Socioeconomic status and time in glucose target range in people with type 2 diabetes: a baseline analysis of the GP-OSMOTIC study.

BACKGROUND: Optimal glycaemia, reflected by glycated haemoglobin (HbA1c) levels, is key in reducing type 2 diabetes (T2D) complications. However, most people with T2D have suboptimal recall and understanding of HbA1c. Continuous glucose monitoring (CGM) measures glucose levels every 5 to 15-min over days and may be more readily understood. Given that T2D is more common in lower socioeconomic settings, we aim to study relationships between socioeconomic status (SES) and percentage time in glucose target range (TIR) which is a key metric calculated from CGM. METHODS: Analysis of baseline data from the General Practice Optimising Structured MOnitoring To Improve Clinical outcomes (GP-OSMOTIC) randomised controlled trial (October 2016 - November 2017) of 300 people with T2D from 25 Victorian General Practices. FreeStyle Libre Pro® sensor patch was used for this study. SES was defined by the Index of Relative Socio-economic Disadvantage (IRSD) and educational attainment. Univariable and multivariable mixed-effects linear regression analyses controlling for age, BMI, diet, exercise and study arm were performed. RESULTS: One hundred and sixty-seven (60.1%) participants were male, the mean (SD) participant age was 61.0 (9.7) years, and the mean (SD) duration of CGM use was 12.3 (2.5) days. The 10th IRSD decile (least disadvantaged) was associated with a 15% higher TIR vs. the 1st decile (most disadvantaged) (95% CI 5, 25; p = 0.003) and a 0.6% lower HbA1c (95% CI 0.1, 1; p = 0.03). There was no evidence of an association between educational attainment and TIR/HbA1c. CONCLUSION: Higher SES measured at an area level is associated with better achievement of glycaemic target using complementary measures of HbA1c and TIR in the GP-OSMOTIC cohort. Given that TIR may be more easily used in patient education and self-management support compared to HbA1c values, the social gradient identified in TIR provides an opportunity for clinicians and policy makers to address health inequities in T2D. TRIAL REGISTRATION: Australian and New Zealand Clinical Trials Registry Trial ACTRN12616001372471 , prospective, Date registered 4/10/2016.

Tissue plasminogen activator does not alter development of acquired epilepsy.

PURPOSE: Tissue plasminogen activator (t-PA), a proven therapy for acute ischemic stroke, is an endogenous serine protease associated with neuronal activity and synaptic plasticity in the brain. Its expression is enhanced after seizures, and is involved in seizure propagation throughout the brain. Therefore, the increased use of t-PA to treat stroke may have important implications for the development of poststroke epilepsy. Using experimental and clinical approaches, we investigated the role of t-PA in the development of epilepsy. METHODS: Mice deficient in t-PA (t-PA(-/-) ) or mice transgenically modified to overexpress neuronal t-PA (T4) underwent amygdala kindling, and seizure threshold and rates of kindling were compared to those in wild-type mice. For the clinical study, we recruited acute ischemic stroke patients who either received intravenous t-PA treatment on admission to hospital (n = 177; cases) or did not (n = 158; controls). We then assessed the incidence of early and late onset seizures and epilepsy in these patients. KEY FINDINGS: T4 mice were more seizure-prone than wild-type mice, exhibiting lower seizure thresholds (p = 0.002), but there were no significant differences observed in the rate of kindling development when comparing either T4 mice, or t-PA(-/-) mice, to their wild-type controls. Furthermore, we found no significant differences between the proportion of poststroke patients experiencing early or late seizures, or developing epilepsy, between those who received t-PA and those who did not. SIGNIFICANCE: Overexpression of endogenous t-PA lowers seizure threshold but does not influence kindling epileptogenesis. Moreover, the therapeutic administration of t-PA in humans does not influence the development of acquired poststroke epilepsy.

Shorter time to intervention improves recanalization success and clinical outcome post intra-arterial intervention for basilar artery thrombosis.

Basilar artery thrombosis is associated with poor clinical outcomes and high mortality rate if untreated. Clinical outcome correlates with recanalization success. As arterial clot composition undergoes organization over time and may become more resistant to recanalization therapy, we postulate that recanalization success is time-dependent. We aim to investigate whether time to intervention predicts recanalization success leading to improved clinical outcomes. Forty-nine consecutive patients with basilar artery thrombosis treated with intra-arterial (IA) therapy between 1993 and 2011 were included. Patient demographics, clinical features, clot location, time to intervention and post-procedural thrombolysis in myocardial infarction (TIMI) scores were collected. Recanalization success was defined as a score of TIMI 2-3. Clinical outcome was measured using the 90-day modified Rankin Scale (mRS) score, with good neurological outcome defined as mRS 0-2. The mean patient age was 59.8 years ± 17.9 and 36.7% were females. IA therapy was commenced within 6 hours of stroke onset in 17/49 (34.7%) patients. Of this 6-hour onset group, 17/17 (100%) demonstrated recanalization success (TIMI 2-3) and 10/17 (58.8%) achieved good neurological outcome at 90-days. IA therapy was commenced after 6 hours of stroke onset in 32/49 (65.3%) patients, with 24/32 (75%) and 6/32 (18.75%) patients achieving recanalization success and good outcome, respectively. A shorter delay to IA therapy is significantly associated with recanalization success (p=0.038) and good neurological outcome at 90 days (p=0.009) in patients with acute basilar artery thrombosis. We recommend a systematic approach to minimize time delay to IA therapy for this condition.