Showing papers on "Pancreatitis published in 2005"

Human pancreatic exocrine response to nutrients in health and disease.

Abstract: Optimal digestion and absorption of nutrients requires a complex interaction among motor and secretory functions of the gastrointestinal tract. Digestion of macronutrients is a prerequisite for absorption and occurs mostly via enzymatic hydrolysis. In this context, pancreatic enzymes, in particular lipase, amylase, trypsin, and chymotrypsin, play the most important role but several brush border enzymes as well as other pancreatic and extrapancreatic enzymes also participate in macronutrient digestion. The crucial importance of pancreatic exocrine function is reflected by the detrimental malabsorption in patients with untreated pancreatic exocrine insufficiency, which is a typical complication of, for example, chronic pancreatitis.1–4 Comprehensive knowledge about the physiological pancreatic exocrine response to normal diets and to individual food components and about alterations in pancreatic exocrine insufficiency is necessary to administer a pancreatic enzyme preparation which imitates physiological conditions closely. Although many efforts have been made to substitute for pancreatic exocrine insufficiency by specially designed pancreatic enzyme preparations, these still have several disadvantages compared with physiological enzyme secretion. In particular lipid absorption is not completely normalised in most patients.5 As a basis for a better understanding of pancreatic exocrine function in health and disease this review will first summarise literature data on pancreatic exocrine response to a normal diet and to administration of individual food components in healthy humans. The next chapter will focus on pancreatic responses to a normal diet and to administration of individual food components in patients with pancreatic diseases, in particular chronic pancreatitits, but also in patients with other pancreatic and non-pancreatic diseases which are associated with intraluminal lack of pancreatic enzymes, for instance coeliac disease and diabetes mellitus. Other evidence of pancreatic involvement and dysfunction in these diseases will also be discussed, particularly if sufficient data on endogenously stimulated pancreatic secretion are lacking. ### 2.1 Introduction The healthy human pancreas adopts …

Cystic pancreatic lesions: A simple imaging-based classification system for guiding management

Abstract: Cystic lesions of the pancreas are increasingly being recognized due to the widespread use of cross-sectional imaging. The initial evaluation of a pancreatic cyst should be directed toward exclusion of a pseudocyst. Patients with pseudocysts generally have a history of acute or chronic pancreatitis, whereas those with cystic tumors most often lack such a history. Several types of cystic lesions are encountered in the pancreas. Because of morphologic overlap at imaging, accurate characterization of these lesions can be difficult. Computed tomography and magnetic resonance imaging are excellent modalities for both initial detection and characterization of cystic pancreatic lesions. An imaging classification system for these lesions has been proposed that is based on the morphologic features of the lesion. This system can be helpful in characterizing lesions, narrowing the differential diagnosis, and making decisions regarding the treatment of affected patients. Endoscopic ultrasonography‐guided aspiration and biopsy is useful in cases that are indeterminate at cross-sectional imaging or that require observation. © RSNA, 2005

Drug-induced pancreatitis: an update.

Abstract: Background and Aims:Many frequently prescribed drugs are suspected to cause acute pancreatitis (AP). The goal of this paper is to bring to light the often occult but real problem of drug-induced pancreatitis (DIP).Methods:We searched the National Library of Medicine/Pubmed for reported cases of DIP

Management of acute pancreatitis: from surgery to interventional intensive care

Abstract: In recent years, treatment of severe acute pancreatitis has shifted away from early surgical treatment to aggressive intensive care. While the treatment is conservative in the early phase, surgery might be considered in the later phase of the disease. Surgical debridement is still the “gold standard” for treatment of infected pancreatic and peripancreatic necrosis. Advances in radiological imaging, new developments in interventional radiology, and other minimal access interventions have revolutionised the management of many surgical conditions over the past decades. Several interventional therapy regimens, including endoscopic retrograde cholangiopancreatography (ERCP) and sphincterotomy, fine needle aspiration for bacteriology (FNAB), percutaneous or endoscopic drainage of peripancreatic fluid collections, pseudocysts, and late abscesses, as well as selective angiography and catheter directed embolisation of acute pancreatitis associated bleeding complications have been well established as diagnostic and therapeutic standards in the management of acute pancreatitis. Secondary to recent technical improvements in interventional therapy and minimally invasive surgery, even infected pancreatic necrosis has successfully been treated in selected patients. However, technical feasibility does not obviate sound clinical judgement. We must be cautious in the application of new technologies in the absence of well designed clinical trials. Thus minimally invasive surgery and interventional therapy for infected necrosis should be limited to clinical trials and specific indications in patients who are critically ill and otherwise unfit for conventional surgery. The management of acute pancreatitis has been controversial over the past decades, varying between a conservative medical approach on the one hand and an aggressive surgical approach on the other. There has been great improvement in knowledge of the natural course and pathophysiology of acute pancreatitis over the past decade.1–4 The clinical course of acute pancreatitis varies from a mild transitory form to a severe necrotising disease. Most episodes of acute pancreatitis (80%) are mild and self limiting, …

Cholelithiasis and cholecystitis.

Abstract: Gallstone disease remains one of the most common medical problems leading to surgical intervention. Every year, approximately 500,000 cholecystectomies are performed in the US. Cholelithiasis affects approximately 10% of the adult population in the United States. It has been well demonstrated that the presence of gallstones increases with age. An estimated 20% of adults over 40 years of age and 30% of those over age 70 have biliary calculi. During the reproductive years, the female-to-male ratio is about 4:1, with the sex discrepancy narrowing in the older population to near equality. The risk factors predisposing to gallstone formation include obesity, diabetes mellitus, estrogen and pregnancy, hemolytic diseases, and cirrhosis. A study of the natural history of cholelithiasis demonstrates that approximately 35% of patients initially diagnosed with having, but not treated for, gallstones later developed complications or recurrent symptoms leading to cholecystectomy. During the last two decades, the general principles of gallstone management have not notably changed. However, methods of treatment have been dramatically altered. Today, laparoscopic cholecystectomy, laparoscopic common bile duct exploration, and endoscopic retrograde management of common bile duct (CBD) stones play important roles in the treatment of gallstones. These technological advances in the management of biliary tract disease are not infrequently accomplished by a multidisciplinary team of physicians, including surgeons trained in laparoscopic techniques, interventional gastroenterologists, and interventional radiologists. With the evolution of laparoscopic cholecystectomy, there has been a global reeducation and retraining program of surgeons. However, the treatment of choice for gallstones remains cholecystectomy. In recognition of the revolutionary advances in the treatment of cholelithiasis, it is the purpose of this collective review to describe recent information on the following topics: types of gallstones, asymptomatic gallstones, symptomatic gallstones, chronic cholecystitis, acute cholecystitis, and other complications of gallstones. Gross and compositional analysis of gallstones allows them to be classified as cholesterol, mixed, and pigment gallstones. When asymptomatic gallstones are detected during the evaluation of a patient, a prophylactic cholecystectomy is normally not indicated because of several factors. Only about 30% of patients with asymptomatic cholelithiasis will warrant surgery during their lifetime, suggesting that cholelithiasis can be a relatively benign condition in some people. However, there are certain factors that predict a more serious course in patients with asymptomatic gallstones and warrant a prophylactic cholecystectomy when they are present. These factors include patients with large (>2.5 cm) gallstones, patients with congenital hemolytic anemia or nonfunctioning gallbladders, or during bariatric surgery or colectomy. Epigastric and right upper quadrant pain occurring 30-60 minutes after meals is frequently associated with gallstone disease. The diagnosis of chronic cholecystitis is made by the presence of biliary colic with evidence of gallstones on an imaging study. Ultrasonography is the diagnostic test of choice, being 90-95% sensitive. The surgical literature suggests that 3-10% of patients undergoing cholecystectomy will have CBD stones. Intraoperative laparoscopic ultrasonography has recently replaced cholangiography as the method of choice for detecting CBD stones. Ultrasonography and radionuclide cholescintigraphy (HIDA scan) are useful in establishing a diagnosis of acute cholecystitis. Laparoscopic cholecystectomy should also be used in the treatment of acute cholecystitis. Laparoscopic cholecystectomy is more likely to be successful when performed within 3 days of the onset of symptoms. It is important to remember that gallstones can lead to a variety of other complications including choledocholithiasis, gallstone ileus, and acute gallstone pancreatitis.

Cigarette smoking accelerates progression of alcoholic chronic pancreatitis

Abstract: Background: Smoking is a recognised risk factor for pancreatic cancer and has been associated with chronic pancreatitis and also with type II diabetes. Aims: The aim of this study was to investigate the effect of tobacco on the age of diagnosis of pancreatitis and progression of disease, as measured by the appearance of calcification and diabetes. Patients: We used data from a retrospective cohort of 934 patients with chronic alcoholic pancreatitis where information on smoking was available, who were diagnosed and followed in clinical centres in five countries. Methods: We compared age at diagnosis of pancreatitis in smokers versus non-smokers, and used the Cox proportional hazards model to evaluate the effects of tobacco on the development of calcification and diabetes, after adjustment for age, sex, centre, and alcohol consumption. Results: The diagnosis of pancreatitis was made, on average, 4.7 years earlier in smokers than in non-smokers (p = 0.001). Tobacco smoking increased significantly the risk of pancreatic calcifications (hazard ratio (HR) 4.9 (95% confidence interval (CI) 2.3–10.5) for smokers v non-smokers) and to a lesser extent the risk of diabetes (HR 2.3 (95% CI 1.2–4.2)) during the course of pancreatitis. Conclusions: In this study, tobacco smoking was associated with earlier diagnosis of chronic alcoholic pancreatitis and with the appearance of calcifications and diabetes, independent of alcohol consumption.

Role of hydrogen sulfide in acute pancreatitis and associated lung injury

Abstract: Hydrogen sulfide (H2S) is a naturally occurring gas with potent vasodilator activity. Cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS) utilize L-cysteine as substrate to form H2S. Of these two enzymes, cystathionine-gamma-lyase (CSE) is believed to be the key enzyme that forms H2S in the cardiovascular system. Whilst H2S has been reported to relax precontracted rat arteries in vitro and to lower blood pressure in the rat, its effect in an inflammatory condition such as acute pancreatitis has not previously been reported. In this paper, we report the presence of H2S synthesizing enzyme activity and CSE (as determined by mRNA signal) in the pancreas. Also, prophylactic, as well as therapeutic, treatment with the CSE inhibitor, DL-propargylglycine (PAG), significantly reduced the severity of caerulein-induced pancreatitis and associated lung injury, as determined by 1) hyperamylasemia [plasma amylase (U/L) (control, 1204+/-59); prophylactic treatment: placebo, 10635+/-305; PAG, 7904+/-495; therapeutic treatment: placebo, 10427+/-470; PAG, 7811+/-428; P<0.05 PAG c.f. placebo; n=24 animals in each group]; 2) neutrophil sequestration in the pancreas [pancreatic myeloperoxidase oxidase (MPO) activity (fold increase over control) (prophylactic treatment: placebo, 5.78+/-0.63; PAG, 2.97+/-0.39; therapeutic treatment: placebo, 5.48+/-0.52; PAG, 3.03+/-0.47; P<0.05 PAG c.f. placebo; n=24 animals in each group)]; 3) pancreatic acinar cell injury/necrosis; 4) lung MPO activity (fold increase over control) [prophylactic treatment: placebo, 1.99+/-0.16; PAG, 1.34+/-0.14; therapeutic treatment: placebo, 2.03+/-0.12; PAG, 1.41+/-0.97; P<0.05 PAG c.f. placebo; n=24 animals in each group]; and 5) histological evidence of lung injury. These effects of CSE blockade suggest an important proinflammatory role of H2S in regulating the severity of pancreatitis and associated lung injury and raise the possibility that H2S may exert similar activity in other forms of inflammation.

Necrosectomy and postoperative local lavage in necrotizing pancreatitis.

Abstract: Necrosectomy with postoperative continuous local lavage was performed in a prospective study involving 95 patients with necrotizing pancreatitis. In the same period 567 patients with oedematous-interstitial pancreatitis were treated non-operatively with a hospital mortality rate of 0.7 per cent. In patients with necrotizing pancreatitis the median Ranson criteria score was 4.5 points; operation was required at a median of 7 days after the onset of symptoms because of non-response to conservative treatment. In all, 59 per cent of the patients (56 out of 95) developed extended intrapancreatic parenchymal necrosis, 70 per cent had ascites, and 66 per cent had intra- and extrapancreatic necrosis; 42 per cent of the patients had bacterial infection of the necrotic tissue. For lavage a median of 8 l/24 h of fluid were instilled postoperatively for 25 days (median). The lavage fluid showed high levels of immunoreactive trypsin, phospholipase A2, and endotoxin in the early postoperative period. Hospital mortality rate was 8.4 per cent. Necrosectomy and continuous postoperative lavage can achieve high survival rates in patients with necrotizing pancreatitis. Postoperative local lavage allows the continuous non-operative evacuation of biologically active compounds and devitalized tissue, and avoids damage to remaining vital exocrine and endocrine pancreatic tissue.

Pancreatic ischaemia in experimental acute pancreatitis: Mechanism, significance and therapy

Abstract: Much clinical and experimental evidence suggests that pancreatic ischaemia in the early phase of acute pancreatitis is important in the development of pancreatic necrosis. While depletion of intravascular volume has often been assumed to be the main circulatory defect, an additional disturbance of pancreatic microcirculation has been demonstrated experimentally. Possible contributory mechanisms include chemical-induced vasoconstriction, direct injury of vessel wall, intravascular coagulation and increased endothelial permeability resulting in pancreatic oedema, haemoconcentration and impaired venous drainage. Pancreatic ischaemia as a consequence of these local effects seems to be responsible for the transition of mild pancreatitis to parenchymal necrosis. In experimental models the beneficial effect of various drugs and of sympathetic blockade has been ascribed to an improvement in pancreatic perfusion. Although effective volume therapy is generally accepted as the mainstay of conservative treatment in acute pancreatitis, the efficacy of different fluid preparations is still controversial, and simple fluid resuscitation has not been shown to prevent the development of parenchymal necrosis. The specific impairment of pancreatic microcirculation cannot be prevented merely by replenishment of intravascular volume with crystalloids, albumin or plasma despite normalization of macrohaemodynamics. In contrast, partial replacement of blood by dextran preparations has been shown to increase pancreatic perfusion by improving blood fluidity. Isovolaemic haemodilution in conjunction with conventional fluid therapy may provide a new and effective means of protecting the pancreas from secondary injury due to the early ischaemic phase of acute pancreatitis.

Risk factors of pancreatic leakage after pancreaticoduodenectomy.

Abstract: AIM: To analyze the risk factors for pancreatic leakage after pancreaticoduodenectomy (PD) and to evaluate whether duct-to-mucosa pancreaticojejunostomy could reduce the risk of pancreatic leakage. METHODS: Sixty-two patients who underwent PD at our hospital between January 2000 and November 2003 were reviewed retrospectively. The primary diseases of the patients included pancreas cancer, ampullary cancer, bile duct cancer, islet cell cancer, duodenal cancer, chronic pancreatitis, pancreatic cystadenoma, and gastric cancer. Standard PD was performed for 25 cases, PD with extended lymphadenectomy for 27 cases, pylorus-preserving PD for 10 cases. A duct-to-mucosa pancreaticojejunostomy was performed for patients with a hard pancreas and a dilated pancreatic duct, and a traditional end-to-end invagination pancreaticojejunostomy for patients with a soft pancreas and a non-dilated duct. Patients were divided into two groups according to the incidence of postoperative pancreaticojejunal anastomotic leakage: 10 cases with leakage and 52 cases without leakage. Seven preoperative and six intraoperative risk factors with the potential to affect the incidence of pancreatic leakage were analyzed with SPSS10.0 software. Logistic regression was then used to determine the effect of multiple factors on pancreatic leakage. RESULTS: Of the 62 patients, 10 (16.13%) were identified as having pancreatic leakage after operation. Other major postoperative complications included delayed gastric emptying (eight patients), abdominal bleeding (four patients), abdominal abscess (three patients) and wound infection (two patients). The overall surgical morbidity was 43.5% (27/62). The hospital mortality in this series was 4.84% (3/62), and the mortality associated with pancreatic fistula was 10% (1/10). Sixteen cases underwent duct-to-mucosa pancreaticojejunostomy and 1 case (1/16, 6.25%) devel-oped postoperative pancreatic leakage, 46 cases underwent invagination pancreaticojejunostomy and 9 cases (9/46, 19.6%) developed postoperative pancreatic leakage. General risk factors including patient age, gender, history of jaundice, preoperative nutrition, pathological diagnosis and the length of postoperative stay were similar in the two groups. There was no statistical difference in the incidence of pancreatic leakage between the patients who received the prophylactic use of octreotide after surgery and the patients who did not undergo somatostatin therapy. Moreover, multivariate logistic regression analysis showed that none of the above factors seemed to be associated with pancreatic fistula. Two intraoperative risk factors, pancreatic duct size and texture of the remnant pancreas, were found to be significantly associated with pancreatic leakage. The incidence of pancreatic leakage was 4.88% in patients with a pancreatic duct size greater than or equal to 3 mm and was 38.1% in those with ducts smaller than 3 mm (P = 0.002). The pancreatic leakage rate was 2.94% in patients with a hard pancreas and was 32.1% in those with a soft pancreas (P = 0.004). Operative time, blood loss and type of resection were similar in the two patient groups. The incidence of pancreatic leakage was 6.25% (1/16) in patients with duct-to-mucosa anastomosis, and was 19.6% (9/46) in those with traditional invagination anastomosis. Although the difference of pancreatic leakage between the two groups was obvious, no statistical signific-ance was found. This may be due to the small number of patients with duct-to-mucosa anastomosis. By further analyzing with multivariate logistic regression, both pancreatic duct size and texture of the remnant pancreas were demonstrated to be independent risk factors (P = 0.007 and 0.017, OR = 11.87 and 15.45). Although anastomotic technique was not a significant factor, pancreatic leakage rate was much less in cases that underwent duct-to-mucosa pancreaticojejunostomy. CONCLUSION: Pancreatic duct size and texture of the remnant pancreas are risk factors influencing pancreatic leakage after PD. Duct-to-mucosa pancreaticojejunostomy, as a safe and useful anastomotic technique, can reduce pancreatic leakage rate after PD.

Serum concentrations of inflammatory mediators related to organ failure in patients with acute pancreatitis

Abstract: Leucocyte activation and proinflammatory cytokine release (tumour necrosis factor (TNF) and interleukin 6 (IL-6)) are thought to contribute to the induction of a systemic inflammatory response, an acute-phase response and multiple organ failure in patients with acute pancreatitis. The serum concentration of TNF, soluble TNF receptors (sTNFR55 and sTNFR75), IL-6 and C-reative protein (CRP) in 58 patients with acute pancreatitis was assessed during the first 2 days of admission. Thirty patients had mild disease and 28 severe disease, of whom 18 developed local pancreatic complications alone (Atlanta classification) and ten developed organ failure (a Goris score of 1 or more). TNF was detected in only 17 patients on the first day of admission, while soluble TNF receptors were detected in all patients and IL-6 in 34. On the first and second days of admission there was a progressive and significant (P < 0.03) increase in the median concentration of sTNFR55, sTNFR75 and IL-6 in patients eventually classified into those with mild disease, a local pancreatic complication alone, or organ failure. This pattern was also evident in CRP levels from the second but not the first day of admission. These findings suggest that proinflammatory cytokines or their soluble receptors may be more accurate early predictors of outcome than CRP, Moreover, markers of inflammation in the sera of patients with acute pancreatitis are highest in those who subsequently develop organ failure.

Acute pancreatitis: models, markers, and mediators.

Abstract: Acute pancreatitis has an incidence of approximately 40 cases per year per 100,000 adults. Although usually self-limiting, 10% to 20% of afflicted patients will progress to severe pancreatitis. The mortality rate among patients with severe pancreatitis may approach 30% when they progress to multisystem organ failure. The development of acute pancreatitis illustrates the requirement for understanding the basic mechanisms of disease progression to drive the exploration of therapeutic options. The pathogenesis of acute pancreatitis involves the interplay of local and systemic immune responses that are often difficult to characterize, particularly when results from animal models are used as a foundation for human trials. Experimental studies suggest that the prognosis for acute pancreatitis depends upon the degree of pancreatic necrosis and the intensity of multisystem organ failure generated by the systemic inflammatory response. This suggests an intricate balance between localized tissue damage with proinflammatory cytokine production and a systemic, anti-inflammatory response that restricts the inappropriate movement of proinflammatory agents into the circulation. The critical players of this interaction include the proinflammatory cytokines IL-1β, TNF-a, IL-6, IL-8, and platelet activating factor (PAF). The anti-inflammatory cytokines IL-10, as well as TNF-soluble receptors and IL-1 receptor antagonist, have also been shown to be intimately involved in the inflammatory response to acute pancreatitis. Other compounds implicated in disease pathogenesis in experimental models include complement, bradykinin, nitric oxide, reactive oxygen intermediates, substance P, and higher polyamines. Several of these mediators have been documented to be present at increased concentrations in the plasma of patients with severe, acute pancreatitis. Preclinical work has shown that some of these mediators are markers for disease activity, whereas other inflammatory components may actually drive the disease process as important mediators. Implication of such mediators suggests that interruption or blunting of an inappropriate immune response has the potential to improve outcome. Although the manipulations of specific mediators in animal models may be promising, they may not transition well to the human clinical setting. However, continued reliance on experimental animal models of acute pancreatitis may be necessary to determine the underlying causes of disease. Full understanding of these basic mechanisms involves determining not only which mediators are present, but also closely documenting the kinetics of their appearance. Measurement of the inflammatory response may also serve to identify diagnostic markers for the presence of acute pancreatitis and provide insight into prognosis. Understanding the models, documenting the markers, and deciphering the mediators have the potential to improve treatment of acute pancreatitis.

Deficiency of UBR1, a ubiquitin ligase of the N-end rule pathway, causes pancreatic dysfunction, malformations and mental retardation (Johanson-Blizzard syndrome).

Abstract: Johanson-Blizzard syndrome (OMIM 243800) is an autosomal recessive disorder that includes congenital exocrine pancreatic insufficiency, multiple malformations such as nasal wing aplasia, and frequent mental retardation. We mapped the disease-associated locus to chromosome 15q14-21.1 and identified mutations, mostly truncating ones, in the gene UBR1 in 12 unrelated families with Johanson-Blizzard syndrome. UBR1 encodes one of at least four functionally overlapping E3 ubiquitin ligases of the N-end rule pathway, a conserved proteolytic system whose substrates include proteins with destabilizing N-terminal residues. Pancreas of individuals with Johanson-Blizzard syndrome did not express UBR1 and had intrauterine-onset destructive pancreatitis. In addition, we found that Ubr1(-/-) mice, whose previously reported phenotypes include reduced weight and behavioral abnormalities, had an exocrine pancreatic insufficiency, with impaired stimulus-secretion coupling and increased susceptibility to pancreatic injury. Our findings indicate that deficiency of UBR1 perturbs the pancreas' acinar cells and other organs, presumably owing to metabolic stabilization of specific substrates of the N-end rule pathway.

Randomized, double-blind phase II trial of lexipafant, a platelet-activating factor antagonist, in human acute pancreatitis

Abstract: The aims of the study were to determine whether the platelet-activating factor antagonist Lexipafant could alter the clinical course and suppress the inflammatory response of human acute pancreatitis. In a double-blind, placebo-controlled study 83 patients were randomized to receive Lexipafant 60 mg intravenously for 3 days, or placebo. Clinical progression was assessed by daily Acute Physiology And Chronic Health Evaluation (APACHE) II score and organ failure score (OFS). The magnitude of the inflammatory response on days 1-5 was assessed by serial measurement of interleukin (IL) 8, IL-6, E-selectin, polymorphonuclear elastase-alpha1-antitrypsin (PMNE-alpha 1-AT), and C-reactive protein (CRP). At entry, patients receiving Lexipafant (n = 42) or placebo (n = 41) were matched for age and sex, aetiology, APACHE II score and OFS. The disease was classified as severe in 29 patients (APACHE II score eight or more). There was a significant reduction in the incidence of organ failure (P = 0.041) and in total OFS (P = 0.048) at the end of medication (72 h). During this time seven of 12 patients with severe acute pancreatitis who had Lexipafant recovered from an organ failure; only two of 11 with severe acute pancreatitis who had placebo recovered from an organ failure and two others developed new organ failure. Lexipafant treatment significantly reduced serum IL-8 (P = 0.038), and IL-6 declined on day 1. Plasma PMNE-alpha 1-AT complexes peaked on day 1; the gradual fall to baseline over 5 days observed in controls did not occur in patients given Lexipafant. No effect was observed on serum CRP. This study provides a rationale for further clinical trials with the potent PAF antagonist Lexipafant in human acute pancreatitis.

Efficacy of octreotide in the prevention of complications of elective pancreatic surgery

Abstract: A placebo-controlled double-blind multicentre study, with randomization into parallel groups, was performed to determine whether perioperative subcutaneous administration of octreotide 01 mg every 8 h reduces the rate of complications specifically related to pancreatic surgery In all, 252 patients were evaluated (153 men, 99 women; mean(sem) age 531(08) years) who had pancreatic or periampullary tumour or other duodenal disease (157 patients) or chronic pancreatitis (95) and were undergoing elective pancreatic resection (100 Whipple's procedure, 60 distal resection, 12 others), pancreaticojejunostomy (66) or enucleation of pancreatic lesions (14) The proportion of patients with complications was significantly lower in the group treated with octreotide than in the placebo group (156 versus 292 per cent, P = 001) Octreotide thus appears to reduce substantially the risk of complications related to elective pancreatic surgery Moreover, treatment acceptability was high

Biliary surgery in the same admission for gallstone‐associated acute pancreatitis

Abstract: The clinical course of 47 patients with gallstone-associated acute pancreatitis who had surgery during the same admission has been reviewed. In 37 patients, when the signs and symptoms of pancreatitis settled on conservative management, biliary tract surgery was safely performed during that admission without mortality. The 10 patients whose clinical condition failed to settle prior to surgery had a complicated hospital stay and a 50 per cent mortality. A revised prognostic factor grading system has been outlined in which the age factor is removed and serum transaminase levels are considered of prognostic significance only if greater than 200 u/l within 48 h of admission. This revised system gives a more accurate assessment of the severity of individual attacks of gallstone-associated acute pancreatitis.

Multicentre audit of death from acute pancreatitis

Abstract: A prospective audit of acute pancreatitis involving nine hospitals in the North-West Thames Region recruited 631 patients over 54 months. There were 57 deaths (9 per cent); a diagnosis had been reached in 50 patients (88 per cent) before death and in seven (12 per cent) at autopsy. Eighteen patients (32 per cent) died within the first week, usually as a result of multisystem organ failure (15 patients). Thirty-nine patients (68 per cent) died after the first week from complications related to infection (26 patients) co-morbid conditions (nine) or non-infective complications (four). Twenty-one patients (42 per cent) had been inadequately evaluated by Ranson's criteria, and only 22 (44 per cent) of 50 with a premortem diagnosis of pancreatitis had undergone computed tomography (CT). Fifteen of 26 patients who died from infection-related complications had CT and only nine underwent necrosectomy or surgical drainage. These data suggest that improved diagnosis, investigation and management of patients with acute pancreatitis is possible, and may result in improved clinical outcome.

Mesothelin Is Overexpressed in Pancreaticobiliary Adenocarcinomas but Not in Normal Pancreas and Chronic Pancreatitis

Abstract: Mesothelin, a cell surface glycoprotein present on normal mesothelial cells, has been reported to be expressed in pancreatic adenocarcinomas. We conducted this study to fully characterize mesothelin expression in surgically resected, formalin-fixed, paraffin-embedded tissue specimens of 18 pancreatic adenocarcinomas, 9 adenocarcinomas of the ampulla of Vater, 12 adenocarcinomas of the common bile duct, and 17 cases of chronic pancreatitis. Mesothelin immunostaining was performed using the antimesothelin monoclonal antibody 5B2. All 18 cases (100%) of pancreatic adenocarcinomas showed mesothelin expression, as did 8 (89%) of 9 cases of ampullar adenocarcinoma and all 12 cases (100%) of common bile duct adenocarcinoma. In all cases of pancreaticobiliary adenocarcinoma, the adjacent normal pancreas did not stain for mesothelin. Of 17 specimens of chronic pancreatitis, 16 were negative for mesothelin expression, and 1 case showed weak mesothelin staining of fewer than 5% of normal pancreatic ducts. Our results demonstrated mesothelin expression in the majority of pancreaticobiliary adenocarcinomas and no expression in normal pancreatic tissues and in chronic pancreatitis.

Pancreatic infection complicating acute pancreatitis

Abstract: Pancreatic infection is the leading cause of death from acute pancreatitis. Patients with severe necrotizing pancreatitis are most at risk. Early computed tomography and percutaneous fine-needle aspiration microbiology of areas of pancreatic necrosis enable early diagnosis. Pancreatic infection should be treated surgically, although sterile necrosis may be managed conservatively. The role of antimicrobial drugs is uncertain.

Randomized controlled multicentre study of the prevention of complications by octreotide in patients undergoing surgery for chronic pancreatitis

Abstract: A randomized double-blind placebo-controlled multicentre trial was carried out in 247 patients undergoing major elective surgery for chronic pancreatitis to clarify whether the perioperative application of octreotide prevents postoperative complications. Eleven complications were defined, including death, anastomotic leakage, pancreatic fistula, abscess, fluid collection, shock, sepsis, bleeding, pulmonary insufficiency, renal insufficiency and postoperative pancreatitis. A total of 124 patients underwent pancreatic head resection, 55 left resection, 61 pancreaticojejunostomy and seven had other procedures. The overall mortality rate was 1.2 per cent (octreotide group 1.6 per cent, placebo group 0.8 per cent [corrected] (P not significant)). The postoperative complication rate in the octreotide group was 16.4 per cent (20 of 122 patients) and in the placebo group 29.6 per cent (37 of 125) (P < 0.007). The perioperative application of octreotide substantially reduces the risk of postoperative complications in patients undergoing major pancreatic surgery for chronic pancreatitis.

Obesity: an important prognostic factor in acute pancreatitis

Abstract: Ninety-nine patients with acute pancreatitis in whom body mass index (BMI = weight (kg)/height2 (m2)) was measured were studied prospectively to determine the importance of obesity as a prognostic factor in this disease. Of 19 obese patients (BMI > or = 30 kg/m2), 12 developed severe pancreatitis; seven had abscesses, of whom five died, and two further patients died. In 80 non-obese patients, the incidence of severe pancreatitis (n = 5), abscess formation (n = 4) and death (n = 4) was significantly less (P = 0.0007). The mean(s.d.) BMI of 17 patients with severe acute pancreatitis was significantly higher than that in 82 patients with mild acute disease (31.2(5.6) versus 23.3(5.6) kg/m2, P < 0.001). As a single prognostic factor, obesity had a sensitivity of 63 per cent and a specificity of 95 per cent for predicting disease severity. When five obese women with gallstone pancreatitis were excluded, the sensitivity of obesity increased to 86 per cent. Severe pancreatitis occurred in all eight obese patients with disease of an alcoholic aetiology. These data suggest that increased fat deposits in the peripancreatic and retroperitoneal spaces in obese patients may increase the risk of peripancreatic fat necrosis, abscess and death. Consideration should be given to including obesity as a prognostic factor in acute pancreatitis.