No abstract available

THE ABSTRACT IS AVAILABLE AT THE CLINICAL PANCREATIC DISORDER I: Acute pancreatitis. North Am J Med Sci 2011; 3: 316-319. doi: 10.4297/najms.2011.3316.

Acute renal injury caused by acute necrotizing pancreatitis (ANP) is a common complication that is associated with a high rate of mortality. Paeoniflorin is the active ingredient of paeonia radix and exhibits a number of pharmacological effects, such as anti‑inflammatory, anticancer, analgesic and immunomodulatory effects. The present study detected the potential treatment effects of paeoniflorin on acute renal injury induced by ANP in a rat model. The optimal dose of paeoniflorin for preventing acute renal injury induced by ANP was determined. Then, the possible protective mechanism of paeoniflorin was investigated. The serum levels of tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β and IL‑6 were measured with enzyme‑linked immunosorbent assay kits. Renal inflammation and apoptosis were measured by immunohistochemistry and terminal deoxynucleotidyl transferase‑mediated dUTP nick end labeling assay. The expression of nitric oxide in kidney tissues was also evaluated. The p38 mitogen‑activated protein kinases (MAPKs) were measured by western blotting. The results shown that paeoniflorin may ameliorate acute renal injury following ANP in rats by inhibiting inflammatory responses and renal cell apoptosis. These effects may be associated with the p38MAPK and nuclear factor‑κB signal pathway.

This paper investigated the potential effects of zerumbone pretreatment on an acute necrotizing pancreatitis rat model induced by sodium taurocholate. The pancreatitis injury was evaluated by serum AMY, sPLA2, and pancreatic pathological score. Pancreatitis-induced hepatic injury was measured by ALT, AST, and hepatic histopathology. The expression of I-κBα and NF-κB protein was evaluated by western blot and immunohistochemistry assay while ICAM-1 and IL-1β mRNA were examined by RT-PCR. The results showed that AMY, sPLA2, ALT, and AST levels and histopathological assay of pancreatic and hepatic tissues were significantly reduced following administration of zerumbone. Applying zerumbone also has been shown to inhibit NF-κB protein and downregulation of ICAM-1 and IL-1β mRNA. The present paper suggests that treatment of zerumbone on rat attenuates the severity of acute necrotizing pancreatitis and pancreatitis-induced hepatic injury, via inhibiting NF-κB activation and downregulating the expression of ICAM-1 and IL-1β.

To identify causal mutations in certain genes in children with acute recurrent pancreatitis (ARP) or chronic pancreatitis (CP).

The rapid production and release of a large number of inflammatory cytokines can cause excessive local and systemic inflammation in severe acute pancreatitis (SAP) and multiple organ dysfunction syndrome (MODS), especially pancreatitis-associated acute lung injury (P-ALI), which is the main cause of early death in patients with SAP. The NLRP3 inflammasome plays an important role in the maturation of IL-1β and the inflammatory cascade. Here, we established a model of SAP using wild-type (NLRP3+/+) and NLRP3 knockout (NLRP3-/-) mice by intraperitoneal injections of caerulein (Cae) and lipopolysaccharide (LPS). Pathological injury to the pancreas and lungs, the inflammatory response, and neutrophil infiltration were significantly mitigated in NLRP3-/- mice. Furthermore, INF-39, an NLRP3 inflammasome inhibitor, could reduce the severity of SAP and P-ALI in a dose-dependent manner. Our results suggested that SAP and P-ALI were alleviated by NLRP3 deficiency in mice, and thus, reducing NLRP3 expression may mitigate SAP-associated inflammation and P-ALI.

Autoimmune pancreatitis (AIP) is a chronic fibro-inflammatory disorder of the pancreas. Recent clinicopathological analysis revealed that most cases of AIP are pancreatic manifestations of systemic IgG4-related disease (IgG4-RD), a newly established disease characterized by enhanced IgG4 antibody responses and the involvement of multiple organs. Although the immuno-pathogenesis of AIP and IgG4-RD has been poorly defined, we recently showed that activation of plasmacytoid dendritic cells (pDCs) with the ability to produce large amounts of IFN-α and IL-33 mediates chronic fibro-inflammatory responses in experimental and human AIP. Moreover, M2 macrophages producing a large amount of IL-33 play pathogenic roles in the development of human IgG4-RD. Interestingly, recent studies including ours provide evidence that compositional alterations of gut microbiota are associated with the development of human AIP and IgG4-RD. In addition, intestinal dysbiosis plays pathological roles in the development of chronic pancreatic inflammation as dysbiosis mediates the activation of pDCs producing IFN-α and IL-33, thereby causing experimental AIP. In this Mini Review, we focus on compositional alterations of gut microbiota in AIP and IgG4-RD to clarify the mechanisms by which intestinal dysbiosis contributes to the development of these disorders.

Infected pancreatic necrosis (IPN) is a significant complication of acute necrotizing pancreatitis (ANP). Early identification of patients at high risk of IPN would enable appropriate treatment, but there is a lack of valid tools. This study aimed to assess the performance of the Pancreatitis Activity Scoring System (PASS) and its modifications (by removing or reducing the weight of opioid usage) in predicting IPN in a cohort of predicted severe ANP patients.

Purpose: The present retrospective study aimed to explore the relationship between pancreatitis and pancreatic cancer in the population cohort of the UK Biobank (UKB) (https://www.ukbiobank.ac.uk). Methods: From the 500 thousand population cohort of UKB, according to the age and gender of patients with pancreatic cancer 1:10, matching the control without pancreatic cancer, the binary Logistic regression model was used to analyze the relationship between pancreatitis and pancreatic cancer, and subgroup analyses were used to identify potential effect modifiers. Results: A total of 1538 patients with pancreatic cancer were compared with 15 380 controls. In the fully adjusted model, patients with pancreatitis had a significantly increased risk of pancreatic cancer compared with no pancreatitis. The risk of pancreatitis and pancreatic cancer increased with the age of pancreatitis, and the risk of pancreatic cancer was highest in the 61 to 70 age group. In addition, in the first 3 years of acute pancreatitis, the risk of pancreatic cancer increased significantly with the increase in the duration of the disease (odds ratio [OR] 29.13, 95% confidence interval [CI]: 16.34-51.93), after 3 years, the trend of increase decreased. After more than 10 years, there was no significant correlation between the risk of acute pancreatitis and pancreatic cancer. However, patients with chronic pancreatitis were significantly associated with an increased risk of pancreatic cancer only in the first 3 years (OR 28.14, 95% CI: 14.86-53.31). Conclusion: Pancreatitis may associate with an increased risk of pancreatic cancer. The older the age of pancreatitis, the higher the risk of pancreatic cancer. The risk of pancreatic cancer increases significantly in the first 3 years of the course of pancreatitis. This may provide an alternative strategy for the early identification of individuals at high risk of pancreatic cancer.

Autoimmune pancreatitis (AIP) is a rare disease. There are two distinct types of AIP: AIP type 1 (AIP-1), a pancreatic manifestation of a multi-organ disease linked to immunoglobulin (Ig)G4, and AIP type 2 (AIP-2), a pancreas-specific disease unrelated to IgG4. The usual course of treatment for AIP is oral corticosteroid medication. Rituximab has also been recommended for recurrent AIP-1 in order to initiate remission and provide ongoing treatment. Immunomodulators such as azathioprine are used to keep certain patients in remission. Evaluation also takes into account a number of pharmacological alternatives, including biologic drugs like anti-tumor necrosis factor therapy, a safe and efficient second-line treatment for AIP-2 relapse or steroid dependence. Corticosteroids and immunosuppressants, which are poorly tolerated due to considerable side effects, are being replaced by other biologic drugs, which may offer a beneficial therapeutic alternative.

Chronic pancreatitis represents a condition that is challenging for clinicians secondary to the difficulty in making an accurate diagnosis and the less than satisfactory means of managing chronic pain. This review emphasises the various manifestations that patients with chronic pancreatitis may have and describes recent advances in medical and surgical therapy. It is probable that many patients with chronic abdominal pain are suffering from chronic pancreatitis that is not appreciated. As the pathophysiology of this disorder is better understood it is probable that the treatment will be more successful.

Hypertriglyceridemia is an uncommon but a well-established etiology of acute pancreatitis leading to significant morbidity and mortality. The risk and severity of acute pancreatitis increase with increasing levels of serum triglycerides. It is crucial to identify hypertriglyceridemia as the cause of pancreatitis and initiate appropriate treatment plan. Initial supportive treatment is similar to management of other causes of acute pancreatitis with additional specific therapies tailored to lower serum triglycerides levels. This includes plasmapheresis, insulin, heparin infusion, and hemofiltration. After the acute episode, diet and lifestyle modifications along with hypolipidemic drugs should be initiated to prevent further episodes. Currently, there is paucity of studies directly comparing different modalities. This article provides a comprehensive review of management of hypertriglyceridemia induced acute pancreatitis. We conclude by summarizing our treatment approach to manage hypertriglyceridemia induced acute pancreatitis.

The management of cystic dystrophy of the duodenal wall (CDDW), or groove pancreatitis (GP), remains controversial. Although pancreatoduodenectomy (PD) is considered the most suitable operation for CDDW, pancreas-preserving duodenal resection (PPDR) has also been suggested as an alternative for the pure form of GP (isolated CDDW). There are no studies comparing PD and PPDR for this disease.

To assess the value of pleural effusion volume (PEV) quantified on chest computed tomography (CT) in patients with early stage acute pancreatitis (AP).

The Annual American Pancreas Club is an important event for communicating around clinical pancreatic disorders, just as the European, Japanese, Indian, and the International Pancreatic association. Even though the meeting is only 1½ day there were 169 different abstracts and a "How do I do it session." Among all these abstracts on the pancreas there are some real pearls, but they are almost always well hidden, never highlighted - all abstracts are similarly presented - and will too soon be forgotten. The present filing of the abstracts is one way (not the way) to get the pancreatic abstracts a little more read and a little more remembered - and perhaps a little more cited. It should also be understood that most of the abstracts are short summaries of hundreds of working hours (evenings, nights, weekends, holidays, you name them …) in the laboratory or in the clinic, often combined with blood, sweat and tears. The authors should be shown at least some respect, and their abstracts should not only be thought of as "just another little abstract" - and the best respect they can be shown are that they will be remembered to be another brick in our scientific wall.Now the pancreatic abstracts of American Pancreas Club 2011 are gathered and filed with the aim to give them a larger audience than they have had in their original abstract book. However, it is obvious that most of clinical fellows do not have time to read all the abstracts. For them I have made a "clinical highlight section" of 10 percent of all the pancreatic abstracts. If someone else should have done some collection of abstract, there should probably have been other selections, but as this is not the case, the editor's choices are the highlighted ones.The article as series I of clinical highlight section is present, and more series will be present in the following issues. If readers will remember some of the abstracts better after reading this "abstract of abstracts", it was worth the efforts - and without efforts there will be little progress.

Objective: To investigate the difference in the characteristics between patients with emphysematous pancreatitis (EP) who survived and those who died. Methods: PubMed search was performed to gather EP cases from March 1959 to February 2019. Forty-two articles with 58 EP cases were identified and met the study's inclusion criteria. The elderly were defined as individuals aged >65 years. Data on patients' demographics, clinical symptoms, laboratory results, treatments, outcomes, and mortality were collected and analyzed by chi-square test and Student's t-test. p-Value <.05 (2-tailed) was set as the significance level. Results: Forty-seven men and eleven women aged 61.3 ± 15.9 (mean ± standard deviation) years were included. The elderly accounted for 43.1% (n = 25) of cases. There were 20 mortality cases, and 38 cases survived, with an overall mortality rate of 34.5%. Sex, underlying diseases, etiologies, and laboratory results were not significantly related to mortality. Older age was significantly related to mortality (p = .001). The shock was more commonly seen in the mortality group (100%) than in the survival group (21%) (p < .001). In contrast, fever was less frequent in the mortality group than in the survival group (25 vs. 71%, p = .002). Conclusions: EP patients have a high mortality rate (34.5%). Older age, afebrile status, and presence of shock are associated with high mortality. To improve the survival of this aggressive group, a further prospective investigation involving a larger sample size is necessary.

The necrosis-fibrosis hypothesis describes a continuum between single attacks of acute pancreatitis (SAP), recurrent acute pancreatitis (RAP) and chronic pancreatitis (CP) with endocrine and exocrine pancreatic insufficiency. For prevention purposes we evaluated clinico-radiological parameters and pancreatic volumetry to compare SAP and RAP and provide prognostic relevance on short-term mortality, need for intervention and the hospitalization duration.

Acute pancreatitis (AP) is characterized by disturbances of pancreatic microcirculation. It remains unclear whether platelets contribute to these perfusion disturbances. The aim of our study was to investigate platelet activation and function in experimental AP. Acute pancreatitis was induced in rats: (1) control (n=18; Ringer's solution), (2) mild AP (n=18; cerulein), and (3) severe AP (n=18; glycodeoxycholic acid (GDOC)+cerulein). After 12 h, intravital microscopy was performed. Rhodamine-stained platelets were used to investigate velocity and endothelial adhesion in capillaries and venules. In addition, erythrocyte velocity and leukocyte adhesion were evaluated. Serum amylase, thromboxane A2, and histology were evaluated after 24 h in additional animals of each group. Results showed that 24 h after cerulein application, histology exhibited a mild AP, whereas GDOC induced severe necrotizing AP. Intravital microscopy showed significantly more platelet-endothelium interaction, reduced erythrocyte velocity, and increased leukocyte adherence in animals with AP compared to control animals. Thromboxane levels were significantly elevated in all AP animals and correlated with the extent of platelet activation and severity of AP. In conclusion, platelet activation plays an important role in acute, especially necrotizing, pancreatitis. Mainly temporary platelet-endothelium interaction is observed during mild AP, whereas severe AP is characterized by firm adhesion with consecutive coagulatory activation and perfusion failure.

We conducted a systematic review in order to summarize the available data on pancreatitis associated with viral hepatitis.

No abstract available