BACKGROUND: Hand hygiene (HH) is central in prevention of health care-associated infections. In low resource settings, models to improve HH compliance are needed. We implemented a continuous quality improvement (CQI) program targeting HH in two hospitals in Kenya. OBJECTIVE: To determine the impact of the HH CQI program and identify factors associated with HH compliance between 2018 and 2019. METHODS: A CQI project targeting the improvement of hand hygiene was implemented, including training and mentorship. Data were collected monthly between April 2018 and December 2019 in Thika and Kitale Hospitals. Healthcare workers trained on Infection Prevention and Control (IPC) observed and recorded HH opportunities and subsequent compliance among staff, including nurses, clinicians, and auxiliary staff, using the World Health Organization's "My Five Moments for Hand Hygiene" tool. Covariates were explored using mixed-effects logistic regression with random department-level intercepts. RESULTS: Hand hygiene compliance improved from 27% at baseline to 44% after 21 months. Indication/moment for HH was significantly associated with compliance. Adjusting for site, professional category and department, compliance was higher after a moment of body fluid exposure (aOR 1.43, 95% CI 1.17–1.74, p value < 0.001) and lower before an aseptic procedure (aOR 0.12, 95% CI 0.08–0.17, p value < 0.001) compared to after patient contact. Wearing of gloves often replaced proper HH in surgical departments, which although not significant, had lower compliance compared to departments for internal medicine (aOR 0.93, 95% CI 0.85–1.02). Adjusted HH compliance from all quarters improved from baseline, but comparing each quarter to the previous quarter, the improvement fluctuated over time. CONCLUSION: Training and mentorship on the importance of HH for all moments is needed to improve overall HH compliance. CQI with regular monitoring and feedback of HH performance can be an effective approach in improving HH compliance in public hospitals ...
Funder: Victorian Cancer Agency ; Funder: NIHR Manchester Biomedical Research Centre ; Funder: Cancer Research UK ; Funder: Cancer Council Tasmania ; Funder: Instituto de Salud Carlos III ; Funder: Cancer Australia ; Funder: NIHR Oxford Biomedical Research Centre ; Funder: Fundación Científica de la Asociación Española Contra el Cáncer ; Funder: Cancer Council South Australia ; Funder: Swedish Cancer Society ; Funder: NIHR Cambridge Biomedical Research Centre ; Funder: Institut Català de la Salut ; Funder: Cancer Council Victoria ; Funder: Prostate Cancer Foundation of Australia ; Funder: National Institutes of Health ; BACKGROUND: Lynch syndrome is a rare familial cancer syndrome caused by pathogenic variants in the mismatch repair genes MLH1, MSH2, MSH6, or PMS2, that cause predisposition to various cancers, predominantly colorectal and endometrial cancer. Data are emerging that pathogenic variants in mismatch repair genes increase the risk of early-onset aggressive prostate cancer. The IMPACT study is prospectively assessing prostate-specific antigen (PSA) screening in men with germline mismatch repair pathogenic variants. Here, we report the usefulness of PSA screening, prostate cancer incidence, and tumour characteristics after the first screening round in men with and without these germline pathogenic variants. METHODS: The IMPACT study is an international, prospective study. Men aged 40-69 years without a previous prostate cancer diagnosis and with a known germline pathogenic variant in the MLH1, MSH2, or MSH6 gene, and age-matched male controls who tested negative for a familial pathogenic variant in these genes were recruited from 34 genetic and urology clinics in eight countries, and underwent a baseline PSA screening. Men who had a PSA level higher than 3·0 ng/mL were offered a transrectal, ultrasound-guided, prostate biopsy and a histopathological analysis was done. All participants are undergoing a minimum of 5 years' annual screening. The primary endpoint was to determine the incidence, stage, and pathology of screening-detected prostate cancer in carriers of pathogenic variants compared with non-carrier controls. We used Fisher's exact test to compare the number of cases, cancer incidence, and positive predictive values of the PSA cutoff and biopsy between carriers and non-carriers and the differences between disease types (ie, cancer vs no cancer, clinically significant cancer vs no cancer). We assessed screening outcomes and tumour characteristics by pathogenic variant status. Here we present results from the first round of PSA screening in the IMPACT study. This study is registered with ClinicalTrials.gov, NCT00261456, and is now closed to accrual. FINDINGS: Between Sept 28, 2012, and March 1, 2020, 828 men were recruited (644 carriers of mismatch repair pathogenic variants [204 carriers of MLH1, 305 carriers of MSH2, and 135 carriers of MSH6] and 184 non-carrier controls [65 non-carriers of MLH1, 76 non-carriers of MSH2, and 43 non-carriers of MSH6]), and in order to boost the sample size for the non-carrier control groups, we randomly selected 134 non-carriers from the BRCA1 and BRCA2 cohort of the IMPACT study, who were included in all three non-carrier cohorts. Men were predominantly of European ancestry (899 [93%] of 953 with available data), with a mean age of 52·8 years (SD 8·3). Within the first screening round, 56 (6%) men had a PSA concentration of more than 3·0 ng/mL and 35 (4%) biopsies were done. The overall incidence of prostate cancer was 1·9% (18 of 962; 95% CI 1·1-2·9). The incidence among MSH2 carriers was 4·3% (13 of 305; 95% CI 2·3-7·2), MSH2 non-carrier controls was 0·5% (one of 210; 0·0-2·6), MSH6 carriers was 3·0% (four of 135; 0·8-7·4), and none were detected among the MLH1 carriers, MLH1 non-carrier controls, and MSH6 non-carrier controls. Prostate cancer incidence, using a PSA threshold of higher than 3·0 ng/mL, was higher in MSH2 carriers than in MSH2 non-carrier controls (4·3% vs 0·5%; p=0·011) and MSH6 carriers than MSH6 non-carrier controls (3·0% vs 0%; p=0·034). The overall positive predictive value of biopsy using a PSA threshold of 3·0 ng/mL was 51·4% (95% CI 34·0-68·6), and the overall positive predictive value of a PSA threshold of 3·0 ng/mL was 32·1% (20·3-46·0). INTERPRETATION: After the first screening round, carriers of MSH2 and MSH6 pathogenic variants had a higher incidence of prostate cancer compared with age-matched non-carrier controls. These findings support the use of targeted PSA screening in these men to identify those with clinically significant prostate cancer. Further annual screening rounds will need to confirm these findings. FUNDING: Cancer Research UK, The Ronald and Rita McAulay Foundation, the National Institute for Health Research support to Biomedical Research Centres (The Institute of Cancer Research and Royal Marsden NHS Foundation Trust; Oxford; Manchester and the Cambridge Clinical Research Centre), Mr and Mrs Jack Baker, the Cancer Council of Tasmania, Cancer Australia, Prostate Cancer Foundation of Australia, Cancer Council of Victoria, Cancer Council of South Australia, the Victorian Cancer Agency, Cancer Australia, Prostate Cancer Foundation of Australia, Asociación Española Contra el Cáncer (AECC), the Instituto de Salud Carlos III, Fondo Europeo de Desarrollo Regional (FEDER), the Institut Català de la Salut, Autonomous Government of Catalonia, Fundação para a Ciência e a Tecnologia, National Institutes of Health National Cancer Institute, Swedish Cancer Society, General Hospital in Malmö Foundation for Combating Cancer.
Background: Prostate-specific antigen (PSA) and PSA-velocity (PSAV) have been used to identify men at risk of prostate cancer (PrCa). The IMPACT study is evaluating PSA screening in men with a known genetic predisposition to PrCa due to BRCA1/2 mutations. This analysis evaluates the utility of PSA and PSAV for identifying PrCa and high-grade disease in this cohort. Methods: PSAV was calculated using logistic regression to determine if PSA or PSAV predicted the result of prostate biopsy (PB) in men with elevated PSA values. Cox regression was used to determine whether PSA or PSAV predicted PSA elevation in men with low PSAs. Interaction terms were included in the models to determine whether BRCA status influenced the predictiveness of PSA or PSAV. Results: 1634 participants had 3 PSA readings of whom 174 underwent PB and 45 PrCas diagnosed. In men with PSA >3.0 ng ml−l, PSAV was not significantly associated with presence of cancer or high-grade disease. PSAV did not add to PSA for predicting time to an elevated PSA. When comparing BRCA1/2 carriers to non-carriers, we found a significant interaction between BRCA status and last PSA before biopsy (P=0.031) and BRCA2 status and PSAV (P=0.024). However, PSAV was not predictive of biopsy outcome in BRCA2 carriers. Conclusions: PSA is more strongly predictive of PrCa in BRCA carriers than non-carriers. We did not find evidence that PSAV aids decision-making for BRCA carriers over absolute PSA value alone. ; This research is coordinated by the Institute of Cancer Research, London, UK and is supported by grants from Cancer Research UK (Grant references (C5047/A21332, C5047/A13232 and C5047/A17528) and The Ronald and Rita McAulay Foundation. Mr and Mrs Jack Baker for the study in NorthShore University HealthSystem, Evanston, Illinois and Myriad Genetics Laboratory, Salt Lake City, Utah, for providing research BRCA testing rates for NorthShore University HealthSystem participants. We acknowledge funding from the NIHR to the Biomedical Research Center at The Institute of Cancer Research and The Royal Marsden NHS Foundation Trust, at Central Manchester Foundation Trust and the Oxford Biomedical Research Centre Program. We acknowledge that in Australia, this project was co-funded by Cancer Council Tasmania and Cancer Australia, grant number 1006349 (2011–2013), Prostate Cancer Foundation of Australia, grant number PCFA PRO4 (2008) and Cancer Councils of Victoria and South Australia, grant number 400048 (2006–2008), The Victorian Cancer Agency Clinical Trial Capacity CTCB08_14, Cancer Australia & Prostate Cancer Foundation of Australia (2014–2016) grant number 1059423, and Translational grants EOI09_50. The Association of International Cancer Research funded data collection in The Netherlands (AICR 10–0596). We acknowledge funding from the Basser Center for BRCA (to S Domchek). We acknowledge funding from the National Cancer Institute [P30-CA008748], the Sidney Kimmel Center for Prostate and Urologic Cancers, and David H. Koch through the Prostate Cancer Foundation, the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre Program in UK, Swedish Cancer Society (Cancerfonden project no. 11–0624), and the Swedish Research Council (VR-MH project no. 2016–02974). We acknowledge funding from the Slovenian Research Agency, Research programme P3–0352. Elena Castro acknolwedges funding from a Juan de la Cierva' fellowship from MINIECO (grant reference IJCI- 2014–19129). We acknowledge the support of the Asociación Española Contra el Cáncer (AECC), the Instituto de Salud Carlos III (organismo adscrito al Ministerio de Economía y Competitividad) and 'Fondo Europeo de Desarrollo Regional (FEDER), una manera de hacer Europa' (PI10/01422, PI13/00285, PIE13/00022, PI16/00563 and CIBERONC) and the Institut Català de la Salut and Autonomous Government of Catalonia (2009SGR290, 2014SGR338 and PERIS Project MedPerCan). ; Peer Reviewed