sitagliptin-phosphate and Acute-Disease

Data on the possible relationship of gliptin treatment with the incidence of acute pancreatitis have been controversial. The aim of the current study was to combine data on the incidence of acute pancreatitis from three large randomized controlled trials.. Three trials designed to test cardiovascular safety and efficacy of add-on treatment with a gliptin were included in the analysis, as follows: SAVOR-TIMI 53 (saxagliptin), EXAMINE (alogliptin), and TECOS (sitagliptin). The trials included 18,238 gliptin-treated patients and 18,157 placebo-treated patients. Data were combined using a random-effects model meta-analysis.. The incidence of acute pancreatitis was significantly increased in the gliptin-treated patients when compared with the control groups (odds ratio 1.79 [95% CI 1.13-2.82], P = 0.013). The difference in the absolute risk was small (0.13%).. Treatment with gliptins significantly increased the risk for acute pancreatitis in a combined analysis of three large controlled randomized trials.

Topics: Acute Disease; Adamantane; Diabetes Mellitus, Type 2; Dipeptides; Dipeptidyl-Peptidase IV Inhibitors; Humans; Incidence; Pancreatitis; Piperidines; Randomized Controlled Trials as Topic; Sitagliptin Phosphate; Uracil

Recent case reports of acute pancreatitis in patients with type 2 diabetes (T2DM) treated with incretin-based therapies have triggered interest regarding the possibility of a mechanism-based association between pancreatitis and glucagon-like peptide-1 mimetics or dipeptidyl peptidase-4 (DPP-4) inhibitors. The objective of this review was to describe the controlled preclinical and clinical trial data regarding the incidence of pancreatitis with sitagliptin, the first DPP-4 inhibitor approved for use in patients with T2DM. Tissue samples from multiple animal species treated with sitagliptin for up to 2 years at plasma exposures substantially in excess of human exposure were evaluated to determine whether any potential gross or histomorphological changes suggestive of pancreatitis occurred. Sections were prepared by routine methods, stained with haematoxylin and eosin and examined microscopically. A pooled analysis of 19 controlled clinical trials, comprising 10,246 patients with T2DM treated for up to 2 years, was performed using patient-level data from each study for the evaluation of clinical and laboratory adverse events. Adverse events were encoded using the Medical Dictionary for Regulatory Activities (MedDRA) version 12.0 system. Incidences of adverse events were adjusted for patient exposure. Tissue samples from preclinical studies in multiple animal species did not reveal any evidence of treatment-related pancreatitis. The pooled analysis of controlled clinical trials revealed similar incidence rates of pancreatitis in patients treated with sitagliptin compared with those not treated with sitagliptin (0.08 events per 100 patient-years vs. 0.10 events per 100 patient-years, respectively). Preclinical and clinical trial data with sitagliptin to date do not indicate an increased risk of pancreatitis in patients with T2DM treated with sitagliptin.

Topics: Acute Disease; Diabetes Mellitus, Type 2; Dipeptidyl-Peptidase IV Inhibitors; Humans; Hypoglycemic Agents; Pancreatitis; Pyrazines; Randomized Controlled Trials as Topic; Risk Factors; Sitagliptin Phosphate; Triazoles

We evaluated the incidence of acute pancreatitis and pancreatic cancer in patients with type 2 diabetes and cardiovascular disease who were treated with sitagliptin, a dipeptidyl peptidase-4 inhibitor (DPP-4i).. In the Trial Evaluating Cardiovascular Outcomes with Sitagliptin (TECOS) study, a cardiovascular safety study of sitagliptin, all suspected cases of acute pancreatitis and pancreatic cancer were collected prospectively for 14,671 participants during a median follow-up time of 3 years, and were adjudicated blindly.. Baseline differences were minimal between participants confirmed to have no pancreatic events, acute pancreatitis, or pancreatic cancer. Among those participants randomized to receive sitagliptin, 23 (0.3%) (vs. 12 randomized to receive placebo [0.2%]) had pancreatitis (hazard ratio 1.93 [95% CI 0.96-3.88], P = 0.065; 0.107 vs. 0.056/100 patient-years), with 25 versus 17 events, respectively. Severe pancreatitis (two fatal) occurred in four individuals allocated to receive sitagliptin. Cases of pancreatic cancer were numerically fewer with sitagliptin (9 [0.1%]) versus placebo (14 [0.2%]) (hazard ratio 0.66 [95% CI 0.28-1.51], P = 0.32; 0.042 vs. 0.066 events/100 patient-years). Meta-analysis with two other DPP-4i cardiovascular outcome studies showed an increased risk for acute pancreatitis (risk ratio 1.78 [95% CI 1.13-2.81], P = 0.01) and no significant effect for pancreatic cancer (risk ratio 0.54 [95% CI 0.28-1.04], P = 0.07).. Pancreatitis and pancreatic cancer were uncommon events with rates that were not statistically significantly different between the sitagliptin and placebo groups, although numerically more sitagliptin participants developed pancreatitis and fewer developed pancreatic cancer. Meta-analysis suggests a small absolute increased risk for pancreatitis with DPP-4i therapy.

Topics: Acute Disease; Aged; Cardiovascular Diseases; Diabetes Mellitus, Type 2; Dipeptidyl-Peptidase IV Inhibitors; Double-Blind Method; Female; Follow-Up Studies; Humans; Male; Middle Aged; Pancreatic Neoplasms; Pancreatitis; Proportional Hazards Models; Risk Factors; Sitagliptin Phosphate; Treatment Outcome

Topics: Acute Disease; Acute Lung Injury; Aldehydes; Animals; Autophagy; Autophagy-Related Protein 5; Beclin-1; Down-Regulation; Inflammation; Kelch-Like ECH-Associated Protein 1; Lung; Mice, Inbred C57BL; Mice, Knockout; NF-E2-Related Factor 2; Oxidative Stress; Pancreatitis; Protective Agents; Reactive Oxygen Species; Sequestosome-1 Protein; Signal Transduction; Sitagliptin Phosphate

Dipeptidyl peptidase 4 (DPP-4) inhibitors are incretin-based medications used as oral antidiabetic agents for the treatment of type 2 diabetes. However, DPP-4 inhibitors produce side effects like acute pancreatitis, upper respiratory tract infection, nasopharyngitis, urinary tract infection, serious allergies, cardiovascular diseases, hemolysis, and retinopathy. Hence, the development of a fast and simple method to detect DPP-4 inhibitors in body fluids is important. In this study, we developed a derivatization-assisted microextraction method to enhance the detection sensitivity for trace levels of a DPP-4 inhibitor, sitagliptin, from a small volume (10 μL) of human plasma by using matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS). Subjecting the analyte to 100 W microwave irradiation after derivatization using a quinoline alkylating reagent (8-bromomethyl quinilone, BrMQ) shortened the reaction time to ~120 s and allowed the target analyte to be easily extracted to a small volume of the organic layer (20 μL). The analyte was then detected by MALDI-TOF MS using α-cyano-4-hydroxycinnamic acid as the matrix. The relative standard deviation and relative error were below 10% in intra- and inter-day assays. Using sitagliptin-d4 as an internal standard, the limits of quantitation and detection were found to be 0.03 μg/mL and 0.01 μg/mL, respectively. All the derivatization and extraction procedures described herein were of microliter grade. This method could effectively reduce the use of organic chemicals and solvents, thereby proving to be an eco-friendly strategy that will cause no harm to the environment.

Topics: Acute Disease; Diabetes Mellitus, Type 2; Humans; Pancreatitis; Quinolines; Sitagliptin Phosphate; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

Severe acute pancreatitis (SAP) is a challenging disease with high morbidity and mortality, often complicated by multiple organ dysfunction syndrome (MODS). The intestine, a major organ involved in MODS, correlates strongly with the evolution of the disease. In this study, we demonstrated that the DPP4 inhibitor, sitagliptin, protects SAP-associated intestinal injury both in vitro and in vivo. These beneficial effects were achieved by suppressing oxidative stress and inflammatory responses. Moreover, in sitagliptin-treated SAP mice, expression of Nrf2 was induced and that of NF-

Topics: Acute Disease; Animals; Cell Proliferation; Dipeptidyl-Peptidase IV Inhibitors; Inflammation; Interleukin-6; Intestines; Lipopolysaccharides; Malondialdehyde; Mice; Mice, Inbred C57BL; Mice, Knockout; NF-E2-Related Factor 2; NF-kappa B; Oxidative Stress; Pancreatitis; Reactive Oxygen Species; Signal Transduction; Sitagliptin Phosphate; Superoxide Dismutase

Angiogenesis is regulated in a tissue-specific manner in all patients, especially those with diabetes. In this study, we describe a novel molecular pathway of angiogenesis regulation in diabetic rats with myocardial infarction (MI) and examine the cardioprotective effects of different doses of sitagliptin. Male rats were divided into 5 groups: normal vehicle group, diabetic group, diabetic + MI, diabetic + MI + 5 mg/kg sitagliptin, and diabetic + MI + 10 mg/kg sitagliptin. Isoproterenol in diabetic rats resulted in significant (

Topics: Acute Disease; Animals; Blood Glucose; Body Weight; Cyclooxygenase 2; Diabetes Mellitus, Experimental; Dose-Response Relationship, Drug; Electrocardiography; Heart Ventricles; Insulin-Like Growth Factor I; Interleukin-6; Male; Myocardial Infarction; Neovascularization, Physiologic; Organ Size; Rats; Sitagliptin Phosphate; Vascular Endothelial Growth Factor A

The cardiovascular safety of saxagliptin, a dipeptidyl-peptidase 4 inhibitor, compared with other antihyperglycemic treatments is not well understood. We prospectively examined the association between saxagliptin use and acute myocardial infarction (AMI).. We identified patients aged ≥18 years, starting from the approval date of saxagliptin in 2009 and continuing through August 2014, using data from 18 Mini-Sentinel data partners. We conducted seven sequential assessments comparing saxagliptin separately with sitagliptin, pioglitazone, second-generation sulfonylureas, and long-acting insulin, using disease risk score (DRS) stratification and propensity score (PS) matching to adjust for potential confounders. Sequential testing kept the overall chance of a false-positive signal below 0.05 (one-sided) for each pairwise comparison.. We identified 82,264 saxagliptin users and more than 1.5 times as many users of each comparator. At the end of surveillance, the DRS-stratified hazard ratios (HRs) (95% CI) were 1.08 (0.90-1.28) in the comparison with sitagliptin, 1.11 (0.87-1.42) with pioglitazone, 0.79 (0.64-0.98) with sulfonylureas, and 0.57 (0.46-0.70) with long-acting insulin. The corresponding PS-matched HRs were similar. Only one interim analysis of 168 analyses met criteria for a safety signal: the PS-matched saxagliptin-pioglitazone comparison from the fifth sequential analysis, which yielded an HR of 1.63 (1.12-2.37). This association diminished in subsequent analyses.. We did not find a higher AMI risk in saxagliptin users compared with users of other selected antihyperglycemic agents during the first 5 years after U.S. Food and Drug Administration approval of the drug.

Topics: Acute Disease; Adamantane; Dipeptides; Dipeptidyl-Peptidase IV Inhibitors; Female; Follow-Up Studies; Humans; Hypoglycemic Agents; Incidence; Insulin, Long-Acting; Male; Middle Aged; Myocardial Infarction; Pioglitazone; Product Surveillance, Postmarketing; Propensity Score; Proportional Hazards Models; Prospective Studies; Sitagliptin Phosphate; Sulfonylurea Compounds; Thiazolidinediones; United States

Topics: Abdominal Pain; Acute Disease; Aged; Diabetes Mellitus, Type 2; Female; Humans; Hypoglycemic Agents; Magnetic Resonance Imaging; Nausea; Pancreas; Pancreatitis; Sitagliptin Phosphate; Treatment Outcome; Vomiting

To assess the risk of acute pancreatitis during treatment with glucagon-like peptide 1 receptor agonist dulaglutide, placebo, and active comparators across phase 2/3 dulaglutide trials.. A total of 6,005 patients with type 2 diabetes participated (dulaglutide group. The exposure-adjusted incidence rate of acute pancreatitis in dulaglutide-treated patients was similar to the rates with placebo, with few reported cases during the entire program.

Topics: Acute Disease; Diabetes Mellitus, Type 2; Exenatide; Female; Glucagon-Like Peptide-1 Receptor; Glucagon-Like Peptides; Humans; Hypoglycemic Agents; Immunoglobulin Fc Fragments; Insulin Glargine; Male; Metformin; Middle Aged; Pancreatitis; Peptides; Recombinant Fusion Proteins; Sitagliptin Phosphate; Venoms

There is still lack of definite evidence to establish the association between sitagliptin use and acute pancreatitis. The study aimed to test this issue in Taiwan.. This case-control study was designed to analyze the database of the Taiwan National Health Insurance Program. There were 349 subjects with type 2 diabetes mellitus aged 20-84 with a first-attack of acute pancreatitis from 2009 to 2011 as the case group and 1116 randomly selected subjects with type 2 diabetes mellitus without acute pancreatitis as the control group. Both groups were matched with sex, age, comorbidities, and index year of diagnosing acute pancreatitis. Current use of sitagliptin was defined as subjects who had their last tablet of sitagliptin ≤7 days before the date of diagnosing acute pancreatitis. Late use of sitagliptin was defined as subjects who had their last tablet of sitagliptin between 8 and 30 days before the date of diagnosing acute pancreatitis. Never use of sitagliptin was defined as subjects who never had a sitagliptin prescription. The risk of acute pancreatitis associated with sitagliptin use was estimated by the odds ratio (OR) and 95% confidence interval (CI) using the multivariable logistic regression model.. After statistical correction for potential confounders, the adjusted OR of acute pancreatitis was 2.47 for subjects with current use of sitagliptin (95% CI 0.84, 7.28), when compared with those never using sitagliptin, but without statistical significance. The adjusted OR decreased to 1.14 for subjects with late use of sitagliptin (95% CI 0.66, 1.98), but without statistical significance.. No significant association is detected between sitagliptin use and acute pancreatitis in type 2 diabetes mellitus.

Topics: Acute Disease; Adult; Aged; Aged, 80 and over; Case-Control Studies; Comorbidity; Databases, Factual; Diabetes Mellitus, Type 2; Female; Humans; Hypoglycemic Agents; Logistic Models; Male; Middle Aged; Multivariate Analysis; Odds Ratio; Pancreatitis; Risk Factors; Sitagliptin Phosphate; Taiwan; Young Adult

To analyze the association between use of DPP-4 inhibitors and acute pancreatitis in high-risk type 2 diabetic patients. A retrospective nationwide cohort study was conducted using the Taiwan National Health Insurance claim database. The risk associated with sitagliptin was compared to that with acarbose, a second-line antidiabetic drug prescribed for patients with similar diabetes severity and with a known neutral effect on pancreatitis. Between January 1, 2009 and December 31, 2010, a total of 8526 sitagliptin initiators and 8055 acarbose initiators who had hypertriglyceridemia or prior hospitalization history for acute pancreatitis were analyzed for the risk of hospitalization due to acute pancreatitis stratified for baseline propensity score. In the crude analysis, sitagliptin was associated with a decreased risk of acute pancreatitis (hazard ratio [HR] 0.74; 95% confidence interval [CI]: 0.62-0.88) compared to acarbose in diabetic patients with prior history of hospitalization for pancreatitis or hypertriglyceridemia. The association was abolished after stratification for propensity score quintiles (adjusted HR 0.95; 95% CI: 0.79-1.16). Similar results were found separately in both patients' histories of prior hospitalization of acute pancreatitis (adjusted HR 0.97; 95% CI: 0.76-1.24) and those with hypertriglyceridemia (adjusted HR 0.86; 95% CI: 0.65-1.13). No significant association was found for different durations or accumulative doses of sitagliptin. In the stratified analysis, no significant effect modification was found in relation to patients' characteristics. Use of sitagliptin was not associated with an increased risk of acute pancreatitis in high-risk diabetic patients with hypertriglyceridemia or with history of acute pancreatitis.

Topics: Acarbose; Acute Disease; Adult; Aged; Aged, 80 and over; Comorbidity; Diabetes Mellitus, Type 2; Dipeptidyl-Peptidase IV Inhibitors; Female; Humans; Hypoglycemic Agents; Male; Middle Aged; Pancreatitis; Proportional Hazards Models; Retrospective Studies; Risk Assessment; Risk Factors; Severity of Illness Index; Sitagliptin Phosphate; Taiwan

To evaluate the risk of acute pancreatitis hospitalization with sitagliptin use in patients with type 2 diabetes mellitus (T2DM).. This retrospective cohort analysis included newly diagnosed T2DM with onset age ≥25 years between 1999 and 2010 from the National Health Insurance database. Ever users (n = 89,800) and never users (n = 449,000) of sitagliptin were followed until end of 2011. A time-dependent approach was used to calculate event incidence and estimate hazard ratios adjusted for propensity score.. During follow-up, 261 ever users and 5,840 never users were hospitalized for acute pancreatitis (respective incidence, 224.0 and 168.4 per 100,000 person-years), with adjusted hazard ratio of 1.59 (95% CI 1.40-1.81). The respective hazard ratio for the first, second, and third tertile of time since starting sitagliptin <9.5, 9.5-21.0, and >21.0 months was 8.10 (6.80-9.65), 1.70 (1.38-2.11), and 0.41 (0.30-0.56); 3.26 (2.67-3.98), 1.86 (1.52-2.27), and 0.76 (0.59-0.98) for cumulative duration <3.7, 3.7-10.3, and >10.3 months; and 3.21 (2.65-3.90), 1.89 (1.54-2.32), and 0.73 (0.57-0.95) for cumulative dose <9,000, 9,000-28,000, and >28,000 mg.. Sitagliptin is associated with a higher risk of acute pancreatitis within the first 2 years of its initiation. The risk diminishes thereafter, probably due to the depletion of susceptible patients.

Topics: Acute Disease; Adult; Aged; Cohort Studies; Databases, Factual; Diabetes Mellitus, Type 2; Female; Follow-Up Studies; Hospitalization; Humans; Hypoglycemic Agents; Incidence; Male; Middle Aged; Pancreatitis; Retrospective Studies; Risk; Sitagliptin Phosphate; Taiwan; Time Factors

Glucagon Like Peptide-1 (GLP-1) drugs are currently used to treat type-2 diabetes. Safety concerns for increased risk of pancreatitis and pancreatic ductal metaplasia have accompanied these drugs. High fat diet (HFD) is a type-2 diabetes risk factor that may affect the response to GLP-1 drug treatment. The objective of the present study was to investigate the effects of diet and GLP-1 based drugs on the exocrine pancreas in mice. Experiments were designed in a mouse model of insulin resistance created by feeding a HFD or standard diet (STD) for 6weeks. The GLP-1 drugs, sitagliptin (SIT) and exenatide (EXE) were administered once daily for additional 6weeks in both mice fed HFD or STD. The results showed that body weight, blood glucose levels, and serum levels of pro-inflammatory cytokines (TNFα, IL-1β, and KC) were significantly greater in HFD mice than in STD mice regardless of GLP-1 drug treatment. The semi-quantitative grading showed that pancreatic changes were significantly greater in EXE and SIT-treated mice compared to control and that HFD exacerbated spontaneous exocrine pancreatic changes seen in saline-treated mice on a standard diet. Exocrine pancreatic changes identified in this study included acinar cell injury (hypertrophy, autophagy, apoptosis, necrosis, and atrophy), vascular injury, interstitial edema and inflammation, fat necrosis, and duct changes. These findings support HFD as a risk factor to increased susceptibility/severity for acute pancreatitis and indicate that GLP-1 drugs cause pancreatic injury that can be exacerbated in a HFD environment.

Topics: Acute Disease; Animals; Apoptosis; Atrophy; Diet, High-Fat; Exenatide; Glucagon-Like Peptide-1 Receptor; Hypoglycemic Agents; Male; Mice; Mice, Inbred C57BL; Necrosis; Pancreas; Pancreatitis; Peptides; Pyrazines; Receptors, Glucagon; Sitagliptin Phosphate; Triazoles; Venoms

Endothelial injuries regularly occur in atherosclerosis and during interventional therapies of the arterial occlusive disease. Disturbances in the endothelial integrity can lead to insufficient blood supply and bear the risk of thrombus formation and acute vascular occlusion. At present, effective therapeutics to restore endothelial integrity are barely available. We analyzed the effect of pharmacological DPP-4-inhibition by Sitagliptin on endogenous progenitor cell-based endothelial regeneration via the SDF-1α/CXCR4-axis after acute endothelial damage in a mouse model of carotid injury.. Induction of a defined endothelial injury was performed in the carotid artery of C57Bl/6 mice which led to a local upregulation of SDF-1α expression. Animals were treated with placebo, Sitagliptin or Sitagliptin+AMD3100. Using mass spectrometry we could prove that Sitagliptin prevented cleavage of the chemokine SDF-1α. Accordingly, increased SDF-1α concentrations enhanced recruitment of systemically applied and endogenous circulating CXCR4+ progenitor cells to the site of vascular injury followed by a significantly accelerated reendothelialization as compared to placebo-treated animals. Improved endothelial recovery, as well as recruitment of circulating CXCR4+ progenitor cells (CD133+, Flk1+), was reversed by CXCR4-antagonization through AMD3100. In addition, short-term Sitagliptin treatment did not significantly promote neointimal or medial hyperplasia.. Sitagliptin can accelerate endothelial regeneration after acute endothelial injury. DPP-4 inhibitors prevent degradation of the chemokine SDF-1α and thus improve the recruitment of regenerative circulating CXCR4+ progenitor cells which mediate local endothelial cell proliferation without adversely affecting vessel wall architecture.

Topics: Acute Disease; Animals; Arterial Occlusive Diseases; Carotid Arteries; Cell Movement; Cell Proliferation; Dipeptidyl Peptidase 4; Dipeptidyl-Peptidase IV Inhibitors; Disease Models, Animal; Endothelium, Vascular; Male; Mice; Mice, Inbred C57BL; Pyrazines; Regeneration; Signal Transduction; Sitagliptin Phosphate; Stem Cells; Triazoles; Tunica Intima

Acute pancreatitis has significant morbidity and mortality. Previous studies have raised the possibility that glucagonlike peptide 1 (GLP-1)-based therapies, including a GLP-1 mimetic (exenatide) and a dipeptidyl peptidase 4 inhibitor (sitagliptin phosphate), may increase the risk of acute pancreatitis.. To test whether GLP-1-based therapies such as exenatide and sitagliptin are associated with an increased risk of acute pancreatitis. We used conditional logistic regression to analyze the data.. Population-based case-control study.. A large administrative database in the United States from February 1, 2005, through December 31, 2008.. Adults with type 2 diabetes mellitus aged 18 to 64 years. We identified 1269 hospitalized cases with acute pancreatitis using a validated algorithm and 1269 control subjects matched for age category, sex, enrollment pattern, and diabetes complications.. Hospitalization for acute pancreatitis.. The mean age of included individuals was 52 years, and 57.45% were male. Cases were significantly more likely than controls to have hypertriglyceridemia (12.92% vs 8.35%), alcohol use (3.23% vs 0.24%), gallstones (9.06% vs 1.34), tobacco abuse (16.39% vs 5.52%), obesity (19.62% vs 9.77%), biliary and pancreatic cancer (2.84% vs 0%), cystic fibrosis (0.79% vs 0%), and any neoplasm (29.94% vs 18.05%). After adjusting for available confounders and metformin hydrochloride use, current use of GLP-1-based therapies within 30 days (adjusted odds ratio, 2.24 [95% CI, 1.36-3.68]) and recent use past 30 days and less than 2 years (2.01 [1.37-3.18]) were associated with significantly increased odds of acute pancreatitis relative to the odds in nonusers.. In this administrative database study of US adults with type 2 diabetes mellitus, treatment with the GLP-1-based therapies sitagliptin and exenatide was associated with increased odds of hospitalization for acute pancreatitis.

Topics: Acute Disease; Adolescent; Adult; Case-Control Studies; Diabetes Mellitus, Type 2; Dipeptidyl-Peptidase IV Inhibitors; Exenatide; Female; Glucagon-Like Peptide 1; Hospitalization; Humans; Logistic Models; Male; Middle Aged; Pancreatitis; Peptides; Pyrazines; Risk Factors; Sitagliptin Phosphate; Triazoles; Venoms

Topics: Acute Disease; Dipeptidyl-Peptidase IV Inhibitors; Exenatide; Glucagon-Like Peptide 1; Humans; Hypoglycemic Agents; Incretins; Metaphor; Pancreatitis; Peptides; Pyrazines; Sitagliptin Phosphate; Treatment Outcome; Triazoles; Venoms

Topics: Acute Disease; Animals; Diabetes Mellitus, Type 2; Evidence-Based Medicine; Exenatide; Humans; Hypoglycemic Agents; Pancreatitis; Peptides; Pyrazines; Risk Assessment; Risk Factors; Sitagliptin Phosphate; Triazoles; Venoms

Topics: Acute Disease; Humans; Hypoglycemic Agents; Pancreatitis; Pyrazines; Sitagliptin Phosphate; Triazoles