Background: Plasma oxalate measurements can be used for the screening and therapeutic monitoring of primary hyperoxaluria. We developed a gas chromatography-mass spectrometry (GC-MS) assay for plasma oxalate measurements with high sensitivity and suitable testing volumes for pediatric populations. Methods: Plasma oxalate was extracted, derivatized, and analyzed by GC-MS. We measured the ion at m/z 261.10 to quantify oxalate and the 13 C 2-oxalate ion (m/z: 263.15) as the internal standard. Method validation included determination of the linear range, limit of blank, limit of detection, lower limit of quantification, precision, recovery, carryover, interference, and dilution effect. The cut-off value between primary and non-primary hyperoxaluria in a pediatric population was analyzed. Results: The detection limit was 0.78 μmol/L, and the linear range was up to 80.0 μmol/L.The between-day precision was 5.7% at 41.3 μmol/L and 13.1% at 1.6 μmol/L. The carry-over was < 0.2%. The recovery rate ranged from 90% to 110%. Interference analysis showed that Hb did not interfere with plasma oxalate quantification, whereas intralipidsand bilirubin caused false elevation of oxalate concentrations. A cut-off of 13.9 μmol/L showed 63% specificity and 77% sensitivity, whereas a cut-off of 4.15 μmol/L showed 100% specificity and 20% sensitivity. The minimum required sample volume was 250 μL.The detected oxalate concentrations showed interference from instrument conditioning, sample preparation procedures, medications, and various clinical conditions. Conclusions GC-MS is a sensitive assay for quantifying plasma oxalate and is suitable for pediatric patients. Plasma oxalate concentrations should be interpreted in a clinical context.

Background: Cerebral vasospasm has been reported following various forms of bacterial meningitis; however, there have been no prior reports of meningitis caused by the non-K1 strain of Escherichia coli. Case Report: A 63-year-old man with chronic thrombocytopenia presented with new-onset seizures that progressed to coma. Cerebrospinal fluid (CSF) analysis showed Gram-negative rods, but CSF culture and the Biofire FilmArray Meningitis/Encephalitis Panel were negative. Additional 16S ribosomal ribonucleic acid (rRNA) polymerase chain reaction and sequencing of the CSF sample indicated E. coli meningitis when correlated with the results of urine culture. The patient eventually developed diffuse cerebral arterial vasospasms with multifocal brain infarcts that progressed to brain death. Conclusion E. coli meningitis in adults may be missed if diagnostic tests include only K1 strains. Clinicians should be aware of cerebral vasospasm as a potentially serious complication of E. coli meningitis, and should consider screening for it, particularly in patients with associated risk factors.

Background: Cerebral vasospasm has been reported following various forms of bacterial meningitis; however, there have been no prior reports of meningitis caused by the non-K1 strain of Escherichia coli. Case Report: A 63-year-old man with chronic thrombocytopenia presented with new-onset seizures that progressed to coma. Cerebrospinal fluid (CSF) analysis showed Gram-negative rods, but CSF culture and the Biofire FilmArray Meningitis/Encephalitis Panel were negative. Additional 16S ribosomal ribonucleic acid (rRNA) polymerase chain reaction and sequencing of the CSF sample indicated E. coli meningitis when correlated with the results of urine culture. The patient eventually developed diffuse cerebral arterial vasospasms with multifocal brain infarcts that progressed to brain death. Conclusion E. coli meningitis in adults may be missed if diagnostic tests include only K1 strains. Clinicians should be aware of cerebral vasospasm as a potentially serious complication of E. coli meningitis, and should consider screening for it, particularly in patients with associated risk factors.

Background: Cerebral vasospasm has been reported following various forms of bacterial meningitis; however, there have been no prior reports of meningitis caused by the non-K1 strain of Escherichia coli. Case Report: A 63-year-old man with chronic thrombocytopenia presented with new-onset seizures that progressed to coma. Cerebrospinal fluid (CSF) analysis showed Gram-negative rods, but CSF culture and the Biofire FilmArray Meningitis/Encephalitis Panel were negative. Additional 16S ribosomal ribonucleic acid (rRNA) polymerase chain reaction and sequencing of the CSF sample indicated E. coli meningitis when correlated with the results of urine culture. The patient eventually developed diffuse cerebral arterial vasospasms with multifocal brain infarcts that progressed to brain death. Conclusion E. coli meningitis in adults may be missed if diagnostic tests include only K1 strains. Clinicians should be aware of cerebral vasospasm as a potentially serious complication of E. coli meningitis, and should consider screening for it, particularly in patients with associated risk factors.

We hypothesized that the administration of amantadine would increase awakening of comatose patients resuscitated from cardiac arrest. Methods We performed a prospective, randomized, controlled pilot trial, randomizing subjects to amantadine 100 mg twice daily or placebo for up to 7 days. The study drug was administered between 72 and 120 hours after resuscitation and patients with absent N20 cortical responses, early cerebral edema, or ongoing malignant electroencephalography patterns were excluded. Our primary outcome was awakening, defined as following two-step commands, within 28 days of cardiac arrest. Secondary outcomes included length of stay, awakening, time to awakening, and neurologic outcome measured by Cerebral Performance Category at hospital discharge. We compared the proportion of subjects awakening and hospital survival using Fisher exact tests and time to awakening and hospital length of stay using Wilcoxon rank sum tests. Results After 2 years, we stopped the study due to slow enrollment and lapse of funding. We enrolled 14 subjects (12% of goal enrollment), seven in the amantadine group and seven in the placebo group. The proportion of patients who awakened within 28 days after cardiac arrest did not differ between amantadine (n=2, 28.6%) and placebo groups (n=3, 42.9%; P>0.99). There were no differences in secondary outcomes. Study medication was stopped in three subjects (21.4%). Adverse events included a recurrence of seizures (n=2; 14.3%), both of which occurred in the placebo group. Conclusion We could not determine the effect of amantadine on awakening in comatose survivors of cardiac arrest due to small sample size.

Background/Aims: The global proportion of hepatocellular carcinoma (HCC) attributable to metabolic dysfunction-associated fatty liver disease (MAFLD) is unclear. The MAFLD diagnostic criteria allows objective diagnosis in the presence of steatosis plus defined markers of metabolic dysfunction, irrespective of concurrent liver disease. We aimed to determine the total global prevalence of MAFLD in HCC cohorts (total-MAFLD), including the proportion with MAFLD as their sole liver disease (single-MAFLD), and the proportion of those with concurrent liver disease where MAFLD was a contributary factor (mixed-MAFLD). Methods: This systematic review and meta-analysis included studies systematically ascertaining MAFLD in HCC cohorts, defined using international expert panel criteria including ethnicity-specific BMI cut-offs. A comparison of clinical and tumour characteristics was performed between single-MAFLD, mixed-MAFLD, and non-MAFLD HCC. Results: 22 studies (56,565 individuals with HCC) were included. Total and single-MAFLD HCC prevalence was 48.7% (95% confidence interval [CI] 34.5–63.0%) and 12.4% (95% CI 8.3–17.3%), respectively. In HCC due to chronic hepatitis B, C, and alcohol-related liver disease, mixed-MAFLD prevalence was 40.0% (95% CI 30.2–50.3%), 54.1% (95% CI 40.4–67.6%) and 64.3% (95% CI 52.7–75.0%), respectively. Mixed-MAFLD HCC had significantly higher likelihood of cirrhosis and lower likelihood of metastatic spread compared to single-MAFLD HCC, and a higher platelet count and lower likelihood of macrovascular invasion compared to non-MAFLD HCC. Conclusions MAFLD is common as a sole aetiology, but more so as a co-factor in mixed-aetiology HCC, supporting the use of positive diagnostic criteria.

Perianeurysmal cysts are a rare and poorly understood finding in patients both with treated and untreated aneurysms. While the prior literature suggests that a minority of perianeurysmal cysts develop 1-4 years following endovascular aneurysm treatment, this updated review demonstrates that nearly half of perianeurysmal cysts were diagnosed following aneurysm coiling, with the other half diagnosed concurrently with an associated aneurysm prior to treatment. 64% of perianeurysmal cysts were surgically decompressed, with a 39% rate of recurrence requiring re-operation. We report a case of a 71-year-old woman who presented with vertigo and nausea and was found to have a 3.4 cm perianeurysmal cyst 20 years after initial endovascular coiling of a ruptured giant ophthalmic aneurysm. The cyst was treated with endoscopic fenestration followed by open fenestration upon recurrence. The case represents the longest latency from initial aneurysm treatment to cyst diagnosis reported in the literature and indicates that the diagnosis of perianeurysmal cyst should remain on the differential even decades after treatment. Based on a case discussion and updated literature review, this report highlights proposed etiologies of development and management strategies for a challenging lesion.