Sulyok Mihály, Ferenci Tamás, Makara Mihály, Horváth Gábor, Szlávik János, Rupnik Zsófia, Kormos Luca, Gerlei Zsuzsanna, Sulyok Zita, Vályi-Nagy István
Doctoral School for Clinical Medicine, Semmelweis University, Budapest, Hungary; Institute for Tropical Medicine, Eberhard Karls University, Tuebingen, Germany.
John von Neumann Faculty of Informatics, Physiological Controls Group, Óbuda University , Budapest , Hungary.
PeerJ. 2017 Jan 11;5:e2867. doi: 10.7717/peerj.2867. eCollection 2017.
Liver disease has become an important cause of morbidity and mortality even in those HIV-infected individuals who are devoid of hepatitis virus co-infection. The aim of this study was to evaluate the degree of hepatic fibrosis and the role of associated factors using liver stiffness measurement in HIV mono-infected patients without significant alcohol intake.
We performed a cross-sectional study of 101 HIV mono-infected patients recruited prospectively from March 1, 2014 to October 30, 2014 at the Center for HIV, St István and St László Hospital, Budapest, Hungary. To determine hepatic fibrosis, liver stiffness was measured with transient elastography. Demographic, immunologic and other clinical parameters were collected to establish a multivariate model. Bayesian Model Averaging (BMA) was performed to identify predictors of liver stiffness.
Liver stiffness ranged from 3.0-34.3 kPa, with a median value of 5.1 kPa (IQR 1.7). BMA provided a very high support for age (Posterior Effect Probability-PEP: 84.5%), moderate for BMI (PEP: 49.3%), CD4/8 ratio (PEP: 44.2%) and lipodystrophy (PEP: 44.0%). For all remaining variables, the model rather provides evidence against their effect. These results overall suggest that age and BMI have a positive association with LS, while CD4/8 ratio and lipodystrophy are negatively associated.
Our findings shed light on the possible importance of ageing, overweight and HIV-induced immune dysregulation in the development of liver fibrosis in the HIV-infected population. Nonetheless, further controlled studies are warranted to clarify causal relations.
即使在未合并感染肝炎病毒的HIV感染者中,肝脏疾病也已成为发病和死亡的重要原因。本研究的目的是在无大量酒精摄入的HIV单感染患者中,使用肝脏硬度测量评估肝纤维化程度及相关因素的作用。
我们对2014年3月1日至2014年10月30日在匈牙利布达佩斯圣伊什特万和圣拉兹洛医院HIV中心前瞻性招募的101例HIV单感染患者进行了横断面研究。为确定肝纤维化,采用瞬时弹性成像测量肝脏硬度。收集人口统计学、免疫学和其他临床参数以建立多变量模型。采用贝叶斯模型平均法(BMA)确定肝脏硬度的预测因素。
肝脏硬度范围为3.0 - 34.3 kPa,中位数为5.1 kPa(四分位间距1.7)。BMA对年龄提供了很高的支持度(后效应概率-PEP:84.5%),对BMI、CD4/8比值和脂肪代谢障碍提供了中度支持度(PEP分别为49.3%、44.2%和44.0%)。对于所有其余变量,该模型反而提供了反对其作用的证据。这些结果总体表明,年龄和BMI与肝脏硬度呈正相关,而CD4/8比值和脂肪代谢障碍与肝脏硬度呈负相关。
我们的研究结果揭示了衰老、超重和HIV诱导的免疫失调在HIV感染人群肝纤维化发展中可能的重要性。尽管如此,仍需要进一步的对照研究来阐明因果关系。