OBJECTIVE: The study aims to determine and quantify the stratified risk of recurrent pancreatitis (RP) after the first episode of acute pancreatitis in relation to etiology and severity of disease.
METHODS: A systematic review and meta-analysis in compliance with PRISMA statement standards was conducted. A search of electronic information sources was conducted to identify all studies investigating the risk of RP after the first episode of acute pancreatitis. Proportion meta-analysis models using random effects were constructed to calculate the weighted summary risks of RP. Meta-regression was performed to evaluate the effect of different variables on the pooled outcomes.
RESULTS: Analysis of 57,815 patients from 42 studies showed that the risk of RP after first episode was 19.8% (95% confidence interval [CI] 17.5-22.1%). The risk of RP was 11.9% (10.2-13.5%) after gallstone pancreatitis, 28.7% (23.5-33.9%) after alcohol-induced pancreatitis, 30.3% (15.5-45.0%) after hyperlipidemia-induced pancreatitis, 38.1% (28.9-47.3%) after autoimmune pancreatitis, 15.1% (11.6-18.6%) after idiopathic pancreatitis, 22.0% (16.9-27.1%) after mild pancreatitis, 23.9% (12.9-34.8%) after moderate pancreatitis, 21.6% (14.6-28.7%) after severe pancreatitis, and 6.6% (4.1-9.2%) after cholecystectomy following gallstone pancreatitis. Meta-regression confirmed that the results were not affected by the year of study (P = 0.541), sample size (P = 0.064), length of follow-up (P = 0.348), and age of patients (P = 0.138) in the included studies.
CONCLUSIONS: The risk of RP after the first episode of acute pancreatitis seems to be affected by the etiology of pancreatitis but not the severity of disease. The risks seem to be higher in patients with autoimmune pancreatitis, hyperlipidemia-induced pancreatitis, and alcohol-induced pancreatitis and lower in patients with gallstone pancreatitis and idiopathic pancreatitis.

Excessive alcohol consumption has long been known to be the primary cause of chronic pancreatitis (CP) but genetic risk factors have been increasingly identified over the past 25 years. The scale and scope of gene-alcohol interactions in CP nevertheless remain unclear.
All studies that had obtained genetic variant data concurrently on alcoholic CP (ACP) patients, non-ACP (NACP) patients and normal controls were collated. Employing normal controls as a common baseline, paired ORACP and ORNACP (odds ratios associated with ACP and NACP, respectively) values were calculated and used to assess gene-alcohol interactions.
Thirteen variants involving PRSS1, SPINK1, CTRC, CLDN2, CPA1, CEL and CTRB1-CTRB2, and varying from very rare to common, were collated. Seven variants had an ORACP > ORNACP, which was regarded as an immediate indicator of gene-alcohol interactions in CP. Variants with an ORACP < ORNACP were also found to interact with alcohol consumption by virtue of their impact on age at first pancreatitis symptoms in ACP.
This study revealed evidence for extensive gene-alcohol interactions in CP. Our findings lend support to the hypothesis that alcohol affects the expression of genetically determined CP and highlight a predominant role of weak-effect variants in the development of ACP.

BACKGROUND: Available estimates of coexistent alcohol-related pancreatitis (ALP) and alcohol-related liver disease (ALD) vary widely, and factors that determine coexistent disease are largely unknown. We performed a systematic review of published literature with the primary aim to generate robust estimates for coexistent alcohol-related chronic pancreatitis (ACP) and alcohol-related cirrhosis (ALC).
METHODS: We searched PubMed, EMBASE, and Web of Science databases from inception until February 2018. Studies included were those in English-language, sample size ≥25 and allowed calculation of the coexistent disease. Pooled estimates were calculated using a random-effects model approach.
RESULTS: Twenty-nine (including 5 autopsy studies) of 2000 eligible studies met inclusion criteria. Only 6.9% included patients were female. Fifteen studies enabled calculation of ACP in ALC, and 11 for ALC in ACP. Pooled prevalence of ACP in ALC was 16.2% (95% CI 10.4-24.5) overall, and 15.5% (95% CI 8.0-27.7) when data were limited to clinical studies. Corresponding prevalence for ALC in ACP was 21.5% (95% CI 12.0-35.6) and 16.9% (95% CI 11.5-24.3), respectively. There was significant heterogeneity among studies (I2 - 65-92%). Pooled prevalence for ALP in ALD or ALD in ALP in clinical studies were 15.2% and 39%, respectively. None of the studies reported outcomes in patients with coexistent disease.
CONCLUSIONS: A sizeable fraction of patients with ACP or ALC have coexistent disease. Future studies should define the prevalence of coexistent disease in women and minority populations, and the consequences of coexistent disease on clinical presentation and short- and long-term outcomes.

Genetic predisposition plays an important role in the development of alcoholic pancreatitis (AP), with previous studies suggesting that genetics variants in certain genes, such asCYP2E1 and CTRC, partially explain individual susceptibility to this disease. Therefore, the aim of this work was to conduct a systematic review and meta-analysis of existing studies that analyzed how polymorphisms within CYP2E1 and CTRC genes influence the risk of AP.
We performed a systematic review of studies that analyzed the genotype distribution of CYP2E1 and CTRC allelic variants among patients with AP and a group of controls. A meta-analysis was conducted using a random effects model. Odds ratios (ORs) and their confidence intervals (CIs) were calculated.
The T allele of theCTRC 180 C > T variant was significantly more prevalent among patients with AP compared to all controls (OR = 1.79, 95% CI = 1.43-2.24; P < 0.00001) and healthy subjects (OR = 1.84, 95% CI = 1.46-2.31; P < 0.00001). The Trp variant of CTRC Arg254Trp polymorphism was also more prevalent in patients with AP; however, these results were not significant after excluding one study. We found no clear evidence that CYP2E1-DraI or of CYP2E1-RsaI/PstI polymorphisms modulate the risk of developing AP.
Our meta-analysis supports that the T allele ofCTRC 180C > T polymorphisms modulates the risk of alcoholic pancreatitis. No clear evidence was found for the remaining SNPs being associated with this disease.

The aim of this study was to assess the occurrence of new-onset diabetes mellitus (DM) after chronic pancreatitis (CP) diagnosis via systematic review and meta-analysis.
A systematic review of literature and meta-analysis of relevant reports were performed. The primary outcome measures studied were newly diagnosed DM and DM treated with insulin. For the binary outcomes, pooled prevalence and 95% confidence interval (CI) were calculated.
Fifteen studies involving 8970 patients were eligible. The incidence of new-onset DM after CP diagnosis was 30% (95% CI, 27%-33%). Among all patients, 17% (95% CI, 13%-22%) developed insulin-dependent new-onset DM. The prevalence of newly diagnosed DM after CP diagnosis increased from 15% within 36 months to 33% after 60 months. The proportion of alcoholic CP, sex, age, and body mass index had minimal effect on the studied outcomes.
This systematic review identified a clinically relevant risk of new-onset DM after CP diagnosis. Therefore, patients should be informed of the risk of DM and monitored.

Diabetes mellitus (DM) is a common disease involving insulin resistance or deficit that, when left unchecked, may cause severe hyperglycemia and subsequent end-organ damage. Acute pancreatitis (AP) is inflammation of the pancreas that can lead to significant morbidity and mortality. AP and DM both account for a significant amount of sudden deaths, and rarely both disease processes may be present in the same decedent, causing some difficulty in wording the cause of death statement. Although much research has been directed at studying the causes and risk factors for AP and DM, there is a complex interplay between these diseases that is not fully understood. This study presents two autopsy cases of sudden, natural deaths that illustrate this interplay, along with a review of the literature. An algorithm for differentiating AP and DM is then discussed in the context of the presented cases as a proposed aid for forensic pathologists in the certification of such deaths.

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Haemosuccus Pancreaticus is defined as upper gastro intestinal (GI) bleeding from the ampula of vater via the pancreatic duct. It is most commonly associated with pancreatic inflammation, erosion of the pancrease by aneurysm or pseudo-aneurysm of the splenic artery. We report a 69 year old man with previous history of acute pancreatitis who was admitted with recurrent haematemesis. Initial upper GI endocopy was normal, while admitted, he collapse with abdominal pain and hypotension. He was resuscitated with blood and intravenous fluid. Repeat upper GI endocopy showed fresh blood in the duodenum, but no active bleeding site was demonstrated. An urgent coeliac axis CT angiogram was done which showed an splenic artery pseudo-aneurysm, which was successfully embolized. Patient is well 9 months after the procedure. This case highlights the importance of considering coeliac axis CT angiogram as part of investigation for obscure GI bleeding.

Reports of pulmonary embolism in the setting of acute pancreatitis are rare. We present three cases of acute pancreatitis associated with pulmonary embolism and review the literature. Two of the three patients had severe acute pancreatitis with bilateral pulmonary emboli, and to our knowledge, these cases represent the first report of pulmonary embolism occurring in the setting of pancreatic ascites and pleural effusion. All patients experienced abdominal pain, though in one patient, symptoms suggestive of a pulmonary embolism were lacking. All three patients were successfully treated with unfractionated heparin and conservative management. Pulmonary thrombosis may occur in the setting of severe acute pancreatitis as the result of systemic inflammatory response. We review the literature and provide microvascular explanations for the occurrence of pulmonary complications and thrombosis in the setting of acute pancreatitis. We also review prior cases of pulmonary embolism in acute pancreatitis. Our experience suggests that pulmonary embolism may be an under-recognized complication of severe acute pancreatitis.

Pseudocysts containing activated enzymes are a common complication of pancreatitis. Pseudocysts can rupture into adjacent structures including the peritoneal cavity, adjacent organs, and rarely vascular structures. While arterial pseudoaneurysms and venous thrombosis or occlusion are well known complications of acute and chronic pancreatitis, only 17 cases of pancreas-portal venous fistula have been encountered in review of the literature. A patient with chronic pancreatitis presented with a history of weight loss, fatigue and was found to have a pancreatic duct-portal vein fistula. The patient was treated surgically with good outcome.