Accuracy of computed tomographic angiography in the diagnosis of patients with inferior vena cava partial obstruction in Budd-Chiari syndrome.

BACKGROUND AND AIM: The diagnosis of the partially obstructed inferior vena cava (IVC) in Budd-Chiari syndrome (BCS) patients has received little attention. We aimed to evaluate the diagnostic accuracy of computed tomographic angiography (CTA) for patients with BCS and a partially obstructed IVC. METHODS: A total of 329 patients with BCS and an obstructed IVC were endovascularly treated with balloon dilation and/or stent placement. All patients underwent a CTA examination prior to endovascular treatment, and the data were retrospectively reviewed. The presence of a round, oval, irregular shape or jet sign low-density area without enhancement within the enhanced proximal IVC was considered a sign of a partially obstructed IVC. Digital subtraction angiography was used as the gold standard. RESULTS: The results from the digital subtraction angiography revealed a partially obstructed IVC in 108 BCS patients and a complete obstruction in 221 patients. The CTA discovered a partially obstructed IVC in 99 patients and a completely obstructed IVC in 230 patients. From the CTA results, 15 were false negatives, and six were false positives. The patient-based evaluation yielded an accuracy of 93.6%, a sensitivity of 86.1%, specificity of 97.3%, positive predictive value of 93.9%, and negative predictive value of 93.5% for the detection of BCS patients with a partial IVC obstruction. CONCLUSIONS: Computed tomographic angiography offered a high diagnostic accuracy and sensitivity in BCS patients with a partially obstructed IVC. The low-density area within the enhanced proximal IVC above the membrane in artery phase can be considered a reliable indicator of a stenotic IVC in BCS patients.

MicroRNA-29a Promotes Pancreatic Cancer Growth by Inhibiting Tristetraprolin.

BACKGROUND/AIMS: The microRNA (miR) 29 family has been studied extensively for its involvement in several diseases, and aberrant expression of its members is associated with tumorigenesis and cancer progression. Here, we examined the role of miR-29a in pancreatic cancer and the involvement of tristetraprolin (TTP). METHODS: We monitored miR-29a and TTP expression in pancreatic cancer by qRT-PCR and western blotting. The effect of miR-29a on pancreatic cancer was determined through MTT assay and migration assay. The results were validated in the tumorigenesis model. RESULTS: We found that miR-29a was up regulated in pancreatic tumor tissues and cell lines and positively correlated with metastasis. Ectopic expression of miR-29a increased the expression of pro-inflammatory factors and epithelial-mesenchymal transition (EMT) markers, through down regulating TTP. TTP was down regulated in tumor tissues, and its ectopic expression decreased cell viability and migration in vitro, inhibited tumor growth and the EMT phenotype in vivo, and reversed the effect of miR-29a on tumor cell proliferation and invasion in vitro and in vivo. CONCLUSION: Our results suggest that miR-29a acts as an oncogene by down regulating TTP and provide the basis for further studies exploring the potential of miR-29a and TTP as biomarkers and targets for the treatment of pancreatic cancer.

Placement of a duodenal stents bridge the duodenal papilla may predispose to acute pancreatitis.

BACKGROUND/AIMS: To retrospective evaluate the incidence, predictive factors, and management of acute pancreatitis after placement of duodenal stent in patients with malignant gastroduodenal obstruction. METHODOLOGY: Among 242 patients with symptomatic malignant gastroduodenal obstruction successfully treated with duodenal stent placement, acute pancreatitis occurred in 10 (4.1%) of the patients 1-7 days after stent placement. The variables were analyzed. Univariate and multivariate analysis was performed to evaluate factors predictive of acute pancreatitis. Management of acute pancreatitis also was evaluated. RESULTS: All patients with acute pancreatitis were presented with abdominal pain and distention with vomiting 1-7 days after stent placement, in which 7 patients developed acute janudice. Four patients were cured by fasting and intravenous nutrition, and the remaining 6 cases were managed with percutaneous cholangiography and drain placement (PTCD). Univariate analysis showed acute pancreatitis was associated with location in the descending duodenum (p = 0.001) and stent bridge the duodenal papilla (p < 0.001). Multivariate analysis exhibited that the presence of stent bridged the duodenal papilla (odds ratio (OR), 18.48; 95% CI, 2.298-148.48; p = 0.006) was independent predictors of acute pancreatitis. CONCLUSIONS: Acute pancreatitis is an uncommon early complication of placement of duodenal stents in patients with malignant gastroduodenal obstruction. Acute pancreatitis occurred most commonly in descending duodenum, and in patients with stent bridged the duodenal papilla. Stent bridged the duodenal papilla may be the most important predictors for acute pancreatitis. Acute pancreatitis can be managed conservatively or by PTCD when developed to acute jaundice.

SPARC regulates ferroptosis induced by sorafenib in human hepatocellular carcinoma.

BACKGROUND: Secreted protein acidic and rich in cysteine (SPARC) is implicated in cancer progression, but its role and associated molecular mechanism in the sorafenib sensitivity of hepatocellular carcinoma cells (HCC) remains elusive. METHODS: Human HCC cell lines Hep3B and HepG2 were treated with sorafenib alone or combined with activator or inhibitor of ferroptosis. Cell viability assay, reactive oxygen species (ROS) assay, lactate dehydrogenase (LDH) assay and western blot were used to study the regulatory mechanism of SPARC on HCC cells. RESULTS: Overexpression of SPARC enhanced the cytotoxic effect of sorafenib in Hep3B and HepG2 cells compared with parental cells. Depletion of SPARC decreased the cytotoxic effect of sorafenib in Hep3B and HepG2 cells compared with parental cells. Moreover, overexpression of SPARC significantly induced LDH release, whereas depletion of SPARC suppressed the release of LDH in Hep3B and HepG2 cells. Inhibition of ferroptosis exerted a clear inhibitory role against LDH release, whereas activation of ferroptosis promoted the release of LDH in HCC cells, as accompanied with deregulated expression of ferroptosis-related proteins. Furthermore, overexpression of SPARC induced oxidative stress, whereas depletion of SPARC suppressed the production of ROS. Deferoxamine (DFX)-induced inhibition of ferroptosis suppressed the production of ROS, while activation of ferroptosis promoted the contents of ROS in HCC cells exposed to sorafenib. CONCLUSION: Our findings give a better understanding of ferroptosis and its molecular mechanism in HCC cells that is regulated by SPARC in response to sorafenib.

Percutaneous needle decompression in treatment of malignant small bowel obstruction.

AIM: To investigate the efficacy and safety of percutaneous needle decompression in the treatment of malignant small bowel obstruction (MSBO). METHODS: A prospective analysis of the clinical data of 52 MSBO patients undergoing percutaneous needle decompression was performed. RESULTS: Percutaneous needle decompression was successful in all 52 patients. Statistically significant differences were observed in symptoms such as vomiting, abdominal distension and abdominal pain before and after treatment (81.6% vs 26.5%, 100% vs 8.2%, and 85.7% vs 46.9%, respectively; all P < 0.05). The overall significantly improved rate was 19.2% (11/52) and the response rate was 94.2% (49/52) using decompression combined with nasal tube placement, local arterial infusion of chemotherapy and nutritional support. During the one-month follow-up period, puncture-related complications were acceptable. CONCLUSION: Percutaneous needle intestinal decompression is a safe and effective palliative treatment for MSBO.