Obesity and the risk of severe acute pancreatitis.

Acute pancreatitis is an acute inflammatory response to pancreatic injury. In humans, the magnitude of the response and complications are highly variable and unpredictable. Recent clinical studies demonstrate that all major complications are more common and more severe in patients who are obese. This raises the question of how adipose tissue interacts with the immune response to worsen the severity of acute pancreatitis. Here we review the results of a series of new studies focusing on various fat-associated cytokines (adipokines) that are produced and released in proportion to the amount of visceral adipose tissue in the body. The primary adipokines that have been studied in acute pancreatitis include adiponectin, leptin, visfatin, resistin, and adipose tissue related MCP-1, TNF-a and IL-6. These new data provide strong evidence that susceptibility and severity in acute pancreatitis are associated with a number of these adipokines. Although no specific therapy exists to block the effects of these factors, recognizing the high risk and anticipating inflammation-associated complications of adipokine release is an important part of optimal patient management. For this review, a PubMed search was performed with the terms "acute pancreatitis", "severe acute pancreatitis", and "obesity". Additional searches were conducted to identify recent reviews on adipokines, Finally, PubMed searches on specific adipokines, including adiponectin, leptin, visfatin and resistin were conducted focusing on acute pancreatitis and systemic inflammation.

Frequency of visualization of presumed celiac ganglia by endoscopic ultrasound.

BACKGROUND AND STUDY AIMS: Celiac ganglia can be visualized by endoscopic ultrasound (EUS). It is unknown how often ganglia are visualized during EUS, and what clinical factors are associated with ganglion visualization. The aim of this study was to prospectively evaluate the frequency of visualization of presumed celiac ganglia by EUS and to identify factors that predict their visualization. PATIENTS AND METHODS: Clinical, demographic, EUS, and cytologic data were collected prospectively from 200 unselected patients who were undergoing EUS in a tertiary referral centre. When presumed celiac ganglia were visualized, their size, number, location, and echo features were noted. When presumed ganglia were aspirated, the results of cytology were recorded. RESULTS: The most common indication for EUS was investigation of a pancreatic mass or cyst (25 %). Presumed celiac ganglia were identified in 81 % of patients overall. Logistic regression analysis determined that female sex and having no prior history of gastrointestinal surgery were independently associated with ganglion visualization. Among patients whose ganglia were visualized, more ganglia were seen per patient with linear echo endoscopes (2, range 0 - 5) than with radial echo endoscopes (1, range 0 - 4) ( P = 0.001). Presumed celiac ganglia were aspirated in 10 patients; and cytologic examination revealed neural ganglia in all of these. CONCLUSIONS: Celiac ganglia can be visualized by EUS in most patients who undergo upper gastrointestinal EUS examinations, and are best seen with linear-array echo endoscopes. Ganglia can usually be differentiated from lymph nodes on the basis of their endosonographic appearance.

Endoscopic transmural entry into pancreatic fluid collections using a dedicated aspiration needle without endoscopic ultrasound guidance: success and complication rates.

BACKGROUND: Endoscopic drainage of pancreatic fluid collections (PFC) is performed with increasing frequency. A variety of techniques for performing transmural entry have been described. However, data are lacking on the technical success and safety of transmural entry using a single technique. The authors describe the largest experience in transmural entry of PFCs without endoscopic ultrasound (EUS) guidance using a dedicated aspiration needle. METHODS: All patients who underwent endoscopic transmural drainage of PFC from October 1998 to May 2006 were identified from the endoscopy database. Data were abstracted from the endoscopic procedure report and the patient records then placed in a JMP drive. All drainages were performed without EUS guidance after visualization of an obvious intraluminal bulge using a dedicated large-bore aspiration needle. The transmural tract into the PFC was dilated using a balloon with a diameter of 6 to 20 mm followed by subsequent placement of one or two 10-Fr double pigtail stents with or without nasocystic irrigation tubes. Successful entry was defined as entry allowing for the placement of stents. RESULTS: No significant difference in the complication rates was observed when they were analyzed for the following variables: age, gender, balloon diameter, presence of endoscopic impression, drainage approach, and size and type of fluid collection. CONCLUSION: Endoscopic transmural drainage of pancreatic fluid collections can be performed safely and effectively via the Seldinger technique without endoscopic ultrasound guidance. The study data will allow sample size calculations to be made if direct comparisons with this technique and others are undertaken.

The MAPK-AP-1/-Runx2 signalling axes are implicated in chondrosarcoma pathobiology either independently or via up-regulation of VEGF.

AIMS: To investigate whether and how the JNK/ERK-AP-1/-Runx2 signalling pathways and vascular endothelial growth factor (VEGF) are engaged in the pathogenesis of cartilaginous tumours. Chondrosarcoma is the third most common primary skeletal malignancy. Nevertheless, the molecular events underlying its pathogenesis remain elusive. JNK/ERK MAPKs and their downstream effectors, c-Jun and c-Fos (AP-1), are involved in chondroblastic differention/proliferation. These proteins interact with the Runx2 transcription factor, which is also implicated in chondroblast biology. VEGF, a key angiogenic factor, is up-regulated in human chondrosarcomas. METHODS AND RESULTS: Normal cartilage and neoplastic cells from 45 chondrosarcomas and 21 enchondromas were investigated immunohistochemically. We evaluated the cellular levels of JNK2, p-JNK2 (phosphorylated/activated JNK2), its main substrate, c-Jun, pc-Jun (phosphorylated/activated c-Jun) and c-Fos. Moreover, the levels of p-ERK (phosphorylated/activated ERK), Runx2 and VEGF were assessed. Positive immunostaining for all proteins was observed in the majority of the examined chondrosarcomas and in a small fraction of enchondromas. The expression levels of all proteins were positively and significantly correlated with each other. These levels were substantially augmented in high-grade compared with low-grade chondrosarcomas and in low-grade tumours compared with benign enchondromas, implying a potential use as molecular markers for prediction of high-grade neoplasms. CONCLUSIONS: The JNK/ERK-AP-1/-Runx2 signal transduction 'network' is associated with chondroblastic malignant transformation and chondrosarcoma development, either separately or through coordinated induction of VEGF.