Kawasaki disease with peritonsillar abscess as the first symptom: A case report.

BACKGROUND: Kawasaki disease (KD), also known as mucocutaneous lymph node syndrome, is an acute, self-limiting vasculitis of unknown aetiology that mainly involves the medium and small arteries and can lead to serious cardiovascular complications, with a 25% incidence of coronary artery aneurysms. Periton-Sillar abscesses are a rare symptom of KD and is easily misdiagnosed at its early stages. CASE SUMMARY: A 5-year-old boy who presented to a community hospital with a 3-d fever, difficulty in opening his mouth, and neck pain and was originally treated for throat infection without improvement. On the basis of laboratory tests, ultrasound of submandibular and superficial lymph nodes and computed tomography of the neck, the clinician diagnosed the periamygdala abscess and sepsis that did not resolve after antibiotic therapy. On the fifth day of admission, the child developed conjunctival congestion, prune tongue, perianal congestion and desquamation, and slightly stiff and swollen bunions on both feet. A diagnosis of KD was reached with complete remission after intravenous immunoglobulin treatment. CONCLUSION: Children with neck pain, lymph node enlargement, or airway obstruction as the main manifestations are poorly treated with intravenous broad-spectrum antibiotics. Clinicians should not rush invasive operations such as neck puncture, incision, and drainage and should be alert for KD when it cannot be explained by deep neck space infection and early treatment with aspirin combined with gammaglobulin.

Pharmacokinetic Study of Nalbuphine in Surgical Patients Undergoing General Anesthesia with Varying Degrees of Liver Dysfunction.

Purpose: This study aimed to characterize the pharmacokinetics of nalbuphine in patients undergoing general anesthesia with varying degrees of liver dysfunction. Patients and Methods: Twenty-four patients were enrolled and divided into three cohorts based on liver function: normal liver function (n = 13), mild liver dysfunction (n = 5), and moderate/severe liver dysfunction (n = 6). During the induction of anesthesia, they received 15 mg of nalbuphine intravenously. Venous blood samples were collected from each patient. The plasma concentration of nalbuphine was determined using ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). The pharmacokinetic parameters of nalbuphine were calculated by non-compartmental analysis (NCA) using Phoenix WinNonlin software. Results: Compared with the normal liver function group, the plasma elimination half-life (T1/2) of nalbuphine was increased by approximately 33% in the moderate/severe liver dysfunction group (2.66 h vs 3.54 h, P<0.05), and the volume of distribution (Vd) increased by approximately 85% (100.08 L vs 184.95 L, P<0.05). Multivariate analysis revealed that weight and platelet were associated with clearance (CL); total bilirubin as an independent factor was associated with T1/2, and weight associated with area under the curve (AUC(0→∞)) independently. Conclusion: The T1/2, mean residence time, and Vd of nalbuphine in patients with moderate/severe liver dysfunction were prolonged or increased significantly compared with those in the normal liver function group. These data suggest that it may need to be used with caution when nalbuphine is administered to patients with moderate or severe liver dysfunction.

DL0410, a novel dual cholinesterase inhibitor, protects mouse brains against Aß-induced neuronal damage via the Akt/JNK signaling pathway.

AIM: 1,1'-([1,1'-Biphenyl]-4,4'-diyl)bis(3-(piperidin-1-yl)propan-1-one)dihydrochloride (DL0410) is a novel synthetic dual acetylcholinesterase (AChE)/butyrocholinesterase (BuChE) inhibitor, which has shown a potential therapeutic effect on Alzheimer's disease (AD). In this study we examined whether DL0410 produced neuroprotective effects in an AD cellular model and an Aß1-42-induced amnesia mouse model. METHODS: The in vitro inhibitory activities against AChE and BuChE were estimated using Ellman's assay. Copper-induced toxicity in APPsw-SY5Y cells was used as AD cellular model, the cell viability was assessed using MTS assay, and cell apoptosis was evaluated based on mitochondrial membrane potential detection. Aß1-42-induced amnesia mouse model was made in male mice by injecting aggregated Aß1-42 (2 µg in 2 µL 0.1% DMSO) into the right cerebral ventricle. Before and after Aß1-42 injection, the mice were orally administered DL0410 (1, 3, 9 mg·kg-1·d-1) or rivastigmine (2 mg·kg-1·d-1) for 3 and 11 d, respectively. Memory impairments were examined using Morris water maze (MWM) test and passive avoidance test. The expression levels of APP, CREB, BDNF, JNK and Akt in the mouse brains were measured with either immunohistochemistry or Western blotting. RESULTS: DL0410 exhibited in vitro inhibitory abilities against AChE and BuChE with IC50 values of 0.286±0.004 and 3.962±0.099 µmol/L, respectively, which were comparable to those of donepezil and rivastigmine. In APPsw-SY5Y cells, pretreatment with DL0410 (1, 3, and 10 µmol/L) decreased the phosphorylation of JNK and increased the phosphorylation of Akt, markedly decreased copper-stimulated Aß1-42 production, reversed the loss of mitochondrial membrane potential, and dose-dependently increased the cell viability. In Aß1-42-treated mice, DL0410 administration significantly ameliorated learning and memory deficits in MWM test and passive avoidance test. Furthermore, DL0410 administration markedly decreased Aß1-40/42 deposits in mouse cerebral cortices, and significantly up-regulated neurotrophic CREB/BDNF. Meanwhile, Akt/JNK signaling pathway may play a key role in the neuroprotective effect of DL0410. CONCLUSION: DL0410 ameliorates cognitive deficit and exerts neuronal protection in AD models, implicating this compound as a candidate drug for the prevention and therapy of AD.

[Pharmacokinetics of salvianolic acid A after single intravenous administration in Rhesus monkey].

Salvianolic acid A (Sal A) is one of the most effective compounds isolated from the root of Salvia miltiorrhiza. Up to now, several studies regarding the pharmacokinetic profiles of Sal A have been reported, however there is no such study reported in monkeys, the species which is more similar to human. The aim of this study is to develop a LC-MS method for the determination of Sal A in monkey plasma and apply it to the pharmacokinetic studies of monkeys. After single intravenous administration of Sal A, the plasma concentration-time curves were observed and the main pharmacokinetic parameters were calculated. The plasma concentration at 2 min (C2 (min)) values were (28.343 ± 6.426), (45.679 ± 12.301) and (113.293 ± 24.360) mg x L(-1) for Rhesus monkeys treated with Sal A at 2.5, 5 and 10 mg x kg(-1). The area under the concentration-time curve (AUC(0-∞)) values were (3.316 ± 0.871), (5.754 ± 2.150) and (13.761 ± 2.825) µg x L(-1) x h, respectively. Furthermore, this method was improved and applied to the simultaneous determination of Sal A, Sal B and Sal C, which provided useful information for preclinical studies and clinical trials of Sal A, Sal B and Sal C.