Xue Y, Sheng Y, Dai H, et al. Risk of development of acute pancreatitis with pre-existing diabetes: a meta-analysis
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.
Available from: Aura Reghina
- "In a metaanalysis , prediabetes and/or DM were observed in 37% of individuals after acute pancreatitis, and newly diagnosed DM developed in 15% of individuals within 12 months after pancreatitis, with an increased risk at 5 years . Conversely, diabetic individuals have a 92% increased risk of development of acute pancreatitis, independent of obesity, alcohol use, gallstones, and hyperlipidemia   "
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ABSTRACT: A 30-year-old obese male patient had been diagnosed with diabetes mellitus due to acute hyperglycemia and ketonuria. He also presented with severe hypertriglyceridemia and high levels of serum lipase. He was initially misdiagnosed with type 1 diabetes and treated with insulin for one month. At two months from first presentation, pancreatic antibodies were negative, and the C-peptide level was normal. A1c level was 5.9% without insulin treatment. The association between diabetes mellitus and acute pancreatitis is well established. We reported a case of severe transient hyperglycemia during mild acute pancreatitis in a metabolically ill patient.
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ABSTRACT: To describe clinical and epidemiological characteristics of patients with very high hypertriglyceridemia (HTG) who were attended in lipid units of the Spanish Society of Atherosclerosis (SEA).
Patients of the HTG Registry of SEA with at least one triglyceride concentration greater than 1,000mg/dL (n=298, HTG severe group) and those whose baseline triglycerides were between 200 and 246mg/dL (HTG control group, n=272) were included.
Patients with very high triglyceride levels were younger (46.9±11.5 years vs 52.7±13 years; p<0.0001), with a larger waist circumference (100.5±10.6cm vs 98.5±11.1cm; p=0.0426), higher alcohol intake (170.7±179.1g/wk vs 118.8±106.4g/wk; p=0,0473), active smoking status (45.6% vs 26.8%; p<0.0001) and a higher frequency of pancreatitis (10.2% vs 3%; p=0.0006) than HTG control group. There was a higher percentage of patients with atherogenic dietary pattern in severe HTG group compared with the control group (138 [46.3%] vs. 94 [34.5%]; p=0,001). The multivariate analysis showed that factors associated with a triglyceride concentration greater than 1,000mg/dl were age, male sex, weight, waist circumference, alcohol, physical inactivity in non-business hours and the presence of diabetes mellitus.
Patients with very high HTG were usually men in the fourth decade of life, with abdominal obesity, smoking and alcohol consumption. In 60% of cases the HTG was primary, and pancreatitis the most frequently complication.
Available from: Ahmad Al-Sarraf
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ABSTRACT: Severe hypertriglyceridemia (HTG) is one cause of acute pancreatitis, yet the level of plasma triglycerides likely to be responsible for inducing pancreatitis has not been clearly defined.
A retrospective cohort study was conducted on patients presenting non-acutely to the Healthy Heart Program Lipid Clinic at St. Paul's Hospital with a TG level > 20 mM (1772 mg/dl) between 1986 and 2007. Ninety-five patients with TG > 20 mM at the time of referral were identified, in who follow up data was available for 84. Fifteen patients (15.8%), with a mean outpatient TG level of 38.1 mM, had a history of acute pancreatitis. Among 91 additional patients with less severe HTG, none had a history of pancreatitis when TG were between 10 and 20 mM. Among patients with TG > 20 mM on presentation, 8 (8.5%), with a mean TG level of 67.8 mM, exhibited eruptive xanthomata. A diet high in carbohydrates and fats (79%) and obesity (47.6%) were the two most frequent secondary causes of HTG at initial visit. By 2009, among patients with follow up data 53% exhibited either pre-diabetes or overt Type 2 diabetes mellitus. Upon referral only 23 patients (24%) were receiving a fibrate as either monotherapy or part of combination lipid-lowering therapy. Following initial assessment by a lipid specialist this rose to 84%, and remained at 67% at the last follow up visit.
These results suggest hypertriglyceridemia is unlikely to be the primary cause of acute pancreatitis unless TG levels are > 20 mM, that dysglycemia, a diet high in carbohydrates and fats, and obesity are the main secondary causes of HTG, and that fibrates are frequently overlooked as the drug of first choice for severe HTG.
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