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Gender-based fatal violence (femicide) is a preventable cause of premature death. The Counting Dead Women Australia (CDWA) campaign is a femicide census counting violent deaths of women in Australia from 2014. We conducted a cross-sectional in-depth review of CDWA cases Jan-Dec 2014 to establish evidence of antecedent factors and describe femicide in Australia. Victim (n = 81) and perpetrator (n = 83) data were extracted from the CDWA register, law databases and coronial reports. Mixed methods triangulation of socio-demographic and incident characteristics. Women ranged in age from 20 to 82 years of age (44 ± 15.4). There were 83 perpetrators, of which 13 were unknown (not yet apprehended). Known perpetrators (n = 70) ranged in age from 16 to 72 years of age (40 ± 12.7) and 89% were male (62/70). The location of the crime was most frequently the victim’s home (49/70). In cases where the relationship between the victim and perpetrator was known (n = 59), over half of femicides were committed by intimate-partners (33/59). Intimate-partner perpetrators were more likely to have a history of violence and commit murder-suicide than other perpetrators. Femicide is overwhelmingly perpetrated by males, with women most vulnerable in their own home and with their intimate partners. Furthermore, intimate-partner femicide is associated with modifiable risk factors, including previous violence and mental health issues, which represents opportunities for early intervention within healthcare settings as practitioners are well-placed to identify risk and provide support. In line with recommendations for multi-sectoral approach, future research should target identification of risk and protective factors, and improved coordination of data collection.

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked Files. This article is open access. To identify common variants contributing to normal variation in two specific domains of cognitive functioning, we conducted a genome-wide association study (GWAS) of executive functioning and information processing speed in non-demented older adults from the CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) consortium. Neuropsychological testing was available for 5429-32 070 subjects of European ancestry aged 45 years or older, free of dementia and clinical stroke at the time of cognitive testing from 20 cohorts in the discovery phase. We analyzed performance on the Trail Making Test parts A and B, the Letter Digit Substitution Test (LDST), the Digit Symbol Substitution Task (DSST), semantic and phonemic fluency tests, and the Stroop Color and Word Test. Replication was sought in 1311-21860 subjects from 20 independent cohorts. A significant association was observed in the discovery cohorts for the single-nucleotide polymorphism (SNP) rs17518584 (discovery P-value=3.12 × 10(-8)) and in the joint discovery and replication meta-analysis (P-value=3.28 × 10(-9) after adjustment for age, gender and education) in an intron of the gene cell adhesion molecule 2 (CADM2) for performance on the LDST/DSST. Rs17518584 is located about 170 kb upstream of the transcription start site of the major transcript for the CADM2 gene, but is within an intron of a variant transcript that includes an alternative first exon. The variant is associated with expression of CADM2 in the cingulate cortex (P-value=4 × 10(-4)). The protein encoded by CADM2 is involved in glutamate signaling (P-value=7.22 × 10(-15)), gamma-aminobutyric acid (GABA) transport (P-value=1.36 × 10(-11)) and neuron cell-cell adhesion (P-value=1.48 × 10(-13)). Our findings suggest that genetic variation in the CADM2 gene is associated with individual differences in information processing speed. National Foundation for Alzheimer's disease and related disorders Institut Pasteur de Lille Centre National de Genotypage Inserm FRC (fondation pour la recherche sur le cerveau) Rotary LABEX (laboratory of excellence program investment for the future) DISTALZ grant (Development of Innovative Strategies for a Transdisciplinary approach to ALZheimer's disease) MEDIALZ Project - ERDF (European Regional Development Fund) 11001003 Conseil Regional Nord Pas de Calais Fondation pour la Recherche Medicale Caisse Nationale Maladie des Travailleurs Salaries Direction Generale de la Sante MGEN Institut de la Longevite Agence Francaise de Securite Sanitaire des Produits de Sante Aquitaine and Bourgogne Regional Councils Fondation de France joint French Ministry of Research/INSERM 'Cohortes et collections de donnees biologiques' program Eisai Wellcome Trust British Heart Foundation Chief Scientist Office of the Scottish Executive NIA N01-AG-12100 National Heart, Lung and Blood Institute Contracts HHSN268201100005C HHSN268201100006C HHSN268201100007C HHSN268201100008C HHSN268201100009C HHSN268201100010C HHSN268201100011C HHSN268201100012C R01HL70825 R01HL087641 R01HL59367 R01HL086694 National Human Genome Research Institute U01HG004402 NIH Roadmap for Medical Research Austrian Science Fond (FWF) P20545-P05 P13180 Intramural Research Program of the NIH, National Institute on Aging NHLBI HHSN268201200036C HHSN268200800007C N01HC55222 N01HC85079 N01HC85080 N01HC85081 N01HC85082 N01HC85083 N01HC850863 U01HL080295 R01HL087652 R01HL105756 R01HL103612 R01HL120393 National Institute of Neurological Disorders and Stroke (NINDS) National Institute on Aging (NIA) R01AG023629 R01AG15928 R01AG20098 R01AG027058 National Center for Advancing Translational Sciences CTSI UL1TR000124 National Institute of Diabetes and Digestive and Kidney Disease Diabetes Research Center (DRC) DK063491 Medical Research Council (UK) European Commission Framework 6 project EUROSPAN LSHG-CT-2006-018947 Republic of Croatia Ministry of Science, Education and Sports 108-1080315-0302 Netherlands Organization for Scientific Research (NWO) Internationale Stichting Alzheimer Onderzoek (ISAO) Hersenstichting Nederland (HSN) Centre for Medical Systems Biology (CMSB) in the framework of the Netherlands Genomics Initiative (NGI) Russian Foundation for Basic Research (RFBR) National Heart, Lung and Blood Institute's Framingham Heart Study N01-HC-25195 Affymetrix, Inc N02-HL-6-4278 U01 HL096917 R01 HL093029 Robert Dawson Evans Endowment of the Department of Medicine at Boston University School of Medicine Boston Medical Center National Institute of Neurological Disorders and Stroke NS17950 National Institute of Aging U01 AG049505 AG033193 AG008122 AG16495 Agence National de la Recherche Leducq Foundation National Heart, Lung and Blood Institute HL054464 HL054457 HL054481 HL071917 HL87660 HL043851 HL080467 National Institute of Neurological Disorders and Stroke of the National Institutes of Health NS041558 Chief Scientist Office of the Scottish Government Health Directorates CZD/16/6 Scottish Funding Council HR03006 Academy of Finland Finnish Diabetes Research Society Folkhalsan Research Foundation Novo Nordisk Foundation Finska Lakaresallskapet Signe and Ane Gyllenberg Foundation University of Helsinki Ministry of Education Ahokas Foundation Emil Aaltonen Foundation Juho Vainio Foundation Wellcome Trust WT089062 University of Newcastle's Strategic Initiative Fund Vincent Fairfax Family Foundation Hunter Medical Research Institute Italian Ministry of Health ICS 110.1RS97.71 US National Institute on Aging N01[AG]916413 N01[AG]821336 263 MD 9164 13 263 MD 821336 Intramural Research Program, National Institute on Aging, National Institutes of Health BBSRC Royal Society Chief Scientist Office of the Scottish Government Research Into Ageing UK Biotechnology and Biological Sciences Research Council (BBSRC) Engineering and Physical Sciences Research Council (EPSRC) Economic and Social Research Council (ESRC) MRC NHMRC 401184 Australian National Health & Medical Research Council 350833 568969 Capacity Building Grant 568940 NHMRC Project 525453 National Institutes of Health CA87969 CA49449 HL34594 U01HG004399 DK058845 CA65725 CA67262 CA50385 5UO1CA098233 EY09611 EY015473 HG004728 HL35464 CA55075 CA134958 DK070756 MRC Human Genetics Unit Arthritis Research UK European Union LSHG-CT-2006-018947 Bristol-Myers Squibb Netherlands Heart Foundation 2001 D 032 European commission 223004 Netherlands Genomics Initiative (Netherlands Consortium for Healthy Aging) 050-060-810 Netherlands Organisation of Scientific Research NWO Investments 175.010.2005.011 911-03-012 Research Institute for Diseases in the Elderly 014-93-015 Netherlands Genomics Initiative (NGI)/Netherlands Organisation for Scientific Research (NWO) project 050-060-810 Erasmus Medical Center Erasmus University, Rotterdam Netherlands Organization for the Health Research and Development (ZonMw) Research Institute for Diseases in the Elderly (RIDE) Ministry of Education, Culture and Science Ministry for Health, Welfare and Sports European Commission 49 (DG XII) Municipality of Rotterdam ZonMW Veni Grant 916.13.054 NIA Grants P30AG10161 R01AG15819 R01AG17917 R01AG30146 K08AG34290 K25AG41906 Federal Ministry of Education and Research 01ZZ9603 01ZZ0103 01ZZ0403 Ministry of Cultural Affairs Social Ministry of the Federal State of Mecklenburg-West Pomerania National Cancer Institute CA047988 Donald W Reynolds Foundation Fondation Leducq Amgen info:eu-repo/grantAgreement/EC/FP7/223004

Publisher's version (útgefin grein), Carotid artery intima media thickness (cIMT) and carotid plaque are measures of subclinical atherosclerosis associated with ischemic stroke and coronary heart disease (CHD). Here, we undertake meta-analyses of genome-wide association studies (GWAS) in 71,128 individuals for cIMT, and 48,434 individuals for carotid plaque traits. We identify eight novel susceptibility loci for cIMT, one independent association at the previously-identified PINX1 locus, and one novel locus for carotid plaque. Colocalization analysis with nearby vascular expression quantitative loci (cis-eQTLs) derived from arterial wall and metabolic tissues obtained from patients with CHD identifies candidate genes at two potentially additional loci, ADAMTS9 and LOXL4. LD score regression reveals significant genetic correlations between cIMT and plaque traits, and both cIMT and plaque with CHD, any stroke subtype and ischemic stroke. Our study provides insights into genes and tissue-specific regulatory mechanisms linking atherosclerosis both to its functional genomic origins and its clinical consequences in humans., The work was supported by the following grants: National Institute of Health grants: R21HL123677, R21-HL140385, DK104806-01A1, R01-MD012765-01A1 (NF), National Institutes of Health awards R01HG009120, R01HG006399, U01CA194393, T32NS048004 (CG), the American Heart Association Grant #17POST33350042 (PV), the British Heart Foundation (RG/13/5/30112) and the National Institute for Health Research University College London Hospitals Biomedical Research Centre (RCL and RPH), the British Heart Foundation FS/14/55/30806 (JCH), the German Federal Ministry of Education and Research (BMBF) in the context of the e:Med program (e:AtheroSysMed), the DFG as part of the CRC 1123 (B3), and the FP7/2007-2103 European Union project CVgenes@target (grant agreement number Health-F2-2013-601456). We thank Li-Ming Gan for assistance with the STARNET study and Jon White for assistance with UCLEB analyses. Additional acknowledgements are included in Supplementary Note 2.

Intimate-partner femicide is a preventable cause of premature death, however in many countries the incidence is not monitored or accessible. In Australia, one woman is murdered each week at the hands of a current or former intimate-partner; however there is scant empirical evidence that investigates femicide, thus little is known about progression of violence and opportunities for intervention. The Counting Dead Women Australia (CDWA) campaign is a femicide census counting violent deaths of women in Australia from 2014. We conducted a cross-sectional in-depth review of CDWA cases Jan-Dec 2014 to establish evidence of antecedent factors and trajectories of intimate-partner femicide. Victim (n=81) and perpetrator (n=83) data were extracted from the CDWA register, law databases and coronial reports. Mixed methods triangulation of socio-demographic and incident characteristics. Women ranged in age from 20–82 years (44±15.8). Known perpetrators ranged in age from 16–72 years (40±12.8) and 89% were male (n=62). Where victim and perpetrator relationship was known, over half were intimate-partners (n=33). One third of cases were in the most disadvantaged Socio-Economic Indexes for Areas (SEIFA) quintile, and this was higher among intimate-partner femicides where approximately 40% were in the most disadvantaged quintile. Intimate-partner perpetrators were more likely to have history of violence and commit murder-suicide than other perpetrators. Conversely, there were lower rates of substance misuse and criminal history among intimate-partner perpetrators. Femicide is overwhelmingly perpetrated by males, with women most vulnerable in their own home and with their intimate-partners. High rates of perpetrator violence, mental health issues and antisocial behaviour are opportunities for early intervention within primary healthcare as practitioners are well-placed to identify victim and perpetrator risk. Perpetration of intimate-partner femicide is associated with modifiable risk factors that should be targeted through a risk-sensitive multi-sectoral approach that can be embedded within healthcare settings.

© Media International Australia Editorial Board. A number of studies have examined why students choose to study journalism at university, but overall, this area is still relatively underexplored. Yet, understanding why students choose journalism, and what career expectations they hold, is important not only for educators but also for wider society and public debates about the future of journalism and the value of tertiary journalism education. This article examines the motivations of 1884 Australian journalism students enrolled across 10 universities. It finds that hopes for a varied lifestyle and opportunities to express their creativity are the most dominant motivations among students. Public service ideals are somewhat less important, while financial concerns and fame are least important. These motivations also find expression in students' preferred areas of specialisation (referred to in Australia as rounds): lifestyle rounds are far more popular than politics and business rounds or science and development rounds.

SummaryBackgroundA high circulating concentration of interleukin 6 is associated with increased risk of coronary heart disease. Blockade of the interleukin-6 receptor (IL6R) with a monoclonal antibody (tocilizumab) licensed for treatment of rheumatoid arthritis reduces systemic and articular inflammation. However, whether IL6R blockade also reduces risk of coronary heart disease is unknown.MethodsApplying the mendelian randomisation principle, we used single nucleotide polymorphisms (SNPs) in the gene IL6R to evaluate the likely efficacy and safety of IL6R inhibition for primary prevention of coronary heart disease. We compared genetic findings with the effects of tocilizumab reported in randomised trials in patients with rheumatoid arthritis.FindingsIn 40 studies including up to 133 449 individuals, an IL6R SNP (rs7529229) marking a non-synonymous IL6R variant (rs8192284; p.Asp358Ala) was associated with increased circulating log interleukin-6 concentration (increase per allele 9·45%, 95% CI 8·34–10·57) as well as reduced C-reactive protein (decrease per allele 8·35%, 95% CI 7·31–9·38) and fibrinogen concentrations (decrease per allele 0·85%, 95% CI 0·60–1·10). This pattern of effects was consistent with IL6R blockade from infusions of tocilizumab (4–8 mg/kg every 4 weeks) in patients with rheumatoid arthritis studied in randomised trials. In 25 458 coronary heart disease cases and 100 740 controls, the IL6R rs7529229 SNP was associated with a decreased odds of coronary heart disease events (per allele odds ratio 0·95, 95% CI 0·93–0·97, p=1·53×10−5).InterpretationOn the basis of genetic evidence in human beings, IL6R signalling seems to have a causal role in development of coronary heart disease. IL6R blockade could provide a novel therapeutic approach to prevention of coronary heart disease that warrants testing in suitably powered randomised trials. Genetic studies in populations could be used more widely to help to validate and prioritise novel drug targets or to repurpose existing agents and targets for new therapeutic uses.FundingUK Medical Research Council; British Heart Foundation; Rosetrees Trust; US National Heart, Lung, and Blood Institute; Du Pont Pharma; Chest, Heart and Stroke Scotland; Wellcome Trust; Coronary Thrombosis Trust; Northwick Park Institute for Medical Research; UCLH/UCL Comprehensive Medical Research Centre; US National Institute on Aging; Academy of Finland; Netherlands Organisation for Health Research and Development; SANCO; Dutch Ministry of Public Health, Welfare and Sports; World Cancer Research Fund; Agentschap NL; European Commission; Swedish Heart-Lung Foundation; Swedish Research Council; Strategic Cardiovascular Programme of the Karolinska Institutet; Stockholm County Council; US National Institute of Neurological Disorders and Stroke; MedStar Health Research Institute; GlaxoSmithKline; Dutch Kidney Foundation; US National Institutes of Health; Netherlands Interuniversity Cardiology Institute of the Netherlands; Diabetes UK; European Union Seventh Framework Programme; National Institute for Healthy Ageing; Cancer Research UK; MacArthur Foundation.

Item does not contain fulltext AIMS/HYPOTHESIS: The aim of this work was to investigate whether measurement of the mean common carotid intima-media thickness (CIMT) improves cardiovascular risk prediction in individuals with diabetes. METHODS: We performed a subanalysis among 4,220 individuals with diabetes in a large ongoing individual participant data meta-analysis involving 56,194 subjects from 17 population-based cohorts worldwide. We first refitted the risk factors of the Framingham heart risk score on the individuals without previous cardiovascular disease (baseline model) and then expanded this model with the mean common CIMT (CIMT model). The absolute 10 year risk for developing a myocardial infarction or stroke was estimated from both models. In individuals with diabetes we compared discrimination and calibration of the two models. Reclassification of individuals with diabetes was based on allocation to another cardiovascular risk category when mean common CIMT was added. RESULTS: During a median follow-up of 8.7 years, 684 first-time cardiovascular events occurred among the population with diabetes. The C statistic was 0.67 for the Framingham model and 0.68 for the CIMT model. The absolute 10 year risk for developing a myocardial infarction or stroke was 16% in both models. There was no net reclassification improvement with the addition of mean common CIMT (1.7%; 95% CI -1.8, 3.8). There were no differences in the results between men and women. CONCLUSIONS/INTERPRETATION: There is no improvement in risk prediction in individuals with diabetes when measurement of the mean common CIMT is added to the Framingham risk score. Therefore, this measurement is not recommended for improving individual cardiovascular risk stratification in individuals with diabetes.

Introduction Patients with chronic liver disease (CLD) and, in particular, non-alcoholic fatty liver disease (NAFLD) are known to have both higher all-cause mortality and cardiovascular (CV) mortality rates than the general population. Beyond investigation of GGT there has been little exploration of the relationship between CV disease (CVD) and other markers of liver disease (non-specific liver injury, steatosis, steatohepatitis, liver fibrosis or portal hypertension). We examined the association of prevalent and incident CV disease with CLD in a cohort of community-based people with type 2 diabetes (T2DM) in order to determine the relationship between these two important conditions. Method 1066 participants of the Edinburgh Type 2 Diabetes Study, a large, randomly-selected population of patients with T2DM aged 60–75 years were invited for liver assessment. A range of liver disease markers (non-specific liver injury – serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT); steatosis – liver ultrasound; steatohepatitis – serum cytokeratin-18; fibrosis – serum AST to Platelet Ratio Index (APRI), AST:ALT ratio, Enhanced Liver Fibrosis (ELF) panel, Fibrosis-4 Score, NAFLD Fibrosis Score; portal hypertension – platelet count) were measured. Subjects were followed-up using patient and GP questionnaires and record linkage for incident CV events (coronary artery disease (CAD), cerebrovascular disease and peripheral vascular disease). Results At baseline there were 372/1035 patients with prevalent CVD, including 319/1035 with CAD. After mean follow-up of 4.4 years there were 121/1035 incident CVD events, including 76/121 CAD events. There were 30/82 CVD related deaths. However, risk of dying from or developing CVD was no higher in subjects with steatosis than without (HR 1.31 95% CI 0.78–2.20, p > 0.05). The only significant relationship was with GGT (U/L log 2 incident CVD, adjusted HR 1.18 95% CI 1.00–1.39, p = 0.045; incident CAD, adjusted HR 1.24 95% CI 1.02–2.51, p = 0.032). Conclusion We conducted the first comprehensive population-based study of older people with T2DM and found no association between non-invasive markers of hepatic steatosis, steatohepatitis, or fibrosis with the development of, or mortality from, CVD. Our finding of a significant independent association between GGT and CVD warrants further evaluation as a potentially useful addition to current CV risk prediction models in T2DM. Disclosure of interest None Declared.

Background Recent data have suggested that plasma aminotransferases may be of limited use in the diagnosis of non-alcoholic fatty liver disease. However, data on the use of aminotransferases to monitor change in hepatosteatotic state are lacking. Methods 394 participants, aged 63–79 years, from the Edinburgh Type 2 Diabetes Study, a large, randomly-selected population of patients with Type 2 diabetes, were assessed on two occasions approximately 3 years apart. Liver ultrasonography was undertaken and both plasma alanine aminotransferase (ALT) and aspartateaminotransferase (AST)) were measured. Hepatic steatosis was graded as either “normal”, “mild” or “moderate/severe” according to findings on ultrasound. Change in steatosis was classified as either regression or progression by 1 or 2 categories. ANOVA (with trend) analysis was used to assess the association between change in steatosis and change in aminotransferase levels. Results Mean follow-up was 2.7 years. 5.1% (n=20) of participants regressed two categories, 14.7% (n=58) regressed one category, 60.7% (n=239) showed no change, 12.4% (n=49) progressed one category and 7.1% (n=28) progressed two categories. There was a statistically significant linear trend for both ALT and AST ( F (4,3)=4.76, p=0.03 and F (4,3)=10.70, p=0.01 respectively) indicating that as the hepatosteatosis stage changed the aminotransferase level increased or decreased proportionally. Conclusion In a relatively large sample of patients with type 2 diabetes representative of patients with type 2 diabetes in general, we have shown that change in aminotransferase levels are proportionally associated with change in levels of hepatosteatosis. This suggests that aminotransferases may be useful in monitoring progression of steatosis.

Background Both cardiovascular disease and liver disease are particularly common in people with type 2 diabetes and it is possible that the two conditions are inter-related. Non-invasive biomarkers are increasingly used to estimate liver inflammation and fibrosis. In this study the association of these biomarkers with cardiovascular risk factors and disease was explored in a large, representative population of people with type 2 diabetes mellitus. Methods Cytokeratin 18 (CK18, biomarker of hepatic inflammation) and the European Liver Fibrosis panel (ELF, biomarker of hepatic fibrosis) were measured in a random subgroup of 564 adults, aged 60–75 years at recruitment, participating in the Edinburgh Type 2 Diabetes Study (ET2DS). Data on conventional CV risk factors (body-mass index [BMI], waist circumference, blood pressure, total cholesterol, triglycerides, smoking status) and prevalent cardiovascular disease (validated myocardial infarction, angina, stroke and transient ischaemic attack events) were also available. Findings Median CK18 was 102 U/L [IQR 76–137, range 29–993] and mean ELF was 8·9 U/L [SD 0·8, range 6·9–11·6]. After adjustment for age and sex, increased CK18 was significantly associated with higher triglyceride levels ( r =0·157, p=0·002). Increased ELF score was associated with higher BMI ( r =0·202, p r =0·139, p=0·008), and diastolic blood pressure (r=–0·045, p=0·025). Despite these associations, neither biomarker was significantly associated with prevalent cardiovascular disease (prevalent cardiovascular disease vs no cardiovascular disease, mean CK18 108·1 U/L [SD 26·2] vs 105·5 [22·6], p=0·473 and mean ELF 8·94 [0·77] vs 8·89 [0·76], p=0·442). Interpretation In people with type 2 diabetes, non-invasive biomarkers of hepatic inflammation and fibrosis are associated with a number of cardiovascular risk factors but do not appear to associate with pre-existing vascular disease. Further investigation is required to determine whether liver biomarkers predict incident cardiovascular disease in this high risk group. Funding Diabetes UK.

Introduction People with type 2 diabetes mellitus (T2DM) have a higher prevalence of and higher mortality rates from liver-associated disease than the non-diabetic population of equivalent age. Early identification of liver disease followed by appropriate surveillance and intervention should be beneficial to the expanding population of older people with T2DM. We aimed to determine the prevalence and progression of hepatic fibrosis in a representative sample of older adults with T2DM. Methods 1066 participants of the Edinburgh Type 2 Diabetes Study, a large, randomly-selected population of patients with T2DM aged 60–75 years were invited to assessment on two occasions. At baseline, the Enhanced Liver Fibrosis Panel (ELF) was measured and demographics and diabetes history were recorded. ELF was repeated approximately 3 years later. The presence of fibrosis was determined as: none/mild Results Average follow-up was 2.7 years. At baseline (n=530), 3.1% subjects had no/mild fibrosis, 85.1% moderate fibrosis and 11.9% severe fibrosis. Follow-up prevalences (n=806) were 1.9%, 79.3%, and 18.9% respectively. 489 subjects had both baseline and follow-up ELF results. 61 (12.5%) patients progressed to the most severe fibrosis stage between baseline and follow-up. None of the factors investigated were independently associated with progression to severe fibrosis: age, sex, social deprivation, diabetes-related factors (fasting glucose, HbA1c, diabetes duration, treatment type or location) or alcohol use. Conclusion These preliminary data suggest that considerable hepatic fibrosis is present in older patients with T2DM. ELF is well validated for diagnosing severe hepatic fibrosis and it is of concern that in Competing interests None declared.