OHDSI MEETINGS THIS WEEK
The Book of OHDSI working group meeting - Tuesday at 11am ET
Zoom URL: https://columbiauniversity.zoom.us/j/258043190
OHDSI Community Call - Tuesday at 12pm ET
ATLAS workgroup meeting - Wednesday at 10am ET
Psychiatry Work Group - Thursday at 8am ET
Population-Level Estimation WG (Eastern Hemisphere) - Thursday at 3am ET
EHR Work Group Meeting - Friday at 10am ET
You can find a full list of upcoming OHDSI meetings here:
Looking for presenters for upcoming OHDSI community calls We are looking for collaborators to share their work on upcoming OHDSI calls. If you are interested in presenting on an upcoming OHDSI call please email me at email@example.com
OHDSI study published in Lancet! The LEGEND hypertension study been published in the Lancet! To check out the paper, click here:
For more info on the study, check out our press release:
OHDSI Symposium Page - A full recap of the 2019 OHDSI U.S. Symposium, including photos, videos, collaborator showcase posters, and more, is available here https://www.ohdsi.org/2019-us-symposium-page/. You can find it on the front page under the Symposium recap video, or as the first dropdown under the “2019 OHDSI Symposium” menu. Presentation slides are available there, and Symposium talks will begin to be posted this week, starting with the morning plenary session.
OHDSI Social Showcase We are in the second week of posting one poster/demo/lightning talk from the Collaborator Showcase ( #OHDSISocialShowcase) each weekday on both our Twitter and LinkedIn pages. Please check these out if you are on either, and share to promote all the great work OHDSI is doing. If you took part in the Collaborator Showcase, you’ll get an email on the Monday of the week you will be included to help you promote it.
2019 OHDSI Symposium - Videos Videos from the 2019 OHDSI symposium, including presentations from the main symposium, tutorials and the Women in Real-World Analytics leadership forum are current in post-production and will be made available shortly.
Words have no power to impress the mind without the exquisite horror of their reality.
Edgar Allan Poe COMMUNITY PUBLICATIONS
Comprehensive comparative effectiveness and safety of first-line antihypertensive drug classes: a systematic, multinational, large-scale analysis
Distributed Analytics on Sensitive Medical Data: The Personal Health Train
Adherence to clinical practice guidelines for the prevention of acute chemotherapy-induced nausea and vomiting in children, adolescents, and young adults with cancer receiving their first cycle of highly emetogenic chemotherapy.
Comparison of First-Line Dual Combination Treatments in Hypertension: Real-World Evidence from Multinational Heterogeneous Cohorts.
SC You, S Jung, JN Swerdel, PB Ryan, MJ Schuemie, MA Suchard, S Lee, J Cho, G Hripcsak, RW Park and S Park,
Korean circulation journal, Aug 28 2019
2018 ESC/ESH Hypertension guideline recommends 2-drug combination as initial anti-hypertensive therapy. However, real-world evidence for effectiveness of recommended regimens remains limited. We aimed to compare the effectiveness of first-line anti-hypertensive treatment combining 2 out of the following classes: angiotensin-converting enzyme (ACE) inhibitors/angiotensin-receptor blocker (A), calcium channel blocker (C), and thiazide-type diuretics (D).Treatment-naïve hypertensive adults without cardiovascular disease (CVD) who initiated dual anti-hypertensive medications were identified in 5 databases from US and Korea. The patients were matched for each comparison set by large-scale propensity score matching. Primary endpoint was all-cause mortality. Myocardial infarction, heart failure, stroke, and major adverse cardiac and cerebrovascular events as a composite outcome comprised the secondary measure.A total of 987,983 patients met the eligibility criteria. After matching, 222,686, 32,344, and 38,513 patients were allocated to A+C vs. A+D, C+D vs. A+C, and C+D vs. A+D comparison, respectively. There was no significant difference in the mortality during total of 1,806,077 person-years: A+C vs. A+D (hazard ratio [HR], 1.08; 95% confidence interval [CI], 0.97-1.20; p=0.127), C+D vs. A+C (HR, 0.93; 95% CI, 0.87-1.01; p=0.067), and C+D vs. A+D (HR, 1.18; 95% CI, 0.95-1.47; p=0.104). A+C was associated with a slightly higher risk of heart failure (HR, 1.09; 95% CI, 1.01-1.18; p=0.040) and stroke (HR, 1.08; 95% CI, 1.01-1.17; p=0.040) than A+D.There was no significant difference in mortality among A+C, A+D, and C+D combination treatment in patients without previous CVD. This finding was consistent across multi-national heterogeneous cohorts in real-world practice.
Incidence, prevalence, and management of plantar heel pain: a retrospective cohort study in Dutch primary care.
N Rasenberg, SM Bierma-Zeinstra, PJ Bindels, J van der Lei and M van Middelkoop,
The British journal of general practice : the journal of the Royal College of General Practitioners, Oct 21 2019
Plantar heel pain (PHP) is a common cause of foot complaints in general practice. However, information on the occurrence and practical management is scarce.The aim of this study was to determine the incidence and prevalence of PHP in Dutch primary care and to gain insight into the types of treatments provided to patients with PHP in primary care.A cohort study was conducted using a healthcare database containing the electronic general practice medical records of approximately 1.9 million patients throughout the Netherlands.A search algorithm was defined and used to identify cases of PHP from January 2013 to December 2016. Descriptive statistics were used to obtain the incidence and prevalence. Data on the management of PHP were manually validated in a random sample of 1000 patients.The overall incidence of PHP was 3.83 cases (95% confidence interval [CI] = 3.77 to 3.89) per 1000 patient-years, the incidence in females was 4.64 (95% CI = 4.55 to 4.72), and 2.98 (95% CI = 2.91 to 3.05) in males. The overall prevalence of PHP was 0.4374% (95% CI = 0.4369 to 0.4378%). Incidence of PHP peaked in September and October of each calendar year. The most commonly applied strategies were a wait-and-see policy (18.0%, n = 168), use of non-steroidal anti-inflammatory drugs (NSAIDs) (19.9%, n = 186), referral to a paramedical podiatric specialist (19.7%, n = 184), and advice to wear insoles (16.4%, n = 153). Treatment strategies varied greatly among GPs.There was large variation in treatment strategies of GPs for patients with PHP. GPs should be aware of conflicting evidence for interventions, such as insoles, and focus more on exercises for which there is evidence for effectiveness.
Non-alcoholic fatty liver disease and risk of incident acute myocardial infarction and stroke: findings from matched cohort study of 18 million European adults.
M Alexander, AK Loomis, J van der Lei, T Duarte-Salles, D Prieto-Alhambra, D Ansell, A Pasqua, F Lapi, P Rijnbeek, M Mosseveld, P Avillach, P Egger, NN Dhalwani, S Kendrick, C Celis-Morales, DM Waterworth, W Alazawi and N Sattar,
BMJ (Clinical research ed.), 2019 10 08
To estimate the risk of acute myocardial infarction (AMI) or stroke in adults with non-alcoholic fatty liver disease (NAFLD) or non-alcoholic steatohepatitis (NASH).Matched cohort study.Population based, electronic primary healthcare databases before 31 December 2015 from four European countries: Italy (n=1 542 672), Netherlands (n=2 225 925), Spain (n=5 488 397), and UK (n=12 695 046).120 795 adults with a recorded diagnosis of NAFLD or NASH and no other liver diseases, matched at time of NAFLD diagnosis (index date) by age, sex, practice site, and visit, recorded at six months before or after the date of diagnosis, with up to 100 patients without NAFLD or NASH in the same database.Primary outcome was incident fatal or non-fatal AMI and ischaemic or unspecified stroke. Hazard ratios were estimated using Cox models and pooled across databases by random effect meta-analyses.120 795 patients with recorded NAFLD or NASH diagnoses were identified with mean follow-up 2.1-5.5 years. After adjustment for age and smoking the pooled hazard ratio for AMI was 1.17 (95% confidence interval 1.05 to 1.30; 1035 events in participants with NAFLD or NASH, 67 823 in matched controls). In a group with more complete data on risk factors (86 098 NAFLD and 4 664 988 matched controls), the hazard ratio for AMI after adjustment for systolic blood pressure, type 2 diabetes, total cholesterol level, statin use, and hypertension was 1.01 (0.91 to 1.12; 747 events in participants with NAFLD or NASH, 37 462 in matched controls). After adjustment for age and smoking status the pooled hazard ratio for stroke was 1.18 (1.11 to 1.24; 2187 events in participants with NAFLD or NASH, 134 001 in matched controls). In the group with more complete data on risk factors, the hazard ratio for stroke was 1.04 (0.99 to 1.09; 1666 events in participants with NAFLD, 83 882 in matched controls) after further adjustment for type 2 diabetes, systolic blood pressure, total cholesterol level, statin use, and hypertension.The diagnosis of NAFLD in current routine care of 17.7 million patient appears not to be associated with AMI or stroke risk after adjustment for established cardiovascular risk factors. Cardiovascular risk assessment in adults with a diagnosis of NAFLD is important but should be done in the same way as for the general population.
Patient-reported gout attack frequency and allopurinol use in general practice in the Netherlands: a prospective observational cohort study protocol.
KDB van Leeuwen, AM Bohnen, ML Jacobs, J van Der Lei, HJEM Janssens, AR Koffeman, PJE Bindels and SMA Bierma-Zeinstra,
BMJ open, 25 2018 11
Gout is the most common inflammatory arthritis in the Dutch general practice population and is often managed with long-term uric acid lowering treatment. The clinical relevance of this treatment in preventing gout attacks is unclear.What is the frequency of self-reported gout attacks and what is the effect of allopurinol use in patients diagnosed with gout in general practice?Adult patients with a diagnostic consultation code for gout in the year 2013, 2014 or 2015 will be invited to participate in this prospective observational cohort study. Patients with a limited life expectancy will be excluded. Baseline measurements will include blood pressure, body mass index and a blood sample (estimated glomerular filtration rate, serum uric acid, cholesterol (low-density lipoprotein (LDL) and high-density lipoprotein), glucose (fasting)). At the 2-year follow-up, patients will receive questionnaires every 3 months. The questionnaires at baseline, 12 months and 24 months assess the frequency of gout attacks, the presence of tophi, comorbidity, medication use, quality of life, diet and lifestyle. The questionnaires in between only assess the frequency of gout attacks and medication use for gout. Descriptive statistics will be used to calculate the mean frequency of self-reported gout attacks during the 2-year follow-up. The propensity score for each patient being offered allopurinol is estimated and used to match patients with and without allopurinol treatment. We will compare the frequency of gout attacks in these groups using multilevel Poisson regression analyses. With this type of analysis, we can calculate the corrected estimated effect of allopurinol on gout attack frequency.The research protocol was approved by the Medical Ethical Committee of the Erasmus Medical Centre in Rotterdam. The knowledge generated by this study will be transferred to the Dutch College of General Practitioners, conferences and to (inter)national peer-reviewed journals.NTR6329; Pre-results.
Missense variants in TAF1 and developmental phenotypes: challenges of determining pathogenicity.
H Cheng, S Capponi, E Wakeling, E Marchi, Q Li, M Zhao, C Weng, PG Stefan, H Ahlfors, R Kleyner, A Rope, A Lumaka, P Lukusa, K Devriendt, J Vermeesch, JE Posey, EE Palmer, L Murray, E Leon, J Diaz, L Worgan, A Mallawaarachchi, J Vogt, SA de Munnik, L Dreyer, G Baynam, L Ewans, Z Stark, S Lunke, AR Gonçalves, G Soares, J Oliveira, E Fassi, M Willing, JL Waugh, L Faivre, JB Riviere, S Moutton, S Mohammed, K Payne, L Walsh, A Begtrup, MJ Guillen Sacoto, G Douglas, N Alexander, MF Buckley, PR Mark, LC Adès, SA Sandaradura, JR Lupski, T Roscioli, PB Agrawal, AD Kline, K Wang, HTM Timmers and GJ Lyon,
Human mutation, Oct 23 2019
We recently described a new neurodevelopmental syndrome (TAF1/MRXS33 intellectual disability syndrome) (MIM# 300966) caused by pathogenic variants involving the X-linked gene TAF1, which participates in RNA polymerase II transcription. The initial study reported eleven families, and the syndrome was defined as presenting early in life with hypotonia, facial dysmorphia, and developmental delay that evolved into intellectual disability (ID) and/or autism spectrum disorder (ASD). We have now identified an additional 27 families through a genotype-first approach. Familial segregation analysis, clinical phenotyping, and bioinformatics were capitalized on to assess potential variant pathogenicity, and molecular modelling was performed for those variants falling within structurally characterized domains of TAF1. A novel phenotypic clustering approach was also applied, in which the phenotypes of affected individuals were classified using 51 standardized Human Phenotype Ontology (HPO) terms. Phenotypes associated with TAF1 variants show considerable pleiotropy and clinical variability, but prominent among previously unreported effects were brain morphological abnormalities, seizures, hearing loss, and heart malformations. Our allelic series broadens the phenotypic spectrum of TAF1/MRXS33 intellectual disability syndrome and the range of TAF1 molecular defects in humans. It also illustrates the challenges for determining the pathogenicity of inherited missense variants, particularly for genes mapping to chromosome X. This article is protected by copyright. All rights reserved.