Florina Romanciuc

Lyso‐phosphatidylcholine: A potential metabolomic biomarker for alcoholic liver disease?

We read with great interest the work of Michelena et al., which demonstrated that in patients with alcoholic hepatitis the presence of a systemic inflammatory response, with or without infection, precipitates development of complications and death. By identifying lipopolysaccharide (LPS) as an important player in the inflammatory response, the authors open a novel gateway for identifying the inflammatory mediators that cause this systemic response. Historic reports found an inverse association between lyso-phosphatidylcholine (LYPC) and the amount of liver fibrosis in an experimental model of alcoholic liver disease (ALD). More recently lower LYPC levels were found in nonalcoholic fatty liver disease/nonalcoholic steatohepatitis patients compared with controls. The link between LPS and LYPC is considered to be phosphatidylcholine-specific phospholipase C, the levels and activity of which are increased by LPS. Therefore, we hypothesized that LYPC may be a biomarker for severity and short-term prognosis in patients with ALD. Thirty consecutive patients admitted for ALD were included. Of them, 17 were known to have cirrhosis and 7 had previous clinical liver-related decompensation (LRD) events. Patients were followed for 30 days for the development of LRD and/or death. At inclusion 16 patients (12 of whom were known to have cirrhosis) had an alcoholic steatohepatitis test score (BioPredictive, France) 0.18, indicating at least minimal activity; the test was used in addition to clinical and biological criteria for the diagnosis of alcoholic hepatitis: recent alcohol abuse, leukocytosis, aspartate aminotransferase/alanine aminotransferase >1. Highperformance liquid chromatography-mass spectrometry was used to determine baseline levels of two LYPC serum metabolites: 16:1 and 20:4. Twelve patients decompensated during follow-up, 6 of them having multiple LRDs; 2 patients died. Both LYPCs had lower levels in patients with LRD compared to those without (0.277 [0.19520.737] versus 0.517 [0.16620.987], P 5 0.0001, and 0.564 [0.31222.116] versus 1.302 [0.795-3.492], P 5 0.008, respectively). The performance of the two LYPC metabolites to predict LRD is summarized in Table 1. They also had a good inverse correlation with Model for End-Stage Liver Disease (20.602; 20.619) (see Supporting Fig. S1); Maddrey (20.632; 20.656); and age, serum bilirubin, international normalized ratio, and serum creatinine (ABIC) (20.404; 20.529) scores and with liver stiffness by transient elastography (20.608 and 20.645). No correlation was found with daily alcohol intake (20.384 and 20.321; P 5 0.07 and 0.135, respectively).

Serum metabolomics can predict the outcome of first systematic transrectal prostate biopsy in patients with PSA <10 ng/ml

AIM To assess the predictive value of metabolomic analysis for the presence of prostate cancer (PCa) at first systematic biopsy. PATIENTS & METHODS Ninety serum samples from patients with suspicion for PCa were included. Targeted and nontargeted metabolomic analysis was performed. RESULTS Six metabolites were combined into a predictive score. A cutoff value of 0.528 for the metabolomic score showed a good accuracy for the prediction of PCa at biopsy (Area under the curve (AUC): 0.779; p < 0.001). These results were validated in a subgroup of patients, showing similar accuracy (p = 0.1). For patients with prostate specific antigen (PSA) less than 10 ng/ml, the score showed a Se 80.95%, Sp 64.52% for the detection of PCa at biopsy. CONCLUSION Metabolomic analysis can predict the outcome of the first systematic biopsy.