Added value of intravenous contrast-enhanced ultrasound for characterization of cystic pancreatic masses: a prospective study on 37 patients

Abstract The aim of this study was to evaluate the added value of contrast-enhanced ultrasound (CEUS) in the pancreatic cystic mass (PCM) diagnosis by using a qualitative and quantitative analysis in order to make a relevant characterization. Patients and method: Between December 2008 and November 2011, 37 patients with PCM discovered at ultrasound examination were prospectively followed. A qualitative and quantitative CEUS analysis was performed in order to differentiate etiologies of the PCM. In the quantitative analysis several parameters were followed: Peak Intensity (PI), Time to Peak (TTP), maximum ascending gradient (GRAD), Time to maximum gradient (TTG) and Area Under the Curve (AUC). Normalized ratios were also calculated. In all patients a definite cytological or histological diagnosis was obtained. Results: Thirty-seven patients were studied: 12 with pancreatitis-associated pseudocyst and 25 with cystic tumors (10 serous cystic adenoma, 5 mucinous cystic adenoma, 6 cystadenocarcinomas, 2 solid pseudopapillary tumors and 2 intraductal papillary mucinous neoplasms). There was a significant difference of the nAUC and nTTP between pseudocyst and cystic tumors, p=0.03 and p=0.01, respectively. A normalized TTP value above 7 sec was suggestive for the diagnosis of pseudocysts with 79.16 % accuracy. There was a significant difference of nTTP and nTTG between the benign and malignant lesions. nTTP < 9 sec and nTTG < 8.5 sec rules out malignant cysts in almost 90% of cases. Conclusion: The CEUS is useful in the diagnosis of PCM. The quantitative analysis of the enhancement of the cystic wall may discriminate the different types of the PCM

Pancreatology

BACKGROUND: PRSS1 and PRSS2 constitute the only functional copies of a tandemly-arranged five-trypsinogen-gene cluster (i.e., PRSS1, PRSS3P1, PRSS3P2, TRY7 and PRSS2) on chromosome 7q35. Variants in PRSS1 and PRSS2, including missense and copy number variants (CNVs), have been reported to predispose to or protect against chronic pancreatitis (CP). We wondered whether a common trypsinogen pseudogene deletion CNV (that removes two of the three trypsinogen pseudogenes, PRSS3P2 and TRY7) might be associated with CP causation/predisposition. METHODS: We analyzed the common PRSS3P2 and TRY7 deletion CNV in a total of 1536 CP patients and 3506 controls from France, Germany, India and Japan by means of quantitative fluorescent multiplex polymerase chain reaction. RESULTS: We demonstrated that the deletion CNV variant was associated with a protective effect against CP in the French, German and Japanese cohorts whilst a trend toward the same association was noted in the Indian cohort. Meta-analysis under a dominant model yielded a pooled odds ratio (OR) of 0.68 (95% confidence interval (CI) 0.52-0.89; p = 0.005) whereas an allele-based meta-analysis yielded a pooled OR of 0.84 (95% CI 0.77-0.92; p = 0.0001). This protective effect is explicable by reference to the recent finding that the still functional PRSS3P2/TRY7 pseudogene enhancers upregulate pancreatic PRSS2 expression. CONCLUSIONS: The common PRSS3P2 and TRY7 deletion CNV was associated with a reduced risk for CP. This finding provides additional support for the emerging view that dysregulated PRSS2 expression represents a discrete mechanism underlying CP predisposition or protection

The PRSS3P2 and TRY7 deletion copy number variant modifies risk for chronic pancreatitis

Background PRSS1 and PRSS2 constitute the only functional copies of a tandemly-arranged five-trypsinogen-gene cluster (i.e., PRSS1, PRSS3P1, PRSS3P2, TRY7 and PRSS2) on chromosome 7q35. Variants in PRSS1 and PRSS2, including missense and copy number variants (CNVs), have been reported to predispose to or protect against chronic pancreatitis (CP). We wondered whether a common trypsinogen pseudogene deletion CNV (that removes two of the three trypsinogen pseudogenes, PRSS3P2 and TRY7) might be associated with CP causation/predisposition. Methods We analyzed the common PRSS3P2 and TRY7 deletion CNV in a total of 1536 CP patients and 3506 controls from France, Germany, India and Japan by means of quantitative fluorescent multiplex polymerase chain reaction. Results We demonstrated that the deletion CNV variant was associated with a protective effect against CP in the French, German and Japanese cohorts whilst a trend toward the same association was noted in the Indian cohort. Meta-analysis under a dominant model yielded a pooled odds ratio (OR) of 0.68 (95% confidence interval (CI) 0.52–0.89; p = 0.005) whereas an allele-based meta-analysis yielded a pooled OR of 0.84 (95% CI 0.77–0.92; p = 0.0001). This protective effect is explicable by reference to the recent finding that the still functional PRSS3P2/TRY7 pseudogene enhancers upregulate pancreatic PRSS2 expression. Conclusions The common PRSS3P2 and TRY7 deletion CNV was associated with a reduced risk for CP. This finding provides additional support for the emerging view that dysregulated PRSS2 expression represents a discrete mechanism underlying CP predisposition or protection

The PRSS3P2 and TRY7 deletion copy number variant modifies risk for chronic pancreatitis

International audienc