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Chronic pancreatitis

Chronic pancreatitis is a long-standing inflammation of the pancreas that alters the organ's normal structure and functions.[1] It can present as episodes of acute inflammation in a previously injured pancreas, or as chronic damage with persistent pain or malabsorption. It is a disease process characterized by irreversible damage to the pancreas as distinct from reversible changes in acute pancreatitis.[6][7] Tobacco smoke and alcohol misuse are two of the most frequently implicated causes, and the two risk factors are thought to have a synergistic effect with regards to the development of chronic pancreatitis.[4] Chronic pancreatitis is a risk factor for the development of pancreatic cancer.[4]

Chronic pancreatitis

Pancreatitis – chronic – discharge[1]

Nausea and vomiting[2][3]

Alcohol(ism), Immune disorder[5]

Serum trypsinogen, Fecal fat test[2]

Pain medicines, avoiding alcohol(and smoking), among other possible management efforts[2]

50 per 100,000 persons (prevalence)

Upper abdominal pain: Upper abdominal pain which increases after drinking or eating, lessens when fasting or sitting and leaning forward. Some people may not suffer pain.[3]

[2]

Nausea and vomiting[3]

[2]

Steatorrhea: Frequent, oily, foul-smelling bowel movements. Damage to the pancreas reduces the production of that aid digestion, which can result in malnutrition. Fats and nutrients are not absorbed properly, leading to loose, greasy stool known as steatorrhea.[2][3]

pancreatic enzymes

Weight loss even when eating habits and amounts are normal.

[2]

(pancreatogenic diabetes):[4] Chronic pancreatitis can affect the ability of the pancreatic islets to produce insulin to regulate glucose levels, leading to diabetes type 3c. Symptoms of diabetes type 3c are due to elevated sugar and may include increased hunger and thirst, frequent urination, weight loss, fatigue, and blurry vision.[8]

Type 3c diabetes

There have been three symptom profiles described in those with chronic pancreatitis. Type A involves intermittent, severe symptom flare-ups with or without objective pancreatitis amongst a background of symptom-free periods. The type A symptom profile is usually more common early in the course of chronic pancreatitis.[4] Type B chronic pancreatitis involves chronic pain accompanied by intermittent severe attacks.[4] And, the type C symptom profile of chronic pancreatitis involves chronic, long-term, severe pain without interspersed acute flare-ups or symptom exacerbations.[4]

Diagnosis[edit]

The diagnosis of chronic pancreatitis is made based on the history and characteristics of symptoms combined with findings on radiologic imaging.[4] Serum amylase and lipase may be moderately elevated in cases of chronic pancreatitis.


Symptoms of diarrhea, with oily, bulky, and foul-smelling stools indicated steatorrhea or fat malabsorption due to exocrine pancreatic insufficiency. Exocrine pancreatic insufficiency can be confirmed by also checking a fecal elastase level, with low levels specifying exocrine pancreatic insufficiency.[4] A quantitative fecal fat test can also be done to quantify the fat levels in the stool and confirm the presence of exocrine pancreatic insufficiency.[4]


When chronic pancreatitis is caused by genetic factors, elevations in ESR, IgG4, rheumatoid factor, ANA and anti-smooth muscle antibody may be detected.[11]


Computed tomography, magnetic resonance cholangiopancreatography (MRCP), and endoscopic ultrasound (EUS) all have similar sensitivity and specificity for diagnosing chronic pancreatitis.[4] MRCP is particularly utilized for its sensitivity in imaging the pancreatic ducts and bile ducts for associated changes such as stones or strictures.[4][12] A biopsy of the pancreas is not required for the diagnosis.[4] On imaging, pancreatic and bile duct dilatation, atrophy of the pancreas, multiple calcifications of the pancreas, and enlargement of pancreatic glands can be found.[12]


On MRI scan, there is a low T1 signal due to inflammation, fibrosis, focal lesions, and calcifications. In those who are given a contrast agent, there would be a higher T1 signal with late gadolinium enhancement due to compression from the fibrotic areas. The overall thickness of the pancreas will be reduced.[12]

Epidemiology[edit]

The annual incidence of chronic pancreatitis is 5 to 12 per 100,000 persons, the prevalence is 50 per 100,000 persons.[18] It has been reported that the pancreas is able to absorb radioactive cesium (Cs-134 and Cs-137) in great quantities from environmental contamination, causing chronic pancreatitis and probably pancreatic cancer with damage of pancreatic islets with Type 3c (pancreatogenic) diabetes.[19]

Exocrine pancreatic insufficiency

Yan, M-X; Li, Y-Q (2006-04-01). . Postgraduate Medical Journal. 82 (966): 254–258. doi:10.1136/pgmj.2005.037192. ISSN 0032-5473. PMC 2579631. PMID 16597812.

"Gall stones and chronic pancreatitis: the black box in between"

Lerch, Markus M.; Gorelick, Fred S. (2013). . Gastroenterology. 144 (6): 1180–1193. doi:10.1053/j.gastro.2012.12.043. PMID 23622127. Retrieved 2015-11-29.

"Models of Acute and Chronic Pancreatitis"

Beyer, Georg; ; Werner, Jens; Lerch, Markus M.; Mayerle, Julia (15 August 2020). "Chronic pancreatitis". The Lancet. 396 (10249): 499–512. doi:10.1016/S0140-6736(20)31318-0. ISSN 0140-6736. PMID 32798493. S2CID 221114304. Retrieved 1 January 2021.

Habtezion, Aida