JPN Guidelines for the management of acute pancreatitis: epidemiology, etiology, natural history, and outcome predictors in acute pancreatitis

Abstract

within the first 1-2 weeks and are mainly attributable to multiple organ dysfunction syndrome (MODS). Depending on patient selection, necrotizing pancreatitis develops in approximately 10%-20% of patients and the mortality is high, ranging from 14% to 25% of these patients. Infected pancreatic necrosis develops in 30%-40% of patients with necrotizing pancreatitis and the incidence of MODS in such patients is high. The recurrence rate of acute pancreatitis is relatively high: almost half the patients with acute alcoholic pancreatitis experience a recurrence. When the gallstones are not treated, the risk of recurrence in gallstone pancreatitis ranges from 32% to 61%. After recovering from acute pancreatitis, about one-third to one-half of acute pancreatitis patients develop functional disorders, such as diabetes mellitus and fatty stool; the incidence of chronic pancreatitis after acute pancreatitis ranges from 3% to 13%. Nevertheless, many reports have shown that most patients who recover from acute pancreatitis regain good general health and return to their usual daily routine. Some authors have emphasized that endocrine function disorders are a common complication after severe acute pancreatitis has been treated by pancreatic resection. Abstract Acute pancreatitis is a common disease with an annual incidence of between 5 and 80 people per 100 000 of the population. The two major etiological factors responsible for acute pancreatitis are alcohol and cholelithiasis (gallstones). The proportion of patients with pancreatitis caused by alcohol or gallstones varies markedly in different countries and regions. The incidence of acute alcoholic pancreatitis is considered to be associated with high alcohol consumption. Although the incidence of alcoholic pancreatitis is much higher in men than in women, there is no difference in sexes in the risk involved after adjusting for alcohol intake. Other risk factors include endoscopic retrograde cholangiopancreatography, surgery, therapeutic drugs, HIV infection, hyperlipidemia, and biliary tract anomalies. Idiopathic acute pancreatitis is defined as acute pancreatitis in which the etiological factor cannot be specified. However, several studies have suggested that this entity includes cases caused by other specific disorders such as microlithiasis. Acute pancreatitis is a potentially fatal disease with an overall mortality of 2.1%-7.8%. The outcome of acute pancreatitis is determined by two factors that reflect the severity of the illness: organ failure and pancreatic necrosis. About half of the deaths in patients with acute pancreatitis occur Key words

Acute Pancreatitis as a Possible Indicator of Pancreatic Cancer: The Importance of Mass Detection

“…Pancreatic cancer is included as one of the causes (12)(13)(14). In our study, among patients with acute pancreatitis, 12 (6.8%) had pancreatic cancer.…”

Primary Isolated Case of Drug Induced Pancreatitis Misdiagnosed as Idiopathic Pancreatitis

“…Reports of drug-induced acute pancreatitis (AP) have been published since the 1950s, and each year the list of drugs associated with AP increases. There are many etiological risk factors for AP, including a history of alcohol abuse, gallstones, endoscopic retrograde cholangiopancreatography and manometry, trauma or surgical procedures near the pancreas, certain medications, hyperlipidemia, infection, and chronic hypercalcemia [5]. Knowledge of the true incidence of drug-induced AP is dependent on clinicians excluding other possible causes and reporting the event.…”

Acute Pancreatitis is a Chronic Disease

“…In cases of severe acute pancreatitis, it is generally advised to reserve surgical debridement of necrosis for cases with proven superinfection, in order minimise eventual functional deficits [49,50]. Also, despite the usual recommendations, early cholecystectomy is not advisable for severe acute gallstone-related pancreatitis; [51][52][53] it should be delayed until the acute inflammatory response has settled.…”