What Is Acute Pancreatitis And Who Are At A Higher Risk?

The pancreas is located in the abdominal cavity behind the stomach and produces pancreatic juices which contain digestive enzymes, and these enzymes help to break down food and absorb nutrients in the small intestine. The pancreas also produces hormones (including insulin) that control blood glucose. Common diseases of the pancreas include pancreatitis and pancreatic cancer. Pancreatitis can be further classified into acute and chronic pancreatitis.

Acute pancreatitis is sudden inflammation of the pancreas that can be mild or life-threatening. Pancreatitis often subsides within a week, but some patients (<20%) with severe acute pancreatitis can develop serious complications (e.g. pancreatic necrosis and infection). The main symptom of pancreatitis is severe abdominal pain which develops suddenly in the center of the abdomen. Other typical symptoms include vomiting, diarrhea, indigestion, fever, and jaundice (i.e. yellowing of the eyes and skin).

In high-income countries, the incidence of acute pancreatitis ranges from 4 to 45 per 100,000 persons, with an annual increase of 2-4%. However, there are no large population-based data available in low- and middle-income countries, including China. Acute pancreatitis has a high case fatality rate, with 2-10% of patients dying of complications of the disease.

In high-income countries, gallstones and heavy alcohol intake (‚Č•5 drinks per day) are the major causes of acute pancreatitis. Gallstones cause about 40-60% of acute pancreatitis. Gallstones are crystalline deposits in the gallbladder (mostly cholesterol stones) and can pass into and block the common bile duct which connects the gallbladder and the pancreas. If the blockage remains, the enzymes in pancreatic fluid start to digest the pancreas, leading to severe inflammation. Heavy alcohol intake causes approximately 2-5% of acute pancreatitis. It is not fully understood why alcohol may cause acute pancreatitis. It has been hypothesized that toxic metabolites of alcohol may damage the pancreas. Studies in Western countries and Japan have reported that individuals with gallstones have a 1.6- to 17-fold higher risk of developing acute pancreatitis, while individuals who drank ‚Č•5 drinks per day have a 1.6- to 3.5-fold higher risk.

In our recent study entitled ‚ÄúMetabolic and lifestyle risk factors for acute pancreatitis in Chinese adults: A prospective cohort study of 0.5 million people,‚ÄĚ published in the journal PLOS Medicine, we examined lifestyle and metabolic risk factors for acute pancreatitis in 0.5 million Chinese adults. Our study showed that individuals with gallstones had a 2.4-fold higher risk of developing acute pancreatitis. Men who drank ‚Č•420 g per week (equivalent to 5 drinks per week) had a 50% higher risk of acute pancreatitis, while men who smoked had a 50% higher risk. Analysis of smoking or alcohol in women was not possible, as only less than 3% of Chinese women smoked or drank alcohol on a weekly basis.

In addition to these well-established risk factors in Western populations, our study identified metabolic risk factors for acute pancreatitis, which were physical activity, adiposity, and diabetes. Individuals who were obese (BMI ‚Č•27 kg/m2) had a two-fold higher risk of acute pancreatitis. Active individuals had a 20% lower risk of acute pancreatitis, while individuals with diabetes had a 30% higher risk.

Why do we care about these risk factors? First, patients with acute pancreatitis are at higher risks of death and developing pancreatic cancer. Our study showed that patients with acute pancreatitis had a 50% higher risk of death and an eight-fold higher risk of developing pancreatic cancer. Second, these lifestyle and metabolic risk factors for pancreatitis are potentially modifiable. A Swedish study reported that individuals who quitted smoking for ‚Č•20 years had a similar risk of developing acute pancreatitis as never smokers.

Taking into account the effect of individual risk factors, we may anticipate that individuals with a healthy lifestyle, including no smoking, limited alcohol intake, high physical activity, and no obesity, may have a lower risk of acute pancreatitis. However, it is unclear whether metabolic risk factors for pancreatitis are causal. For example, pancreatitis can induce diabetes. The modifiable nature of the risk factors suggests that, assuming cause and effect, many cases of acute pancreatitis might be prevented with modifications to lifestyle.

These findings are described in the article entitled Metabolic and lifestyle risk factors for acute pancreatitis in Chinese adults: A prospective cohort study of 0.5 million people, recently published in the journal PLOS Medicine. This work was conducted by Yuanjie Pang, Christiana Kartsonaki, Iain Turnbull, Ling Yang, Yiping Chen, Iona Y. Millwood, Fiona Bragg, Michael V. Holmes, and Zhengming Chen from the University of Oxford,  Yu Guo, Zheng Bian, and Liming Li from the Chinese Academy of Medical Sciences, Weiwei Gong from the Provincial Center for Disease Control, Qinai Xu and Quan Kang from the Nangang Center for Disease Control, and Junshi Chen from the National Center for Food Safety Risk Assessment.

About The Author

Yuanjie Pang

Yuanjie Pang is a researcher employed at the Clinical Trial Service Unit and Epidemiological Studies Unit (CTSU) in the Nuffield Department of Population Health, University of Oxford. Yuanjie holds a ScM in Epidemiology from Johns Hopkins University Bloomberg School of Public Health and an MBBs from Peking University Health Science Center. Her DPhil research involves investigating metabolic risk factors (i.e. adiposity, diabetes and physical activity) and cancer in the China Kadoorie Biobank.

Christiana Kartsonaki

Christiana Kartsonaki is a Senior Statistician at the Clinical Trial Service Unit and Epidemiological Studies Unit (CTSU) in the Nuffield Department of Population Health, University of Oxford. She has a degree in Mathematics, an MSc in Applied Statistics and a DPhil in Statistics. She has previously worked in the Department of Oncology of the University of Oxford and at the Centre for Cancer Genetic Epidemiology in the Department of Public Health and Primary Care of the University of Cambridge.

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