Alterations of coagulation and fibrinolysis in patients with blunt splenic injury after splenic artery embolization.

BACKGROUND: Thrombotic complications following splenectomy have been documented. However, there has been sparse literature regarding thrombotic complications following splenic artery embolization (SAE).The objective of this study was to determine changes in coagulation and fibrinolysis and assess the thrombotic risk after SAE in patients with blunt splenic injury (BSI). METHODS: This study included 38 BSI patients who were hemodynamically stable on admission. SAE was performed if the splenic injury was classed as grade III or greater and had no requirement of immediate surgery. Platelet (PLT), fibrinogen (FIB), D-dimers (D-D), fibrinogen/fibrin degradation products (FDP), antithrombin III (AT III), prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), hemoglobin (Hb), and hematocrit (Hct) were measured before SAE procedures and then 1d, 3d, and 7d after SAE. RESULTS: The technical success rate of SAE and the splenic salvage rate were 100%. There was no mortality. Compared with pre-SAE values, the levels of PLT, FIB, D-D, and FDP increased significantly at 3 days and 7 days after SAE (p < 0.05). However, AT III, PT, APTT, TT, Hb, and Hct showed no statistically significant difference at 1d, 3d, and 7d after SAE (p > 0.05). CONCLUSION: Alterations in PLT and hemostatic parameters might contribute to the increased risk of thrombotic complications in BSI patients undergoing SAE. Thromboembolism following SAE should be considered and thrombotic prophylaxis should be recommended.

BACH1 is transcriptionally inhibited by TET1 in hepatocellular carcinoma in a microRNA-34a-dependent manner to regulate autophagy and inflammation.

Hepatocellular carcinoma (HCC), one of the main contributors to cancer-associated deaths globally, is characterized by high invasiveness. Herein, we studied the molecular mechanisms underlying ten-eleven translocation 1 (TET1)-mediated autophagy in HCC. Following data mining using GSE101728, GSE14520 and GSE138178, TET1 was screened out, and the differential expression of TET1 was verified by bioinformatics analysis. TET1, one of the prognostic markers in HCC, was poorly expressed in HCC. Through functional experiments, we determined that upregulation of TET1 inhibited the proliferation, migration, invasion, tumorigenesis, metastasis and inflammatory factors of HCC cells, and promoted cell autophagy and apoptosis. Mechanistically, TET1 activated miR-34a by demethylating miR-34a. BTB domain and CNC homology 1 (BACH1) was identified as the target gene of miR-34a. Notably, Downregulation of miR-34a increased cellular inflammatory factors and decreased autophagy in the presence of TET1, while declines in BACH1 suppressed cellular inflammatory factors and enhanced autophagy in the presence of miR-34a inhibitor. BACH1 negatively regulated the p53 pathway. In conclusion, TET1 is a tumor suppressor in the progression of HCC by regulating the miR-34a/BACH1/p53 axis, and may contribute to the improvement of HCC prognosis and therapy.

Efficacy evaluation of different conservative treatments for blunt spleen rupture.

BACKGROUND: This study aimed to provide a reference for the clinical treatment of patients with spleen ruptures by analyzing and discussing the clinical effects of the conservative treatment. METHODS: The clinical data of 93 patients with blunt spleen rupture treated in the First Affiliated Hospital of University of Science and Technology of China from April 2015 to April 2018 were retrospectively analyzed. Among them, 84 cases were treated conservatively and 9 cases were treated surgically. The general information of conservative treatment and surgical treatment were compared. The relationship between different conservative treatment methods and CT classification of spleen rupture and the changes of abdominal drainage were analyzed. RESULTS: The CT classification grade and trauma score of patients with spleen rupture in surgical treatment were higher than those in conservative treatment group (P<0.05). A total of 90.3% patients were treated conservatively. Among them, 7.1% (83.4% were in CT classification of spleen injury grade 1-2) were from the observation group, 14.3% (83.3% were in CT classification of spleen injury grade 1-2) were from abdominal drainage group, 3.6% were from splenic artery embolization group, and 75% (9.5% were in CT classification of spleen injury grade 2, 77.8% in grade 3 and 12.7% in grade 4) were from splenic artery embolization plus abdominal drainage group. There was no significant difference in the total amount of abdominal drainage on day 1, day 2 and day 3, and the CT classification of spleen rupture (P>0.05). However, there significant differences on the amount of abdominal drainage among day 1, day 2 and day 3 (P<0.05). Meanwhile, 2 complications occurred in the splenic artery embolization plus abdominal drainage group. CONCLUSIONS: Conservative treatment is feasible in blunt spleen rupture patients of CT classification grade of 1-4 with stable hemodynamical. Splenic rupture patients of CT classification grade 4-5 with instable hemodynamical should be treated surgically.

LncRNA TRG-AS1 stimulates hepatocellular carcinoma progression by sponging miR-4500 to modulate BACH1.

BACKGROUND: T cell receptor gamma locus antisense RNA 1 (TRG-AS1) has been reported to involve in the progression of glioblastoma, however the role and its underlying molecular mechanism in hepatocellular carcinoma (HCC) remain unknown. METHODS: Quantitative real-time polymerase chain reaction (RT-qPCR) was applied to detect TRG-AS1 expression in HCC cells. Besides, the proliferation abilities of HCC cells were assessed by colony formation and EdU assays. The migratory and invasive abilities of HCC cells were examined by transwell assays. Imunofluorescence staining (IF) was used to analyze the epithelial-mesenchymal transitions (EMT). The interaction among TRG-AS1, miR-4500 and BTB domain and CNC homolog 1 (BACH1) were proofed by means of RIP and RNA pull down and luciferase reporter assays. RESULTS: TRG-AS1 was conspicuously overexpressed in HCC cells. TRG-AS1 silencing apparently suppressed HCC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT). Mechanism exploration revealed that TRG-AS1 acted as a molecular sponge of miR-4500 to regulate BACH1. MiR-4500 silencing or BACH1 overexpression in BACH1-downregulated cells fully rescued cell proliferation migration, invasion and EMT progress. CONCLUSION: TRG-AS1 regulates HCC progression by targeting miR-4500/BACH1 axis.

Colonic obstruction caused by accessory spleen torsion: A rare case report and literature review.

RATIONALE: Accessory spleen torsion is a rare cause of the acute abdomen. The complications of accessory spleen torsion, such as intestinal obstruction, are rarer. We herein report a case of colonic obstruction caused by accessory spleen torsion because of the unusual condition. PATIENT CONCERNS: A 15-year-old patient presented with acute intestinal obstruction with signs of peritoneal irritation. Abdominal computed tomography (CT) and ultrasonography examinations revealed a soft tissue mass in the left midabdomen. Systemic inflammatory response syndrome (SIRS) was observed in this case. DIAGNOSES: The diagnosis of peritonitis and colonic obstruction secondary to accessory spleen torsion was made. Pathologic examination showed infracted splenic tissue. INTERVENTIONS: We performed emergency laparotomy and found that accessory spleen torsion pressured against splenic flexure and descending colon, and caused colon obstruction. The patient underwent accessory splenectomy and enteral decompression. OUTCOMES: At 6 months follow-up, the patient recovered well with perfect digestion. LESSONS: Accessory spleen torsion and its complications are extremely rare. This entity should be considered in differential diagnosis of acute abdomen. However, in case of acute abdomen with critical clinical situation, emergency surgical intervention is necessary for timely diagnosis and treatment.

[Nonoperative management of blunt splenic injury].

OBJECTIVE: To investigate the monitoring and therapeutic methods of nonoperative management of blunt splenic injury. METHODS: Eighty-two cases with nonoperative management of 95 patients of blunt splenic injury from September 2005 to April 2008 were analyzed retrospectively. Percutaneous peritoneal drainage was applied to 75 cases, and auto-blood transfusion was applied to 38 cases. Eighty-two cases were followed up from 3 weeks to 8 months. RESULTS: Eighty-two patients with nonoperative management were treated successfully, including 34 cases classified as grade III to IV, 6 cases over 55-years-old, 14 cases with severe multiple injury (ISS > or = 16) and 37 cases whose drained peritoneal blood volume were over 500 ml. The drained peritoneal blood volume was 30 to 2400 ml. The total volume of auto-blood transfusion was 22 300 ml and the average volume was 613 ml. All cases were followed up without delayed hematocele or peritoneal infection. CONCLUSIONS: Most hemodynamically stable patients with blunt splenic injury can be healed with nonoperative management. The treatments including percutaneous peritoneal drainage and transfusion of auto-blood can significantly increase the performance rate and the achievement ratio of nonoperative management of blunt splenic injury.