Lupus nephritis in Indigenous Australians: a single-centre study.

BACKGROUND: The incidence, presentation and outcomes of lupus nephritis (LN) vary with geography, ethnicity, socioeconomic status and gender. There are relatively few data on LN in the non-Caucasian populations in Australia. AIMS: To describe the clinical presentation, histological features, natural history, and outcomes of a historical cohort of Aboriginal and Torres Strait Islanders people in Far North Queensland with biopsy-proven LN. METHODS: This is a retrospective observational study, and the study was conducted in Cairns and Hinterland Hospital and Health Service, Queensland, Australia. The study included Aboriginal and Torres Strait Islander patients with biopsy-proven LN treated between 1990 and 2013. The main outcome measures were renal replacement therapy and overall patient survival. RESULTS: Aboriginal and Torres Strait Islander people represented a substantial proportion (n = 16/40, 40%) of all patients diagnosed with LN during the observation period. The frequency of nephrotic range proteinuria (n = 11/14, 78.5%), estimated glomerular filtration rate <60 mL/min/1.73 m2 (n = 6/14, 42.8%) and proliferative LN (n = 13/16, 81.25%) was high at the time of presentation. Despite use of multiple immunosuppressive agents, the overall rate of remission was poor (n = 4/14, 28.5%) and incidence of end-stage kidney disease (n = 4/14, 28.5%) and death (n = 5/16, 31.25%) was high. CONCLUSIONS: The clinical presentation of LN in Aboriginal and Torres Strait Islanders in Far North Queensland is severe and the response to standard immunosuppressive therapy is unsatisfactory. Larger prospective multi-centre studies are required to better understand ethnic disparities in prognosis and response to immunosuppressive therapy in this specific population.

Access to imaging investigation and neurosurgical care is delayed in regional Queensland for paediatric primary brain tumours.

Central nervous system tumours are the leading oncology cause of paediatric mortality. The aim of this research was to identify stages within the diagnostic process of a primary paediatric brain tumour that could be improved resulting in better outcomes. METHODS: The electronic medical records of Queensland Children's Hospital patients with central nervous system tumours between the 17/12/2014 till 11/12/2019 were retrospectively accessed. Time intervals of symptom onset to first medical review,location, time till medical imaging,subspecialty or neurosurgical review, timing of surgery, diagnosis and mortality status were recorded then analysed. RESULTS: A total of 168 patients were included. Mean age to 7.5, 65% male, with pilocytic astrocytoma representing 31%. 71.4% of the population were from a major city as determined by Remoteness Area classification, ABS, with 19% inner regional and 9.5% being outer regional and remote. The average time from first medical review to diagnostic imaging was significantly different when comparing remoteness classification (p = 0.044). There was also a statistically significant difference in the duration of time from medical imaging to specialist review comparing major city and outer regional/remote (p = 0.016) and inner regional versus outer regional/remote areas (p = 0.026). CONCLUSIONS: Delays in imaging in outer regional and remote Queensland are contributing to a delay in diagnosis and intervention in paediatric brain tumours. Service provision for neurosurgery in outer regional and remote Queensland is currently on par with inner regional and city areas. Suspicion of paediatric brain tumours is needed with clear referral pathways for general practitioners to access diagnostic imaging.

Posttraumatic Amnesia: A Systematic Review and Meta-Analysis. Proposal for a New Severity Classification.

BACKGROUND: Posttraumatic amnesia (PTA) duration is used to predict outcome after traumatic brain injury (TBI): however, no meta-analysis exists. METHODS: A systematic review was performed following PRISMA reporting guidelines. The databases Scopus-1966, PubMed/MEDLINE, CINAHL, PsycINFO, and Embase were searched for relevant texts. Random effects meta-analysis derived pooled estimates of the odds ratio of outcomes of interest and sensitivity and specificity of PTA at different cutoffs, and subsequently a summary receiver operating curve was derived. PTA prediction of Glasgow Outcome Scale (GOS) and Glasgow Outcome Scale-Extended (GOSE) scores was assessed both qualitatively and quantitatively by pooled odds ratio regarding both a good outcome (GO: GOS-5 or GOSE-7/GOSE-8) and a severe disability outcome (SDO: GOS-3 or a GOSE-3/GOSE-4). Summary receiver operating curve analysis was performed in the prediction of composite of a moderate disability outcome (MDO: GOS-4 or GOSE-5/GOSE-6) and SDO. RESULTS: Twenty-four studies were included in qualitative synthesis, and 9 (12,386 patients; males, 64%-84%) in meta-analysis. The odds of a GO and SDO were significantly different between PTA >56 days and PTA <7 days (P = 0.04 and P = 0.03). PTA <7 days (mild TBI) excluded MDO/SDO and SDO alone with 87% and 90% sensitivity. PTA of 43-86 days (severe TBI) predicted MDO/SDO or SDO with 90%-96% and 80%-90% specificity. However, PTA of 7-42 days (moderate TBI) predicted MDO/SDO or SDO with only 38%-89% and 30%-80% specificity. CONCLUSIONS: PTA duration was reliable in predicting outcome when <7 days, and especially when >42 days but was often unreliable between 7 and 42 days duration.

Blood Biomarkers and Structural Imaging Correlations Post-Traumatic Brain Injury: A Systematic Review.

BACKGROUND: Blood biomarkers are of increasing importance in the diagnosis and assessment of traumatic brain injury (TBI). However, the relationship between them and lesions seen on imaging remains unclear. OBJECTIVE: To perform a systematic review of the relationship between blood biomarkers and intracranial lesion types, intracranial lesion injury patterns, volume/number of intracranial lesions, and imaging classification systems. METHODS: We searched Medical Literature Analysis and Retrieval System Online, Excerpta Medica dataBASE, and Cumulative Index to Nursing and Allied Health Literature from inception to May 2021, and the references of included studies were also screened. Heterogeneity in study design, biomarker types, imaging modalities, and analyses inhibited quantitative analysis, with a qualitative synthesis presented. RESULTS: Fifty-nine papers were included assessing one or more biomarker to imaging comparisons per paper: 30 assessed imaging classifications or injury patterns, 28 assessed lesion type, and 11 assessed lesion volume or number. Biomarker concentrations were associated with the burden of brain injury, as assessed by increasing intracranial lesion volume, increasing numbers of traumatic intracranial lesions, and positive correlations with imaging classification scores. There were inconsistent findings associating different biomarkers with specific imaging phenotypes including diffuse axonal injury, cerebral edema, and intracranial hemorrhage. CONCLUSION: Blood-based biomarker concentrations after TBI are consistently demonstrated to correlate burden of intracranial disease. The relation with specific injury types is unclear suggesting a lack of diagnostic specificity and/or is the result of the complex and heterogeneous nature of TBI.

Chronic Traumatic Encephalopathy: The cellular sequela to repetitive brain injury.

This review aims to integrate current literature on the pathogenic mechanisms of Chronic Traumatic Encephalopathy (CTE) to create a multifactorial understanding of the disease. CTE is a progressive neurodegenerative disease, classed as a tauopathy, although it appears the pathogenic mechanisms are more complex than this. It affects those with a history of repetitive mild traumatic brain injury. Currently, there are no treatments for CTE and the disease can only be affirmatively diagnosed in post mortem. Understanding the pathogenesis of the disease will provide an avenue to explore possible treatment and diagnostic modalities. The pathological hallmarks of CTE have been well characterised and have been linked to the pathophysiologic mechanisms in this review. Human studies are limited due to ethical implications of exposing subjects to head trauma. Phosphorylation of tau, microglial activation, TAR DNA-binding protein 43 and diffuse axonal injury have all been implicated in the pathogenesis of CTE. The neuronal loss and axonal dysfunction mediated by these pathognomonic mechanisms lead to the broad psycho-cognitive symptoms seen in CTE.