The prognosis of NAFLD depends heavily on the histopathological severity . Although liver biopsy has traditionally been considered the only reference method for evaluation of tissue damage, problem is that liver biopsy only gives a snapshot and not an insight into the dynamic changes during the process . Moreover, it is invasive, difficult to accept, and susceptible to significant sampling variability and has a risk of severe complications . Therefore, an ideal noninvasive surrogate marker or tests is urgently needed.
Several blood biomarkers and scores systems have been proposed for differential diagnosis of simple steatosis from NASH. Among the clinical and laboratory parameters, the best representative biomarker is cytokeratin-18 with 66% of Sen and 82% of Spe . Besides, NAFIC score (AUROC = 0.851) were reported to be useful for diagnosing the early stage of NASH via the combination with blood markers such as Palekar’s score [32, 33]. However, the use of laboratory indexes above is unusual and costly. Moreover, none of them are liver specific and their results may be influenced by changes in clearance and excretion of each individual parameter. Therefore, more longitudinally verifiable data are needed. It is known that the best-studied imaging modality was magnetic resonance elastography (MRE), demonstrating the high accuracy (AUROC = 0.93) for discriminating patients with NASH from those with simple steatosis, with 94% of Sen and 73% of Spe . However, the group design utilized in this study lacked the clear histological diagnosis between NASH and not-NASH disease. To date, noninvasive tests have not been validated for diagnosing NASH because of the small number of studies.
SWE is an emerging noninvasive method based on shear waves implemented on the diagnostic ultrasound system to provide quantitative analysis of tissue stiffness. In the present study, we evaluated the performance of SWE on the diagnosis of NAFLD and compared it with the four serum fibrosis scores using histopathology as reference. The LSMs on SWE was proved to be a reliable method that can not only bring up potentially steatohepatitis hint, but also roughly determine the stage of liver fibrosis and would not been influenced by the presence of steatosis at the same time.
In the present study, we evaluated the performance of SWE in indentifying NASH in NAFLD patients and confirmed the good performance of SWE to diagnose NASH with an AUROC of 0.85 (0.73–0.92) at a cutoff of 7.55 kPa. To the best of our knowledge, this is the first study to evaluated SWE in a clinic concerned NASH, which was deemed to steatosis with lobular and portal area inflammation rather than minor inflammation.
As for staging fibrosis, dozens of noninvasive models composed of blood biochemical biomarkers were reported to be useful, including NFS , FIB-4 , APRI , enhanced liver fibrosis (ELF)  and CA index . However, APRI and FIB-4 were initially established for patients with hepatitis C virus (HCV) infection or HIV/HCV coinfection. ELF and CA index need some special tests. In this study, the AUROC of SWE LSMs on detection of fibrosis is superior to those of four scoring systems (NFS, FIB-4, APRI and BARD). This is reasonable because some blood markers of the scoring systems would be affected by races and diets, whereas the SWE LSMs is directly reflect stiffness of the liver and guided by a higher frame-rate B-mode image that can yield a more accurate measurement. Transient elastography (TE) was initially shown to be reliable for assessing fibrosis in patients with chronic hepatitis C . TE also was reported to be useful to assess fibrosis in patients with NAFLD [21, 37]. However, there were some limitations of TE. The first is its one-dimensional imaging that may fail to obtain reliable LSMs. Besides, TE has poor performance related to obesity, narrow intercostal space, and ascites . SWE is a more accuracy method to staging fibrosis than TE. Ferraioli et al. showed that SWE was more accurate than TE in assessing significant fibrosis (≥ F2) in chronic hepatitis C . Similarly, a recent meta-analysis studied for NAFLD patients  showed the pooled Sen and Spe for diagnosing F ≥ 2, F ≥ 3, and F = 4 disease, TE were 76% and 65%, 75% and 74%, 88% and 82%, respectively, SWE were higher than TE, were 85% and 94%, 90% and 92%, 100% and 86%, respectively.
As for NAFLD disease, some animal studies have reported that SWE is an efficient technique to differentiate NASH from less severe NAFL [39, 40]. However, limited human data were available on NAFLD. Samir AE et al.’s study showed that the use of SWE provided an AUROC of 0.77 (95% CI: 0.68, 0.86), with an optimal cutoff of 7.29 kPa (Sen = 91.4%, Spe = 52.5%) for ≥ F2 patients with a varied spectrum of liver diseases (NAFLD included) . Garcovich et al. assessed SWE for diagnosing NASH in pediatric population and reported an AUROC of 0.96 to diagnose ≥ F2 with a cutoff value of 6.7 kPa (Sen = 87%, Spe = 96%) . Arinc ozturk et al  demonstrated the higher threshold of 8.37 kPa than that of 7.65 kPa in this study to diagnose high risk NASH (F ≥ 2). This result may be accounted for different histopathological outcome markers or different patient samples. To date, apart from this study, no reliably diagnostic threshold to detect NASH in general population.
In the present retrospective study, the LSMs between the normal control group and NAFL group was no statistically difference (P = 1.0). Similarly, Suh et al. used SWE to study liver LSMs and demonstrated no statistical difference between the normal control group and NAFL group (P = 0.694) , suggesting that steatosis would not affect liver LSMs. Samir AE et al. also proved steatosis did not show any correlation with LSMs , consistent with our results. However, it cannot be ignored that the influence of severe steatosis on LSMs, because fatty attenuation of severe steatosis may lead to SWE measurement failure . Nevertheless, several literatures had inconsistent conclusions. In some transient elastography studies, steatosis has been reported to have an effect on TE LSMs [45–47].
One of the strengths of the study is that we consulted clinically concerned NAFLD classifications : steatosis with minor inflammation is regarded as non-progressive and assigned to the NAFL group, rather than early NASH. So we can make a more clear diagnosis between NASH and non-NASH. Furthermore, we derived threshold to detect NASH and stage fibrosis. This result can be used for consensus establishment in clinical practice on thresholds or strategies for diagnosing NASH and differentiating fibrosis stage, or further trying to avoid liver biopsy. In addition, we evaluated in this study four fibrosis scoring biochemical systems in Chinese population. However, our study has some limitations such as limited sample size, bias of retrospective study, sampling error of needle biopsy, et al. Larger studies are needed to define the effect of these and other confounders and to establish SWE thresholds for various fibrosis stages in distinct diffuse liver disease.