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Mechanistic studies of acute pancreatitis require animal models because clinical material is generally not available during the early phases of the disease. Here we describe a protocol to induce biliary pancreatitis by retrogradely infusing bile acids into the pancreatic duct of anesthetized mice. The resulting model replicates events believed to be responsible for the onset of clinical biliary (i.e., gallstone) pancreatitis and creates highly reproducible pancreatitis with a severity that depends on the concentration of infused bile acid. Pancreatitis reaches its maximal level of severity within 24 h of induction, and it resolves over the subsequent week. This protocol enables the investigator to use genetically modified strains of mice, and it requires only relatively simple and easily learned techniques of small animal surgery. With practice and gentle technique, the surgery (from induction of anesthesia to completion of the infusion) can be completed within 25 min per animal.

Objective:Most mechanistic studies of pancreatitis in mice employ the secretagogue-induced model. The currently reported studies were designed to develop an alternative, and possibly more clinically relevant, mouse model of pancreatitis.Design:Na-taurocholate (10–50 μl, 1–5%) in saline, or saline alone, was retrogradely infused into the mouse pancreatic duct. The animals were killed 6–24 hours later and the severity of pancreatitis in the pancreatic head and tail was examined by quantitating hyperamylasemia, pancreatic edema, acinar cell necrosis, and pancreatic inflammation. In addition, intrapancreatic activation of trypsinogen, generation of IL-6, intrapulmonary sequestration of neutrophils, and alterations in lung compliance were evaluated. The effects of Na-taurocholate on in-vitro acinar cell calcium transients, viability, and trypsinogen activation were examined.Results:Little or no evidence of pancreatitis was observed in mice infused with saline alone or in the tail of pancreata removed from animals infused with Na-taurocholate. In the head of the pancreas, evidence of pancreatitis was observed 12–24 hours after infusion of 20–50 μl 2–5% Na-taurocholate and the earliest morphological changes involved terminal duct and acinar cells. Intrapancreatic trypsin activity was transiently elevated within 5 minutes of Na-taurocholate infusion and pancreatic IL-6 levels were elevated 24 hours later. Under in-vitro conditions, Na-taurocholate triggered pathological acinar cell calcium transients, cell death, and calcium-dependent trypsinogen activation.Conclusion:This clinically relevant model of acute biliary pancreatitis yields reproducible results and its severity can be easily manipulated. It is ideally suited for use in mechanistic studies employing genetically modified mouse strains.

In 1788 Cawley reported on a “free living young man” who had died of emaciation and diabetes and whose postmortem examination revealed multiple pancreatic calculi. 1 In the two centuries since that early description of chronic pancreatitis, literally thousands of reports dealing with this disease have been published, yet chronic pancreatitis remains an enigmatic process of uncertain pathogenesis, unpredictable clinical course, and unclear treatment. Classification and Pathology Acute and chronic pancreatitis are distinguished from each other on the basis of structural and functional criteria. In acute pancreatitis, the gland is normal before the attack and can return to normal after resolution . . .

Accompagnateurs are trained to administer medications, monitor patients for complications or adverse reactions to medications, answer questions about medical conditions, and help patients seek medical care.5 These workers will need to be trained in diagnosing and monitoring complications of surgery and in administering basic wound care, and PIH and ZL will have to make a long-term commitment to \"accompanying\" patients who received injuries necessitating surgery.

ACUTE pancreatitis is usually distinguished from chronic pancreatitis by assessing whether the pancreas was normal in structure or function before the onset of the disease. 1 In the United States, chronic pancreatitis is most often associated with chronic alcohol abuse, whereas acute pancreatitis is usually associated with biliary tract stones. A number of studies, most notably that by Acosta and Ledesma, 2 have shown that attacks of \"gallstone pancreatitis\" occur when the stones become impacted in the terminal common bile duct or pass through the sphincter of Oddi into the duodenum. How stones that pass through or become lodged in the terminal . . .

Acute pancreatitis is an inflammatory disease, which varies in severity from mild to severe. Factors determining the severity of pancreatitis are not known. It is generally believed that the earliest events in the evolution of acute pancreatitis lead to premature intra-acinar cell activation of digestive zymogens and that those enzymes, once activated cause acinar cell injury. Recent studies have suggested that the ultimate severity of resulting pancreatitis may be determined by events which occur subsequent to acinar cell injury. These include inflammatory cell recruitment and activation as well as the generation and release of cytokines and other chemical mediators of inflammation. Recently, we have undertaken studies to elucidate the role of various inflammatory agents in determining the severity of pancreatitis. Results from these ongoing studies indicate that substance P acting via neurokinin-1 (NK1) receptors, chemokines interacting with CCR1 receptors and platelet activating factor play an important pro-inflammatory role in regulating the severity of pancreatitis and associated lung injury. On the other hand, complement factor 5a (C5a) acts as an anti-inflammatory agent during the development of pancreatitis.

In our view this seems insufficient evidence to recommend carbapenems as first-choice agents, given the availability of other agents with adequate pancreatic tissue penetration.4 UK guidelines for the management of acute pancreatitis are not conclusive with regard to choice of agent or duration of therapy. [...] with selective use (ie, only in patients with severe pancreatitis and using more appropriate antibiotics), the data suggested a benefit.1 Later, other prospective and randomised trials as well as meta-analyses showed a weak benefit, no benefit, or even disadvantage of antibiotic prophylaxis because antibiotics might induce bacterial resistance and favour fungal infections.2 However, the I international Association of Pancreatology clearly stated in 2002 that prophylaxis with broadspectrum antibiotics reduces infection rates in patients with pancreatic necrosis seen on CT, although survival is not modified.3 By contrast, a recent publication,4 not available when our paper was in press, included 100 patients with severe disease selected from 32 centres and showed no advantage in infection or mortality between patients receiving early antibiotic treatment or placebo.

The optimal preoperative evaluation of periampullary neoplasms remains controversial. The aim of this study was to analyze the accuracy of helical computed tomography (CT) and CT angiography with three-dimensional reconstruction in predicting resectability. Between March 1996 and May 1999, a total of 100 patients with periampullary neoplasms were prospectively staged by helical CT and CT angiography with three-dimensional reconstruction. Vascular involvement was graded from 0 to 4, with grade 0 representing no vascular involvement and grade 4 total encasement of either the superior mesenteric vein or artery. Patients with grade 4 lesions were considered unresectable. Sixty-eight patients underwent surgical exploration with intent to perform a pancreaticoduodenectomy. Forty-four lesions were grade 0, five were grade 1, eight were grade 2, and 11 were grade 3. Resectability for grades 0 to 3 was 96%, 100%, 50%, and 9%, respectively, for an overall resectability rate of 76%. Resectability in patients with vascular encroachment (grade 2) is usually determined by the extent of local disease rather than the presence of extrapancreatic disease. Resection is rarely possible in patients with evidence of vascular encasement (grade 3). Additional imaging modalities such as diagnostic laparoscopy are superfluous in patients with no evidence of local vascular involvement on CT angiography (grades 0 and 1) because of the high resectability rate and infrequency of unsuspected distant metastatic deposits.