Overwork as a concept to understand health inequities for ethnicised patients in health care.

Health inequities for ethnically minoritised patients are well-documented. In this ethnographic study, we follow thirteen patients categorised as 'ethnic minorities' in Danish health care during hospitalisation in three orthopaedic wards across two hospitals. The categorisation of 'ethnic minority patient' has been problematised for its Eurocentric origin and practices within Westernised health care. We use ethnicised to emphasise the process of becoming minoritised based on markers of physical appearance, religious symbols, language or names. Access to health care also rely on perceived legitimacy as health-care recipients which requires work by patients. We demonstrate the workings patients categorised as 'ethnic minorities' engage in by (re)producing othering ideas about non-Danishness, including distancing from other patients perceived as problematic. These were then (counter)produced by positioning oneself as the opposite, as deserving health-care receivers by displaying welfare reciprocity, supporting egalitarian ideas by discounting discriminatory experiences, showing gratitude and identifying staff with good vibes. We propose these doings as creating overwork. This theoretical approach enables a sensitivity towards subtle and covert workings for patients placed in the margins of health care. In this study, overwork is closely related to notions of Danishness and takes on specific forms within a modernised and universalised Danish health-care system.

The use of artificial intelligence to assess diabetic eye disease among the Greenlandic population.

Background: Retina fundus images conducted in Greenland are telemedically assessed for diabetic retinopathy by ophthalmological nurses in Denmark. Applying an AI grading solution, in a Greenlandic setting, could potentially improve the efficiency and cost-effectiveness of DR screening.Method: We developed an AI model using retina fundus photos, performed on persons registered with diabetes in Greenland and Denmark, using Optos® ultra wide-field scanning laser ophthalmoscope, graded according to ICDR.Using the ResNet50 network we compared the model's ability to distinguish between different images of ICDR severity levels in a confusion matrix.Results: Comparing images with ICDR level 0 to images of ICDR level 4 resulted in an accuracy of 0.9655, AUC of 0.9905, sensitivity and specificity of 96.6%.Comparing ICDR levels 0,1,2 with ICDR levels 3,4, we achieved a performance with an accuracy of 0.8077, an AUC of 0.8728, a sensitivity of 84.6% and a specificity of 78.8%. For the other comparisons, we achieved a modest performance.Conclusion: We developed an AI model using Greenlandic data, to automatically detect DR on Optos retina fundus images. The sensitivity and specificity were too low for our model to be applied directly in a clinical setting, thus optimising the model should be prioritised.

Non-steroidal anti-inflammatory drugs and risk of pulmonary embolism in patients with inflammatory joint disease-results from the nationwide Norwegian Cardio-rheuma registry.

AIMS: Patients with inflammatory joint diseases (IJD), including rheumatoid arthritis (RA), psoriatic arthritis (PsA), and axial spondyloarthritis (axSpA) have increased rates of pulmonary embolism (PE). Non-steroidal anti-inflammatory drugs (NSAIDs) use is associated with PE in the general population. Our aim was to evaluate the association between NSAIDs use and PE in IJD patients. METHODS AND RESULTS: Using individual-level registry data from the whole Norwegian population, including data from the Norwegian Patient Registry and the Norwegian Prescription Database, we: (1) evaluated PE risk in IJD compared to non-IJD individuals, (2) applied the self-controlled case series method to evaluate if PE risks were associated with use of traditional NSAIDs (tNSAIDs) and selective cox-2 inhibitors (coxibs). After a one-year wash-out period, we followed 4 660 475 adults, including 74 001 with IJD (RA: 39 050, PsA: 20 803, and axSpA: 18 591) for a median of 9.0 years. Crude PE incidence rates per 1000 patient years were 2.02 in IJD and 1.01 in non-IJD individuals. Age and sex adjusted hazard ratios for PE events were 1.57 for IJD patients compared to non-IJD. Incidence rate ratios (IRR) [95% confidence interval (CI)] for PE during tNSAIDs use were 0.78 (0.64-0.94, P = 0.010) in IJD and 1.68 (1.61-1.76, P < 0.001) in non-IJD. IRR (95% CI) for PE during coxibs use was 1.75 (1.10-2.79, P = 0.018) in IJD and 2.80 (2.47-3.18, P < 0.001) for non-IJD. CONCLUSION: Pulmonary embolism rates appeared to be higher in IJD than among non-IJD subjects in our study. Traditional NSAIDs may protect against PE in IJD patients, while coxibs may associated with increased PE risk.

Beyond the insider/outsider debate in "at-home" ethnographies: Diffractive methodology and the onto-epistemic entanglement of knowledge production.

In this article, we discuss the practice of conducting research in one's own field, in this case, from a position as a researcher with a nursing background doing fieldwork in a hospital and in one's own organization, an orthopedic surgical department. We show how an "insider" researcher position paves the way for analytical insights about sleep as an institutional phenomenon in the orthopedic surgical infrastructure and how acute and elective patient trajectories differ but build on the same logic, creating the same dynamics of inclusion and exclusion. Through a situated and sociomaterial perspective, we analyze different clinical interactions in which we follow the hospital bed as an example of a central relational element that co-creates sleep as an institutional phenomenon. Inspired by Karen Barad, we demonstrate how to move diffractively when doing and analyzing fieldwork and argue how moving diffractively as a researcher doing fieldwork "at home" is productive and challenges the concept and demand of "distance" as the phenomenological exercise in fieldwork.

Risk Factors for Bleeding in Cancer Patients Treated with Conventional Dose Followed by Low-Dose Apixaban for Venous Thromboembolism.

BACKGROUND: Incidence of and risk factors for bleeding in cancer patients with venous thromboembolism (VTE) treated with apixaban are poorly described. METHODS: We analyzed data from the prospective CAP study where 298 cancer patients with any type of VTE received 5 mg apixaban twice daily for 6 months, and then 2.5 mg apixaban twice daily for 30 months. For most analyses, major bleedings and clinically relevant nonmajor bleedings were merged to "clinically relevant bleedings." Risk factors were estimated by odds ratios (OR) and 95% confidence intervals (CIs). RESULTS: The incidence of clinically relevant bleedings was 38% per person-year during the first 6 months of treatment, 21% per person-year from 7 to 12 months, and between 4 and 8% per person-year from 13 to 36 months. Clinically relevant bleedings were associated with age above 74 years (OR: 2.0, 95% CI: 1.0-4.1), body mass index (BMI) below 21.7 (OR: 2.3, 95% CI: 1.1-4.8), and hemoglobin at baseline below 10.5 for females (OR: 2.8, 95% CI: 1.1-7.3) and 11.1 for males (OR: 3.3, 95% CI: 1.3-8.4) during the first 6 months. Gastrointestinal (GI) or urogenital cancer was not associated with clinically relevant bleedings compared with other cancers. Among patients with luminal GI cancer, nonresected cancer had increased risk of bleeding (OR: 3.4, 95% CI: 1.0-11.6) compared with resected GI cancer. CONCLUSION: There were very few bleedings while patients were on low-dose apixaban. Factors associated with bleeding in patients treated with full-dose apixaban were high age, low BMI, and low hemoglobin, and probably nonresected luminal GI cancer.

Trans-Regulation of Alternative PD-L1 mRNA Processing by CDK12 in Non-Small-Cell Lung Cancer Cells.

Immunotherapy using checkpoint inhibitors targeting the interaction between PD-1 on T cells and PD-L1 on cancer cells has shown significant results in non-small-cell lung cancer (NSCLC). Not all patients respond to the therapy, and PD-L1 expression heterogeneity is proposed to be one determinant for this. The alternative processing of PD-L1 RNA, which depends on an alternative poly-A site in intron 4, generates a shorter mRNA variant (PD-L1v4) encoding soluble PD-L1 (sPD-L1), relative to the canonical PD-L1v1 mRNA encoding membrane-associated PD-L1 (mPD-L1). This study aimed to identify factors influencing the ratio between these two PD-L1 mRNAs in NSCLC cells. First, we verified the existence of the alternative PD-L1 RNA processing in NSCLC cells, and from in silico analyses, we identified a candidate list of regulatory factors. Examining selected candidates showed that CRISPR/Cas9-generated loss-of-function mutations in CDK12 increased the PD-L1v4/PD-L1v1 mRNA ratio and, accordingly, the sPD-L1/mPD-L1 balance. The CDK12/13 inhibitor THZ531 could also increase the PD-L1v4/PD-L1v1 mRNA ratio and impact the PD-L1 transcriptional response to IFN-γ stimulation. The fact that CDK12 regulates PD-L1 transcript variant formation in NSCLC cells is consistent with CDK12's role in promoting transcriptional elongation over intron-located poly-A sites. This study lays the groundwork for clinical investigations to delineate the implications of the CDK12-mediated balancing of sPD-L1 relative to mPD-L1 for immunotherapeutic responses in NSCLC.

General practitioners' assessment of interventions applied to optimize laboratory test utilization: a cross-sectional survey study.

General practitioners (GPs) in the Region of Southern Denmark were randomly allocated to a range of interventions to optimize their use of Vitamin D tests over one year. The aim of the current survey study was to investigate GPs assessment of the interventions. Using REDCap web-platform, we invited 638 GPs to participate in a survey about their experiences of guidelines, feedback reports, non-interruptive alerts, and interruptive alerts. The questions were customized for the different interventions. We received responses from only 131 GPs (21%), but no differences in gender, age, or type of GP clinic were observed between responders and invited GPs. Approximately half of the GPs found that guidelines were helpful, and a similar proportion of GPs read the feedback reports 'often' or 'always'. The pop-up alerts were accepted when used for maximum three months for often-used tests. In contrast, alerts were accepted for long periods for rarely-used tests. The groups that were exposed to the interruptive alert found it 'problematic' that it appeared every time vitamin D was requested. Guidelines and feedback reports on tests numbers were accepted, but it was previously found, that they had little effect on improving the use of biochemical tests. Pop-up alerts in the requesting IT system can produce alert fatigue. Future research should focus on developing feedback reports that - when possible - also include relevant clinical information, and pop-up alerts should for often used tests be displayed only for weeks or a few months, but can be repeated.

RGMb impacts partial epithelial-mesenchymal transition and BMP2-Induced ID mRNA expression independent of PD-L2 in nonsmall cell lung cancer cells.

PD-1/PD-ligand-axis immunotherapy-mediated activation of T-cells for cancer cell elimination is a promising treatment of nonsmall cell lung cancer (NSCLC). However, the effect of immunotherapy on intracellular signaling pathways in cancer cells still needs further delineation. Repulsive Guidance Molecule b (RGMb), a regulator of Bone Morphogenetic Proteins (BMPs) signaling, interacts with the PD-ligand, PD-L2, at cancer cell membranes. Accordingly, a clarification of the functions of RGMb and its relation to PD-L2 might provide insight into NSCLC cell signaling responses to PD-1/PD-ligand-axis immunotherapy. In this study, the functions of RGMb and PD-L2 were examined using the two NSCLC cell lines HCC827 and A549. CRISPR/Cas9 was used to decrease the expression of RGMb and PD-L2, while lentiviral vectors were used to increase their expression. Downstream effects were examined by RT-qPCR and immunoassays. Ectopic expression of RGMb impacted BMP2-induced expression of ID1 and ID2 messenger RNA (mRNA) independently of PD-L2, while RGMb depletion by CRISPR/Cas9 did not affect the BMP2-mediated induction of ID1, ID2, and ID3 mRNA. However, depletion of RGMb resulted in a partial epithelial-mesenchymal transition (EMT) gene expression profile in HCC827 cells, which was not mimicked by PD-L2 depletion. The results show that RGMb is a coregulator of BMP signaling and hence, ID mRNA expression and that RGMb can control the EMT balance in NSCLC cells. However, RGMb appears to exert these functions independently of PD-L2, and accordingly, the PD-1/PD-ligand axis for immune surveillance in NSCLC cells.

Arterial events in cancer patients treated with apixaban for venous thrombosis.

INTRODUCTION: In a recent interventional study of cancer patients with newly diagnosed venous thrombosis (VT), we found a high risk of arterial thrombotic events (AT) during treatment with therapeutic doses of apixaban. METHODS: Total 298 cancer patients with VT received apixaban as treatment and secondary prophylaxis for up to 36 months. AT was registered as a serious adverse event, and this is a post hoc analysis of risk factors for AT. Clinical risk factors and concomitant medication were assessed through odds ratios (OR) with 95 % confidence interval using multivariate logistic regression. Biomarkers were assessed by non-parametric testing. RESULTS: AT occurred in 16/298 patients (5.4 %, 95 % confidence interval (CI) 3.1-8.6 %). Median leucocyte count at baseline was higher in patients with AT compared with patients without AT (11 vs. 6.8·109/L, p < 0.01). Clinical factors associated with AT were pancreatic cancer (OR 13.7, 95 % CI 4.3-43.1), ovarian cancer (OR 19.3, 95 % CI 2.3-164.4), BMI <25 percentile (OR 3.1, 95 % CI 1.1-8.8) and previous VT (OR 4.4, 95 % CI 1.4-13.7). Pancreatic cancer had a cumulative incidence of AT of 36 % compared with 0.8 % for all other cancers at 6 months (p < 0.01). Non-steroidal anti-inflammatory drugs (OR 4.9, 95 % CI 1.0-26) and antiplatelet treatment (OR 3.8, 95 % CI 1.2-12.2) were associated with AT. CONCLUSION: In cancer patients with apixaban treated VT, pancreatic cancer was strongly associated with AT. In addition, ovarian cancer, BMI < 25 percentile, previous VT, antiplatelet treatment, non-steroidal anti-inflammatory drug use and high leucocyte count at baseline were associated with AT. The CAP study is registered with the unique identifier NCT02581176 in ClinicalTrials.gov.

PD-L1 and PD-L2 immune checkpoint protein induction by type III interferon in non-small cell lung cancer cells.

INTRODUCTION: Despite the clinical success of PD-1/PD-1-ligand immunotherapy in non-small cell lung cancer (NSCLC), the appearance of primary and acquired therapy resistance is a major challenge reflecting that the mechanisms regulating the expression of the PD-1-ligands PD-L1 and PD-L2 are not fully explored. Type I and II interferons (IFNs) induce PD-L1 and PD-L2 expression. Here, we examined if PD-L1 and PD-L2 expression also can be induced by type III IFN, IFN-λ, which is peculiarly important for airway epithelial surfaces. METHODS: In silico mRNA expression analysis of PD-L1 (CD274), PD-L2 (PDCD1LG2), and IFN- λ signaling signature genes in NSCLC tumors and cell lines was performed using RNA sequencing expression data from TCGA, OncoSG, and DepMap portals. IFN-λ-mediated induction of PD-L1 and PD-L2 expression in NSCLC cell lines was examined by real-time quantitative polymerase chain reaction and flow cytometry. RESULTS: IFNL genes encoding IFN- λ variants are expressed in the majority of NSCLC tumors and cell lines along with the IFNLR1 and IL10R2 genes encoding the IFN-λ receptor subunits. The expression of PD-L1 and PD-L2 mRNA is higher in NSCLC tumors with IFNL mRNA expression compared to tumors without IFNL expression. In the NSCLC cell line HCC827, stimulation with IFN-λ induced both an increase in PD-L1 and PD-L2 mRNA expression and cell surface abundance of the corresponding proteins. In the NSCLC cell line A427, displaying a low basal expression of PD-L1 and PD-L2 mRNA and corresponding proteins, stimulation with IFN-λ resulted in an induction of the former. CONCLUSION: The type III IFN, IFN- λ, is capable of inducing PD-L1 and PD-L2 expression, at least in some NSCLC cells, and this regulation will need acknowledgment in the development of new diagnostic procedures, such as gene expression signature profiles, to improve PD-1/PD-1-ligand immunotherapy in NSCLC.

Examination of the Functional Relationship between PD-L1 DNA Methylation and mRNA Expression in Non-Small-Cell Lung Cancer.

Immunotherapy targeting the interaction between programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1) is a treatment option for patients with non-small-cell lung cancer (NSCLC). The expression of PD-L1 by the NSCLC cells determines treatment effectiveness, but the relationship between PD-L1 DNA methylation and expression has not been clearly described. We investigated PD-L1 DNA methylation, mRNA expression, and protein expression in NSCLC cell lines and tumor biopsies. We used clustered regularly interspaced short palindromic repeats-associated protein 9 (CRISPR-Cas9) to modify PD-L1 genetic contexts and endonuclease deficient Cas9 (dCas9) fusions with ten-eleven translocation methylcytosine dioxygenase 1 (TET1) and DNA (cytosine-5)-methyltransferase 3A (DNMT3A) to manipulate PD-L1 DNA methylation. In NSCLC cell lines, we identified specific PD-L1 CpG sites with methylation levels inversely correlated with PD-L1 mRNA expression. However, inducing PD-L1 mRNA expression with interferon-γ did not decrease the methylation level for these CpG sites, and using CRISPR-Cas9, we found that the CpG sites did not directly confer a negative regulation. dCas9-TET1 and dCas9-DNMT3A could induce PD-L1 hypo- and hyper-methylation, respectively, with the latter conferring a decrease in expression showing the functional impact of methylation. In NSCLC biopsies, the inverse correlation between the methylation and expression of PD-L1 was weak. We conclude that there is a regulatory link between PD-L1 DNA methylation and expression. However, since these measures are weakly associated, this study highlights the need for further research before PD-L1 DNA methylation can be implemented as a biomarker and drug target for measures to improve the effectiveness of PD-1/PD-L1 immunotherapy in NSCLC.

Genome-wide epigenetic and mRNA-expression profiling followed by CRISPR/Cas9-mediated gene-disruptions corroborate the MIR141/MIR200C-ZEB1/ZEB2-FGFR1 axis in acquired EMT-associated EGFR TKI-resistance in NSCLC cells.

Background: Epithelial-mesenchymal-transition (EMT) is an epigenetic-based mechanism contributing to the acquired treatment resistance against receptor tyrosine kinase inhibitors (TKIs) in non-small cell lung cancer (NSCLC) cells harboring epidermal growth factor receptor (EGFR)-mutations. Delineating the exact epigenetic and gene-expression alterations in EMT-associated EGFR TKI-resistance (EMT-E-TKI-R) is vital for improved diagnosis and treatment of NSCLC patients. Methods: We characterized genome-wide changes in mRNA-expression, DNA-methylation and the histone-modification H3K36me3 in EGFR-mutated NSCLC HCC827 cells in result of acquired EMT-E-TKI-R. CRISPR/Cas9 was used to functional examine key findings from the omics analyses. Results: Acquired EMT-E-TKI-R was analyzed with three omics approaches. RNA-sequencing identified 2,233 and 1,972 up- and down-regulated genes, respectively, and among these were established EMT-markers. DNA-methylation EPIC array analyses identified 14,163 and 7,999 hyper- and hypo-methylated, respectively, differential methylated positions of which several were present in EMT-markers. Finally, H3K36me3 chromatin immunoprecipitation (ChIP)-sequencing detected 2,873 and 3,836 genes with enrichment and depletion, respectively, and among these were established EMT-markers. Correlation analyses showed that EMT-E-TKI-R mRNA-expression changes correlated better with H3K36me3 changes than with DNA-methylation changes. Moreover, the omics data supported the involvement of the MIR141/MIR200C-ZEB1/ZEB2-FGFR1 signaling axis for acquired EMT-E-TKI-R. CRISPR/Cas9-mediated analyses corroborated the importance of ZEB1 in acquired EMT-E-TKI-R, MIR200C and MIR141 to be in an EMT-E-TKI-R-associated auto-regulatory loop with ZEB1, and FGFR1 to mediate cell survival in EMT-E-TKI-R. Conclusions: The current study describes the synchronous genome-wide changes in mRNA-expression, DNA-methylation, and H3K36me3 in NSCLC EMT-E-TKI-R. The omics approaches revealed potential novel diagnostic markers and treatment targets. Besides, the study consolidates the functional impact of the MIR141/MIR200C-ZEB1/ZEB2-FGFR1-signaling axis in NSCLC EMT-E-TKI-R.

Challenges facing the clinical adoption of a new prognostic biomarker: a case study.

In this article, we show how a particular biomarker comes into being in an emergency department in a hospital in Copenhagen, Denmark. We explore the contextual becoming of this biomarker, suPAR, through interviews with nurses and physicians and through relational ontology. We find that as a prognostic biomarker suPAR is challenged in it becoming as an object for clinical practice in the emergency department by the power of diagnostic practices and the desire for experience-based scripts that quickly enable the clinician to reach the right diagnosis. Although suPAR is enacted as a promising triage strategy suggesting a low or high risk of disease, the inability to rule out specific diagnoses and producing the notion of secure clinical actions make its non-specificity and prognostic character problematic in clinical practices. Specific diagnostic criteria versus prognostic interpretation and non-specificity risk profiling challenges the way healthcare workers in an emergency department understand the tasks they are set to solve and how to solve them. We discuss how the becoming of suPAR is strengthened through enactments of specificity and engagement in triage strategies and we reflect on it's becoming through new diagnostic practices with the need to accommodate diagnostic ambiguity.

[Factor Xa inhibitors in the prevention and treatment of venous thromboembolism in cancer patients]. / Faktor Xa-hemmere til forebygging og behandling av venøs tromboembolisme ved kreft.

Venous thromboembolism is a common complication of cancer. The prevalence varies according to cancer type and increases proportionally with the stage of cancer. In the past 15-20 years, low molecular weight heparin has been recommended as the first-line treatment. New international guidelines now allow for use of direct factor Xa inhibitors both as prophylaxis and treatment for venous thromboembolism. Prophylaxis should as a general rule only be initiated in patients with moderate to high risk. Bleeding risk assessment is important before starting anticoagulation. Both thrombosis and bleeding risk can change and should therefore be assessed on an ongoing basis. In this clinical review, use of anticoagulation therapy in cancer patients is discussed with particular emphasis on the use of direct factor Xa inhibitors.

An Extended PD-L2 Cytoplasmic Domain Results From Alternative Splicing in NSCLC Cells.

Antibody-based immunotherapy targeting the interaction between programmed cell death 1 (PD-1) and its ligand PD-L1 has shown impressive clinical outcomes in various cancer types, including nonsmall cell lung cancer (NSCLC). However, regulatory mechanisms in this immune checkpoint pathway still needs clarification. PD-L2 is structurally homologous to PD-L1 and is a second PD-1 ligand. Alternative mRNA splicing from the CD274 and PDCD1LG2 genes holds the potential to generate PD-L1 and PD-L2 isoforms, respectively, with novel functionality in regulation of the PD-1 immune checkpoint pathway. Here, we describe alternative splicing in NSCLC cells potentially generating eight different PD-L2 isoforms from the PDCD1LG2 gene. Extension of exon 6 by four nucleotides is the most prominent alternative splicing event and results in PD-L2 isoform V with a cytoplasmic domain containing a 10 amino acid extension. On average 13% of the PDCD1LG2 transcripts in NSCLC cell lines and 22% of the transcripts in NSCLC tumor biopsies encode PD-L2 isoform V. PD-L2 isoform V localizes to the cell surface membrane but less efficiently than the canonical PD-L2 isoform I. The cytoplasmic domains of PD-1 ligands can affect immune checkpoint pathways by conferring membrane localization and protein stability and thereby represent alternative targets for immunotherapy. In addition, cytoplasmic domains are involved in intracellular signalling cascades in cancer cells. The presented observations of different cytoplasmic domains of PD-L2 will be important in the future delineation of the PD-1 immune checkpoint pathway.

Labor Market Affiliation of Marginal Part-Time Workers in Denmark-A Longitudinal Study.

This longitudinal study examined the labor market affiliations of marginal part-time workers (<15 working hours/week) compared with full-time workers (32−40 working hours/week) within gender and age groups. Analyses were based on 1,492,187 Danish employees with marginal part-time or full-time work at baseline using register data of working hours and labor market affiliation from the Labor Market Account. We used the Expected Labor Market Affiliation method within gender and age groups to estimate the time spent in different labor market states over a 5-year follow-up from 2012−2017. The multistate model included five recurrent labor market states: work, unemployment, long-term sickness absence, studying, and temporarily out, and the results were adjusted for education level, morbidity, and ethnicity. A marginal part-time worker generally had fewer days of work without social benefits and spent more days studying during follow-up compared with a full-time worker. In addition, marginal part-time workers ≥ 25 years old had more days of unemployment and more days of long-term sickness absence. These findings suggest that marginal part-time workers have fewer paid workdays without social benefits compared with full-time workers, depending on age. Further studies should explore whether marginal part-time work is a stepping stone into or out of the labor market.

The Greenland population health survey 2018 - methods of a prospective study of risk factors for lifestyle related diseases and social determinants of health amongst Inuit.

Since 1993, regular population health surveys in Greenland have supported and monitored the public health strategy of Greenland and have monitored cardiometabolic and lung diseases. The most recent of these surveys included 2539 persons aged 15+ from 20 communities spread over the whole country. The survey instruments included personal interviews, self-administered questionnaires, blood sampling, anthropometric measurements, blood pressure, ECG, oral glucose test, pulmonary function, hand grip strength and chair stand test. Blood samples were analysed for glucose, glycated haemoglobin (HbA1c), insulin, incretin hormones, cholesterol, kidney function, fatty acids in erythrocyte membranes and mercury, urine for albumin-creatinine ratio, and aliquots were stored at -80°C for future use. Data were furthermore collected for studies of the gut microbiome and diabetes complications. Survey participants were followed up with register data. The potential of the study is to contribute to the continued monitoring of risk factors and health conditions as part of Greenland's public health strategy and to study the epidemiology of cardiometabolic diseases and other chronic diseases and behavioural risk factors. The next population health survey is planned for 2024. The emphasis of the article is on the methods of the study and results will be presented in other publications.

Low dose apixaban as secondary prophylaxis of venous thromboembolism in cancer patients - 30 months follow-up.

BACKGROUND: There are no data on the effect of low-dose anticoagulation as secondary prophylaxis for venous thromboembolism (VTE) in cancer patients. We assessed the efficacy and safety of low-dose apixaban for 30 months, after initial 6 months of full-dose treatment. METHODS: We included 298 patients with cancer and any type of VTE in a single arm interventional clinical trial. All patients were treated with full-dose apixaban (5 mg twice daily) for 6 months. Total 196 patients with active cancer after 6 months treatment continued with apixaban 2.5 mg twice daily for another 30 months. The main endpoints were recurrent VTE, major bleeding and clinically relevant non-major bleeding. RESULTS: During the 30 months of treatment with low-dose apixaban 14 (7.6%; 95% confidence interval (CI) 4.0%-11.7%) patients experienced recurrent VTE, six (3.1%; 95% CI 1.1%-6.5%) experienced major bleeding and 16 (8.1%, 95% CI: 4.7%-12.8%) experienced clinically relevant non-major bleeding. The incidence rate per person month of recurrent VTE was 0.8% (95% CI 0.41-1.6) at 2-6 months with full-dose apixaban, and 1.0% (95% CI 0.5-1.9) at 7-12 months with low-dose apixaban. The incidence rate of major bleeding was 1.1% (95% CI 0.6-2.0) at 2-6 months, and 0.3% (95% CI 0.1-1.0) at 7-12 months. Between 12 and 36 months the incidence rate of recurrent VTE and major bleedings remained low. CONCLUSION: Dose reduction of apixaban to 2.5 mg twice daily seems safe after 6 months of full-dose treatment. After 12 months the incidence rate of recurrent VTE and major bleeding remained low.