The pancreas is one of the most important organs in the body, especially when it comes to the breakdown of dietary fats and lipids. It is known as one of the body’s main source of lipases (enzymes that break down fat into simpler molecules) which is why it can have such dire consequences when infected. Because the pancreas is so vital to something as important as fat digestion, it comes as no surprise how it can be affected by a myriad of pathologic events.
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Most often when people think of a pancreatic infection, they think of something like acute pancreatitis. Acute pancreatitis is a disease of the pancreas involving swelling as well as necrosis, and it happens to be the most common gastrointestinal disease leading to acute hospitalization.3 The disease itself is becoming more commonly seen in today’s society, and cases have only seen an increase within the last two decades.7
Looking at the pancreas specifically, one might wonder how the organ keeps itself from getting digested on an everyday basis. To keep autodigestion from occurring in a healthy pancreas, the body has multiple mechanisms in place. These protective mechanisms are maintained intracellularly due to the presence of a mucous film for added protection around the duct epithelium, through the use of zymogens (inactive precursors) which do not become activated until a specific set of criteria are met, and through a system of enzyme inhibitors circulating throughout the bloodstream in case pancreatic juices happen to escape.1 Although these methods are all equally important to ensure pancreatic enzymes are maintained, one of the most significant protective mechanisms involved is the use of a one-way permeability system to ensure the enzymes, once they are cleaved and activated, cannot return to the pancreatic cells from which they came.1
Having all these protective systems in place, it would seem as if there were no possible way of causing damage to the pancreas nor to the areas around it. Seeing as how pancreatitis exists, however, shows evidence these systems can and will be avoided depending on the pathology being looked at. Whenever these digestive enzymes leak out and cause autodigestion to surrounding cells, this usually points to a breakdown of the protective mechanisms listed above. Most often, the cause of acute pancreatitis is due to damage of the pancreatic ducts leading to changes in the vasculature permeability.6 In a healthy pancreas, the ducts are only permeable to contents of a certain size, but when alcohol or some other damaging agent comes into play, the cells of the pancreatic duct experience increased permeability allowing enzymes and other similarly sized molecules to leak out into the surrounding interstitial space. This may be one of the reasons why heavy alcohol consumption is seen as one of the causes for acute pancreatitis- because it can change the permeability of the ducts in such a drastic way.
Once the permeability of the ducts has been altered and the enzymes have leaked out into the extracellular space, many damaging events take place. As mentioned earlier, pancreatic enzymes are created and stored in the pancreas as inactive zymogens before being sent out to the duodenum of the small intestine where a majority of the body’s digestion takes place. Once in the small intestine, the zymogens undergo a conformational change as a result of the physiological aspects of the duodenum and become activated. If these zymogens leak out into the interstitial space separate from the small intestine though (such as in acute pancreatitis), they become activated simply due to the physiological conditions maintained within that particular space. As it turns out, the proteolytic zymogens and other enzymes residing in the pancreatic juice are extremely easy to activate, especially in patients with pancreatitis who have an overactive amount of proteolytic activity.4 This increased activity only leads to a greater amount of inflammation and damage, so unless scientists find more efficient ways to inactivate leaked zymogens, the break-down of cellular components at and near the pancreas will only continue.
Whenever patients are suffering from acute pancreatitis, one of two things can happen. The patient can either be labeled as having edematous interstitial pancreatitis or, in more severe cases, as having necrotizing pancreatitis.2 In most cases when the pancreatitis is on the milder side (as is the case with edematous interstitial pancreatitis) it is able to resolve within a few months of treatment. If a patient has a more intense form of the disease, however, then a fatal outcome including multiple organ failures can result. On a positive note, only about 20% of patients suffering from pancreatitis will have it progress to the more aggressive form3 with the remaining 80% having a rapid improvement within days of receiving treatment.2
Referring to the unlucky few who have their pancreatitis progress to the necrotizing form, the pancreatitis becomes a lot more difficult to treat. When someone is suffering from necrotizing pancreatitis, a complicated course follows along with the release of multiple toxic, septic, and vasoactive agents from the infected pancreatic gland.2 This release of agents leads to many drastic effects and can even cause injury to systems separate from the digestive system such as the cardiovascular and renal systems.
Not only does pancreatitis damage other systems, but the fat storage cells surrounding the pancreatic area as well. When acute pancreatitis reaches its necrotizing form, it is often referred to by physicians as peripancreatic fat necrosis,3 and the reason for this may be because of the fat necrosis that occurs in the area surrounding the pancreas once pancreatic lipases are released. These lipid digesting enzymes, once activated, will break down any kind of triglyceride storing cell it comes into contact with- most notably the adipocytes residing in adipose tissue. After these cells have been destroyed, the dead cells will accumulate and cause further damage to the area as fat necrosis begins to occur, and as fat necrosis continues to worsen in the pancreatic area, infected patients become increasingly at risk for persistent systemic inflammatory response syndrome and, in some cases, organ failure.3
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One specific way fat necrosis associated with acute pancreatitis can be characterized is if there are any ghost cells present. Ghost cells are simply cells damaged by pancreatic enzymes and can be viewed microscopically after taking a sample from the patient.8 Along with the presence of ghost cells, an increase in calcium and free floating fatty acid molecules to the affected area are excellent indicators for fat necrosis as well, which is why doctors often look for these before diagnosing someone with pancreatitis. The reason this is such a great indicator is because once cells lose their membrane integrity due to the presence of digestive enzymes, their intracellular storages of calcium and fatty acids get released and may even combine to form basophilic calcium deposits- yet another characteristic of acute pancreatitis. This means evidence for pancreatitis cannot just be diagnosed through the presence of ghost cells, but through histological stains as well.
Another more obvious yet vague component of identifying pancreatic fat necrosis is the presence of inflammation. One would expect the inflammation to be a result of inflammatory infiltration but seeing as how there is an absence of infiltrate in the area7 of an infected patient, a more likely cause for this could be the presence of all the necrotic cells in the area. One other possible cause for the inflammation of these cells is STING signaling. STING signaling, when studied in patients with acute pancreatitis, has been found to promote inflammation of the cells, at least at the experimental level.Researchers were able to find how STING (a transmembrane protein found in macrophages) causes inflammation in pancreatic cells after sensing acinar cell death in the area.9 This seems to act as a safety mechanism to keep inflammation from occurring before acinar cell death has been detected. If the macrophages could promote inflammation whenever they wanted, many harmful effects could arise.
Although most people can be treated for acute pancreatitis within a matter of months, scientists are still looking for ways to treat the more advanced form of the disease within a shorter period. Currently, researchers are working on discovering new strategies to overcome this disease, some of which involve nutritional intervention due to its possibility of maintaining gut barrier functionality.5 Researchers are consistently trying to discover therapeutic agents that will allow for the maintenance of the small intestine barrier due to how necessary it is for everyday function and in keeping intestinal bacteria from spreading. If the gut barrier is unable to be sustained, further damage will result as well as the progression of the disease overall.
Noting how acute pancreatitis and its progression can be the result of multiple etiological factors, it can be said further research needs to be done both on stopping it from spreading and in preventing it from occurring in the first place. Albeit some forms of treatment have been discovered, scientists have yet to find an agent that targets acute pancreatitis specifically, which may be a reason as to why it is such a common gastrointestinal disorder. It should be of utmost importance to discover an overall cure for the disease seeing as how so many people are affected by it, and until specific treatment can be found, people are only going to continue to suffer.
- Becker, V. “Acute Pancreatitis: A Brief Introduction of the Pathology.” Acute Pancreatitis, 1987, pp. 3–6., doi:10.1007/978-3-642-83027-3_1.
- Beger, H. G., et al. “Prognostic Criteria in Necrotizing Pancreatitis.” Acute Pancreatitis, 1987, pp. 198–200., doi:10.1007/978-3-642-83027-3_26.
- Bouwense SAW, Gooszen HG, van Santvoort HC, Besselink MGH, Chapter 91 – Acute Pancreatitis, Editor(s): Charles J. Yeo, Shackelford’s Surgery of the Alimentary Tract, 2 Volume Set (Eighth Edition), Content Repository Only!, 2019, 1076-1084, ISBN 9780323402323, https://doi.org/10.1016/B978-0-323-40232-3.00091-1.
- Figarella, C., et al. “Enzyme Activation and Liberation: Intracellular/Extracellular Events.” Acute Pancreatitis, 1987, pp. 53–60., doi:10.1007/978-3-642-83027-3_8.
- Li-Long Pan, Jiahong Li, Muhammad Shamoon, Madhav Bhatia, Jia Sun. Corrigendum: Recent Advances on Nutrition in Treatment of Acute Pancreatitis. Frontiers in Immunology, Vol 9 (2018). 2018. doi:10.3389/fimmu.2018.00849/full.
- Reber, H. A. “Changes in Duct and Vascular Permeability: The Key to the Development of Acute Pancreatitis.” SpringerLink, Springer, Berlin, Heidelberg, 1 Jan. 1987, link.springer.com/chapter/10.1007/978-3-642-83027-3_7.
- Sepúlveda EVF, Guerrero-Lozano R, Acute pancreatitis and recurrent acute pancreatitis: an exploration of clinical and etiologic factors and outcomes, Jornal de Pediatria, 2018, ISSN 0021-7557, https://doi.org/10.1016/j.jped.2018.06.011.
- Smith J, Arnoletti J, Varadarajulu S, Morgan D, Post-pancreatitis Fat Necrosis Mimicking Carcinomatosis, Radiology Case Reports, Volume 3, Issue 2, 2008, 192, ISSN 1930-0433, https://doi.org/10.2484/rcr.v3i2.192.
- Zhao Q, Wei Y, Pandol SJ, Li L, Habtezion A. Original Research: STING Signaling Promotes Inflammation in Experimental Acute Pancreatitis. Gastroenterology. 2018;154:1822-1835.e2. doi:10.1053/j.gastro.2018.01.065.
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