Abstract：Objective To study the efficacy and safety of double plasma molecular absorption system (DPMAS) in the treatment of pediatric acute liver failure (PALF). Methods A prospective analysis was performed on the medical data of children with PALF who were hospitalized in the Intensive Care Unit (ICU), Hunan Children's Hospital, from March 2018 to June 2020. The children were randomly divided into two groups:plasma exchange group (PE group) and DPMAS group (n=18 each). The two groups were compared in terms of clinical indices after treatment, laboratory markers before and after treatment, and adverse events after treatment. Results Compared with the PE group, the DPMAS group had a significantly lower number of times of artificial liver support therapy and a significantly shorter duration of ICU stay (P < 0.05), while there was no significant difference in the 12-week survival rate between the two groups (P > 0.05). There was no significant difference in laboratory markers between the two groups before treatment (P > 0.05). After treatment, both groups had reductions in the levels of total bilirubin, interleukin-6, and tumor necrosis factor-α, and the DPMAS group had significantly greater reductions than the PE group (P < 0.05). Both groups had a significant reduction in alanine aminotransferase (P < 0.05), while there was no significant difference between the two groups (P > 0.05). The PE group had a significant increase in albumin, while the DPMAS group had a significant reduction in albumin (P < 0.05). The PE group had a significant reduction in prothrombin time, while the DPMAS group had a significant increase in prothrombin time (P < 0.05). There was no significant difference between the two groups in the rebound rate of total bilirubin and the overall incidence rate of adverse events after treatment (P > 0.05). Conclusions DPMAS is safe and effective in the treatment of PALF and can thus be used as an alternative to artificial liver support therapy.
HE Jie,ZHANG Xin-Ping,ZHOU Xiong et al. Application of double plasma molecular adsorption system in children with acute liver failure[J]. CJCP, 2021, 23(2): 180-185.
Newland CD. Acute liver failure[J]. Pediatr Ann, 2016, 45(12):e433-e438.
[2]
Kathemann S, Bechmann LP, Sowa JP, et al. Etiology, outcome and prognostic factors of childhood acute liver failure in a German single center[J]. Ann Hepatol, 2015, 14(5):722-728.
[3]
Zhao P, Wang CY, Liu WW, et al. Acute liver failure in Chinese children:a multicenter investigation[J]. Hepatobiliary Pancreat Dis Int, 2014, 13(3):276-280.
[4]
Ng VL, Li RS, Loomes KM, et al. Outcomes of children with and without hepatic encephalopathy from the pediatric acute liver failure study group[J]. J Pediatr Gastroenterol Nutr, 2016, 63(3):357-364.
[5]
Pham YH, Miloh T. Liver transplantation in children[J]. Clin Liver Dis, 2018, 22(4):807-821.
[6]
Firl DJ, Sasaki K, McVey J, et al. Improved survival following living donor liver transplantation for pediatric acute liver failure:analysis of 20 years of US national registry data[J]. Liver Transpl, 2019, 25(8):1241-1250.
[7]
Jain V, Dhawan A. Extracorporeal liver support systems in paediatric liver failure[J]. J Pediatr Gastroenterol Nutr, 2017, 64(6):855-863.
Roth K, Strickland J, Copple BL. Regulation of macrophage activation in the liver after acute injury:role of the fibrinolytic system[J]. World J Gastroenterol, 2020, 26(16):1879-1887.
[13]
Wree A, Holtmann TM, Inzaugarat ME, et al. Novel drivers of the inflammatory response in liver injury and fibrosis[J]. Semin Liver Dis, 2019, 39(3):275-282.
[14]
Triantafyllou E, Woollard KJ, Mcphail MJW, et al. The role of monocytes and macrophages in acute and acute-on-chronic liver failure[J]. Front Immunol, 2018, 9:2948.
[15]
Weiskirchen R, Tacke F. Cellular and molecular functions of hepatic stellate cells in inflammatory responses and liver immunology[J]. Hepatobiliary Surg Nutr, 2014, 3(6):344-363.
[16]
Chastre A, Bélanger M, Beauchesne E, et al. Inflammatory cascades driven by tumor necrosis factor-alpha play a major role in the progression of acute liver failure and its neurological complications[J]. PLoS One, 2012, 7(11):e49670.
[17]
Lai HS, Lin WH, Lai SL, et al. Interleukin-6 mediates angiotensinogen gene expression during liver regeneration[J]. PLoS One, 2013, 8(7):e67868.
[18]
Zhao SM, Jiang JH, Jing YY, et al. The concentration of tumor necrosis factor-α determines its protective or damaging effect on liver injury by regulating Yap activity[J]. Cell Death Dis, 2020, 11(1):70.
[19]
Lai WY, Wang JW, Huang BT, et al. A novel TNF-α-targeting aptamer for TNF-α-mediated acute lung injury and acute liver failure[J]. Theranostics, 2019, 9(6):1741-1751.
[20]
Gao DD, Fu J, Qin B, et al. Recombinant adenovirus containing hyper-interleukin-6 and hepatocyte growth factor ameliorates acute-on-chronic liver failure in rats[J]. World J Gastroenterol, 2016, 22(16):4136-4148.
[21]
Tan EX, Wang MX, Pang JX, et al. Plasma exchange in patients with acute and acute-on-chronic liver failure:a systematic review[J]. World J Gastroenterol, 2020, 26(2):219-245.
[22]
Stahl K, Hadem J, Schneider A, et al. Therapeutic plasma exchange in acute liver failure[J]. J Clin Apher, 2019, 34(5):589-597.
