The gold standard in diagnosing NAFLD is liver biopsy by which discrimination between steatosis and NASH is possible [
27]. Given its invasive nature with risks such as haemorrhagic complications and pain, liver biopsy is not useful as an epidemiological screening tool [
28]. As a result, current cross-sectional epidemiological data are mainly based on surrogate markers such as imaging rather than on histopathological data. Considering the higher sensitivity, lower costs and wide availability, ultrasound is preferred over CT-scanning for diagnosing NAFLD [
29]. However, its sensitivity is limited in the setting of mild NAFLD and in morbidly obese patients [
30,
31]. Magnetic resonance spectroscopy proton density fat fraction (MRS-PDFF) is a very sensitive imaging modality, with a sensitivity up to 100% [
31]. Due to its wider availability and low risk for sampling error, magnetic resonance imaging proton density fat fraction (MRI-PDFF) is increasingly used in research. In a recent review by Caussy et al., the differences and impact of MRS-PDFF and MRI-PDFF were extensively discussed. Considering the high costs and limited availability, MRI-based imaging is currently still not a useful screening tool and its use remains limited to research [
32]. In 2010, a new non-invasive tool for the detection of steatosis, called controlled attenuation parameter (CAP), was introduced [
33]. It is an addition to the Fibroscan (Echosens, Paris, France) and measures steatosis simultaneously with fibrosis. CAP determines the total ultrasonic attenuation at a frequency of 3.5 MHz and is reported in decibel/meter (dB/m). In a meta-analysis by Wang et al., CAP provided good sensitivity and specificity [
34]. For example, the sensitivity for the detection of ≥ S1 steatosis (≥ 5% of the hepatocytes affected with lipid accumulation) was 0.78 with an area under the curve (AUC) of 0.86 (95% CI 0.82–0.88). For stage S3 (> 66% of the hepatocytes affected), the sensitivity was 0.86 with an AUC of 0.94 (95% CI 0.91–0.96). It should be emphasized that none of the above-mentioned imaging modalities can assess the degree of NAFLD/NASH as assessed by the histological Brunt classification [
35]. Differentiating between NAFLD and NASH is important since 25–35% of patients with NASH eventually progress to liver fibrosis or even cirrhosis [
36,
37]. Using serum alanine aminotransferase (ALT) levels in addition to imaging to discriminate between steatosis and NASH turns out to be disappointing. Several studies showed that a significant proportion of the patients with biopsy-proven NASH had normal ALT values, although some studies suggested that the common laboratory cut-off value for ALT was too high [
38‐
40]. There are several risk scores—such as the NAFLD Fibrosis score—available to evaluate which patients with NAFLD are at risk for (advanced) fibrosis, but its utility still needs to be evaluated in the HIV-positive population [
41]. There are currently no guidelines that recommend universal screening for NAFLD in the general population or in specific subpopulations. In contrast, the European AIDS Clinical Society (EACS) guideline recommends screening for NAFLD in HIV-infected patients with metabolic syndrome using ultrasound [
42]. Since the prevalence of NAFLD among HIV-infected patients with persistent liver enzyme elevations is high, ultrasound screening should also be considered in this population.