I read with interest the recent paper by Campos and coworkers,1 who developed a novel clinical scoring system for predicting nonalcoholic steatohepatitis (NASH) in patients with morbid obesity (median body mass index: 48 kg/m2). The authors identified hypertension, type 2 diabetes, the presence of sleep apnea, elevated aspartate aminotransferase and alanine aminotransferase activities, and non-Black race as independent predictors of NASH in a cohort of 200 obese patients.1 Based on the significant prognosticators identified, the authors developed an original NASH Clinical Scoring System to predict the probability of NASH according to different risk categories (low, intermediate, high, and very high). The positive predictive value for the presence of NASH in the very-high-risk group was 93%. Conversely, the negative predictive values for the presence of NASH were 87% and 71% in patients at low risk and intermediate risk, respectively.1
Besides clinical predictors of NASH, demand is growing for biomarkers that can reliably identify patients with NASH in the setting of obesity. Of interest, a very recent laboratory study has shown that, among obese individuals, NASH can be predicted reliably by measuring serum levels of adiponectin, resistin, and cleaved CK-18 fragments, a product of hepatocyte apoptosis during liver injury.2 This biomarker panel yielded a sensitivity of 95.45%, specificity of 70.21%, and an area under curve of 0.908 for the presence of NASH.2 Another study by Trak-Smayra and colleagues3 has identified by surface-enhanced laser desorption/ionization–time-of-flight analysis significant changes in serum protein profiles in obese patients that varied according to severity of liver lesions (steatosis and NASH).3 Specifically, three novel putative biomarkers of liver damage in the setting of obesity (termed CM10-7558.4, CM10-7924.2, and Q10-7926.9) were discovered.3 Altogether, these findings suggest and highlight two potentially important future research directions in the setting of obesity-associated NASH. First, the existence of serum-based marker panels with sufficient sensitivity and specificity2 may actually improve the clinical screening of obese individuals at high risk for developing NASH. Accordingly, it would be very interesting to investigate whether the concomitant measurements of adiponectin, resistin, and cleaved CK-18 fragments2 may ameliorate the diagnostic performance of the clinical scoring system developed by Campos and coworkers.1 Second, the establishing of a noninvasive strategy to identify biomarkers by proteomic profiling leading to the identification of novel proteins predictive of NASH in obesity3 will be helpful in the future for the definition of nonalcoholic fatty liver disease subphenotypes, as well as in the measurement of response to therapy in clinical studies. This might ultimately lead to a reduction in the rate of liver biopsies to screen for NASH in morbidly obese patients, as well as for choosing and tailoring treatments for obesity-associated liver disease.