Platelet count/spleen volume ratio has a good predictive value for esophageal varices in patients with hepatitis B liver cirrhosis.

BACKGROUND & AIMS: Platelet count/spleen longest diameter ratio (PSDR) is widely used in clinical practice due to its good performance in predicting esophageal varices (EV). We obtained spleen volume (SV) by magnetic resonance examination, the purpose of this study was to evaluate the clinical value of platelet count/spleen volume ratio (PSVR) and spleen volume in predicting EV in patients with hepatitis B cirrhosis. Methods: This study was a diagnostic accuracy experiment and retrospective, 199 patients with hepatitis B cirrhosis who met the criteria were selected as the research subjects. All patients were collected blood samples in the morning on an empty stomach within 2 days, and related indicators were tested. Within 10 days, they received electronic gastroscopy and abdominal magnetic resonance examination. According to the Child-Pugh score, the patients were divided into groups with or without EV and with or without high-risk esophageal varices (HRV), then statistical analysis of the two groups was performed. RESULTS: The area under the curve (AUC) of PSVR in predicting EV or HRV in each group (85.5%-92.6%) was higher than PSDR, SV, spleen diameter, and platelet count. The AUC of PSDR in diagnosing HRV was higher than SV, and the AUC of SV in diagnosing EV was higher than PSDR, but the difference was not significant (P>0.05). In Child-Pugh A patients, Multivariate logistic regression analysis showed PSVR could be a predictor of HRV (P<0.05), SV was a reliable predictor of EV (P<0.05). CONCLUSION: PSVR is better than PSDR, spleen diameter, platelet count in predicting EV; in the absence of serological results, SV could be used instead of PSDR. Both can predict EV or HRV of patients with hepatitis B cirrhosis.

Long noncoding RNA small nucleolar RNA host gene 15 deteriorates liver cancer via microRNA-18b-5p/LIM-only 4 axis.

Extensive studies have explored the involvements of long noncoding RNAs (lncRNAs) in liver cancer. Limitedly, the concrete function of lncRNA small nucleolar RNA host gene 15 (SNHG15) is still elusive. Therefore, the work was initiated to unearth SNHG15-oriented mechanism in liver cancer. Liver cancer tissues were resected. The connection between SNHG15 expression with prognosis and clinicopathological traits of liver cancer patients was evaluated. Liver cancer cells SMMC-7721 were transfected with restored microRNA (miR)-18b-5p or depleted SNHG15 to discover their effects on the proliferation, migration, invasion, cycle arrest, and apoptosis of SMMC-7721 cells. The transfected SMMC-7721 cells were injected into nude mice for further investigation. SNHG15, miR-18b-5p, and LIM-only 4 (LMO4) expressions in tissues and cells were tested. The regulatory connections among SNHG15, miR-18b-5p, and LMO4 were detected. SNHG15 and LMO4 were overexpressed while miR-18b-5p was downregulated in liver cancer tissues and cells. Up-regulated SNHG15 was connected with inferior prognosis and aggressive behaviors of liver cancer patients. SNHG15 knockdown or miR-18b-5p restoration depressed SMMC-7721 cell growth in vivo and in vitro. SNHG15 bound to miR-18b-5p and miR-18b-5p targeted LMO4. The work has illuminated that silencing SNHG15 represses liver cancer progression by modulating miR-18b-5p and LMO4, indicating the therapeutic potency of SNHG15/miR-18b-5p/LMO4 axis in liver cancer.