Kohlhaas Anna, Durango Esteban, Millonig Gunda, Bastard Cecile, Sandrin Laurent, Golriz Mohammad, Mehrabi Arianeb, Büchler Markus W, Seitz Helmut Karl, Mueller Sebastian
Department of Medicine and Center for Alcohol Research, Liver Disease and Nutrition, Salem Medical Center, University of Heidelberg, Heidelberg, Germany.
Department of Research and Development, Echosens, Paris, France.
Hepat Med. 2012 May 1;4:11-8. doi: 10.2147/HMER.S30256. eCollection 2012.
In contrast with other elastographic techniques, ascites is considered an exclusion criterion for assessment of fibrosis stage by transient elastography. However, a normal liver stiffness could rule out hepatic causes of ascites at an early stage. The aim of the present study was to determine whether liver stiffness can be generally determined by transient elastography through an ascites layer, to determine whether the ascites-mediated increase in intra-abdominal pressure affects liver stiffness, and to provide initial data from a pilot cohort of patients with various causes of ascites.
Using the XL probe in an artificial ascites model, we demonstrated (copolymer phantoms surrounded by water) that a transient elastography-generated shear wave allows accurate determination of phantom stiffness up to a water lamella of 20 mm. We next showed in an animal ascites model that increased intra-abdominal pressure does not affect liver stiffness. Liver stiffness was then determined in 24 consecutive patients with ascites due to hepatic (n = 18) or nonhepatic (n = 6) causes. The cause of ascites was eventually clarified using routine clinical, imaging, laboratory, and other tools. Valid (75%) or acceptable (25%) liver stiffness data could be obtained in 23 patients (95.8%) with ascites up to an ascites lamella of 39 mm. The six patients (25%) with nonhepatic causes of ascites (eg, pancreatitis, peritoneal carcinomatosis) had a significantly lower liver stiffness (<8 kPa) as compared with the remaining patients with hepatic ascites (>30 kPa). Mean liver stiffness was 5.4 kPa ± 1.3 versus 66.2 ± 13.3 kPa.
In conclusion, the presence of ascites and increased intra-abdominal pressure does not alter underlying liver stiffness as determined by transient elastography. We suggest that, using the XL probe, transient elastography can be used first-line to identify patients with nonhepatic ascites at an early stage.
与其他弹性成像技术不同，腹水被视为瞬时弹性成像评估纤维化阶段的排除标准。然而，正常的肝脏硬度可在早期排除腹水的肝脏病因。本研究的目的是确定肝脏硬度是否可通过腹水层由瞬时弹性成像总体确定，确定腹水介导的腹腔内压力增加是否影响肝脏硬度，并提供来自不同病因腹水患者的初步数据。
在人工腹水模型中使用XL探头，我们证明（被水包围的共聚物体模）瞬时弹性成像产生的剪切波可准确测定高达20mm水层的体模硬度。接下来我们在动物腹水模型中表明腹腔内压力增加不影响肝脏硬度。然后对24例因肝脏（n = 18）或非肝脏（n = 6）病因导致腹水的连续患者测定肝脏硬度。最终使用常规临床、影像学、实验室及其他工具明确腹水病因。在23例（95.8%）腹水厚度达39mm的患者中可获得有效（75%）或可接受（25%）的肝脏硬度数据。与其余肝性腹水患者（>30kPa）相比，6例（25%）非肝脏病因腹水患者（如胰腺炎、腹膜癌）的肝脏硬度显著更低（<8kPa）。平均肝脏硬度为5.4kPa±1.3，而肝性腹水患者为66.2±13.3kPa。
总之，腹水的存在及腹腔内压力增加不会改变瞬时弹性成像测定的基础肝脏硬度。我们建议，使用XL探头时，瞬时弹性成像可作为一线方法在早期识别非肝性腹水患者。
