ABSTRACT Introduction Men with prostate cancer (PCa) and their support providers face challenges in accessing high‐quality, impartial information tailored to their specific needs to enhance their overall care and decision‐making. We describe the development, piloting and evaluation of the co‐designed web portal ‘BroSupPORT’. Methods IT teams developed and integrated BroSupPORT into the Victorian Prostate Cancer Outcomes Registry (PCOR‐Vic) electronic patient‐reported outcome follow‐up process. A comparator tool was built enabling men to compare their patient‐reported outcome results against men of similar age, risk profile and after the same treatment. PCOR‐Vic participants were invited to access BroSupPORT after 12 months of follow‐up patient‐reported outcome measure completion. Factors associated with consent to BroSupPORT were determined using logistic regression. Portal access data were gathered from PCOR‐Vic data extracts and Google Analytics. A survey on portal exit and 2 weeks after consent was used to collect feedback. Results Over a 4‐month pilot, 331/583 (57%) men consented to accessing BroSupPORT. Among those men who accessed the portal, the majority (209/331 =63%) were diagnosed in a private hospital and resided in a major city (214/331=65%). On average, men spent 3:20 min on the portal, with sexual function aspects receiving the most attention. Twenty‐three percent of men revisited the portal during the pilot. Most men found the portal easy to use, reassuring and informative, while 9% found the patient‐reported comparisons difficult to interpret. Conclusion A patient portal—enabling men to compare their patient‐reported outcomes with other similar men and providing access to information and resources—may be a scalable solution in addressing the complex supportive care needs of men with PCa on a population basis.
To investigate whether a range of previously identified biopsychosocial risk factors were associated with poorer health-related quality of life after transport-related injuries.This study involved 1,574 participants who sustained a transport-related injury, claimed compensation through the Victorian compensation scheme (in the Australian state of Victoria), and contributed to their cross-sectional outcome survey. Health-related quality of life was assessed using the EQ-5D-3L instrument.Of the 1,574 participants (mean age 44.8 (standard deviation 16.6) years, 61% reported poor recovery expectations, 55% reported high pain intensity, 54% reported poor satisfaction with care provided, and 41% reported no improvement in their recovery. Poor quality of life was defined as EQ-5D-3L summary score 0-0.70. Predictors of self-reported poor health-related quality of life included older age (65+ years) patients (adjusted odds ratios (aOR) = 1.73, 95% confidence interval (95% CI) 1.04-2.87), higher pain intensity (aOR = 2.17, 95% CI 1.27-3.71), self-reported pre-injury chronic pain (aOR = 1.47, 95% CI 1.00-2.17), self-reported pre-injury mental health issues (aOR = 2.62, 95% CI 1.80-3.82), no improvement in recovery in the last 3 months (aOR = 1.54, 95% CI 1.15-2.06), longer hospital stay (>7 days) (aOR = 2.34, 95% CI 1.43-4.21) and no support from the family (aOR = 2.37, 95% CI 1.62-3.46).Biopsychosocial risk factors were associated with poorer health-related quality of life, regardless of the time since injury. Early assessment of these risk factors and tailored interventions will go some way towards improving outcomes among compensable patients with minor to moderate transport-related injuries. Key words: recovery; health outcomes; road trauma; non-catastrophic injuries; compensation.
Objectives: To assess the effectiveness of an intervention package comprising intense education, a range of reporting options, changes in report management and enhanced feedback, in order to improve incident-reporting rates and change the types of incidents reported. Design, setting and participants: Non-equivalent group controlled clinical trial involving medical and nursing staff working in 10 intervention and 10 control units in four major cities and two regional hospitals in South Australia. Main outcome measures: Comparison of reporting rates by type of unit, profession, location of hospital, type of incident reported and reporting mechanism between baseline and study periods in control and intervention units. Results: The intervention resulted in significant improvement in reporting in inpatient areas (additional 60.3 reports/10 000 occupied bed days (OBDs); 95% CI 23.8 to 96.8, p<0.001) and in emergency departments (EDs) (additional 39.5 reports/10 000 ED attendances; 95% CI 17.0 to 62.0, p<0.001). More reports were generated (a) by doctors in EDs (additional 9.5 reports/10 000 ED attendances; 95% CI 2.2 to 16.8, p = 0.001); (b) by nurses in inpatient areas (additional 59.0 reports/10 000 OBDs; 95% CI 23.9 to 94.1, p<0.001) and (c) anonymously (additional 20.2 reports/10 000 OBDs and ED attendances combined; 95% CI 12.6 to 27.8, p<0.001). Compared with control units, the study resulted in more documentation, clinical management and aggression-related incidents in intervention units. In intervention units, more reports were submitted on one-page forms than via the call centre (1005 vs 264 reports, respectively). Conclusions: A greater variety and number of incidents were reported by the intervention units during the study, with improved reporting by doctors from a low baseline. However, there was considerable heterogeneity between reporting rates in different types of units.
The role of nitric oxide (NO) formed by the inducible isoform of NO synthase (NOS) in the generation of indomethacin‐induced intestinal microvascular leakage was investigated in the rat. 2 Indomethacin (10 mg kg −1 , s.c.) provoked an elevation of vascular leakage of radiolabelled human serum albumin in the jejunum over 48 h, commencing 18 h after its administration. This was associated with the induction of a calcium‐independent NOS, as assessed by the conversion of radiolabelled L‐arginine to citrulline. 3 Pretreatment with the glucocorticoid, dexamethasone (1 mg kg −1 day −1 , s.c.) inhibited the induction of NOS and reduced jejunal microvascular leakage, determined 24 and 48 h after indomethacin. 4 Administration of the broad‐spectrum antibiotic, ampicillin (800 mg kg −1 day −1 , p.o.) likewise inhibited both the induction of NOS and the plasma leakage observed 24 and 48 h after indomethacin. 5 Ampicillin pretreatment did not, however, inhibit the induction of NOS, determined 5 h following endotoxin (3 mg kg −1 i.v.) challenge. Furthermore, incubation with ampicillin (1 mM, 10 min) did not inhibit the activity of the calcium‐independent isoform in vitro . 6 Administration of the NOS inhibitor, N G ‐nitro‐L‐arginine methyl ester (L‐NAME, 2–10 mg kg −1 , s.c.), at the time of the detectable expression of the inducible NOS (18 h after indomethacin), dose‐dependently attenuated the plasma leakage, determined 6 later. This effect was reversed by pretreatment with L‐arginine (300 mg kg −1 , s.c.) 15 min before L‐NAME. 7 These findings suggest that induction of a calcium‐independent NOS following indomethacin administration involves gut bacteria and leads to microvascular injury in the rat jejunum.
Prostate cancer is the most commonly diagnosed and prevalent malignancy reported to Australian cancer registries, with numerous studies from single institutions summarizing patient outcomes at individual hospitals or States. In order to provide an overview of patterns of care of men with prostate cancer across multiple institutions in Australia, a specialized dataset was developed. This dataset, containing amalgamated data from South Australian and Victorian prostate cancer registries, is called the South Australian-Victorian Prostate Cancer Health Outcomes Research Dataset (SA-VIC PCHORD). A total of 13,598 de-identified records of men with prostate cancer diagnosed and consented between 2008 and 2013 in South Australia and Victoria were merged into the SA-VIC PCHORD. SA-VIC PCHORD contains detailed information about socio-demographic, diagnostic and treatment characteristics of patients with prostate cancer in South Australia and Victoria. Data from individual registries are available to researchers and can be accessed under individual data access policies in each State. The SA-VIC PCHORD will be used for numerous studies summarizing trends in diagnostic characteristics, survival and patterns of care in men with prostate cancer in Victoria and South Australia. It is expected that in the future the SA-VIC PCHORD will become a principal component of the recently developed bi-national Australian and New Zealand Prostate Cancer Outcomes Registry to collect and report patterns of care and standardised patient reported outcome measures of men nation-wide in Australia and New Zealand.
To perform a systematic review and meta-analysis of the literature to understand the variation in the reporting of neuroendocrine staining and determine the influence of reporting neuroendocrine staining at diagnosis on patient outcomes.Medical databases were searched to identify studies in which adenocarcinoma specimens were stained with any of the following four neuroendocrine markers: chromogranin A (CgA), neuron-specific enolase (NSE), synaptophysin and CD56. The prevalence of neuroendocrine staining and correlation of the prevalence of neuroendocrine staining to patient outcomes were analysed using a random-effects model. All statistical tests were two-sided.Sixty-two studies spanning 7616 patients were analysed. The pooled prevalence for the most common marker, CgA (41%), was similar to that of NSE (39%) and higher than that of synaptophysin (31%). The prevalence of CgA staining was significantly influenced by reporting criteria, where objective thresholds reduced the variation in prevalence to 26%. No correlation was found between CgA prevalence and tumour grade. Patients positive for CgA staining using objective criteria had more rapid biochemical progression (hazard ratio [HR] 1.98, 95% confidence interval [CI] 1.49 to 2.65) and poorer prostate cancer-specific survival (HR 7.03, 95% CI 2.55 to 19.39) compared to negative patients, even among those with low-risk cancers.Discrepancies in the reported prevalence of neuroendocrine cells in adenocarcinoma are driven by the inconsistent scoring criteria. This study unequivocally demonstrates that when neuroendocrine cell staining is assessed with objective criteria it identifies patients with poor clinical outcomes. Future studies are needed to determine the exact quantifiable thresholds for use in reporting neuroendocrine cell staining to identify patients at higher risk of progression.
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