熊去氧胆酸对婴儿肝炎综合征患儿血清炎症因子和肝功能的影响
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摘要
目的:探讨熊去氧胆酸对婴儿肝炎综合征患儿血清炎症因子和肝功能的影响。方法:选取我院自2013年5月-2015年5月收治的婴儿肝炎综合征患儿91例,随机分为对照组(n=47)和观察组(n=44),对照组患儿给予常规护肝、利胆等治疗,观察组患儿在对照组的基础上给予熊去氧胆酸治疗,两组均治疗3周。比较两组患儿治疗前后的血清炎症因子及肝功能指标水平,观察两组患儿用药后的临床治疗效果及不良反应发生情况。结果:治疗后,所有患儿的血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、总胆红素(TBil)、直接胆红素(DBil)、丙氨酸转氨酶(ALT)、谷氨酰转肽酶(GGT)、总胆汁酸(TBA)水平均低于治疗前,且观察组低于对照组(P<0.05)。观察组患儿治疗后总有效率高于对照组(P<0.05)。两组患儿总不良反应发生率比较差异无统计学意义(P>0.05)。结论:熊去氧胆酸可以减轻婴儿肝炎综合征患儿的炎症反应,改善其肝功能,疗效显著且安全性好。
Objective: To investigate the effect of ursodeoxycholic acid on serum inflammatory factors and liver function in infants with infantile hepatitis syndrome. Methods: 91 infants with infantile hepatitis syndrome who were treated in our hospital from May 2013 to May 2015 were selected, and they were randomly divided into control group(n=47) and observation group(n=44), the control group were given routine liver protection and gallbladder treatment, the observation group were given ursodeoxycholic acid on the basis of the control group, and the two groups were treated for 3 weeks. The levels of serum inflammatory factors and liver function indexes were compared between the two groups before and after treatment. The clinical effects and adverse reactions of two groups after medication were observed. Results: After treatment, the levels of serum tumor necrosis factor-ɑ(TNF-α), interleukin-6(IL-6), total bilirubin(TBil),direct bilirubin(DBil), alanine transaminase(ALT), glutamyl transaminopeptidase(GGT) and total bile acid(TBA) in all infants were lower than those before treatment, and the observation group was lower than the control group(P<0.05). The total effective rate of the observation group after treatment was higher than that of the control group(P<0.05). There was no significant difference in the incidence of the total adverse reactions between the two groups(P>0.05). Conclusion: Ursodeoxycholic acid can reduce the inflammatory reaction and improve the liver function of infants with hepatitis syndrome, the curative effect is remarkable, and the safety is good.
Objective: To investigate the effect of ursodeoxycholic acid on serum inflammatory factors and liver function in infants with infantile hepatitis syndrome. Methods: 91 infants with infantile hepatitis syndrome who were treated in our hospital from May 2013 to May 2015 were selected, and they were randomly divided into control group(n=47) and observation group(n=44), the control group were given routine liver protection and gallbladder treatment, the observation group were given ursodeoxycholic acid on the basis of the control group, and the two groups were treated for 3 weeks. The levels of serum inflammatory factors and liver function indexes were compared between the two groups before and after treatment. The clinical effects and adverse reactions of two groups after medication were observed. Results: After treatment, the levels of serum tumor necrosis factor-ɑ(TNF-α), interleukin-6(IL-6), total bilirubin(TBil),direct bilirubin(DBil), alanine transaminase(ALT), glutamyl transaminopeptidase(GGT) and total bile acid(TBA) in all infants were lower than those before treatment, and the observation group was lower than the control group(P<0.05). The total effective rate of the observation group after treatment was higher than that of the control group(P<0.05). There was no significant difference in the incidence of the total adverse reactions between the two groups(P>0.05). Conclusion: Ursodeoxycholic acid can reduce the inflammatory reaction and improve the liver function of infants with hepatitis syndrome, the curative effect is remarkable, and the safety is good.
引文
[1] Wang G, Feng D. Dynamic relationship between infantile hepatitissyndrome and cytomegalovirus infection[J]. Exp Ther Med, 2017, 13(6):3443-3447
[2] Wang X, Qian L, Jia L, et al. Utility of Shear Wave Elastography forDifferentiating Biliary Atresia From Infantile Hepatitis Syndrome[J].J Ultrasound Med, 2016, 35(7):1475-1479
[3] Yasmeen S, Siddique N, Athar Abbas M, et al. Fiber gene basedmolecular and biological characterization of hydropericardium-hepatitis syndrome associated avian adenoviruses[J]. Iran J Vet Res,2017, 18(3):190-196
[4] Sugiura A, Wada S, Mori H, et al. Successful Treatment for ChronicHepatitis C-Autoimmune Hepatitis Overlap Syndrome due toDaclatasvir and Asunaprevir[J]. Case Rep Gastroenterol, 2017, 11(2):305-311
[5] Sun Y, Du T, Liu B, et al. Seroprevalence of avian hepatitis E virusand avian leucosis virus subgroup J in chicken flocks with hepatitissyndrome, China[J]. BMC Vet Res, 2016, 12(1):261
[6] Leonardsson H, Hreinsson JP, L觟ve A, et al. Hepatitis due toEpstein-Barr virus and cytomegalovirus:clinical features andoutcomes[J]. Scand J Gastroenterol, 2017, 52(8):893-897
[7] Lei JH, Tian Y, Luo HY, et al. Guillain-Barrésyndrome followingacute co-super-infection of hepatitis E virus and cytomegalovirus in achronic hepatitis B virus carrier[J]. J Med Virol, 2017, 89(2):368-372
[8] Zhang Xiao-jun, Yang Yun. To observe the curative effect of He-Nelaser irradiation in the treatment of infantile hepatitis syndrome inchildren[J]. Laser Journal, 2014, 35(8):99-100
[9] Zhang H, Li S, Yang J, et al. A meta-analysis of ursodeoxycholic acidtherapy versus combination therapy with corticosteroids forPBC-AIH-overlap syndrome:evidence from 97 monotherapy and 117combinations[J]. Prz Gastroenterol, 2015, 10(3):148-155
[10] Fang YQ, Lv DX, Jia W, et al. Case-control study on prednisolonecombined with ursodeoxycholic acid and azathioprine in pure primarybiliary cirrhosis with high levels of immunoglobulin G andtransaminases:efficacy and safety analysis[J]. Medicine(Baltimore),2014, 93(20):e104
[11] Peng Hong, Dong Guo-qing. Etiological examination and clinicalanalysis of infantile hepatitis syndrome[J]. Chinese Journal ofMisdiagnostics, 2003, 3(5):686-687
[12] Cho HH, Kim WS, Choi YH, et al. Ultrasonography evaluation ofinfants with Alagille syndrome:In comparison with biliary atresia andneonatal hepatitis[J]. Eur J Radiol, 2016, 85(6):1045-1052
[13] Serghini M, Labidi A, Khsiba A, et al. Cytomegalovirus infectionsimulating an overlap syndrome:autoimmune hepatitis-primarybiliary cirrhosis[J]. Tunis Med, 2014, 92(10):652-653
[14] Chan A, Bazerbachi F, Hanson B, et al. Cytomegalovirus hepatitisand pancreatitis in the immunocompetent[J]. Ochsner J, 2014, 14(2):295-299
[15] Quigley G, Al Ani M, Nadir A. Occurrence of Jaundice FollowingSimultaneous Ursodeoxycholic Acid Cessation and Obeticholic AcidInitiation[J]. Dig Dis Sci, 2018, 63(2):529-532
[16] Harms MH, Lammers WJ, Thorburn D, et al. Major HepaticComplications in Ursodeoxycholic Acid-Treated Patients WithPrimary Biliary Cholangitis:Risk Factors and Time Trends inIncidence and Outcome[J]. Am J Gastroenterol, 2018, 113(2):254-264
[17] Di Guida F, Pirozzi C, Magliocca S, et al. Galactosylated Pro-Drug ofUrsodeoxycholic Acid:Design, Synthesis, Characterization, andPharmacological Effects in a Rat Model of Estrogen-InducedCholestasis[J]. Mol Pharm, 2018, 15(1):21-30
[18] Alaca N,?zbeyli D, Uslu S, et al. Treatment with milk thistle extract(Silybum marianum), ursodeoxycholic acid, or their combinationattenuates cholestatic liver injury in rats:Role of the hepatic stemcells[J]. Turk J Gastroenterol, 2017, 28(6):476-484
[19] Reig A, SeséP, Parés A. Effects of Bezafibrate on Outcome andPruritus in Primary Biliary Cholangitis With SuboptimalUrsodeoxycholic Acid Response[J]. Am J Gastroenterol, 2018, 113(1):49-55
[20] Sombetzki M, Fuchs CD, Fickert P, et al. 24-nor-ursodeoxycholicacid ameliorates inflammatory response and liver fibrosis in a murinemodel of hepatic schistosomiasis[J]. J Hepatol, 2015, 62(4):871-878
[21] Wu X, Xu W, Feng X, et al. TNF-αmediated inflammatorymacrophage polarization contributes to the pathogenesis ofsteroid-induced osteonecrosis in mice[J]. Int J ImmunopatholPharmacol, 2015, 28(3):351-361
[22] Wang Jie, Sun Hao-miao, Wang Hong-qing, et al. Serum IL-18 andTNF-αlevels change before and after treatment in CMV hepatitisbaby and its significance[J]. Anhui Medical Journal, 2015, 36(12):1517-1519
[23] Motawi T, Shaker OG, Hussein RM, et al. Polymorphisms ofα1-antitrypsin and Interleukin-6 genes and the progression of hepaticcirrhosis in patients with a hepatitis C virus infection[J]. Balkan JMed Genet, 2017, 19(2):35-44
[24] Chen Z, Li YX, Fu HJ, et al. Hepatitis B Virus Core AntigenStimulates IL-6 Expression via p38, ERK and NF-κB Pathways inHepatocytes[J]. Cell Physiol Biochem, 2017, 41(1):91-100
[25] Schleker T, Jacobsen EM, Mayer B, et al. Preserved in vitroimmunoreactivity in children receiving long-term immunosuppressivetherapy due to inflammatory bowel disease or autoimmune hepatitis[J]. Mol Cell Pediatr, 2018, 5(1):1
[26] Li J, Yang C, Zhang S, et al. Ginsenoside Rg1 inhibits inflammatoryresponses via modulation of the nuclear factor-κB pathway andinhibition of inflammasome activation in alcoholic hepatitis[J]. Int JMol Med, 2018, 41(2):899-907
[27] Wang Z, Sheng L, Yang Y, et al. The Management of AutoimmuneHepatitis Patients with Decompensated Cirrhosis:Real-WorldExperience and a Comprehensive Review[J]. Clin Rev AllergyImmunol, 2017, 52(3):424-435
[28] Arain SQ, Talpur FN, Channa NA, et al. Serum lipids as an indicatorfor the alteration of liver function in patients with hepatitis B[J].Lipids Health Dis, 2018, 17(1):36
[29]赵攀,熊艺茹,陈婧,等.肝纤维化程度及自身抗体表达对熊去氧胆酸单药治疗自身免疫性肝病重叠综合征患者临床疗效的影响[J].现代生物医学进展, 2016, 16(8):1521-1523Zhao Pan, Xiong Yi-ru, Chen Jing, et al. Impact of Fibrosis andAutoantibody on the Efficacy of Ursodeoxycholic Acid Monotherapyin Patients with Autoimmune Hepatitis and Primary Biliary CirrhosisOverlap Syndrome[J]. Progress in Modern Biomedicine, 2016, 16(8):1521-1523
[30] Torisu Y, Nakano M, Takano K, et al. Clinical usefulness ofursodeoxycholic acid for Japanese patients with autoimmune hepatitis[J]. World J Hepatol, 2017, 9(1):57-63
[2] Wang X, Qian L, Jia L, et al. Utility of Shear Wave Elastography forDifferentiating Biliary Atresia From Infantile Hepatitis Syndrome[J].J Ultrasound Med, 2016, 35(7):1475-1479
[3] Yasmeen S, Siddique N, Athar Abbas M, et al. Fiber gene basedmolecular and biological characterization of hydropericardium-hepatitis syndrome associated avian adenoviruses[J]. Iran J Vet Res,2017, 18(3):190-196
[4] Sugiura A, Wada S, Mori H, et al. Successful Treatment for ChronicHepatitis C-Autoimmune Hepatitis Overlap Syndrome due toDaclatasvir and Asunaprevir[J]. Case Rep Gastroenterol, 2017, 11(2):305-311
[5] Sun Y, Du T, Liu B, et al. Seroprevalence of avian hepatitis E virusand avian leucosis virus subgroup J in chicken flocks with hepatitissyndrome, China[J]. BMC Vet Res, 2016, 12(1):261
[6] Leonardsson H, Hreinsson JP, L觟ve A, et al. Hepatitis due toEpstein-Barr virus and cytomegalovirus:clinical features andoutcomes[J]. Scand J Gastroenterol, 2017, 52(8):893-897
[7] Lei JH, Tian Y, Luo HY, et al. Guillain-Barrésyndrome followingacute co-super-infection of hepatitis E virus and cytomegalovirus in achronic hepatitis B virus carrier[J]. J Med Virol, 2017, 89(2):368-372
[8] Zhang Xiao-jun, Yang Yun. To observe the curative effect of He-Nelaser irradiation in the treatment of infantile hepatitis syndrome inchildren[J]. Laser Journal, 2014, 35(8):99-100
[9] Zhang H, Li S, Yang J, et al. A meta-analysis of ursodeoxycholic acidtherapy versus combination therapy with corticosteroids forPBC-AIH-overlap syndrome:evidence from 97 monotherapy and 117combinations[J]. Prz Gastroenterol, 2015, 10(3):148-155
[10] Fang YQ, Lv DX, Jia W, et al. Case-control study on prednisolonecombined with ursodeoxycholic acid and azathioprine in pure primarybiliary cirrhosis with high levels of immunoglobulin G andtransaminases:efficacy and safety analysis[J]. Medicine(Baltimore),2014, 93(20):e104
[11] Peng Hong, Dong Guo-qing. Etiological examination and clinicalanalysis of infantile hepatitis syndrome[J]. Chinese Journal ofMisdiagnostics, 2003, 3(5):686-687
[12] Cho HH, Kim WS, Choi YH, et al. Ultrasonography evaluation ofinfants with Alagille syndrome:In comparison with biliary atresia andneonatal hepatitis[J]. Eur J Radiol, 2016, 85(6):1045-1052
[13] Serghini M, Labidi A, Khsiba A, et al. Cytomegalovirus infectionsimulating an overlap syndrome:autoimmune hepatitis-primarybiliary cirrhosis[J]. Tunis Med, 2014, 92(10):652-653
[14] Chan A, Bazerbachi F, Hanson B, et al. Cytomegalovirus hepatitisand pancreatitis in the immunocompetent[J]. Ochsner J, 2014, 14(2):295-299
[15] Quigley G, Al Ani M, Nadir A. Occurrence of Jaundice FollowingSimultaneous Ursodeoxycholic Acid Cessation and Obeticholic AcidInitiation[J]. Dig Dis Sci, 2018, 63(2):529-532
[16] Harms MH, Lammers WJ, Thorburn D, et al. Major HepaticComplications in Ursodeoxycholic Acid-Treated Patients WithPrimary Biliary Cholangitis:Risk Factors and Time Trends inIncidence and Outcome[J]. Am J Gastroenterol, 2018, 113(2):254-264
[17] Di Guida F, Pirozzi C, Magliocca S, et al. Galactosylated Pro-Drug ofUrsodeoxycholic Acid:Design, Synthesis, Characterization, andPharmacological Effects in a Rat Model of Estrogen-InducedCholestasis[J]. Mol Pharm, 2018, 15(1):21-30
[18] Alaca N,?zbeyli D, Uslu S, et al. Treatment with milk thistle extract(Silybum marianum), ursodeoxycholic acid, or their combinationattenuates cholestatic liver injury in rats:Role of the hepatic stemcells[J]. Turk J Gastroenterol, 2017, 28(6):476-484
[19] Reig A, SeséP, Parés A. Effects of Bezafibrate on Outcome andPruritus in Primary Biliary Cholangitis With SuboptimalUrsodeoxycholic Acid Response[J]. Am J Gastroenterol, 2018, 113(1):49-55
[20] Sombetzki M, Fuchs CD, Fickert P, et al. 24-nor-ursodeoxycholicacid ameliorates inflammatory response and liver fibrosis in a murinemodel of hepatic schistosomiasis[J]. J Hepatol, 2015, 62(4):871-878
[21] Wu X, Xu W, Feng X, et al. TNF-αmediated inflammatorymacrophage polarization contributes to the pathogenesis ofsteroid-induced osteonecrosis in mice[J]. Int J ImmunopatholPharmacol, 2015, 28(3):351-361
[22] Wang Jie, Sun Hao-miao, Wang Hong-qing, et al. Serum IL-18 andTNF-αlevels change before and after treatment in CMV hepatitisbaby and its significance[J]. Anhui Medical Journal, 2015, 36(12):1517-1519
[23] Motawi T, Shaker OG, Hussein RM, et al. Polymorphisms ofα1-antitrypsin and Interleukin-6 genes and the progression of hepaticcirrhosis in patients with a hepatitis C virus infection[J]. Balkan JMed Genet, 2017, 19(2):35-44
[24] Chen Z, Li YX, Fu HJ, et al. Hepatitis B Virus Core AntigenStimulates IL-6 Expression via p38, ERK and NF-κB Pathways inHepatocytes[J]. Cell Physiol Biochem, 2017, 41(1):91-100
[25] Schleker T, Jacobsen EM, Mayer B, et al. Preserved in vitroimmunoreactivity in children receiving long-term immunosuppressivetherapy due to inflammatory bowel disease or autoimmune hepatitis[J]. Mol Cell Pediatr, 2018, 5(1):1
[26] Li J, Yang C, Zhang S, et al. Ginsenoside Rg1 inhibits inflammatoryresponses via modulation of the nuclear factor-κB pathway andinhibition of inflammasome activation in alcoholic hepatitis[J]. Int JMol Med, 2018, 41(2):899-907
[27] Wang Z, Sheng L, Yang Y, et al. The Management of AutoimmuneHepatitis Patients with Decompensated Cirrhosis:Real-WorldExperience and a Comprehensive Review[J]. Clin Rev AllergyImmunol, 2017, 52(3):424-435
[28] Arain SQ, Talpur FN, Channa NA, et al. Serum lipids as an indicatorfor the alteration of liver function in patients with hepatitis B[J].Lipids Health Dis, 2018, 17(1):36
[29]赵攀,熊艺茹,陈婧,等.肝纤维化程度及自身抗体表达对熊去氧胆酸单药治疗自身免疫性肝病重叠综合征患者临床疗效的影响[J].现代生物医学进展, 2016, 16(8):1521-1523Zhao Pan, Xiong Yi-ru, Chen Jing, et al. Impact of Fibrosis andAutoantibody on the Efficacy of Ursodeoxycholic Acid Monotherapyin Patients with Autoimmune Hepatitis and Primary Biliary CirrhosisOverlap Syndrome[J]. Progress in Modern Biomedicine, 2016, 16(8):1521-1523
[30] Torisu Y, Nakano M, Takano K, et al. Clinical usefulness ofursodeoxycholic acid for Japanese patients with autoimmune hepatitis[J]. World J Hepatol, 2017, 9(1):57-63