摘要:

IntroductionMost cases of chronic pancreatitis are alcohol-related, but not all alcoholics develop pancreatitis.AimTo elucidate historical and biologic risk factors for this disease.MethodologyAlcoholic Japanese men (n = 132) consecutively admitted to the National Alcoholism Center over 24 months, including 54 with chronic pancreatitis (diagnosed by endoscopic retrograde cholangiopancreatography) and 78 without, were surveyed about drinking history, smoking, education, and marital status, and tested for amylase, glycosylated hemoglobin, body mass, alcohol and aldehyde dehydrogenase genotypes, and K-rasgene mutations in pancreatic juice.ResultsHigher risk for chronic pancreatitis was associated with drinking spirits rather than lower-alcohol beverages (odds ratio [OR], 2.58;p= 0.01). Daily ethanol consumption by those who drank spirits was greater than that among those who drank lower-alcohol beverages; however, no differences in either daily ethanol consumption or duration of drinking were observed between alcoholics with and without chronic pancreatitis. Postgastrectomy patients were at higher risk for chronic pancreatitis than unoperated comparison subjects (OR, 4.35,P< 0.05). Elevated glycosylated hemoglobin (OR, 4.62,p< 0.01), decreased amylase (OR 4.20,P<0.02), and low body mass (OR 1.89,P<0.1) were more frequent in alcoholics with chronic pancreatitis. K-rasgene mutations existed in 18.8% of alcoholics with chronic pancreatitis but in only 11.4% of those without the disorder. The frequencies of alcohol and aldehyde dehydrogenase genotypes in alcoholics with and without pancreatitis did not differ significantly.ConclusionOur study strongly suggested that spirits and partial gastrectomy increase the risk for chronic pancreatitis in male alcoholics.

ISSN:0885-3177    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

IntroductionCompared with traditional radiologic methods for the detection of cholelithiasis, early transient hypertransaminasemia had provided a useful prediction of biliary etiology in patients with acute pancreatitis.AimTo investigate whether this application remains valid in the modern era of imaging for microlithiasis.MethodologyThe biochemical detection (LFT) of cholelithiasis was based on an increase in serum alanine transaminase of ≥80 IU/L (normal range, 0–45 IU/L) within 24 hours of admission. We have taken the collective findings of abdominal ultrasound (USS), endoscopic ultrasound (EUS), and postmortem examination to represent the denominator for the diagnosis of cholelithiasis against which comparison with LFT was made.ResultsOf 68 patients with acute pancreatitis who were treated between October 2000 and December 2001, cholelithiasis was the etiological factor in 44 patients (65%). EUS detected microlithiasis in 5 of 10 patients examined. The etiology remained idiopathic in 3 patients (4.4%). The sensitivity, specificity, and positive and negative predictive values for USS were 86%, 100%, 100%, and 80% respectively; for LFT, they were 91%, 100%, 100%, and 86%; and for USS and LFT combined, they were 98%, 100%, 100%, and 96%, respectively.ConclusionsIn patients with acute pancreatitis, the biochemical analysis within 24 hours of admission provided a simple, rapid, and more accurate prediction of cholelithiasis than USS. The combination of LFT and USS detected or excluded a biliary etiology in almost all patients.

ISSN:0885-3177    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

IntroductionA diet containing a high amount of fat has been shown, in short-term studies, to increase the expression of pancreatic lipase and colipase.AimTo investigate the effects of long-term high-fat–feeding (113 days) on the mRNA expression of pancreatic lipase, colipase, pancreatic lipase-related proteins (1 and 2), and uncoupling proteins during the development of obesity and glucose intolerance.MethodologyMice were fed either a high-fat or standard diet and killed after 3, 13, 57, and 113 days. Brown and white adipose tissues from the pancreas were collected for mRNA extraction.ResultsThe high-fat–fed mice became obese and glucose-intolerant by 113 days. The high-fat diet increased lipase (p< 0.05) expression initially. At the end of the experiment, the lipase levels had decreased to the level of the control. Colipase levels did not change during the first 57 days of high-fat feeding but decreased below control levels by 113 days (p< 0.05). The high-fat diet increased brown adipose tissue uncoupling protein 1 (UCP1)(p< 0.005) expression but not the expression of uncoupling protein 2.ConclusionLong-term high-fat feeding, leading to glucose intolerance, occurs with a simultaneous decrease in the mRNA expression of pancreatic lipase and colipase and an increase in UCP1 expression.

ISSN:0885-3177    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

IntroductionStomach changes after major pancreatectomy (Px) are unclear. We previously reported that 90% Px increased stomach weight in rats similarly to endogenous hypergastrinemia by lansoprazole, a proton-pump inhibitor.AimTo investigate the role of endogenous gastrin in gastric hypertrophy after Px.MethodologyIn male Wistar rats, we compared the wet weight of the stomach and serum gastrin levels between normal (n = 10) or sham-operated controls (n = 10) and 90% partially pancreatectomized rats (n = 7). Then, using Northern blot analysis, we compared gene expression of gastrin, cholecystokinin-B (CCK-B) receptor, and somatostatin in the stomach among normal controls (n = 7), sham-operated rats (n = 7), and 90% partially pancreatectomized rats (n = 8). The samples were obtained on the third and seventh postoperative days (POD).ResultsWet weight of the stomach was significantly heavier in the Px rats than in the sham-operated controls (3.90 ± 0.12 mg/g vs 2.63 ± 0.07mg/g;p< 0.0001) on the 14th POD. Serum gastrin levels were also higher in the Px rats than in controls (161.4 ± 13.35 pg/mL vs 110.6 ± 5.67 pg/mL;p< 0.005) on the 14th POD. Gene expression of gastrin in the stomach on the 7th POD was significantly higher in the Px rats than in the sham-operated rats (p< 0.05), and gene expression of CCK-B receptor clearly increased in the Px rats on the 7th POD, when compared with that of controls (p< 0.05). Gastric somatostatin gene expression in both operated groups increased approximately twice as much as in normal controls after operation (p< 0.005). However, on the 7th POD, it returned to control levels only in Px rats and not in sham-operate rats (p< 0.05).ConclusionIncreased gene expression of gastrin and CCK-B receptor suggests that gastrin may act as a trophic factor on the stomach after partial Px. Moreover, the relative decrease in gastric somatostatin gene expression may also influence gastric hypertrophy after Px.

ISSN:0885-3177    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:0885-3177    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

IntroductionEffective triage of patients with acute pancreatitis is dependent on the ability to accurately predict a severe course. Predictors (e.g., APACHE II score of >8) have been tested against wide-ranging definitions of severity (prevalence, 15%–40%). To ensure uniformity in defining a severe course of acute pancreatitis, the Atlanta symposium of 1992 adopted all-encompassing criteria (local complications, systemic complications, need for surgery, or death).AimsTo assess the prevalence of each Atlanta criteria for severe acute pancreatitis and to determine the sensitivity, specificity, and positive and negative predictive values of the APACHE II score as a predictor of these criteria for severe acute pancreatitis.MethodologyWe reviewed records of patients admitted to the University of Cincinnati Medical Center (Cincinnati, OH, U.S.A.) between 1994 and 1998 with acute pancreatitis. Exclusion criteria included referral from an outside hospital, immunocompromised state, and chronic pancreatitis.ResultsSeventy-four consecutive patients met our inclusion criteria. Ten patients (13.5%) had a severe course. Seven patients developed only local complications. Three patients had systemic complications. Pancreatic surgical intervention was required in four patients. No deaths occurred. An APACHE II score of >8 exhibited 50% sensitivity and 69% specificity (positive predictive value, 20%; negative predictive value, 89%). All patients with systemic complications and two of seven patients with only local complications had an APACHE II score of >8.ConclusionsThe prevalence of severity among our nonreferred patients with acute pancreatitis was less than previously reported. The APACHE II scoring system exhibited reasonable sensitivity in predicting systemic complications and/or the need for surgery, with a low positive predictive value. This most certainly is a function of the low pretest probability of severe pancreatitis. Future studies attempting to identify predictive systems that triage patients in a more cost-effective manner should restrict their analysis to Atlanta criteria other than local complications.

ISSN:0885-3177    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

Introduction and aimsWe investigated coagulative disorders, particularly the role of the D-dimer, in acute pancreatitis where coagulation abnormalities related to disease severity are known to occur.MethodologyD-dimer levels in 30 patients with acute pancreatitis were evaluated; pancreatitis was mild and uncomplicated in 11 patients, accompanied by complications in 15, and severe in 4. We attempted to find a relationship between the D-dimer level and the antithrombin III level, prothrombin time, partial thromboplastin time, the C-reactive protein level, and results of routine laboratory tests.ResultsIn the 11 patients with uncomplicated pancreatitis, the D-dimer level increased about 1.5 times over the limit, while in the 15 patients with complications and the four patients with severe pancreatitis, the D-dimer level increased about seven times above the normal limit; this difference was highly significant (p< 0.0001). The rise in the D-dimer level was inversely related to albumin and calcium levels (p= 0.0001) and directly related to the C-reactive protein level, fibrinogen level and leukocyte count (p= 0.0001), prothrombin time (p= 0.006), partial thromboplastin time (p= 0.03), and acute abdominal collections and lung involvement (p= 0.0001). The increase appeared early on, lasting for the entire study and peaking on days 3–6.ConclusionsThe D-dimer is the expression of pancreatitis and the extension of systemic involvement; it may be considered a prominent link in the chain of events leading to severe disease.

ISSN:0885-3177    

出版商:OVID    

年代:2003

数据来源: OVID

ISSN:0885-3177    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

IntroductionAntibiotic treatment represents a cornerstone in the management of severe acute pancreatitis. However, different antibiotic substances are currently used. In this study, we analyzed penetration of cefepime into pancreatic tissue in two models of acute pancreatitis.Aims and MethodologyFollowing induction of acute pancreatitis, animals were treated with a single intravenous dose of cefepime (0.1 mg/g of body weight). At two different time points, blood and tissue samples were obtained for determination of cefepime concentration and microbiologic analysis.ResultsMean pancreatic tissue concentrations ± SEM 30 minutes after drug administration were significantly higher in animals with either mild acute pancreatitis (113 ± 22 mg/kg) or severe acute pancreatitis (75 ± 22 mg/kg) than in control animals (30 ± 6 mg/kg) (p< 0.005). The minimal inhibitory concentrations (MIC90) for organisms usually isolated from infected pancreatic necrosis vary between 0.05 and 8 mg/L, which is between nine and 1,500 times lower than the mean peak concentration found in necrotic pancreatic tissue. Seven hours 30 minutes after antibiotic administration, pancreatic cefepime concentrations were still above the MIC90in 100% and 83% of animals with mild and severe disease, respectively. The infection rate of pancreatic tissue was significantly lower after antibiotic treatment and was similar after imipenem/cilastatin or cefepime treatment.ConclusionBecause of its antibacterial coverage and proven tissue penetration in acute pancreatitis, cefepime should be studied in patients with severe acute pancreatitis.

ISSN:0885-3177    

出版商:OVID    

年代:2003

数据来源: OVID

摘要:

IntroductionThe pathogenesis of acute pancreatitis remains elusive. Sepsis and multiple organ failure continue to cause death (overall mortality rate, ≈10%) despite immense improvements in supportive, radiologic, and surgical therapy. The gut appears to play a key role in the development of these complications.AimTo critically review the evidence implicating the gut in the pathogenesis of acute pancreatitis.MethodsRelevant English-language literature or abstracts cited in the MEDLINE database were reviewed.Results and ConclusionGram-negative enteric organisms account for most infections of pancreatic necrosis and subsequent sepsis, which suggests the gut as a source. Intestinal permeability is increased early in patients with severe acute pancreatitis and correlates with endotoxemia, which suggests translocation as a possible mechanism. The pathogenesis of the deranged function of the gut mucosal barrier and the possible sites of increase in intestinal permeability are discussed. The gut also plays a role in priming neutrophils and the release of inflammatory cytokines, which initiate and propagate nearly all the detrimental consequences of severe inflammation and sepsis. Future research avenues and potential therapeutic measures that may restore and preserve gut barrier function are explored.

ISSN:0885-3177    

出版商:OVID    

年代:2003

数据来源: OVID