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Scientific discovery could lead to treatments for chronic pancreatitis

Pancreatitis is one of the most common gastrointestinal hospital admissions-related illness. Patients with the acute form of the disease show up at hospitals doubled over with severe abdominal pain, a swollen belly that’s tender to the touch, nausea, and vomiting.

For some patients the disease flares up then disappears. For others, it develops into an ongoing, chronic form of the disease with no known cure. Not only is it extremely painful, it also causes malnutrition and carries with it a high risk of leading to pancreatic cancer. Treatment options are pretty much limited to prescription pain killers.

This has great implication in a disease that has no active therapy with no known agents that can alter its natural devastating course

It’s known that chronic pancreatitis is marked by the uncontrolled growth of scar tissue in the pancreas known as fibrosis, which slowly destroys the organ’s ability to function. Since the pancreas is in charge of excreting enzymes to digest food, patients begin to suffer malnutrition. It’s also known that excessive alcohol consumption is the leading cause of pancreatitis but just what is happening at a molecular level to cause the fibrosis is less clear.

Now, Stanford researcher and gastroenterologist Aida Habtezion, MD, and colleagues here and at Cedars-Sinai Medical Center have published research that sheds light on what exactly is happening and could lead to treatments for the severe disease. In a story I wrote on the study, Habtezion discusses their discovery of a new molecular pathway that when blocked by an experimental pharmacological drug can slow the progression of pancreatitis in animal models and in human cells.

As Habtezion told me, her lab's research into just how the immune cells of the pancreas behave when inflamed with pancreatitis unveiled the new pathway:

"For the first time we can show that macrophages interact with pancreatic stellate cells via a particular immune pathway, and by targeting this pathway we show a decrease in chronic pancreatitis/fibrosis progression,” she said. “This has great implication in a disease that has no active therapy with no known agents that can alter its natural devastating course.”

The hope is that researchers will now be able to develop a form of the experimental pharmacological agent used in the study to block the molecular pathway that can be given to humans. Blocking the pathway will block the scar tissue growth, and hopefully either slow the progression of the disease or reverse it altogether.

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