Advances in pediatric non-alcoholic fatty liver disease: From genetics to lipidomics

Table 3 Main results of human proteomics studies in non-alcoholic fatty liver disease

Ref.	Study design	Population (n)	Main findings
Cusi et al[129]	Case-control study	300 subjects with NAFLD (median age 52 ± 1 yr) and 124 without NAFLD (median age 51 ± 1 yr). NAFLD was proven by MRS, biopsy, or US	Increased plasma CK-18 in steatosis, inflammation, and fibrosis
Sookoian et al[130]	Cross- sectional study	101 subjects with simple steatosis (median age 52.3 yr) and 60 NASH patients (median age 54.6 yr). NAFLD was proven by biopsy	sICAM-1 is able to differentiate between patients with simple steatosis and NASH
Rodriguez-Suarez et al[131]	Cross- sectional study	18 controls, 6 obese patients with NAFLD, 6 obese patients with early stage of NASH. Liver disease diagnosis was by biopsy	CPS1 could stratify different phenotypes associated with liver disease severity
Małecki et al[134]	Cross- sectional study	30 children (mean age 10.62 yr), 16 children with NAFLD (mean age 11.06 yr). NAFLD was proven by US	Afamin, retinol-binding protein-4, complement components, and hemopexin were upregulated; serum protease inhibitors, clusterin, immunoglobulin chains, vitamin D binding protein were down-regulated
Bălănescu et al[135]	Cross- sectional study	68 overweight and obese children (mean age 10 yr) and 10 healthy controls. NAFLD was proven by US or elevated alanine transaminase levels	HSP-90 isoforms could be used as NAFLD biomarkers in obese and overweight patients

NASH: Non-alcoholic steatohepatitis; miR: MicroRNA; NAFLD: Non-alcoholic fatty liver disease; MRS: Magnetic resonance spectroscopy; US: Ultrasound; CK-18: Cytokeratin-18; sICAM-1: Soluble intercellular adhesion molecule-1; CPS1: Carbamoyl-phosphate synthase 1; HSP-90: Heat shock protein-90.