The clinical manifestations of acute and chronic pancreatitis and pancreatic insufficiency are protean. Thus, patients may present with hypertriglyceridemia, vitamin B₁₂ malabsorption, hypercalcemia, hypocalcemia, hyperglycemia, ascites, pleural effusions, and chronic abdominal pain with normal blood amylase levels. Indeed, if the clinician considers pancreatitis as a possible diagnosis only when presented with a patient having classic symptoms (i.e., severe, constant epigastric pain that radiates through to the back, along with an elevated blood amylase or lipase level), only a minority of patients with pancreatitis will be diagnosed correctly.

As emphasized in Chap. 307, the etiologies as well as the clinical manifestations of pancreatitis are quite varied. Although it is well appreciated that pancreatitis is frequently secondary to alcohol abuse and biliary tract disease, it can also be caused by drugs, trauma, and viral infections and is associated with metabolic and connective tissue disorders. In ~30% of patients with acute pancreatitis and 25–40% of patients with chronic pancreatitis, the etiology is obscure.

Although good data exist concerning the frequency of acute pancreatitis (about 5000 new cases per year in the United States, with a mortality rate of about 10%), the number of patients who suffer with recurrent acute pancreatitis or chronic pancreatitis is largely undefined. These statistics have not changed over the past 25 years. Only one prospective study on the incidence of chronic pancreatitis is available; it showed an incidence of 8.2 new cases per 100,000 per year and a prevalence of 26.4 cases per 100,000. These numbers probably underestimate considerably the true incidence and prevalence, because non-alcohol-induced pancreatitis was largely ignored. At autopsy, the prevalence of chronic pancreatitis ranges from 0.04 to 5%. The relative inaccessibility of the pancreas to direct examination and the nonspecificity of the abdominal pain associated with pancreatitis make the diagnosis of pancreatitis difficult and usually dependent on elevation of blood amylase and/or lipase levels. Many patients with chronic pancreatitis do not have elevated blood amylase or lipase levels. Some patients with chronic pancreatitis develop signs and symptoms of pancreatic exocrine insufficiency, and thus objective evidence for pancreatic disease can be demonstrated. However, there is a very large reservoir of pancreatic exocrine function. More than 90% of the pancreas must be damaged before maldigestion of fat and protein is manifested. Even the secretin stimulation test, which is the most sensitive method of assessing pancreatic exocrine function, is probably abnormal only when >60% of exocrine function has been lost. Noninvasive, indirect tests of pancreatic exocrine function (fecal elastase, serum trypsinogen) are much more likely to give abnormal results in patients with obvious pancreatic disease, i.e., pancreatic calcification, steatorrhea, or diabetes mellitus, than in patients with occult disease. Thus, the number of patients who have subclinical exocrine dysfunction (<90% loss of function) is unknown.