Cleveland, Ohio 44106

  • Acute Recurrent Pancreatitis

Purpose:

The purpose of this research is to compare intermittent fasting with a standard diet approach for improving the quality of life related to your pancreas disease. Our hope is to improve your symptoms and prevent you from needing to go into the hospital for pancreas-related issues.


Study summary:

Fasting is a classic means for religious discipline, yet recently regaining favor in the medical landscape. Numerous studies have come forth, both in animals and humans outlining the benefit of intermittent fasting (IF) on various disease states and longevity. Though a relatively complex cellular process, fasting for at least 8-12 hours has been shown to lead to fatty acid release from a patient's adipose storage. These fatty acids then shuttle to the liver, where they are converted to ketones such as beta-hydroxybutyrate and acetoacetate. Ketones are then utilized for energy sources in the heart, brain and skeletal muscle tissue. The energy produced (ATP), then leads to increase in the cellular powerhouses, the mitochondria and autophagy or cell recycling. This cellular recycling is one main way in which IF has proven benefit for inflammatory conditions and in cancer care. Furthermore, reductions in amino acids and glucose due to fasting and reliance on ketones as energy, lead to down regulation of the mTOR pathway. Much is known regarding the mTOR pathway. Down regulation of mTOR is associated with increased autophagy (as above), lower protein and lipid synthesis, ribosome and lysosome creation (cell shuttles) and lowered energy use. Specific to the pancreas, mTOR down regulation has been shown to lower protein synthesis with the pancreas, caused by cholecystokinin (CCK), a pancreas stimulating hormone.2 The effect of this leads to lower pancreatic enzymes secretion. Inhibition of mTOR also lowers the generation of fibroblasts, the scar-tissue cells within the pancreas, leading to less scar-formation.3 Scar tissue formation is a vital part of morbidity and complications for patients with chronic pancreatitis. Pancreatic disease-modulation has also been evaluated in regard to the mTOR pathway.4 For pancreatic cancer, rapamycin a mTOR inhibitor have been implicated as targets for chemotherapy. Clinical trials have shown benefit for pancreatic cancer cases given rapamycin in concert with other chemotherapeutic medications.5 For acute, chronic pancreatitis and post-ERCP pancreatitis, mTOR is usually activated.6 In particular, blocking the mTOR pathway can favor autophagy, limit cell death (apoptosis) and hence necrosis of the pancreas. Necrosis in pancreatitis, leads to complex disease, possess a higher mortality, organ failure, and can make the clinical course more complicated. Therefore, the mTOR pathway has been implicated as a potential therapeutic target to ameliorate disease course and severity.4,7,8 The purpose of this study is to evaluate IF as a means for limiting disease severity with people who have recurrent acute pancreatitis and chronic pancreatitis. Our hypothesis is that IF will improve pancreatic-disease related quality of life.1


Criteria:

Inclusion Criteria: Age ≥ 18 year Recurrent acute pancreatitis defined by greater than 2 episodes of pancreatitis, defined by: abdominal pain and either amylase or lipase > 3 x the upper limit of normal, imaging suggestive of, separated by time Anatomy of chronic pancreatitis defined by Rosemont criterion9 or on imaging (CT, MRI) Pancreatic exocrine insufficiency defined by a pancreatic elastase < 200 ug/g stool10 Exclusion Criteria: Age < 18 years Pregnant Patients Age > 80 years Patients who cannot consent for themselves Glycogen storage disease Insulinoma or hypoglycemic state Active alcohol abuse Alcohol induced acute pancreatitis Gallstone induced acute pancreatitis Pancreatic solid neoplasm Patients with diabetes Patients on beta blockers


NCT ID:

NCT04760847


Primary Contact:

Shaffer Mok
Phone: 4404065500
Email: Shaffer.Mok@UHhospitals.org


Backup Contact:

N/A


Location Contact:

Cleveland, Ohio 44106
United States

Shaffer Mok, MD
Phone: 440-406-5500
Email: Shaffer.Mok@UHhospitals.org

Site Status: N/A


Data Source: ClinicalTrials.gov

Date Processed: June 21, 2021

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