【medical-news】The Lancet Diabetes & Endocrinology：肠促胰岛素或不增加急性胰腺炎的风险
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Background
Previous studies have yielded conflicting results about the association between incretin therapies and acute pancreatitis. We aimed to compare the occurrence of acute pancreatitis in a population of patients with type 2 diabetes who received incretins compared with those who received other antidiabetic treatment.
Methods
In our population-based matched case-control study, we extracted information from an administrative database from Piedmont, Italy (containing data for 4·4 million inhabitants). From a dataset of 282 429 patients receiving treatment with antidiabetic drugs for type 2 diabetes, we identified 1003 cases older than 41 years who had been admitted to hospital for acute pancreatitis between Jan 1, 2008, and Dec 31, 2012, and 4012 controls who were matched for sex, age, and time of start of antidiabetic therapy. We compared incretin exposure in cases and controls with a conditional logistic regression model, expressed as odds ratios (ORs [95% CI]). We adjusted all analyses for risk factors of acute pancreatitis, as ascertained by hospital discharge records, and concomitant use of metformin or glibenclamide.
Findings
The mean age of cases and controls (72·2 years [SD 11·1]) was high, as expected in an unselected diabetic population in Europe. After adjustment for available confounders, use of incretins in the 6 months before hospital admission was not associated with increased risk of acute pancreatitis (OR 0·98, 95% CI 0·69—1·38; p=0·8958).
Interpretation
Our findings suggest that, in an unselected population, use of incretins is not associated with an increased risk of acute pancreatitis. Larger studies are needed to clarify whether age or type of incretin therapy could affect the risk of acute pancreatitis in patients with type 2 diabetes.
Incretin-based therapies for type 2 diabetes include twodrug classes. The first class, glucagon-like peptide-1(GLP-1) receptor agonists, includes drugs that mimic theaction of native GLP-1, such as the injectable GLP-1analogues exenatide and liraglutide. The other classincludes drugs that delay the catabolism of native GLP-1mainly through inhibition of the endogenous enzymedipeptidyl peptidase 4 (DPP-4), thus extending the actionof native GLP-1. The DPP-4 inhibitors sitagliptin,vildagliptin, saxagliptin, and linagliptin, in order of theirprevalence of use in the market in Europe, are all takenorally. Although cases of haemorrhagic or necrotizingpancreatitis have been reported in patients taking thesedrugs, a clear-cut pharmacoepidemiological associationbetween incretin treatment and increased risk ofpancreatic damage has not been shown. Incidence ofacute pancreatitis is higher in patients with type 2 diabetesthan in the non-diabetic population, irrespective oftreatment.Further complicating the issue is the fact thatseveral drugs commonly used in the treatment of type 2diabetes (eg, non-incretin anti-diabetes drugs, statins,and angiotensin-converting enzyme inhibitors) havebeen reported to increase the risk of acute pancreatitis.
Previous studies have yielded conflicting results about the association between incretin therapies and acute pancreatitis. We aimed to compare the occurrence of acute pancreatitis in a population of patients with type 2 diabetes who received incretins compared with those who received other antidiabetic treatment.
Methods
In our population-based matched case-control study, we extracted information from an administrative database from Piedmont, Italy (containing data for 4·4 million inhabitants). From a dataset of 282 429 patients receiving treatment with antidiabetic drugs for type 2 diabetes, we identified 1003 cases older than 41 years who had been admitted to hospital for acute pancreatitis between Jan 1, 2008, and Dec 31, 2012, and 4012 controls who were matched for sex, age, and time of start of antidiabetic therapy. We compared incretin exposure in cases and controls with a conditional logistic regression model, expressed as odds ratios (ORs [95% CI]). We adjusted all analyses for risk factors of acute pancreatitis, as ascertained by hospital discharge records, and concomitant use of metformin or glibenclamide.
Findings
The mean age of cases and controls (72·2 years [SD 11·1]) was high, as expected in an unselected diabetic population in Europe. After adjustment for available confounders, use of incretins in the 6 months before hospital admission was not associated with increased risk of acute pancreatitis (OR 0·98, 95% CI 0·69—1·38; p=0·8958).
Interpretation
Our findings suggest that, in an unselected population, use of incretins is not associated with an increased risk of acute pancreatitis. Larger studies are needed to clarify whether age or type of incretin therapy could affect the risk of acute pancreatitis in patients with type 2 diabetes.
Incretin-based therapies for type 2 diabetes include twodrug classes. The first class, glucagon-like peptide-1(GLP-1) receptor agonists, includes drugs that mimic theaction of native GLP-1, such as the injectable GLP-1analogues exenatide and liraglutide. The other classincludes drugs that delay the catabolism of native GLP-1mainly through inhibition of the endogenous enzymedipeptidyl peptidase 4 (DPP-4), thus extending the actionof native GLP-1. The DPP-4 inhibitors sitagliptin,vildagliptin, saxagliptin, and linagliptin, in order of theirprevalence of use in the market in Europe, are all takenorally. Although cases of haemorrhagic or necrotizingpancreatitis have been reported in patients taking thesedrugs, a clear-cut pharmacoepidemiological associationbetween incretin treatment and increased risk ofpancreatic damage has not been shown. Incidence ofacute pancreatitis is higher in patients with type 2 diabetesthan in the non-diabetic population, irrespective oftreatment.Further complicating the issue is the fact thatseveral drugs commonly used in the treatment of type 2diabetes (eg, non-incretin anti-diabetes drugs, statins,and angiotensin-converting enzyme inhibitors) havebeen reported to increase the risk of acute pancreatitis.
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