Early hemoperfusion for emergency treatment of carbamazepine poisoning.

OBJECTIVES: To investigate the clinical value of early hemoperfusion (HP) in emergency treatment of carbamazepine (CBZ) poisoning. METHODS: 104 patients with acute CBZ poisoning treated from August 2004 to October 2015 in the Emergency Department were reviewed. Patients were categorized into three groups: group A, who received HP treatment in the Emergency Department; group B, who received HP treatment in the blood purification room; and group C, who did not received HP treatment. Pharmacokinetic parameters of CBZ and remission of complications were compared among the three groups. RESULTS: Both groups A and B had lower time to peak, area under curve and maximum concentration values than group C (P<0.05), and these kinetics indexes were significantly lower in group A than in group B (P<0.05). The mean retention times were 0.85±0.08, 1.20±0.15 and 2.52±0.29days in the three groups, respectively, and were significantly lower value in group A than in group B (P<0.05). The incidences of respiratory depression and seizure in group A were significantly lower than those of groups B and C (P<0.05). Group A had significantly higher Glasgow coma scale (GCS) scores at 4h after admission than the other two groups (P<0.05), and group B had significantly higher GCS scores than group C at 6h after admission (P<0.05). CONCLUSIONS: Initiation of HP in the early treatment stage of CBZ poisoning upon admission to an emergency department can significantly reduce the plasma concentration and retention period of CBZ, relieve the symptoms and shorten the overall treatment period.

Paraquat poisoning induced pulmonary epithelial mesenchymal transition through Notch1 pathway.

Progressive pulmonary fibrosis is the most characteristic feature of subacute PQ poisoning. Epithelial-to-mesenchymal transition (EMT) is reported to be involved in the pulmonary fibrosis after PQ exposure. Recent evidence suggested Notch signaling is required for EMT. In this study, we investigated whether Notch1 and TGF-ß1/Smad3 signaling was involved in EMT caused by PQ. It is demonstrated that A549 cells underwent EMT after treated with PQ at dose of 300 µmol/L for 6 days, charactered by increasing expression of mesenchymal marker α-SMA and decreasing expression of epithelial marker E-cadherin. We found that there was an apparent increased expression of Notch1 and jagged-1 in PQ induced EMT process. EMT could be enhanced by Jagged-1 ligand of Notch1, and be blocked by DAPT, a γ-secretase inhibitor. Our data also showed that the expression of TGF-ß1/Smad3 increased after Notch1 is elevated in EMT caused by PQ. Jagged-1 significantly induced SMA expression, and this induction was completely inhibited by SB431542 in A549 cells. In conclusion, we demonstrated that Notch1 pathway was important in EMT induced by PQ, and TGF-ß1/Smad3 signaling partly plays a role as the downstream of Notch1.