UNASSIGNED: The 2000HIV study cohort comprises 1895 virally suppressed PHIV that were included between 2019 and 2021 in 4 HIV treatment centers in the Netherlands. The majority (58.5%) underwent vibration-controlled transient elastography for the assessment of liver steatosis and fibrosis. The prevalence of steatosis (controlled attenuation parameter ≥263 dB/m) and fibrosis (liver stiffness measurement ≥7.0 kPa) was estimated. Multiple factors including HIV characteristics and antiretroviral drugs were tested in a logistic regression model for association with steatosis and fibrosis. Analyses were performed separately for lean (Asian descent: BMI < 23 kg/m2, other descent: BMI < 25 kg/m2) and overweight/obese (other BMI) participants.
UNASSIGNED: Of 1050 PHIV including 505 lean and 545 overweight/obese PHIV, liver steatosis was observed in 37.7% of the overall study population, 19.7% of lean, and 54% of overweight/obese PHIV, whereas fibrosis was observed in 9.0% of the overall study population, 5.9% of lean, and 12.0% of overweight/obese PHIV.All associations with fibrosis and most associations with steatosis concerned metabolic factors such as type 2 diabetes mellitus (overall population: adjusted odds ratio [aOR] for steatosis: 2.3 [1.21-4.4], P = .011; aOR for fibrosis: 3.7 [1.82-7.53], P < .001). Furthermore, in lean PLHIV, liver steatosis was associated with CD4 and CD8 counts at enrollment, dual therapy, and history of treatment with raltegravir (aOR: 3.6 [1.53-8.47], P = .003), stavudine (aOR: 3.73 [1.69-8.2], P = .001), and indinavir (aOR: 3.86 [1.59-9.37], P = .003). These associations were not observed in overweight/obese PHIV.
UNASSIGNED: Liver steatosis was highly prevalent, affecting approximately one-fifth of lean PHIV and half of overweight/obese PHIV. Fibrosis was observed in a minority. Both steatosis and fibrosis were associated with traditional metabolic risk factors. In addition, (prior) exposure to specific antiretroviral drugs was associated liver steatosis in lean, but not in overweight/obese PHIV. Implementing increased screening protocols could enhance the identification of steatotic liver disease in lean PHIV.
■2000HIV研究队列包括2019年至2021年在荷兰的4个HIV治疗中心中纳入的1895例病毒抑制的HIV。大多数(58.5%)接受振动控制的瞬时弹性成像评估肝脏脂肪变性和纤维化。估计脂肪变性(受控衰减参数≥263dB/m)和纤维化(肝硬度测量≥7.0kPa)的患病率。在Logistic回归模型中测试了包括HIV特征和抗逆转录病毒药物在内的多种因素与脂肪变性和纤维化的相关性。分别对瘦(亚洲血统:BMI<23kg/m2,其他血统:BMI<25kg/m2)和超重/肥胖(其他BMI)参与者进行分析。
■在1050个PHV中,包括505个瘦瘦的和545个超重/肥胖的PHV,在整个研究人群的37.7%中观察到肝脏脂肪变性,精益的19.7%,和54%的超重/肥胖的艾滋病毒,尽管在整个研究人群的9.0%中观察到纤维化,5.9%的精益,和12.0%的超重/肥胖的艾滋病毒。与纤维化的所有关联和与脂肪变性的大多数关联都涉及代谢因素,例如2型糖尿病(总体人群:脂肪变性的调整比值比[aOR]:2.3[1.21-4.4],P=.011;纤维化的aOR:3.7[1.82-7.53],P<.001)。此外,在精益PLHIV中,入组时肝脏脂肪变性与CD4和CD8计数相关,双重疗法,和雷替格韦治疗史(AOR:3.6[1.53-8.47],P=.003),司他夫定(OR:3.73[1.69-8.2],P=.001),和茚地那韦(AOR:3.86[1.59-9.37],P=.003)。在超重/肥胖的PHV中未观察到这些关联。
■肝脏脂肪变性非常普遍,影响大约五分之一的瘦瘦的PEV和一半的超重/肥胖的PEV。在少数人中观察到纤维化。脂肪变性和纤维化均与传统代谢危险因素相关。此外,(以前)暴露于特定的抗逆转录病毒药物与瘦肝脂肪变性相关,但不是超重/肥胖的艾滋病毒。实施更多的筛查方案可以增强瘦肉型PMiv中脂肪变性肝病的识别。