April 10th, 2014
2014 Annual and Special Pancreas Meetings – Click Here
8th International Symposium on Inherited Diseases of the Pancreas – June 8, 2014 – Jerusalem, Israel.
–> REGISTRATION IS OPEN (Click here)
The a major symposium on inherited diseases of the pancreas will be held immediately BEFORE the ESPGHAN 2014 Annual meeting. The program as of April 10, 2014 includes OUTSTANDING international experts. The program includes the latest updates on all of the major pancreatic genetic advances – plus a focus on CFTR – 25 year anniversary. Download a “save the date” flyer. Travel information is available at the ESPGHAN website. See PancreasFest.org for details.
July 23 (PM) to July 25, 2014. The focus is on complications of chronic pancreatitis – pancreatogenic diabetes (T3cDM) – pancreatic cancer development and detection. Annual meeting of CAPER and INSPPIRE. Brufsky Award and lecture for clinical excellence in pancreatic cancer research. Workshops and working group meetings for INSPPIRE, North American Pancreatic Study Group (NAPS2-AA, NAPS3), Acute Pancreatitis Working Group, and more…! Abstracts submission deadline TBA. “In addition to a fantastic program, the cost of having PancreasFest in Pittsburgh is low enough that I can afford to bring my students and post-docs to learn, present their work and meet the leaders in the field” – Miklos Sahin-Toth MD PhD.
The preliminary program has been posted (click here for PancreasFest home page)
NIDDK Workshop on Total Pancreatectomy and Islet Autotransplantations (TPIAT).
An NIDDK Workshop will be held on the day prior to PancreasFest (July 23, 2014) to discuss challenges, knowledge gaps and research needs for TPIAT. A link to the program will be posted as soon as it is finalized.
Recommendations from PancreasFest:
The Guidance statements from are now published in Pancreatology
“Detection, evaluation and treatment of diabetes mellitus in chronic pancreatitis: Recommendations from PancreasFest 2012“. These specifically address issues surrounding when and how to screen for diabetes, including Type 3c (pancreatogenic diabetes).(Click here for Abstract).
“Total pancreatectomy and islet autotransplantation in chronic pancreatitis: Recommendations from PancreasFest” These recommendations guid physicians in the evaluation and management of patients before, and after TPIAT. Click here for Abstract”
The Carboxypeptidase A1 (CPA1) gene is a chronic pancreatitis susceptibility gene with a novel mechanism of disease.
Mutations in CPA1 are linked to patients with nonalcoholic chronic pancreatitis, especially with early age of onset (see Witt et al, Nature Genetics, PMID 23955596). Carboxypeptidase A1 is pancreatic digestive enzyme that hydrolyzes C-terminal peptide bonds in dietary polypeptides that are exposed by chymotrypsins and elastases. It is the most abundant digestive enzyme after trypsin, and contributes up to 10% of the total protein. Risk of chronic pancreatitis is unrelated to trypsin. DNA sequencing of all ten CPA1 exons in 944 German cases and 3,938 control reveled 35 different mutations. Functional studies in the laboratory of Miklós Sahin-Tóth MD PhD (Boston Univ.) showed that many of the variants had less than 20% of expected activity and were not secreted from experimental cells. This suggests that the mutated peptides were miss-folding, causing stress inside of the endoplasmic reticulum. The low activity mutants were found in 3.1% of cases compared to 0.1% of controls (OR = 25). The finding was replicated in 3 other groups, and found to be especially prevalent in children.
NIDDK-NCI Workshop on Pancreatitis-Diabetes-Pancreatic Cancer: REPORT
June 12-13, 2013. Bethesda MD. By all accounts, the PDPC conference was an overwhelming success. A full report will be published in the November issue of Pancreas. The most important take-away points are that relationship between pancreatitis, diabetes and pancreatic cancer are complex, and that evaluation of human data to assess possible connections requires the proper control population. The problem is further complicated by “reverse causality”; pancreatitis is a risk for pancreatic cancer and pancreatic cancer can cause acute and chronic pancreatitis: diabetes mellitus is a risk for pancreatic cancer, but pancreatic cancer can also cause diabetes – up to two years before it can be seen on CT scan. The combination of pancreatitis and diabetes results in higher risk of pancreatic cancer than either disease alone. Also, it was clear that assessing the effects of diabetes treatment on pancreatic cancer risk was critically dependent on the control population, since the risk of patients with diabetes is independently increase already. The risk may be especially high in patients with pancreatogenic (Type 3c) diabetes, but this type of diabetes has not been tested for in big epidemiology studies.
Data presented from randomized controlled trials of GLP-1 and DPP-4 anti-diabetes agents did not appear to indicate any risk for pancreatic cancer above matched control populations with the same diseases. The FDA also presented their methods of assessing risk in human studies and by assessing and replicating animal studies, and they did not report an increased cancer risk with use of either GLP-1 agonists or DPP-4 antagonists. See Program Link.
Breakthrough: Alcohol, CLDN2 & Chronic Pancreatitis in men:
A genetic link between alcohol drinking and chronic pancreatitis in men has been discovered. An advanced online report has was published (see PMID: 23143602 ) that largely explains why men have chronic alcoholic pancreatitis more often then women. A region on Chromosome X called the “CLDN2 locus” seems to cause a rapid progression from acute pancreatitis to chronic pancreatitis, rather than recovery, in persons who continue to drink alcohol after acute pancreatitis. About 4% of men in the United states are at risk because they have BOTH the X-factor and are drinking alcohol (>4 drinks per day). Men have the XY chromosome pair, while women have XX. Having two X chromosomes, with at least one being normal protects women – only 0.6% of women in the United States are at risk. The study also showed that a genetic factor on chromosome 7 that decreases expression of trypsin reduces the risk of recurrent acute and chronic pancreatitis. (for more information see UPMC Press Release)
CME Program on Chronic Pancreatitis
Drs Whitcomb & Forsmark discuss advances in science that translate into better treatment of chonic pancreatitis.
CME credit for physicians
(click on image to open a new page)
PRSS1 – Website.
A new web site has been launched to provide information on the functional consequence of various cationic trypsinogen (PRSS1) mutations. The site is maintained by Dr. Miklos Sahin-Toth and Dr. Balazs Nemeth. Click here to visit.
Personalized approaches to treatment of Pancreatitis.
David Whitcomb MD PhD and Adam Slivka MD PhD discuss the advances in the treatment of pancreatitis using genetics. (View of the Whitcomb lab, University of Pittsburgh)
PEaRL .:. Pancreatitis Education and Research Letter
PEaRL news letter page – See “Patient Information” link above
- previous PEaRLs - PEaRL Page
Pancreas Eduction and Research News (PEARL) – Winter 2012-13.