Acute pancreatitis varies considerably in its impact on the gland and its metabolism. Pathological findings vary from mild oedema to haemorrhagic necrosis, and the clinical presentation spans a wide spectrum from mild to fulminating or fatal illness.
The most common causes of acute pancreatitis are alcoholism and gallstone disease. Table 1 sets out the causes of acute pancreatitis. It is of interest that diabetes is, in itself, a risk factor for acute pancreatitis, and the use of certain classes of glucose- lowering agents, particularly the glucagon- like peptide- 1 receptor agonists and the dipeptidyl peptidase- 4 inhibitors, has been reported to be associated with acute pancreatitis. Recent systematic reviews have either failed to con firm a link between the use of these agents and acute pancreatitis or have shown only a minor increase in risk. The US Food and Drug Administration (FDA) and the European Medicines Agency (EMA) continue to state that the currently available data do not support a causal relationship between incretin- based drugs and pancreatitis.
Table1. Causes of acute pancreatitis.
Classically, the disease presents with sudden onset of epigastric pain, associated with nausea and vomiting, aggravated by food and partially relieved by sitting up and leaning forward. Physical examination reveals low- grade fever, tachycardia, and hypotension. Jaundice may also be found infrequently. Cullen sign (periumbilical discoloration) and Grey Turner sign (flank discoloration) indicate severe necrotizing pancreatitis.
Commonly found metabolic abnormalities include hyperglycaemia, hypocalcaemia, hyperlipidaemia, hypoalbuminaemia, and coagulation disorders. Serum levels of amylase and lipase are elevated, but these are neither sensitive nor specific. Computed tomography (CT) or magnetic resonance imaging (MRI) shows oedema of the pancreas. Loss of the normal enhancement on dynamic CT scanning indicates pancreatic necrosis.
Most patients with acute pancreatitis develop transient hyperglycaemia, which mostly results from a rise in glucagon levels rather than from β- cell injury [9]. Hyperglycaemia is usually mild and resolves within days to weeks without needing insulin treatment. Permanent diabetes is rare and occurs mostly in cases with fulminant disease and multiorgan failure, in which the incidence approaches 25%. Blood glucose levels exceeding 11.1 mmol/l (200 mg/dl) during the first 24 hours indicate a poor prognosis. Following an episode of acute pancreatitis, individuals have a greater than twofold increased risk of developing diabetes over the next five years.
Non- specific elevations of serum amylase and lipase may also be found in diabetic ketoacidosis. Acute pancreatitis, however, may affect up to 11% of individuals with ketoacidosis, usually with mild or even no abdominal pain.
