Risk of development of acute pancreatitis with pre-existing diabetes: a meta-analysis

Department of Gastroenterology, The Third People's Hospital of Wuxi, Jiangsu, China.
European journal of gastroenterology & hepatology (Impact Factor: 1.66). 06/2012; 24(9):1092-8. DOI: 10.1097/MEG.0b013e328355a487
Source: PubMed

ABSTRACT It is well established that acute pancreatitis (AP) often causes diabetes mellitus. However, whether pre-existing diabetes is associated with the development of AP remains unknown. To clarify the association of pre-existing diabetes and the development of AP, we carried out a meta-analysis of observational studies.
A computerized literature search was performed in MEDLINE (from 1 January 1966) and EMBASE (from 1 January 1974), through 31 January 2012. We also searched the reference lists of relevant articles. Summary relative risks with their corresponding 95% confidence intervals (CIs) were calculated using a random-effects model. Between-study heterogeneity was assessed using Cochran's Q statistic and the I 2.
A total of seven articles (10 523 incident cases of AP) were included in this meta-analysis. Analysis of seven studies indicated that, compared with nondiabetic individuals, diabetic individuals had a 92% increased risk of development of AP (95% CI 1.50-2.47). There was significant evidence of heterogeneity among these studies (P heterogeneity<0.001, I 2=93.0%). These increased risks were independent of alcohol use, gallstones, and hyperlipidemia.
Although the current evidence supports a positive link between pre-existing diabetes and an increased risk of development of AP, additional studies, with a perfect design, are required before definitive conclusions can be drawn.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Background/objective: Signals from the FDA Adverse Event Reporting System (AERS) and pre-clinical and human pancreata obtained from organ donors have suggested that incretin-based therapies used to treat Type 2 Diabetes Mellitus, such as glucagon-like peptide 1 (GLP-1) receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors, may increase the risk of acute pancreatitis (AP) and pancreatic cancer (PC). However, data from observational studies and randomized trials have been conflicting. We conducted a literature review to identify and summarize all observational data published assessing the pancreatic safety of incretins. Methods: Searches were conducted in MEDLINE via PubMed and EMBASE using the key terms for the time period of January 1, 2005, to February 12, 2014. 180 articles were screened in abstract form and 49 were subsequently reviewed in full-text for inclusion. Data from 12 articles are included in this report. Findings: Data from the FDA AERS database suggest increased risk of AP and PC with GLP-1 receptor agonist and DPP-4 inhibitor use. These findings are not supported by population-based observational studies for either AP or PC, however studies assessing the relationship between PC and incretin-based therapies are limited. Conclusions: Current evidence is conflicting and inadequate to conclude if use of incretin-based therapies increases the risk of AP and PC. Further studies, notably with the ability to provide long term follow-up, are needed.
    Current Medical Research and Opinion 09/2014; DOI:10.1185/03007995.2014.960515 · 2.37 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Acute pancreatitis (AP) can lead to a systemic inflammatory response that often results in acute lung injury and single or multiple organ failure. In a previous study we demonstrated that diabetes aggravates the local pathophysiological process during AP. In this study we explore, if diabetes also increases pancreatitis induced systemic inflammation and causes lung injury. Acute pancreatitis was induced in untreated and streptozotocin-treated diabetic mice by injection of cerulein. Systemic inflammation was studied by IL-6 ELISA in blood plasma and white blood cell count. Lung inflammation and lung injury were quantified by chloroacetate esterase staining, evaluation of the alveolar cellularity index and cleaved caspase-3 immunohistochemistry. In normoglycaemic mice AP increased the IL-6 concentration in plasma and caused lymphocytopenia. Diabetes significantly increased the IL-6 concentration in plasma and further reduced the number of lymphocytes during AP, whereas diabetes had little effect on these parameters in the absence of pancreatitis. However, diabetes only marginally increased lung inflammation and did not lead to cell death of the lung epithelium during AP. We conclude that diabetes increases parameters of systemic inflammation during AP, but that this increase is insufficient to cause lung injury.
    International Journal of Experimental Pathology 11/2014; 95(6). DOI:10.1111/iep.12103 · 2.05 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Diabetes mellitus and pancreatitis are two distinct diseases encountered commonly in small animal practice. Whilst the clinical signs of diabetes mellitus are usually unmistakeable, a firm diagnosis of pancreatitis can prove more elusive, as clinical signs are often variable. Over the past 10 to 15 years, despite the fact that the clinical signs of diabetes mellitus are remarkably consistent, it has become more apparent that the underlying pathology of diabetes mellitus in dogs and cats is heterogeneous, with exocrine pancreatic inflammation accompanying diabetes mellitus in a number of cases. However, the question remains as to whether the diabetes mellitus causes the pancreatitis or whether, conversely, the pancreatitis leads to diabetes mellitus – as there is evidence to support both scenarios. The concurrence of diabetes mellitus and pancreatitis has clinical implications for case management as such cases may follow a more difficult clinical course, with their glycaemic control being “brittle” as a result of variation in the degree of pancreatic inflammation. Problems may also arise if abdominal pain or vomiting lead to anorexia. In addition, diabetic cases with pancreatitis are at risk of developing exocrine pancreatic insufficiency in the following months to years, which can complicate their management further.
    Journal of Small Animal Practice 01/2015; 56(1). DOI:10.1111/jsap.12295 · 0.91 Impact Factor