in the CA; however, after excluding extreme values, cumulative costs were slightly higher in the SA. Conclusions: No major cost impacts due to screening were apparent, but the FinRSPC's 20-year follow-up period is too short to provide definitive evidence at this stage. Longer term follow-up will be required to be better informed about the costs of, or savings from, introducing mass PCa screening. (C) 2018 Elsevier Ltd. All rights reserved.Peer reviewe
Prostate cancer risk prediction using a polygenic risk score
Hereditary factors have a strong influence on prostate cancer (PC) risk and poorer outcomes, thus stratification by genetic factors addresses a critical need for targeted PC screening and risk-adapted follow-up. In this Finnish population-based retrospective study 2283 clinically diagnosed and 455 screen-detected patients from the Finnish Randomised Study of Screening for Prostate Cancer (FinRSPC), 2400 healthy individuals have been involved. Individual genetic risk through establishment of a polygenic risk score based on 55 PC risk SNPs identified through the Finnish subset of the Collaborative Oncological Gene-Environment Study was assessed. Men with PC had significantly higher median polygenic risk score compared to the controls (6.59 vs. 3.83, P4 ng/mL in polygenic risk score quartile four compared to quartile one (18.7% vs 8.3%, PPeer reviewe
Antihypertensive drug use and prostate cancer-specific mortality in Finnish men
The aim of this study was to investigate pre- and post-diagnostic use of antihypertensive drugs on prostate cancer (PCa)-specific survival and the initiation of androgen deprivation therapy (ADT). The cohort investigated 8,253 PCa patients with 837 PCa-specific deaths during the median follow-up of 7.6 years after diagnosis. Information on drug use, cancer incidence, clinical features of PCa, and causes of death was collected from Finnish registries. Hazard ratios with 95% confidence intervals were calculated using Cox regression with antihypertensive drug use as a time-dependent variable. Separate analyses were performed on PCa survival related to pre- and post-diagnostic use of drugs and on the initiation of ADT. Antihypertensive drug use overall was associated with an increased risk of PCa-specific death (Pre-PCa: 1.21 (1.04–1.4), Post-PCa: 1.2 (1.02–1.41)). With respect to the separate drug groups, angiotensin II type 1 receptor (ATr) blockers, were associated with improved survival (Post-PCa: 0.81 (0.67–0.99)) and diuretics with an increased risk (Post-PCa: 1.25 (1.05–1.49)). The risk of ADT initiation was slightly higher among antihypertensive drug users as compared to non-users. In conclusion, this study supports anti-cancer effect of ATr blockers on PCa prognosis and this should be investigated further in controlled clinical trials.Peer reviewe
Safety and Antitumour Activity of ODM-201 (BAY-1841788) in Chemotherapy-naĂŻve and CYP17 Inhibitor-naĂŻve Patients : Follow-up from the ARADES and ARAFOR Trials
Background: ODM-201, a new androgen receptor antagonist for treatment of metastatic castration-resistant prostate cancer (mCRPC), demonstrated antitumour activity and acceptable tolerability in phase 1/2 trials. Objective: To determine the antitumour activity and safety profile of extended treatment with ODM-201 in men with mCRPC. Design, setting, and participants: ARADES and ARAFOR trials with ODM-201 enrolled chemotherapy-naïve and CYP17 inhibitor (CYP17i)-naïve mCRPC patients. Both trials had extended follow-up. Here we report results for chemotherapy-naïve and CYP17i-naïve patients from both trials (data cutoff October 2014 for ARADES and April 2015 for ARAFOR) after extended follow-up. Intervention: A total of 41 chemotherapy-naïve and CYP17i-naïve patients received oral ODM-201 twice daily (total daily dose of 1200, 1400 or 1800 mg). Outcome measurements and statistical analysis: Antitumour activity was assessed in terms of prostate-specific antigen (PSA) declines and PSA/radiographic progression. Safety was assessed until disease progression and/or drug discontinuation due to any intolerable adverse event (AE). Results and limitations: ODM-201 safety data after a median treatment time of 13.5 mo (95% confidence interval [CI] 9.7–15.6, interquartile range [IQR] 7.5–22.0) were similar to those reported in the main ARADES and ARAFOR trials. The overall AE incidence was 80.5% (n = 33/41), with 58.5% (n = 24/41) of patients experiencing only grade 1–2 AEs. The most common AEs were fatigue, back pain, diarrhoea, nausea, and pain in extremity. The median times to PSA and radiological progression were 12.4 mo (95% CI 6.3–18.2, IQR 5.5–22.0) and 15.3 mo (95% CI 9.5–not reached [NR], IQR 6.3–NR), respectively. Conclusions: Extended treatment with ODM-201 (1200–1800 mg/d) was well tolerated, with no new safety concerns, and provided evidence of sustained antitumour activity in chemotherapy-naïve and CYP17i-naïve patients with mCRPC. Patient summary: Prolonged treatment with high doses of ODM-201 was well tolerated and provided long-lasting disease control in patients with mCRPC. ODM-201 represents a therapeutic treatment option for mCRPC. The ARAFOR trial (including the follow-up stage) and the follow-up component of the ARADES trial are registered with ClinicalTrials.gov as trial numbers NCT01784757 and NCT01429064. Extended treatment with ODM-201 was well tolerated and provided long-lasting disease control in chemotherapy- naïve and CYP17 inhibitor-naïve patients with metastatic castration-resistant prostate cancer (mCRPC). ODM-201 may represent an additional effective treatment option for mCRPC. © 2017 European Association of UrologyPeer reviewe
Inverse Association between Statin Use and Cancer Mortality Relates to Cholesterol Level
Statins have been associated with a decreased cancer mortality. However, cholesterol level as such may modify the risk of cancer death. To clarify the complex interplay between statins, cholesterol level, and cancer mortality, we conducted a comprehensive analysis to separate the effects of cholesterol level and statin medication on cancer mortality. Our study population consisted of 16,924 men participating in the Finnish Randomized Study of Screening for Prostate Cancer with at least one cholesterol measurement during follow-up (1996–2017). Cox proportional regression was used to estimate hazard ratios. In total, 1699 cancer deaths were observed during the median follow-up of 19 years. When statins’ association with the risk of cancer death was estimated without adjustment for cholesterol level, statin use was associated with a lowered cancer mortality (HR 0.87; 95% CI 0.79–0.97) compared to non-users. However, with further adjustment for total cholesterol level, statin use was no longer associated with a lower cancer mortality (HR 1.08; 95% CI 0.97–1.20). Upon stratified analysis, statin use was associated with a decreased cancer mortality only if the total cholesterol level decreased after the initiation of statin use (HR 0.66; 95% CI 0.58–0.76). The inverse association between statin use and cancer mortality is limited to men with a reduction in total cholesterol level after the commencement of statins, i.e., statin use is associated with a lowered cancer mortality only if the total cholesterol level decreases. This suggests that the effect of statin use on cancer mortality relates to the decreased total cholesterol level
Inverse Association between Statin Use and Cancer Mortality Relates to Cholesterol Level
Statins have been associated with a decreased cancer mortality. However, cholesterol level as such may modify the risk of cancer death. To clarify the complex interplay between statins, cholesterol level, and cancer mortality, we conducted a comprehensive analysis to separate the effects of cholesterol level and statin medication on cancer mortality. Our study population consisted of 16,924 men participating in the Finnish Randomized Study of Screening for Prostate Cancer with at least one cholesterol measurement during follow-up (1996–2017). Cox proportional regression was used to estimate hazard ratios. In total, 1699 cancer deaths were observed during the median follow-up of 19 years. When statins’ association with the risk of cancer death was estimated without adjustment for cholesterol level, statin use was associated with a lowered cancer mortality (HR 0.87; 95% CI 0.79–0.97) compared to non-users. However, with further adjustment for total cholesterol level, statin use was no longer associated with a lower cancer mortality (HR 1.08; 95% CI 0.97–1.20). Upon stratified analysis, statin use was associated with a decreased cancer mortality only if the total cholesterol level decreased after the initiation of statin use (HR 0.66; 95% CI 0.58–0.76). The inverse association between statin use and cancer mortality is limited to men with a reduction in total cholesterol level after the commencement of statins, i.e., statin use is associated with a lowered cancer mortality only if the total cholesterol level decreases. This suggests that the effect of statin use on cancer mortality relates to the decreased total cholesterol level
Cancer mortality does not differ by antiarrhythmic drug use : A population-based cohort of Finnish men
In-vitro studies have suggested that the antiarrhythmic drug digoxin might restrain the growth of cancer cells by inhibiting Na+/K+-ATPase. We evaluated the association between cancer mortality and digoxin, sotalol and general antiarrhythmic drug use in a retrospective cohort study. The study population consists of 78,615 men originally identified for the Finnish Randomized Study of Screening for Prostate Cancer. Information on antiarrhythmic drug purchases was collected from the national prescription database. We used the Cox regression method to analyze separately overall cancer mortality and mortality from the most common types of cancer. During the median follow-up of 17.0 years after the baseline 28,936 (36.8%) men died, of these 8,889 due to cancer. 9,023 men (11.5%) had used antiarrhythmic drugs. Overall cancer mortality was elevated among antiarrhythmic drug users compared to non-users (HR 1.43, 95% CI 1.34-1.53). Similar results were observed separately for digoxin and for sotalol. However, the risk associations disappeared in long-term use and were modified by background co-morbidities. All in all, cancer mortality was elevated among antiarrhythmic drug users. This association is probably non-causal as it was related to short-term use and disappeared in long-term use. Our results do not support the anticancer effects of digoxin or any other antiarrhythmic drug.Peer reviewe
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