Serum level of ceruloplasmin in patients with different liver diseases in Jilin,China

Wang ShaSha; Hua Fang; Jiao YongGeng; Qin ErYun; Zhi YiXiao; Pang MengYuan; Xu HongQin; Chi XiuMei; Niu JunQi; Hua Rui

doi:10.3969/j.issn.1001-5256.2020.09.023

Volume 36 Issue 9

Sep. 2020

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Article Navigation > Journal of Clinical Hepatology > 2020 > 36(9): 2025-2029

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Serum level of ceruloplasmin in patients with different liver diseases in Jilin,China

DOI: 10.3969/j.issn.1001-5256.2020.09.023

Department of Hepatology,The First Hospital of Jilin University
Department of Cardiology,The First Hospital of Jilin University
Department of Anesthesiology,The FAW General Hospital of Jilin Province

Research funding:

Received Date: 2020-05-17
Published Date: 2020-09-20

Abstract

Abstract

Objective To investigate the serum level of ceruloplasmin in patients with different stages and etiologies of liver diseases.Methods A total of 1077 patients with liver diseases who were hospitalized in Department of Hepatology,The First Hospital of Jilin University,from January 2012 to January 2018 were enrolled,and the serum level of ceruloplasmin was analyzed for the patients with different liver diseases. The Kruskal-Wallis H test was used to compare the level of ceruloplasmin between the patients with virus-related liver diseases with different liver functional states,and a Spearman correlation analysis was used to investigate the correlation of ceruloplasmin with other biomarkers. Results In the Wilson's disease group,97. 6%( 41/42) of the patients had a serum ceruloplasmin level of < 0. 2 g/L and88. 1%( 37/42) had a level of < 0. 1 g/L. In the non-Wilson's disease group,24. 3%( 251/1035) of the patients had a ceruloplasmin level of < 0. 2 g/L and 0. 2% had a level of < 0. 1 g/L. There was a significant difference in the serum level of ceruloplasmin between the patients with virus-related liver diseases with different liver functional states,and the patients with chronic viral hepatitis,severe viral hepatitis,and viral hepatitis cirrhosis had a significantly lower level than those with acute viral hepatitis and virus-related liver cancer( P =0. 005,P < 0. 001,P = 0. 001,P = 0. 027,P < 0. 001,and P = 0. 001). In the patients without Wilson's disease,serum ceruloplasmin was positively correlated with albumin and prealbumin( r = 0. 068 and 0. 091,both P < 0. 05) and was negatively correlated with prothrombin time( r =-0. 297,P < 0. 05). Conclusion Ceruloplasmin often decreases significantly in patients with Wilson's disease,with a slight reduction in patients with other types of liver diseases. For these patients,it should be determined whether the reduction in ceruloplasmin is caused by hepatocyte injury or the presence of Wilson's disease.
- ceruloplasmin,
- liver diseases,
- hepatolenticular degeneration

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肝细粒棘球蚴病(hepatic cystic echinococcosis，HCE)又称囊型肝包虫病，是由细粒棘球绦虫的幼虫寄生于人或动物体内引起的人兽共患的寄生虫病，呈世界性分布，包括非洲、南美洲、中亚等多个地区^[1]。在我国以西部地区的新疆、青海、宁夏、甘肃、西藏、四川、内蒙古等地流行为主，平均患病率为1.08%^[2]。

我国慢性HBV感染者约7000万^[3]，2006年调研显示HCV感染者约1000万^[4]。慢性病毒性肝炎发展为肝硬化和肝细胞癌(HCC)的风险更高，故将HBV和HCV归类为“癌病毒”^[5]。但是慢性肝炎病毒感染发展至肝硬化、HCC的机制复杂，此病程很难有效延缓或逆转。

囊型肝包虫病、肝炎病毒感染均为免疫相关性疾病，其病程的发生、发展均与机体的免疫应答有密切的关系^[6-7]。新疆地区是肝包虫病与肝炎病毒感染的流行地区^{[1, 8]}，但在临床工作中发现囊型肝包虫病鲜有与肝癌共患的现象，手术中笔者也发现肝包虫合并肝炎的肝脏与同期肝炎患者肝脏相比，质地较软，很少有肝硬化结节形成。两种疾病之间是否互相影响，目前尚不清楚。因此本研究收集囊型肝包虫患者病例资料，以进一步明确囊型肝包虫病与慢性HBV/HCV感染、肝硬化、HCC的共患状态。

1. 资料与方法

1.1 研究对象

收集2003年—2019年石河子大学医学院第一附属医院住院部收治的401例囊型肝包虫病患者及72例单纯慢性HBV/HCV感染者资料。纳入标准：(1)符合囊型肝包虫病诊断的常规就诊患者；(2)共患病病例需符合慢性HBV/HCV感染、肝硬化、HCC诊断标准；(3)单纯慢性HBV/HCV感染病例符合慢性HBV/HCV感染诊断标准及匹配条件；(4)病例资料完整、齐全，符合质控要求的病例。

1.2 诊断标准

(1) 肝包虫诊断符合《2006年国家包虫病诊断标准(WS257-2006)》，从患者流行病学、临床表现、影像学检查、免疫学检查及手术病理标本等方面综合判断确定的肝包虫临床病例^[9]；(2)慢性HBV/HCV感染诊断符合《慢性乙型肝炎防治指南(2015年更新版)》、《慢性丙型肝炎防治指南(2015版)》^[10-11]；(3)肝硬化诊断符合《肝硬化诊治指南》^[12]；(4)HCC诊断符合《原发性肝癌诊疗规范(2017年版)》^[13]。

1.3 研究方法

由经过专门培训的调查员收集囊型肝包虫病例资料中患者性别、年龄、民族、生活习惯(吸烟史、饮酒史)、实验室检查(肝功能、甲型/乙型/丙型肝炎检测)等数据，了解囊型肝包虫病与HBV/HCV感染、肝硬化、HCC共患病状态。

选取囊型肝包虫合并慢性HBV/HCV感染病例为共患病组，根据共患病组患者的病毒感染类型、病毒感染病程、性别、年龄、生活习惯(吸烟史、饮酒史)、抗病毒治疗情况，按1∶2匹配单纯慢性HBV/HCV感染患者为对照组，分析两组病毒感染状态、肝硬化、HCC的疾病构成。单纯慢性HBV/HCV感染组匹配条件：(1)病毒感染类型一致；(2)病毒感染病程、抗病毒治疗、性别、年龄、生活习惯(吸烟史、饮酒史)构成比与共患病组差异无统计学意义；(3)排除有其他可导致肝脏异常的疾病。

对肝包虫合并慢性HBV/HCV感染病例与单纯肝包虫病例中包虫分型进行比较。

1.4 统计学方法

所有数据采用SPSS 21.0软件进行统计。计数资料两组之间比较采用χ²检验或Fisher确切概率法。P < 0.05为差异有统计学意义。

2. 结果

2.1 一般资料

401例囊型肝包虫患者中男228例(56.9%)，女173例(43.1%)，年龄4~91岁，主要以20~50岁患者为主，有209例(52.1%)，其次是51~70岁患者，有111例(27.7%)，< 20岁12例(3%)，＞70岁69例(17.2%)。其中汉族318例(79.3%)，哈萨克族33例(8.2%)，回族31例(7.7%)，维吾尔族17例(4.2%), 蒙古族2例(0.5%)。既往有长期饮酒史84例(20.9%)，有长期吸烟史123例(30.7%)。

2.2 肝包虫与慢性HBV/HCV感染、肝硬化、HCC共患病情况

401例囊型肝包虫患者中合并慢性HBV/HCV感染患者38例(9.5%)，其中肝包虫合并慢性HBV感染21例(5.2%)，肝包虫合并慢性HCV感染15例(3.7%)，肝包虫同时合并慢性HBV感染和慢性HCV感染2例(0.5%)；肝包虫合并肝硬化4例(1%)，其中慢性HBV感染后肝硬化1例(0.25%)、慢性HBV、HCV共感染后肝硬化1例(0.25%)，其他原因肝硬化2例(0.5%)；合并HBV/HCV感染后HCC 0例，其他原因肝癌1例(0.25%)。

2.3 肝包虫病对病毒感染状态及病程的影响

共患病组与单纯慢性HBV/HCV感染组性别、年龄、肝炎病程、生活习惯(吸烟史、饮酒史)、抗病毒治疗方面比较，差异均无统计学意义(P值均＞0.05)。共患病组的慢性HBV感染者中非活动性HBsAg携带患者占81%，HBeAg阳性CHB患者占9.5%，HBeAg阴性CHB患者占9.5%；单纯慢性HBV/HCV感染组的HBV感染者中非活动性HBsAg携带患者占43%，HBeAg阳性CHB患者占33%，HBeAg阴性CHB患者占19%，差异有统计学意义(P=0.033)；共患病组中HCV感染者的HCV RNA转阴率为73%，与单纯慢性HBV/HCV感染组HCV感染者(40%)比较差异有统计学意义(P=0.035)；共患病组肝硬化占比5.2%，HCC占比0，单纯慢性HBV/HCV感染组肝硬化占比18.4%，HCC占比5.2%，差异有统计学意义(P=0.048)(表 1)。

表 1 肝包虫病对HBV/HCV感染状态及病程影响的比较

指标	共患病组(n=38)	单纯肝炎组(n=76)	χ²值	P值
性别[例(%)]			0.476	0.490
男	26(68)	47(62)
女	12(32)	29(38)
年龄[例(%)]			0.121	0.728
< 35岁	6(16)	14(18)
≥35岁	32(84)	62(82)
肝炎病程[例(%)]			0.650	0.723
<10年	12(31)	19(25)
10~20年	20(53)	42(55)
＞20年	6(16)	15(20)
饮酒史[例(%)]			1.160	0.281
有	7(18)	21(28)
无	31(82)	55(72)
吸烟史[例(%)]			3.254	0.071
有	9(24)	31(41)
无	29(76)	45(59)
规律抗病毒治疗[例(%)]			3.109	0.078
有	2(5)	13(17)
无	36(95)	63(83)
慢性HBV感染[例(%)]	21(55)	42(55)		0.033
慢性HBV携带状态	0(0)	2(5)
HBeAg阳性CHB	2(9.5)	14(33)
非活动性HBsAg携带	17(81)	18(43)
HBeAg阴性CHB	2(9.5)	8(19)
慢性HCV感染[例(%)]	15(40)	30(40)	4.447	0.035
HCV RNA阳性	4(27)	18(60)
HCV RNA转阴	11(73)	12(40)
慢性HBV、HCV共感染[例(%)]		2(5)	4(5)	1.000
HBeAg阴性CHB，HCV RNA阳性	1(50)	1(25)
非活动性HBsAg携带，HCV RNA阴性	1(50)	1(25)
非活动性HBsAg携带，HCV RNA阳性	0(0)	2(50)
病情进展[例(%)]				0.048
单纯HBV/HCV感染	36(95)	58(76)
合并肝硬化	2(5)	14(18)
合并肝癌	0(0)	4(5)

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2.4 肝包虫分型情况

合并HBV/HCV感染的肝包虫和单纯肝包虫的分型构成比差异无统计学意义(P＞0.05)，肝包虫合并HBV/HCV感染后并未发生集中在某型或向某型偏倚(表 2)。

表 2 肝包虫分型情况

包虫分型	共患病患者(n=38)	单纯肝包虫患者(n=363)
单囊型(CL、CE1)	6	81
多子囊型(CE2)	14	155
内囊塌陷型(CE3)	5	52
实变型(CE4)	6	44
钙化型(CE5)	7	31

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3. 讨论

肝细粒棘球蚴病(囊型肝包虫病)是由细粒棘球绦虫的幼虫感染人体而形成的一种寄生虫良性病变，病程较长，部分可随自然病程的进展钙化死亡^[14]，而因HBV和HCV持续感染导致的病毒性肝炎患者主要结局是肝硬化和HCC。目前在我国慢性HBV感染约7000万，其中发展为CHB患者2000~3000万，因输血导致的慢性HCV感染者肝硬化发生率为18%~30%^[3-4]，肝硬化和HCC患者中, 由HBV/HCV感染所致者分别为77%和84%^[15]，可见慢性HBV/HCV感染后疾病进一步进展的比例是较高的。而本次调查401例囊型肝包虫病患者，合并慢性HBV/HCV感染38例，其中仅有2例HBV/HCV感染后肝硬化(5.2%)，而HBV/HCV感染后HCC患者为0。进一步回顾共患病患者，与匹配的单纯HBV/HCV感染者对比，发现共患病组中病毒感染状态为非活动状态比例较高，CHB患者比例下降，HCV RNA转阴率升高，两组病毒感染状态的构成比差异均有统计学意义(P值均 < 0.05)，因此不除外是囊型肝包虫的存在导致了HBV/HCV感染状态的构成比发生了改变，但仍需大样本、前瞻性的队列研究进一步证实。

囊型肝包虫病、慢性肝炎病毒感染、肝硬化、HCC均为免疫相关疾病。肝炎病毒感染后发生肝炎-肝硬化-HCC的病程中，一个重要因素是通过影响不同的免疫细胞，使多种细胞因子共同参与下发生的，例如肝炎病毒影响下T淋巴细胞异常免疫攻击形成慢性肝损伤^[16-17]；抑制辅助性T淋巴细胞(Th)1免疫，增强Th2免疫^[18-19]；刺激巨噬细胞分泌TGFβ和IL-10^[20]；使活化的肝星状细胞免受攻击，加重肝脏的纤维化^[21]等，具体机制不明且复杂。而机体在细粒棘球蚴感染后，可导致机体产生复杂的抗原-抗体免疫反应，该免疫反应在体内持续存在，同时囊型肝包虫对免疫系统的影响也体现在与肝炎密切相关的免疫细胞上^[22]。当两者共存时，可使机体免疫反应更为复杂，目前尚不明确。有动物实验^[23]发现，在囊型肝包虫影响下的免疫环境，对肺癌有一定的抑制作用，但肝包虫是否会对肝炎性HCC产生作用，仍需进一步研究。

本研究为单中心研究，包虫病例数量有限，需要进一步完善多中心研究，来进一步明确肝细粒棘球蚴对肝炎、肝硬化、HCC的影响，同时囊型肝包虫合并病毒性肝炎患者的转归也需要一定时间进一步随访，从而得到更高级别的证据。

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沈阳化工大学材料科学与工程学院沈阳 110142

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Serum level of ceruloplasmin in patients with different liver diseases in Jilin,China

DOI: 10.3969/j.issn.1001-5256.2020.09.023