Spaan Michelle, Carey Ivana, Bruce Matthew, Shang Dazhuang, Horner Mary, Dusheiko Geoff, Agarwal Kosh
Institute of Liver Studies, King's College Hospital, London, United Kingdom; Department of Gastroenterology and Hepatology, Erasmus MC, Rotterdam, the Netherlands.
Institute of Liver Studies, King's College Hospital, London, United Kingdom.
J Hepatol. 2020 Jun;72(6):1097-1104. doi: 10.1016/j.jhep.2019.12.028. Epub 2020 Jan 22.
BACKGROUND & AIMS: Coinfection with HDV causes rapid progression to liver cirrhosis and hepatic decompensation in patients with chronic hepatitis B. Factors that are associated with disease progression are poorly understood. In this study we aim to identify risk factors associated with disease progression and better characterise clinical differences and treatment response between HDV genotype 1 and 5.
In this retrospective study, all patients under our care between 2005 and 2016 with HBV/HDV coinfection (HBsAg+, anti-HDV antibodies positive) were analysed. Patients were excluded if follow-up was less than 6 months, if they had HCV and/or HIV coinfection or an acute HDV infection. Demographic data, stage of liver disease, development of liver complications and treatment response were recorded.
One-hundred seven patients (mean age 36.0 years, 57% male) were followed for a median period of 4.4 years (range 0.6-28.1 years); 64% were of African origin and 17% were of European origin, with 28% of patients being cirrhotic at first visit; 43% patients had actively replicating HDV virus (anti-HDV-IgG+, anti-HDV-IgM+ or HDV RNA+) and 57% of patients were HDV exposed (anti-HDV-IgG+, HDV RNA-). Patients with actively replicating HDV more often developed liver complications than HDV-exposed patients (p = 0.002), but no differences in baseline characteristics were observed. Patients with HDV genotype 5 less often developed cirrhosis or hepatic decompensation compared to patients with HDV genotype 1. Twenty-four patients were treated with peg-IFN and post-treatment response was significantly better in patients infected with genotype 5 (10% GT1 vs. 64% GT5, p = 0.013).
Patients infected with HDV genotype 5 appear to have a better prognosis with fewer episodes of hepatic decompensation and better response to peg-IFN treatment than patients infected with HDV genotype 1.
Hepatitis delta is a virus that affects the liver. The virus is known to have different subtypes, called genotypes. With this research we discovered that hepatitis delta virus genotype 1 behaves differently than genotype 5 and causes faster development of liver disease. This is important for education of our patients and to determine how often we need to check our patients.
丁型肝炎病毒（HDV）合并感染会使慢性乙型肝炎患者迅速发展为肝硬化和肝失代偿。与疾病进展相关的因素尚不清楚。在本研究中，我们旨在确定与疾病进展相关的危险因素，并更好地描述HDV 1型和5型之间的临床差异及治疗反应。
在这项回顾性研究中，我们分析了2005年至2016年间在我们照护下的所有HBV/HDV合并感染患者（HBsAg阳性，抗HDV抗体阳性）。如果随访时间少于6个月、合并丙型肝炎病毒（HCV）和/或人类免疫缺陷病毒（HIV）感染或急性HDV感染，则将患者排除。记录人口统计学数据、肝病分期、肝脏并发症的发生情况及治疗反应。
107例患者（平均年龄36.0岁，57%为男性）接受了中位时间为4.4年（范围0.6 - 28.1年）的随访；64%为非洲裔，17%为欧洲裔，28%的患者初诊时已发生肝硬化；43%的患者HDV病毒处于活跃复制状态（抗HDV-IgG阳性、抗HDV-IgM阳性或HDV RNA阳性），57%的患者曾暴露于HDV（抗HDV-IgG阳性，HDV RNA阴性）。HDV活跃复制的患者比HDV暴露的患者更常发生肝脏并发症（p = 0.002），但在基线特征方面未观察到差异。与HDV 1型患者相比，HDV 5型患者发生肝硬化或肝失代偿的情况较少。24例患者接受了聚乙二醇干扰素治疗，5型感染患者的治疗后反应明显更好（1型为10%，5型为64%，p = 0.013）。
与HDV 1型感染患者相比，HDV 5型感染患者似乎预后更好，肝失代偿发作次数更少，对聚乙二醇干扰素治疗的反应更好。
丁型肝炎是一种影响肝脏的病毒。已知该病毒有不同的亚型，称为基因型。通过本研究我们发现，丁型肝炎病毒1型的表现与5型不同，会导致肝病发展更快。这对于对我们的患者进行教育以及确定我们需要多久检查一次患者非常重要。
