Cocaine-Induced Acute Pancreatitis.
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ABSTRACT:
SUBMITTER: Strzepka J
PROVIDER: S-EPMC8500593 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background/Objectives: The pathogenesis of hyperglycemia during acute pancreatitis (AP) remains unknown due to inaccessibility of human tissues and lack of animal models. We aimed to develop an animal model to study the mechanisms of hyperglycemia and impaired glucose tolerance in AP.MethodsWe injected ferrets with intraperitoneal cerulein (50 μg/kg, 9 hourly injections) or saline. Blood samples were collected for glucose (0, 4, 8, 12, 24h); TNF-α, IL-6 (6h); amylase, lipase, insulin, glucagon, pancreatic polypeptide (PP), glucagon-like peptide-1 (GLP-1), and gastric inhibitory polypeptide (GIP) (24h). Animals underwent oral glucose tolerance test (OGTT), mixed meal tolerance test (MMTT) at 24h or 3 months, followed by harvesting pancreas for histopathology and immunostaining.ResultsCerulein-injected ferrets exhibited mild pancreatic edema, neutrophil infiltration, and elevations in serum amylase, lipase, TNF-α, IL-6, consistent with AP. Plasma glucose was significantly higher in ferrets with AP at all time points. Plasma glucagon, GLP-1 and PP were significantly higher in cerulein-injected animals, while plasma insulin was significantly lower compared to controls. OGTT and MMTT showed abnormal glycemic responses with higher area under the curve. The hypoglycemic response to insulin injection was completely lost, suggestive of insulin resistance. OGTT showed low plasma insulin; MMTT confirmed low insulin and GIP; abnormal OGTT and MMTT responses returned to normal 3 months after cerulein injection.ConclusionsAcute cerulein injection causes mild acute pancreatitis in ferrets and hyperglycemia related to transient islet cell dysfunction and insulin resistance. The ferret cerulein model may contribute to the understanding of hyperglycemia in acute pancreatitis.
| S-EPMC8355067 | biostudies-literature
Project description:Background and aimsDrugs are considered a relatively rare and understudied cause of acute pancreatitis (AP). The lack of convincing and conclusive data on drug-induced AP (DIAP) complicates the diagnosis as well as the identification of the causative drug. The aim of this study is to document causes of DIAP cases that occurred in the Saguenay-Lac-Saint-Jean (SLSJ) population.MethodsWe have conducted a retrospective and descriptive population-based study of DIAP cases that occurred between 2006 and 2014 in the six hospitals serving the entire SLSJ population. Cases were selected from the Quebec Ministry of Health hospitalizations registry (MED-ECHO) administrative public database. A medical chart review was performed in an attempt to characterize DIAP hospitalizations and to identify the imputable drugs.ResultsDuring the studied period, 75 cases (30.7% male, 69.3% female) were included totaling 90 hospitalizations for DIAP. Among them, 50 causative drugs were identified and were distributed in 17 different drug classes. Recurrent DIAPs were documented in 13 cases, and among them, 6 cases have experimented a positive rechallenge. Six drugs (5-fluorouracil, atorvastatin, bortezomib, nilotinib, rosuvastatin, and triamcinolone) were associated with the highest degree of evidence. The most common causative drugs of DIAP hospitalization were azathioprine (n = 7), followed by atorvastatin (n = 6), hydrochlorothiazide (n = 5), rosuvastatin (n = 4), and codeine (n = 4).ConclusionsThis study has added new evidences about potentially pancreatitis-associated drugs in literature. This is the first study to report definite 5-fluorouracil- and triamcinolone-induced AP. An updated version of the evidence-based literature review is needed to support the clinicians in the identification of the causative drugs.
| S-EPMC7655261 | biostudies-literature
Project description:There still is a lack of specific, early markers for acute pancreatitis. We used the gene expression profiling Affimetrix mouse gene 1.0 ST arrays (Affymetrix , Inc. Santa Clara, CA), to cmpare the gene expression between control mice and mice with induced experimental acute pancreatitis, in order to identify new potential biomarkers of acute pancreatitis.
2018-09-12 | GSE109227 | GEO
Project description:AimTo investigate the effect of Gardenia jasminoides (GJ) on cerulein-induced acute pancreatitis (AP) in mice.MethodsC57BL/6 mice weighing 18-20 g were divided into three groups. (1) Normal saline-treated group, (2) treatment with GJ at a dose of 0.1 g/kg, (3) treatment with GJ at a dose of 1 g/kg. GJ was administered orally (n = 6 per group) for 1 wk. Three hours later, the mice were given an intraperitoneal injection of cerulein (50 microg/kg), a stable cholecystokinin (CCK) analogue, every hour for a total of 6 h as described previously. The mice were sacrificed at 6 h after completion of cerulein injections. Blood samples were obtained to determine serum amylase, lipase and cytokine levels. The pancreas was rapidly removed for morphologic examination and scoring. A portion of pancreas was stored at -70 degree and prepared for the measurement of tissue myeloperoxidase (MPO) activity, an indicator of neutrophil sequestration, and for reverse-transcriptase PCR (RT-PCR) and real-time PCR measurements.ResultsTreatment with GJ decreased significantly the severity of pancreatitis and pancreatitis-associated lung injury. Treatment with GJ attenuated the severity of AP compared with saline-treated mice, as shown by reduction in pancreatic edema, neutrophil infiltration, serum amylase and lipase levels, serum cytokine levels, and mRNA expression of multiple inflammatory mediators.ConclusionThese results suggest that GJ attenuated the severity of AP as well as pancreatitis-associated lung injury.
| S-EPMC2761580 | biostudies-literature
Project description:To investigate the role of bone morphogenetic protein (BMP) signaling in acute pancreatitis (AP) by administration of noggin, an endogenous BMP antagonist, in a cerulein-induced AP model.Acute pancreatitis was induced by 9 hourly intraperitoneal injections of cerulein (50 ?g/kg). Control mice received phosphate-buffered saline injections. In a separate group, noggin (0.5 mg/kg) was given intraperitoneally at 1 hour before and 2, 4, and 6 hours after AP induction. The mice were euthanized at 1 hour after completion of AP induction. The blood samples and the pancreas were harvested for analysis. Isolated pancreatic acini from normal mice and AR42J cells were treated with BMP2 and cerulein. AR42J cells were also treated with noggin. Phosphorylation of Smad1/5/8 was measured.Bone morphogenetic protein signaling was up-regulated in AP mouse pancreas. Bone morphogenetic protein 2 and cerulein-induced phosphorylation of Smad1/5/8 in the acinar cells in vitro, which was blocked by noggin. Noggin administration in vivo attenuated AP induction, decreased vacuole formation in acinar cells, blocked LC3-II levels, and partially restored Beclin-1 and lysosomal-associated membrane protein 2 levels.Bone morphogenetic protein signaling seems to promote AP induction and autophagy, as suggested by our study showing that noggin ameliorates AP and partially restores autophagic homeostasis.
| S-EPMC3894737 | biostudies-literature
Project description:BackgroundAR42J are immortalized pancreatic adenocarcinoma cells that share similarities with pancreatic acinar cells. AR42J are often used as a cell-culture model of cerulein (CN)-induced acute pancreatitis (AP). Nevertheless, it is controversial how to treat AR42J for reliable induction of AP-like processes. Gene knockout and/or overexpression often remain challenging, as well. In this study, we demonstrate conditions for a reliable induction of proinflammatory markers upon CN treatment in AR42J and high transfection efficacy using Glyoxalase-I (Glo-I) as a target of interest.MethodsEffects of dexamethasone (dexa) and CN on cell morphology and amylase secretion were analyzed via ELISA of supernatant. IL-6, TNF-α and NF-κB-p65 were measured via qRT-PCR, ELISA and Western Blot (WB). Transfection efficacy was determined by WB, qRT-PCR and immune fluorescence of pEGFP-N1-Glo-I-Vector and Glo-I-siRNA.ResultsTreatment of AR42J with 100 nm dexa is mandatory for differentiation to an acinar-cell-like phenotype and amylase production. CN resulted in secretion of amylase but did not influence amylase production. High levels of CN-induced amylase secretion were detected between 3 and 24 hours of incubation. Treatment with LPS alone or in combination with CN did not influence amylase release compared to control or CN. CN treatment resulted in increased TNF-α production but not secretion and did not influence IL-6 mRNA. CN-induced stimulation of NF-κB was found to be highest on protein levels after 6h of incubation. Transient transfection was able to induce overexpression on protein and mRNA levels, with highest effect after 12 to 24 hours. Gene-knockdown was achieved by using 30 pmol of siRNA leading to effective reduction of protein levels after 72 hours. CN did not induce amylase secretion in AR42J cell passages beyond 35.ConclusionAR42J cells demonstrate a reliable in-vitro model of CN-induced AP but specific conditions are mandatory to obtain reproducible data.
| S-EPMC7833168 | biostudies-literature
Project description:Cerulein induced acute pancreatitis in C57Bl/6J
| PRJNA430220 | ENA
Project description:IntroductionAcute pancreatitis (AP) is a serious inflammatory condition of the pancreas. Hypertriglyceridemia (HTG) is considered an uncommon cause of AP. The current study aims to present a unique case of recurrent seasonal severe HTG-induced AP (HTG-AP); treated with insulin and heparin.Case reportA 36-year-old male presented with recurrent attacks of severe upper abdominal pain that was radiating to the back and associated with repeated vomiting. The condition has being occurring every autumn-winter for the last three years. He had thalassemia minor and had a history of HTG-AP. His TG levels were relatively normal from February to August; however, from September to February, his TG levels highly elevated which has resulted in HTG-AP every year for the past three years. The condition was confirmed via a contrast-enhanced computerized tomography scan of the abdomen. To prevent the next HTG-AP, his TG level was monitored monthly. When TG levels spiked again, the patient was put on an insulin infusion with heparin, glucose, and potassium to rapidly reduce TG level. After two days, serum TG was dramatically reduced (<500 mg/dL).DiscussionDespite multiple theories being proposed, the pathogenesis of HTG-AP is yet to be understood. Usually, HTG-AP is a single episodic, and recurrent HTG-AP is considered uncommon finding. Previous reports are contradictory regarding TG level and seasonal variation. There is currently no standard management approach to treat HTG-AP cases.ConclusionHTG-AP rarely reoccurs on an annual basis, and seasonal variation seems to play a major role in its onset. The condition can be managed with insulin, heparin, and glucose infusions.
| S-EPMC8977940 | biostudies-literature
Project description:ObjectivesWe aimed to evaluate the anti-inflammatory and inhibitory effects of Lithospermum erythrorhizon (LE) on cerulein-induced acute pancreatitis (AP) in a mouse model.MethodsAcute pancreatitis was induced via intraperitoneal injection of cerulein (50 μg/kg) every hour for 6 times. In the LE, water extract (100, 250, or 500 mg/kg) was administered intraperitoneally 1 hour before the first injection of cerulein. Six hours after AP, blood, the pancreas, and the lung were harvested for further examination. In addition, pancreatic acinar cells were isolated using a collagenase method, and then, we investigated the acinar cell viability and cytokine productions.ResultsTreatment with LE reduced pancreatic damage and AP-associated lung injury and attenuated the severity of AP, as evidenced by the reduction in neutrophil infiltration, serum amylase and lipase levels, trypsin activity, and proinflammatory cytokine expression. In addition, treatment with LE inhibited high mobility group box 1 expression in the pancreas during AP. In accordance with in vivo data, LE inhibited the cerulein-induced acinar cell death, cytokine productions, and high-mobility group box 1 expression. Furthermore, LE also inhibited the activation of p38 mitogen-activated protein kinases.ConclusionsThese results suggest that LE plays a protective role during the development of AP by inhibiting the activation of p38.
| S-EPMC4272226 | biostudies-literature
Project description:BackgroundThe differences in outcomes between acute biliary pancreatitis (ABP) and acute alcohol-induced pancreatitis (AAP) have not been well studied. We sought to examine the differences between ABP and AAP as regards to in-hospital outcomes and resource utilization, using a large nationwide database.MethodsWe queried the National Inpatient Sample databases 2016 and 2017 using the International Classification of Diseases, 10th revision, Clinical Modification (ICD-10-CM) coding system to identify the patients with a primary diagnosis of AAP and ABP. The primary outcome was all-cause in-hospital mortality. Secondary outcomes were hospital length of stay (LOS), hospitalization charge/cost, shock, acute kidney injury (AKI), intensive care unit (ICU) admission, and home discharge. Analysis was performed with STATA software.ResultsThere was no significant difference in mortality between patients with AAP and ABP (0.42% vs. 0.82%, adjusted odds ratio [aOR] 0.95, 95% confidence interval [CI] 0.69-1.31; P=0.79). Patients with ABP had a significantly longer LOS (+0.48 days, P<0.001). Patients with ABP had significantly higher adjusted mean hospitalization charges ($+19,958, P<0.001) and costs ($+4,848, P<0.001). Patients with ABP had a significantly lower likelihood of shock (aOR 0.75, 95%CI 0.59-0.95; P=0.02), AKI (aOR 0.76, 95%CI 0.71-0.82; P<0.001) or ICU admission (aOR 0.74, 95%CI 0.62-0.88; P=0.001). They were more likely to be discharged home (aOR 1.26, 95%CI 1.18-1.34; P<0.001).ConclusionAlthough there was no difference in all-cause mortality, patients with ABP had better hospitalization outcomes but greater resource utilization.
| S-EPMC7903563 | biostudies-literature