Mackay Base Hospital,Queensland Health,Queensland Government

Background/Objectives: Traumatic brain injury in elderly patients is a significant public health concern, particularly for those on antithrombotic therapy. A clearer understanding of how different antithrombotic agents affect the likelihood of intracranial hemorrhage in elderly patients with TBI is needed to guide clinical management. Therefore, the objective of this study was to assess the effect of preinjury antithrombotic agents on the incidence of intracranial hemorrhage in elderly patients with traumatic brain injury. Methods: The design was a retrospective cohort study set in a regional Australian hospital emergency department. The study evaluated elderly patients (≥65 years) with head injury cases identified from the integrated electronic medical record using SNOMED codes. Data on patient demographics, antithrombotic use, computed tomography imaging, and outcomes were collected. Results: A total of 152 elderly TBI patients were included in the study. Of these patients, 90.1% had falls leading to TBI. Among the patients, 30.3% were on antiplatelet agents, 23% were on direct oral anticoagulants, 7.2% were on vitamin K antagonists, and 39.5% were not on any antithrombotic agents. Intracranial hemorrhage was found in 26.5% of patients, with both direct oral anticoagulants (aOR 4.87, 95% CI 1.42–16.67, p < 0.01) and vitamin K antagonists (aOR 4.95, 95% CI 1.04–23.55, p < 0.04) demonstrating statistically significant associations with increased odds of ICH. Conclusions: Both vitamin K antagonists and direct oral anticoagulants were associated with a higher odds of intracranial hemorrhage in elderly patients with TBI, while antiplatelet therapy did not show this effect.

ABL2 rearrangements represent a subtype of acute lymphoblastic leukaemia (ALL) associated with poor prognosis and survival. This study reports a high-risk T-cell ALL (T-ALL) case with a novel TPR::ABL2 gene fusion resulting from a chromosomal deletion. Overexpression of TPR::ABL2 in Ba/F3 cells promoted cytokine-independent growth, demonstrating its oncogenic nature. Both primary patient and Ba/F3 cells carrying TPR::ABL2 exhibited kinase activation and sensitivity to tyrosine kinase inhibitors (TKIs). This study expands the repertoire of ABL2 fusions identified in ALL and supports the incorporation of TKIs into T-ALL treatment regimens to improve outcomes for this subtype.

BACKGROUND Fabry disease (FD) is a rare X‑linked lysosomal disorder in which long‑term cardiac outcomes, particularly in heterozygous females, remain incompletely defined. The N224S alpha-galactosidase A gene (GLA) variant is recognized as pathogenic, yet its cardiac phenotype and response to prolonged migalastat therapy are not well characterized. Although clinical trials and observational studies have reported variable cardiac responses to migalastat, real‑world longitudinal data beyond 5 years remain limited. Understanding long‑term structural and functional changes is especially important in patients with pre‑existing cardiac involvement, where distinguishing favorable remodeling from fibrosis‑related progression can be challenging. CASE REPORT We describe a 9‑year follow‑up of a 71‑year‑old heterozygous woman with FD due to the N224S mutation treated with migalastat. Serial transthoracic echocardiography demonstrated a sustained reduction in left ventricular mass index (LVMI) over long‑term therapy. Left ventricular systolic function remained preserved throughout follow‑up, and there was no evidence of progressive structural deterioration. Available Doppler‑derived diastolic indices, including a gradual decline in early diastolic mitral inflow velocity to early diastolic mitral annular velocity (E/e'), suggested improving left ventricular filling pressures over time. Although LVMI showed minor year‑to‑year variability, these changes were consistent with expected technical or physiological variation and did not alter the clear long‑term downward trend. CONCLUSIONS This case provides real‑world evidence of favorable long‑term cardiac remodeling during migalastat therapy in a heterozygous woman with the N224S variant. The sustained reduction in LVMI, preserved systolic function, and improving diastolic indices together indicate a durable cardiac response and extend the limited longitudinal data available for variant‑specific outcomes in FD.

To estimate the effect of restrictive fluid management on renal function and mortality in critically ill patients with acute kidney injury (AKI) at high risk of developing positive fluid balance. We conducted a target trial emulation using data from 12 intensive care units in Queensland, Australia (2015–2021). Adults with AKI within 72 h of intensive care unit (ICU) admission and an AKI-Fluid Balance Risk Score ≥ 32 were included. The intervention comprised conservative crystalloid administration, restricted nutritional fluid intake, and diuretic use for 72 h. We estimated per-protocol effects using a sequential doubly robust estimator for longitudinal modified treatment policies. The primary outcome was AKI Rank at day 7; secondary outcomes included 30-day mortality. Among 8,685 patients, the intervention was associated with substantial reduction in fluid balance (− 2,304 mL at 72 h; 95

Introduction: Diabetic ketoacidosis (DKA) is a common complication of diabetes mellitus characterized by metabolic acidosis, ketogenesis, hypovolemia, hyperglycemia, and electrolyte depletion. During treatment of DKA with intravenous fluids and insulin, some electrolyte disturbances can worsen. Hypophosphatemia is one such electrolyte disturbance that has not been well characterized in patients with severe DKA requiring Intensive Care Unit (ICU) admissions. This study sought to evaluate the incidence, severity, associations, and outcomes of hypophosphatemia in DKA. Methods: This retrospective multicenter study was conducted across DKA admissions to Queensland ICUs from 2016 to 2021. Adult patients (>18 years) requiring ICU admission for management of DKA were included in this study. Patients with DKA were stratified by lowest recorded phosphate level as: normal ≥ 0.80 mmol/L, mild 0.50–0.79 mmol/L, moderate 0.30–0.49 mmol/L and severe < 0.3 mmol/L. Patient demographics, comorbidities, ICU-related supports, and medications (including fluid, insulin administration, phosphate, and other electrolyte replacement) were collected. Univariate analysis was performed between hypophosphatemia severity and normophosphatemia subgroups to determine risk factors, outcomes, replacement, and progression of hypophosphatemia in the ICU. Phosphate replacement and administered insulin was compared to nadir serum phosphate level. Multivariate analysis and linear regression were performed to identify risk factors for the development of hypophosphatemia. Results: A total of 842 admissions of 669 unique patients due to DKA were included; 436 of 842 (51.8%) admissions maintained normophosphatemia in the ICU, while 220 (26.1%, n = 220/842) had mild hypophosphatemia, 124 (14.7%, n = 124/842) had moderate hypophosphatemia and 62 (7.4%, n = 62/842) had severe hypophosphatemia. Patients with higher BMI, higher APACHE II/III score, cerebrovascular disease and all blood gas parameters (excluding PaO2) were found to have more severe hypophosphatemia. Lower serum phosphate was associated with greater replacement and greater insulin administration per kilogram body weight. ICU length of stay, hospital length of stay and mortality were not affected by degree of hypophosphatemia (p > 0.05). Linear regression revealed that standard base excess was strongly associated with the development of hypophosphatemia (β = 0.02, 95% CI 0.01–0.02, p < 0.001). Conclusions: Increasing severity of hypophosphatemia was associated with increasing severity of DKA. Increased ICU length of stay was related to increased severity of hypophosphatemia.