Clinical risk prediction model for 30-day all-cause re-hospitalisation or mortality in patients hospitalised with heart failure.

BACKGROUND: This study aimed to develop a risk prediction model (AUS-HF model) for 30-day all-cause re-hospitalisation or death among patients admitted with acute heart failure (HF) to inform follow-up after hospitalisation. The model uses routinely collected measures at point of care. METHODS: We analyzed pooled individual-level data from two cohort studies on acute HF patients followed for 30-days after discharge in 17 hospitals in Victoria, Australia (2014-2017). A set of 58 candidate predictors, commonly recorded in electronic medical records (EMR) including demographic, medical and social measures were considered. We used backward stepwise selection and LASSO for model development, bootstrap for internal validation, C-statistic for discrimination, and calibration slopes and plots for model calibration. RESULTS: The analysis included 1380 patients, 42.1% female, median age 78.7 years (interquartile range = 16.2), 60.0% experienced previous hospitalisation for HF and 333 (24.1%) were re-hospitalised or died within 30 days post-discharge. The final risk model included 10 variables (admission: eGFR, and prescription of anticoagulants and thiazide diuretics; discharge: length of stay>3 days, systolic BP, heart rate, sodium level (<135 mmol/L), >10 prescribed medications, prescription of angiotensin converting enzyme inhibitors or angiotensin receptor blockers, and anticoagulants prescription. The discrimination of the model was moderate (C-statistic = 0.684, 95%CI 0.653, 0.716; optimism estimate = 0.062) with good calibration. CONCLUSIONS: The AUS-HF model incorporating routinely collected point-of-care data from EMRs enables real-time risk estimation and can be easily implemented by clinicians. It can predict with moderate accuracy risk of 30-day hospitalisation or mortality and inform decisions around the intensity of follow-up after hospital discharge.

Adolescent mental health and behavioural predictors of being NEET: a prospective study of young adults not in employment, education, or training.

BACKGROUND: Young adults who are not in employment, education, or training (NEET) are at risk of long-term economic disadvantage and social exclusion. Knowledge about risk factors for being NEET largely comes from cross-sectional studies of vulnerable individuals. Using data collected over a 10-year period, we examined adolescent predictors of being NEET in young adulthood. METHODS: We used data on 1938 participants from the Victorian Adolescent Health Cohort Study, a community-based longitudinal study of adolescents in Victoria, Australia. Associations between common mental disorders, disruptive behaviour, cannabis use and drinking behaviour in adolescence, and NEET status at two waves of follow-up in young adulthood (mean ages of 20.7 and 24.1 years) were investigated using logistic regression, with generalised estimating equations used to account for the repeated outcome measure. RESULTS: Overall, 8.5% of the participants were NEET at age 20.7 years and 8.2% at 24.1 years. After adjusting for potential confounders, we found evidence of increased risk of being NEET among frequent adolescent cannabis users [adjusted odds ratio (ORadj) = 1.74; 95% confidence interval (CI) 1.10-2.75] and those who reported repeated disruptive behaviours (ORadj = 1.71; 95% CI 1.15-2.55) or persistent common mental disorders in adolescence (ORadj = 1.60; 95% CI 1.07-2.40). Similar associations were present when participants with children were included in the same category as those in employment, education, or training. CONCLUSIONS: Young people with an early onset of mental health and behavioural problems are at risk of failing to make the transition from school to employment. This finding reinforces the importance of integrated employment and mental health support programmes.

Substance use in adulthood following adolescent self-harm: a population-based cohort study.

OBJECTIVE: To determine whether adolescents who self-harm are at increased risk of heavy and dependent substance use in adulthood. METHOD: Fifteen-year prospective cohort study of a random sample of 1943 adolescents recruited from secondary schools across the state of Victoria, Australia. Data pertaining to self-harm and substance use was obtained at seven waves of follow-up, from mean age 15.9 years to mean age 29.1 years. RESULTS: Substance use and self-harm were strongly associated during the adolescent years (odds ratio (OR): 3.3, 95% CI 2.1-5.0). Moreover, adolescent self-harmers were at increased risk of substance use and dependence syndromes in young adulthood. Self-harm predicted a four-fold increase in the odds of multiple dependence syndromes (sex- and wave-adjusted OR: 4.2, 95% CI: 2.7-6.6). Adjustment for adolescent anxiety/depression attenuated but did not eliminate most associations. Adolescent substance use confounded all associations, with the exception of multiple dependence syndromes, which remained robustly associated with adolescent self-harm (fully adjusted odds ratio: 2.0, 95% CI: 1.2-3.2). CONCLUSION: Adolescent self-harm is an independent risk factor for multiple dependence syndromes in adulthood. This level of substance misuse is likely to contribute substantially to the premature mortality and disease burden experienced by individuals who self-harm.

A case-control study to investigate the risk of leukaemia associated with exposure to benzene in petroleum marketing and distribution workers in the United Kingdom.

OBJECTIVES: To investigate the risk of leukaemia in workers in the petroleum distribution industry who were exposed to low levels of benzene. METHODS: From the cohort of distribution workers, 91 cases were identified as having leukaemia on either a death certificate or on cancer registration. These cases were compared with controls (four per case) randomly selected from the cohort, who were from the same company as the respective case, matched for age, and alive and under follow up at the time of case occurrence. Work histories were collected for the cases and controls, together with information about the terminals at which they had worked, fuel compositions, and occupational hygiene measurements of benzene. These data were used to derive quantitative estimates of personal exposure to benzene. Odds ratios (OR) were calculated conditional on the matching, to identify those variables in the study which were associated with risk of leukaemia. Examination of the potential effects of confounding and other variables was carried out with conditional logistic regression. Analyses were carried out for all leukaemia and separately for acute lymphoblastic, chronic lymphocytic, acute myeloid and monocytic, and chronic myeloid leukaemias. RESULTS: There was no significant increase in the overall risk of all leukaemias with higher cumulative exposure to benzene or with intensity of exposure, but risk was consistently doubled in subjects employed in the industry for > 10 years. Acute lymphoblastic leukaemia tended to occur in workers employed after 1950, who started work after the age of 30, worked for a short duration, and experienced low cumulative exposure with few peaks. The ORs did not increase with increasing cumulative exposure. The risk of chronic lymphocytic leukaemia seemed to be related most closely to duration of employment and the highest risk occurred in white collar workers with long service. These workers had only background levels of benzene exposure. There was no evidence of an association of risk with any exposure variables, and no evidence of an increasing risk with increasing cumulative exposure, mean intensity, or maximum intensity of exposure. The patterns of risk for acute myeloid and monocytic leukaemia were different from those of the lymphoid subgroups, in which duration of employment was the variable most closely related to risk. Risk was increased to an OR of 2.8 (95% confidence interval (95% CI) 0.8 to 9.4) for a cumulative exposure between 4.5 and 45 ppm-years compared with < 0.45 ppm-years. For mean intensity between 0.2 and 0.4 ppm an OR of 2.8 (95% CI 0.9 to 8.5) was found compared with < 0.02 ppm. Risk did not increase with cumulative exposure, maximum intensity, or mean intensity of exposure when treated as continuous variables. Cases of acute myeloid and monocytic leukaemia were more often classified as having peaked exposures than controls, and when variables characterising peaks, particularly daily and weekly peaks, were included in the analysis these tended to dominate the other exposure variables. However, because of the small numbers it is not possible to distinguish the relative influence of peaked and unpeaked exposures on risk of acute myeloid and monocytic leukaemia. There was no evidence of an increased risk of chronic myeloid leukaemia with increases in cumulative exposure, maximum intensity, mean intensity, and duration of employment, either as continuous or categorical variables. Analyses exploring the sensitivity of the results to the source and quality of the work histories showed similar patterns in general. However, no increases in ORs for categories of cumulative exposure were found for acute myeloid and monocytic leukaemia in the data set which included work histories obtained from personnel records still in existence, although numbers were reduced. Analyses excluding the last five and 10 years of exposure showed a tendency for ORs to reduce for chronic lymphocytic leukaemia and chronic myeloid leukaemia, and to increase for acute myeloid and monocytic leukaemia. Limitations of the study include uncertainties and gaps in the information collected, and small numbers in subcategories of exposure which can lead to wide CIs around the risk estimates and poor fit of the mathematical models. CONCLUSIONS: There is no evidence in this study of an association between exposure to benzene and lymphoid leukaemia, either acute or chronic. There is some suggestion of a relation between exposure to benzene and myeloid leukaemia, in particular for acute myeloid and monocytic leukaemia. Peaked exposures seemed to be experienced for this disease. However, in view of the limitations of the study, doubt remains as to whether the risk of acute myeloid and monocytic leukaemia is increased by cumulative exposures of < 45 ppm-years. Further work is recommended to review the work histories and redefine their quality, to explore the discrepancies between results for categorical and continuous variables, and to develop ranges around the expose estimates to enable further sensitivity analyses to be carried out.

Comparison of the diagnosis of leukaemia from death certificates, cancer registration and histological reports - implications for occupational case-control studies.

It is essential in occupational case-control studies of rare diseases for ascertainment to be as complete as possible, together with an accurately defined diagnosis. A nested case-control study from a large cohort of UK oil distribution workers followed up since 1950 was carried out to investigate the association between leukaemia, in particular acute myeloid leukaemia, and exposure to benzene. Ninety-one cases occurring before 1993 were identified from death certificates or cancer registrations (available from 1971). Histopathology departments were contacted to obtain material that might confirm the diagnosis of leukaemia and this was received for 39 (43%) cases. The majority of the cases (88) were identified primarily from death certificates, with a cancer registration also being received for 56 (90%) of the 62 deaths occurring after 1971. Discrepancies in the diagnoses from these two sources were found for 12 cases, five being acute myeloid leukaemia. For the majority, the diagnosis on the death certificate was more specific than that on the cancer registration. Histology reports were received for nine of the discrepancies, all confirming the death certificate diagnosis. Although leukaemia appears to be regularly registered as a cancer, records may not be routinely updated when new clinical information becomes available. It is recommended that death certificates, cancer registrations and histology reports are obtained routinely by cancer registries to maximize both numbers of cases and diagnostic accuracy for epidemiological studies.

Occupational risk factors in alcoholism.

This study has investigated the presence and influence of six of the eight risk factors previously identified, which are common to occupations associated with high rates of alcoholism. The factors studied were availability of alcohol at work, social pressure to drink from colleagues, separation from family due to work commitments, lack of supervision, collusion by colleagues, and stresses and strains. The sample was drawn from problem drinkers attending a community drug treatment centre in London. None of the six factors was found to have a significant influence on the development or maintenance of these subjects' alcohol problems. It is concluded that these risk factors, while previously shown to be associated with those who seek medical treatment for the physical consequences of long-term alcohol misuse, are not of significance in the different populations of those who present for psychological alcohol treatment.

Ethnic differences in the consequences of alcohol misuse.

The drinking habits of Asian and indigenous patients receiving in-patient care for alcoholism in West London were studied. Although both racial groups reported similar levels of current alcohol intake, the Asian developed problems and presented for in-patient detoxification with a shorter mean duration of drinking than the indigenous subjects. Values for mean corpuscular volume (MCV) and gamma glutamyl transpeptidase (GGT) were higher in the Asians, suggesting the Asians were at greater risk of alcohol-related physical damage.