Central line-associated bloodstream infections (CLABSIs) result in morbidity and mortality among hospitalized patients. Hospital interventions to reduce the incidence of CLABSI are often broadly applied to all patients with central venous access. Identifying central lines at high risk for CLABSI at time of insertion will allow for a more focused delivery of preventative interventions.

This was an observational cohort study conducted at three hospitals including all patients who received central venous access. CLABSIs were identified using an institutional CLABSI database maintained by the hospital epidemiology team. Logistic regression (LASSO) and machine learning (random forest, XGboost) techniques were applied for the prediction of CLABSI occurrence, adjusting for selected patent and insertion-level characteristics.

A total of 40,008 central venous catheters were included, of which 409 (1.02%) were associated with CLABSI. The random forest and the XGBoost models had the highest discrimination (Area Under the Received Operating Curve [AUC] 0.79) followed by LASSO (0.73). High illness severity, receipt of total parenteral nutrition, receipt of hemodialysis, pre-insertion hospital length-of-stay, and low albumin levels were all predictive of CLABSI occurrence. Precision for all models was poor owing to a high false-positive rate.

CLABSI can be predicted based upon patient and insertion level factors in the electronic health record. In this study, random forest and gradient-boosted models had the highest AUC. Prediction cut-offs for the identification of CLABSI can be adjusted based upon the acceptable rate of false-positives for a given CLABSI preventative intervention.

The association between cannabis and psychosis is established, but the role of underlying genetics is unclear. We used data from the EU-GEI case-control study and UK Biobank to examine the independent and combined effect of heavy cannabis use and schizophrenia polygenic risk score (PRS) on risk for psychosis.

Genome-wide association study summary statistics from the Psychiatric Genomics Consortium and the Genomic Psychiatry Cohort were used to calculate schizophrenia and cannabis use disorder (CUD) PRS for 1098 participants from the EU-GEI study and 143600 from the UK Biobank. Both datasets had information on cannabis use.

In both samples, schizophrenia PRS and cannabis use independently increased risk of psychosis. Schizophrenia PRS was not associated with patterns of cannabis use in the EU-GEI cases or controls or UK Biobank cases. It was associated with lifetime and daily cannabis use among UK Biobank participants without psychosis, but the effect was substantially reduced when CUD PRS was included in the model. In the EU-GEI sample, regular users of high-potency cannabis had the highest odds of being a case independently of schizophrenia PRS (OR daily use high-potency cannabis adjusted for PRS = 5.09, 95% CI 3.08–8.43, p = 3.21 × 10−10). We found no evidence of interaction between schizophrenia PRS and patterns of cannabis use.

Regular use of high-potency cannabis remains a strong predictor of psychotic disorder independently of schizophrenia PRS, which does not seem to be associated with heavy cannabis use. These are important findings at a time of increasing use and potency of cannabis worldwide.

Despite the frequent co-occurrence of depression and diabetes, gender differences in their relationship remain unclear.

This exploratory study examined if gender modifies the association between depressive symptoms, prediabetes and diabetes with cognitive-affective and somatic depressive symptom clusters.

Cross-sectional analyses were conducted on 29 619 participants from the 2007–2018 National Health and Nutrition Examination Survey. Depressive symptoms were measured by the nine-item Patient Health Questionnaire. Multiple logistic regression was used to analyse the relationship between depressive symptoms and diabetes. Multiple linear regression was used to analyse the relationship between depressive symptom clusters and diabetes.

The odds of having depressive symptoms were greater in those with diabetes compared to those without. Similarly, total symptom cluster scores were higher in participants with diabetes. Statistically significant diabetes–gender interactions were found in the cognitive-affective symptom cluster model. Mean cognitive-affective symptom scores were higher for females with diabetes (coefficient = 0.23, CI: 0.10, 0.36, P = 0.001) than males with diabetes (coefficient = −0.05, CI: −0.16, 0.07, P = 0.434) when compared to the non-diabetic groups.

Diabetes was associated with higher cognitive-affective symptom scores in females than in males. Future studies should examine gender differences in causal pathways and how diabetic states interact with gender and influence symptom profiles.

Depression is an independent risk factor for cardiovascular disease (CVD), but it is unknown if successful depression treatment reduces CVD risk.

Using eIMPACT trial data, we examined the effect of modernized collaborative care for depression on indicators of CVD risk. A total of 216 primary care patients with depression and elevated CVD risk were randomized to 12 months of the eIMPACT intervention (internet cognitive-behavioral therapy [CBT], telephonic CBT, and select antidepressant medications) or usual primary care. CVD-relevant health behaviors (self-reported CVD prevention medication adherence, sedentary behavior, and sleep quality) and traditional CVD risk factors (blood pressure and lipid fractions) were assessed over 12 months. Incident CVD events were tracked over four years using a statewide health information exchange.

The intervention group exhibited greater improvement in depressive symptoms (p < 0.01) and sleep quality (p < 0.01) than the usual care group, but there was no intervention effect on systolic blood pressure (p = 0.36), low-density lipoprotein cholesterol (p = 0.38), high-density lipoprotein cholesterol (p = 0.79), triglycerides (p = 0.76), CVD prevention medication adherence (p = 0.64), or sedentary behavior (p = 0.57). There was an intervention effect on diastolic blood pressure that favored the usual care group (p = 0.02). The likelihood of an incident CVD event did not differ between the intervention (13/107, 12.1%) and usual care (9/109, 8.3%) groups (p = 0.39).

Successful depression treatment alone is not sufficient to lower the heightened CVD risk of people with depression. Alternative approaches are needed.

ClinicalTrials.gov Identifier: NCT02458690

Depressive symptoms are common in stroke survivors. While obesity has been associated with stroke and depression, its influence on the association between stroke and depressive symptoms is unknown.

Cross-sectional data from 2015 to 2016 Canadian Community Health Survey was used. History of stroke was self-reported and our outcome of interest was depressive symptoms in the prior 2 weeks, measured using the 9-item Patient Health Questionnaire. Self-reported body mass index (BMI) was modeled as cubic spline terms to allow for nonlinear associations. We used multivariable logistic regression to evaluate the association between stroke and depressive symptoms and added an interaction term to evaluate the modifying effect of BMI.

Of the 47,521 participants, 694 (1.0%) had a stroke and 3314 (6.5%) had depressive symptoms. Those with stroke had a higher odds of depressive symptoms than those without (aOR = 3.13, 95% CI 2.48, 3.93). BMI did not modify the stroke-depressive symptoms association (P interaction = 0.242) despite the observed variation in stroke-depressive symptoms association across BMI categories,: normal BMI [18.5–25 kg/m2] (aOR† = 3.91, 95% CI 2.45, 6.11), overweight [25–30 kg/m2] (aOR† = 2.63, 95% CI 1.58, 4.20), and obese [>30 kg/m2] (aOR† = 2.76, 95% CI 1.92, 3.94). Similar results were found when depressive symptoms were modeled as a continuous measure.

The association between stroke and depressive symptoms is not modified by BMI, needing additional work to understand the role of obesity on depression after stroke.

Parkinson’s disease (PD) is associated with metabolic disorders such as insulin resistance. Pharmacological intervention used to treat insulin resistance, like GLP-1 agonists, may have auspicious results in the treatment for PD. The objective of this clinical trial was to assess the therapeutic effect of liraglutide on non-motor symptoms, such as, but not limited to, cognitive function and emotional well-being, and quality of life for individuals with PD.

In a single-center, randomized, double-blind, placebo-controlled trial, PD patients self-administered liraglutide injections once-daily (1.2 or 1.8 mg, as tolerated) or placebo in a 2:1 study design for 52 weeks after titration. Primary outcomes included adjusted difference in the OFF-state Movement Disorders Society Unified PD Rating Scale (MDS-UPDRS) part III, non-motor symptom scale (NMSS) and Mattis Dementia Rating Scale (MDRS-2). Secondary outcomes included quality of life scores (Parkinson Disease Questionnaire, PDQ-39) and other neuropsychological tests, including Delis-Kaplan Executive Function System (DKEFS), Geriatric Depression Scale (GDS), and Parkinson’s Anxiety Scale (PAS) scores.

Sixty-three subjects were enrolled and randomized to liraglutide (n=42) or placebo (n=21). Mean age in years was 63.5 (9.8) and 64.2 (6.4) for liraglutide and placebo cohorts, respectively (p=0.78), and mean age at symptom onset was 58.9 (10.5) and 59.3 (7.5) for liraglutide and placebo cohorts, respectively (p=0.86). At 54 weeks, NMSS scores had improved by 6.6 points in the liraglutide group and worsened by 6.5 points in the placebo group, a 13.1 point adjusted mean difference (p<0.05). Further analysis showed all nine NMSS sub-domain changes favoring the liraglutide group, with one (attention/memory) reaching statistical significance (p<0.05). Secondary outcome analyses revealed a significant improvement of PDQ-39 (p<0.001) and Parkinson’s Anxiety Scale - Avoidance Behavior scores (p<0.05) in the treatment group. MDRS-2 sub-scores did not further differentiate study groups, while DKEFS letter fluency scores favored placebo group (p<0.05).

Treatment with liraglutide improved self-reported non-motor symptoms of PD, activities of daily living, and quality of life. These results validate similar outcomes reported with other GLP-1 agonists implicating consideration for novel treatment opportunities for individuals with PD. Notably, the absence of significant performance-based cognitive changes over the duration of the trial for the participants in this study has several plausible explanations given participant-related baseline demographic and clinical factors. Implications for neuropsychologists will be discussed.

To compare the nutritional content, serving size and taxation potential of supermarket beverages from four different Western countries.

Cross-sectional analysis. Multivariate regression analysis and χ2 comparisons were used to detect differences between countries.

Supermarkets in New Zealand (NZ), Australia, Canada and the UK.

Supermarket beverages in the following categories: fruit juices, fruit-based drinks, carbonated soda, waters and sports/energy drinks.

A total of 4157 products were analysed, including 749 from NZ, 1738 from Australia, 740 from Canada and 930 from the UK. NZ had the highest percentage of beverages with sugar added to them (52 %), while the UK had the lowest (9 %, P<0·001). Differences in energy, carbohydrate and sugar content were observed between countries and within categories, with UK products generally having the lowest energy and sugar content. Up to half of all products across categories/countries exceeded the US Food and Drug Administration’s reference single serving sizes, with fruit juices contributing the greatest number. Between 47 and 83 % of beverages in the different countries were eligible for sugar taxation, the UK having the lowest proportion of products in both the low tax (5–8 % sugar) and high tax (>8 % sugar) categories.

There is substantial difference between countries in the mean energy, serving size and proportion of products eligible for fiscal sugar taxation. Current self-regulatory approaches used in these countries may not be effective to reduce the availability, marketing and consumption of sugar-sweetened beverages and subsequent intake of free sugars.

Neuropathy is common in Waldenström's macroglobulinemia (WM, an IgM-associated lymphoplasmacytic lymphoma) and in IgM-monoclonal gammopathy of undetermined significance (IgM-MGUS). Paraneoplastic or paraimmune mechanisms are thought to be involved in the pathogenesis of these neuropathies. Attempts at distinguishing WM and IgM-MGUS neuropathies are lacking especially among bone marrow (BM) confirmed patients.

Retrospective analyses were performed on BM confirmed WM (N=30) and IgM-MGUS (N=73) neuropathy patients with neurologic assessments and hematologic features.

The presence of anemia and quantity of IgM monoclonal protein were significantly greater in WM. Based on multiple neurologic assessments differences were not found for: 1) length of time from neurologic symptom onset to evaluation; 2) chief complaint of painless loss of feeling in the feet, Romberg's sign and tremor; and 3) clinical motor, sensory and reflex abnormalities. Autonomic testing was normal in both diseases. Using nerve conduction (NCS) criteria for demyelination, 62% of IgM-MGUS and 27% of WM met this criteria (p=0.013). IgM MGUS patients had greater terminal conduction slowing by ulnar residual latency calculation (<0.01). The degree of axonal loss as measured by summated compound muscle action potentials and available nerve biopsy was not significantly different between diseases.

Although WM and IgM-MGUS must be distinguished for hematologic prognosis and treatment, clinical neuropathy presentations of WM and IgM-MGUS are similar and likely related to comparable axonal loss in both conditions. Despite these similarities, evidence of demyelination was found by electrophysiologic studies much more commonly in IgM-MGUS. This difference may reflect varied immune mechanism(s) in the two disorders.