Long-term outcomes in children with moderate to severe traumatic brain injury: a single-centre retrospective study.

Traumatic brain injury (TBI) is a significant cause of mortality and disability in the pediatric population. Non-accidental trauma (NAT) has specifically been reported to result in more severe injury as compared to accidental mechanisms of injury. We aim to investigate the long-term neurological outcomes in children with moderate to severe traumatic brain injury. Our secondary aim is to evaluate the difference in outcomes between children presenting with NAT and non-NAT, in our study population. We performed a retrospective study in a tertiary pediatric hospital between January 2008 to October 2017 of all patients with TBI <16 years old with a Glasgow Coma Scale (GCS) ≤13. The dual primary outcomes were mortality and Paediatric Functional Independence Measure (WeeFIM) scores, recorded at the start of rehabilitation, discharge, 3 months and 6 months post-injury. The secondary outcome was the development of post-traumatic epilepsy. There were 68 patients with a median age of 4.5 [interquartile range (IQR) 1.0-9.0] years old. The most common presenting symptom was vomiting for children <2 years (11/20, 55.0%) while confusion and disorientation were common for those ≥2 years (27/48, 56.3%). WeeFIM scores at the start of rehabilitation [median 122.0, IQR 33.8-126.0] improved at 6 months post-injury (median 126.0, IQR 98.5-126.0). There was a greater incidence of post-traumatic epilepsy in age <2 years (6/20, 30.0%) compared to age ≥2 years (1/48, 2.1%) (p = .002). When comparing NAT versus non-NAT survivors, cognition WeeFIM scores were significantly different at the start of rehabilitation (p = .017) and at 3 months post-injury (p = .025). NAT predicts for poorer long-term outcomes, specifically in cognition, as measured by WeeFIM scores. Younger children <2 years had a higher incidence of post-traumatic epilepsy compared to older children.

Hypouricemic effects of Mesona procumbens Hemsl. through modulating xanthine oxidase activity in vitro and in vivo.

Uric acid is a metabolite obtained from purine by xanthine oxidase activity (XO) and high levels of serum uric acid leads to hyperuricemia and gout. Mesona procumbens Hemsl. has been used as a healthy beverage and a traditional remedy. In this study, the hypouricemic effects of M. procumbens extracts were evaluated in vitro and in vivo. The 50% ethanol extract of M. procumbens (EE50) showed the strongest inhibitory effect on monosodium urate (MSU)-induced XO activity in THP-1 cells. However, the phenolics and flavonoids in EE50 may not serve as inhibitors of XO. EE50 prevented an increase in the serum uric acid level in potassium oxonate (PO)-challenged ICR mice and streptozocin (STZ)-induced SD rats. EE50 down-regulated STZ-induced liver XO activity, and it restored renal OAT1 and urate transporter expression. STZ-induced renal interleukin-1ß (IL-1ß) and the tumor necrosis factor-α (TNF-α) level were inhibited by EE50 treatment. EE50 exhibits the hypouricemic effect via down-regulation of XO activity, suggesting that EE50 has potential to improve hyperuricemia and its complications.