Origin and outcome of metastatic tumours to the testes:a nationwide study

ObjectivesTo perform a retrospective cohort analysis for metastatic tumours in the testes to explore the timing, presentation and prognosis of this particular type of metastases and the factors that influence outcome.Patients and methodsA nationwide retrospective review of pathology reports of patients with pathologically confirmed metastases to the testis between 1991 and 2021 was performed. Data were collected from the Dutch nationwide pathology databank (PALGA) and the Netherlands Cancer Registry. Log-rank testing and Kaplan–Meier analyses were used to assess overall survival (OS), and Cox proportional hazard models were used for multivariate survival analysis.ResultsA total of 175 patients with a testicular metastasis were included. The median (range) age at diagnosis of testicular metastasis was 67 (3–88) years. Testicular metastases originated from a variety of primary tumours, although most frequently from the prostate (40.6%), kidney (13.7%), colon (10.3%), bladder (7.4%) and skin (5.7%). Synchronous testicular metastasis was detected in 53 cases, while 114 metachronous lesions were found after a median (interquartile range) interval of 22 (1–53) months after the original cancer diagnosis. OS after the diagnosis of a testicular metastasis was poor, with a median survival of 14.2 months (95% confidence interval 10.2–18.3). Primary tumour origin was an independent factor for survival, with worst survival for patients with primary skin, bladder and colon cancer.ConclusionTesticular metastases are very uncommon and arise mainly from primary tumours anatomically close to the testes. Most patients develop metachronous testicular metastasis at an oligometastatic disease stage. These metastases are invariably associated with poor survival

Relationships between the adverse effects of drugs and genetic polymorphism in genes encoding drug metabolizing enzymes

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Peptic ulcerations are related to systemic rather than local effects of low-dose aspirin

Background & Aims: Effervescent calcium carbasalate is a calcium-salt of acetylsalicylic acid causing less local gastric damage than acetylsalicylic acid at high doses in healthy controls. The aim of the study was to investigate the incidence of peptic ulcers in a population-based cohort using bioequivalent low-dose acetylsalicylic acid (80 mg) or effervescent calcium carbasalate (100 mg). Methods: Incident acetylsalicylic acid or effervescent calcium carbasalate users were identified from the Integrated Primary Care Information database. The study cohort comprised 19,819 subjects: 11,891 on acetylsalicylic acid and 7928 on effervescent calcium carbasalate. Incidence rates for documented peptic ulcer disease confirmed by endoscopy were calculated and time-dependent adjusted Cox regression analysis was used to compare the risk of peptic ulcers for patients using acetylsalicylic acid or effervescent calcium carbasalate. Results: During an average 1.85 years of follow-up evaluation, 115 ulcers were found. The risk for developing a peptic ulcer during drug use was: 3.07 per 1000 person-years for acetylsalicylic acid and 4.31 for effervescent calcium carbasalate. The risk of peptic ulcers was not statistically significantly higher in patients using effervescent calcium carbasalate than in acetylsalicylic acid users (adjusted hazard ratio, 1.39; 95% confidence interval, 0.92-2.12). Conclusions: The incidence rate of peptic ulcer disease is similar in patients using low-dose effervescent calcium carbasalate compared with regular low-dose acetylsalicylic acid. This implicates that peptic ulcers seem to be related to systemic rather than to local effects of low-dose acetylsalicylic acid

Primary non-variceal upper gastrointestinal bleeding in NSAID and low-dose aspirin users: development and validation of risk scores for either medication in two large Dutch cohorts

Non-steroidal anti-inflammatory drugs (NSAIDs) and low-dose acetylsalicylic acid (ASA) have several adverse gastrointestinal (GI) effects, including upper GI bleeding. We aimed to develop a simple risk score to identify high risk NSAID and ASA users for primary upper GI bleeding. Using data from two large anonymized health insurance databases, we defined a development and validation cohort with NSAID and ASA users which were followed-up for the occurrence of a primary upper GI bleeding. Cox regression analyses identified risk factors which were combined into simple risk scores. C-statistics were used to evaluate the discriminative ability of these scores in a validation cohort. In total, 421 cases of upper GI bleeding were identified in the initial cohort of 784,263 NSAID users (incidence rate 54.2 per 10,000 person-years), while 1,295 cases of upper GI bleeding were identified in 235,531 ASA users (incidence rate 37.9 per 10,000 person-years). The risk of upper GI bleeding increased with a higher risk score, which for NSAID users included age, male gender, anemia and concomitant use of ASA or anticoagulants. For ASA users, age, anemia, diabetes and concomitant use of other antiplatelet drugs or anticoagulants were included in the risk score. The C-statistics in the validation cohort were 0.68 and 0.63 or NSAID and ASA users, respectively. Risk factors for primary upper GI bleeding are to a large extent similar for NSAID and ASA users. Using a risk score based on these risk factors, patients at the highest risk can be identified with moderate accuracy

Timing of adjuvant chemotherapy and its relation to survival among patients with stage III colon cancer

Background: Currently available data suggest that delaying the start of adjuvant chemotherapy in colon cancer patients has a detrimental effect on survival. We analysed which factors impact on the timing of adjuvant chemotherapy and evaluated the influence on overall survival (OS). Patients and methods: Stage III colon cancer patients who underwent resection and received adjuvant chemotherapy between 2008 and 2013 were selected from the Netherlands Cancer Registry. Timing of adjuvant chemotherapy was subdivided into: 64, 5-6, 7-8, 9-10, 11-12 and 13-16 weeks post-surgery. Multivariable regressions were performed to assess the influence of several factors on the probability of starting treatment within 8 weeks post-surgery and to evaluate the association of timing of adjuvant chemotherapy with 5-year OS. Results: 6620 patients received adjuvant chemotherapy, 14% commenced after 8 weeks. Factors associated with starting treatment after 8 weeks were older age (Odds ratio (OR) 65-74 versus = 75 versus <65 years 1.6 (1.25-1.94)), emergency resection (OR 1.8 (1.41-2.32)), anastomotic leakage (OR 8.1 (6.14-10.62)), referral to another hospital for adjuvant chemotherapy (OR 1.9 (1.36-2.57)) and prolonged postoperative hospital admission (OR 4.7 (3.30-6.68)). Starting 5-8 weeks post-surgery showed no decrease in OS compared to initiation within 4 weeks (Hazard ratio (HR) 5-6 weeks 0.9 (0.79-1.11); HR 7-8 weeks 1.1 (0.91-1.30)). However, commencing beyond 8 weeks was associated with decreased OS compared to initiation within 8 weeks (HR 9-10 weeks 1.4 (1.21-1.68); HR 11-12 weeks 1.3 (1.06-1.59); HR 13-16 weeks 1.7 (1.23-2.23)). Conclusion: Our data support initiating adjuvant chemotherapy in stage III colon cancer patients within 8 weeks post-surgery. (C) 2015 Elsevier Ltd. All rights reserved