Search PubMed⌕ Search

Biomedical subjects

H G Beger

Publications and source records attributed to H G Beger.

At least 73 records · Page 4Linked to original sources

Gallbladder carcinoma and surgical treatment.

Gallbladder carcinoma shows an unusual geographic and demographic distribution. It is relatively uncommon in Europe, but more frequent in Israel, Chile, Bolivia and in Southwestern Native Americans in the United States. Chronic cholecystitis, choledochal cysts, high body mass index, female gender, age, nicotine and industrial exposure to carcinogens are associated risk factors. The frequency of gallbladder cancer in all operations of the biliary tract is about 1-3%, reflecting the commonest biliary tract malignancy. Preoperative imaging, including ultrasound and computed tomography (CT), may reveal signs indicative of the presence of malignancy. However, most patients are not diagnosed prior to surgical intervention. Survival depends on the ability to achieve a curative resection, including hepatectomy and lymph node dissection in patients with local extended tumour according to the stage of the disease. Overall, the curative resection rates for gallbladder carcinoma range from 10% to 30%. Regional and para-aortic lymphadenectomy provides no survival benefit for patients with para-aortic disease, which has a negative influence on prognosis equivalent to that of distant metastases. A survival benefit is seen only in selected patients with metastases limited to the regional nodes. Taking a sample biopsy of the para-aortic nodes before starting surgery is recommended because these nodes are involved more frequently than expected. For those patients with unresectable cancer, palliative surgical, endoscopic or radiological bypass procedures can improve quality of life. Other approaches to the management of advanced tumours include systemic chemotherapy or combined chemo-radiotherapy and need further evaluation. Early-stage tumours are often discovered as an incidental finding during (laparoscopic) cholecystectomy or on histological examination of the gallbladder, mostly necessitating relaparotomy and extensive resection. In the following, management of patients with gallbladder cancer at different stages and situations is discussed.

Carcinoma↗

Short-bowel syndrome - surgical treatment with long-term benefit?

Survival and management of patients with irreversible intestinal failure has been made possible by the development of total parenteral nutrition (TPN). Despite the progress of TPN severe and even fatal complications might occur. Different non-surgical and surgical therapies can be employed to either improve intestinal function or restore enteral autonomy to obviate the need for TPN. A comprehensive review of the pertinent literature on different treatment modalities for short-bowel syndrome and our own experience are presented to judge long-term benefit and make recommendations on up-to-date surgical management.

Disease Management↗

Duodenum-preserving pancreatic head resection in patients with benign and borderline tumors of the pancreatic head.

BACKGROUND: Benign tumors of the pancreas are rare, accounting for only 1-2% of primary pancreatic lesions. Up to now, partial duodenopancreatectomy is still one of the established forms of treatment of benign tumors of the pancreas. We applied duodenum-preserving pancreatic head resection in 12 patients with benign pancreatic tumors to evaluate the feasibility, morbidity and recurrence rates after this less aggressive method. METHODS: Between April 1984 and December 1999, 12 patients with benign and borderline tumors of the pancreatic head were operated on by duodenum-preserving pancreatic head resection. RESULTS: All five patients with serous cystadenoma are free of recurrence 4.4 years after primary resection. One of two patients with mucinous cystadenoma and one of three patients with intraductal papillary mucinous tumor developed recurrent tumor within the former pancreatic head 5 years and 6 years, respectively, after the primary operation. Both patients were resected a second time. One of two patients with gastrinoma still has elevated serum gastrin levels. There was no hospital or long-term mortality. CONCLUSION: For a symptomatic serous cystadenoma, duodenum-preserving pancreatic head resection is a good alternative to partial duodenopancreatectomy. In borderline tumors with malignant potential, we would rather suggest a more radical duodenum-preserving segmental resection. A video clip (3 min) is attached demonstrating the basic steps of duodenum-preserving pancreatic head resection.

Adult↗

Is (18)F-fluorodeoxyglucose positron emission tomography in recurrent colorectal cancer a contribution to surgical decision making?

BACKGROUND: Accuracy of (18)F-fluorodeoxyglucose positron emission tomography (FDG-PET) and contribution to surgical decision making in recurrent or metastatic colorectal cancer were evaluated. METHODS: One hundred whole-body PET tests in colorectal cancer patients (1994 to 1998) were compared with computed tomography (CT), liver ultrasonography, and carcinoembryonic antigen (CEA) test. Mean follow-up was 12 months. RESULTS: Sensitivity, specificity, and accuracy of FDG-PET for malignant findings were, respectively, 98%, 90% and 95%; for 87 CT scans, 91%, 72%, and 82%; for 98 CEA tests, 76%, 90%, and 82%; for detection of liver metastases with PET, 100%, 99%, and 99%; and for 68 ultrasound tests, 87%, 96%, and 93%. PET accuracy for local recurrence was 96%. Additional information was provided by PET in 86% of cases (abdomen, thorax, liver). PET influenced surgical decisions in 61% of cases. CONCLUSION: FDG-PET adds relevant accuracy to the conventional staging of patients with colorectal cancer and may cost-effectively help to select the appropriate treatment.

Abdominal Neoplasms↗

Disturbed bile secretion and cytochrome P450 function during the acute state of experimental colitis in rats.

BACKGROUND/AIMS: A variety of hepatobiliary abnormalities has been described in patients with inflammatory bowel diseases. However, the pathophysiological mechanisms leading to these liver alterations are poorly understood. The aim of the present study was to investigate parameters of liver function in a trinitrobenzenesulfonic acid (TNB)-induced rat colitis model. METHODS: Glucose output, bile acid secretion, bile acid uptake, and the cytochrome P-450 metabolic capacity during TNB-colitis were studied in the perfused liver model. Furthermore, hepatic bile acid- and glycogen content was measured. To evaluate the inflammatory response in the colon and liver, NF-kappaB/Rel was quantified by electrophoretic mobility shift assays. As an NF-kappaB/Rel regulated gene the inducible NO-synthase (NOS2) was evaluated by Western blot analysis. As possible mediators released from the inflamed colon into the portal vein, endotoxin and the stable metabolite of prostaglandin I2 (6-keto-prostaglandin-F1alpha) were determined. RESULTS: Glucose output, bile acid secretion, bile acid uptake, and cytochrome P-450 metabolic capacity decreased on the first and second day of TNB-colitis. Hepatic bile acid content increased at day 14 of colitis. Glycogen content was reduced, most likely due to an inadequate chow intake of these animals. A low level of portal endotoxin was detectable during the first 2 days of colitis. In addition, 6-keto-prostaglandin-F1alpha was clearly increased in portal blood. NF-kappaB/Rel binding activity and inducible NOS2 were strongly positive in the colon during colitis. Although low levels of portal endotoxin were measured during the first 2 days of colitis, no significant NF-kappaB/Rel activity and NOS2 induction were detected in the liver. CONCLUSION: Our results indicate that during the acute state of the TNB-colitis, bile acid secretion and cytochrome P-450 function are disturbed in the absence of distinct inflammatory changes in the liver.

Animals↗

Effects of hepatocellular iron imbalance on nitric oxide and reactive oxygen intermediates production in a model of sepsis.

BACKGROUND/AIMS: In mammals iron homeostasis is most important, as imbalance of iron such as iron overload may lead to severe diseases. Recently, it has been shown that the iron regulatory protein-1 is partially controlled by nitric oxide and reactive oxygen intermediates, molecules frequently seen in inflammatory events. The aim of the present study was to investigate the effects of impaired iron homeostasis on the interaction of nitric oxide, and reactive oxygen intermediate formation in hepatocytes in a model of acute inflammation. METHODS: Hepatocytes isolated from Corynebacterium parvum (C parvum)-injected rats were used to examine the formation of nitrogen and oxygen intermediates by iron deprivation and iron overload in the presence of lipopolysaccharide. In addition, we investigated the RNA binding and aconitase activity of iron regulatory protein-1. RESULTS: In the present study we show that iron overload in lipopolysaccharide-treated C. parvum-primed hepatocytes downregulated the RNA binding of iron regulatory protein-1 and aconitase activity. Subsequently, we observed a reduced formation of nitrite/nitrate and S-nitrosothiols but an increased production of reactive oxygen species, and hepatocellular damage. Moreover, the addition of iron to cell cultures caused a further increase in cellular damage, a drop in the cellular glutathione pool, and an increase in peroxynitrite and hydroxyl-like radicals. In contrast, addition of deferoxamine (an iron chelator) to lipopolysaccharide-treated C. parvum-primed hepatocytes protected cells by stabilizing the GSH content, maintaining the nitric oxide formation, and by reducing Fenton oxidants. CONCLUSIONS: Our results show that the antioxidative effects of iron chelators prevent the formation of toxic Fenton oxidants in severe inflammatory events, which should be considered in the treatment of disorders characterized by an iron imbalance.

Animals↗

Pre-clinical evaluation of the activity of gemcitabine as a basis for regional chemotherapy of pancreatic and colorectal cancer.

AIMS: To estimate the potential activity of gemcitabine for hepatic arterial infusion (HAI) chemotherapy in pancreatic and colorectal cancer. METHODS: The anti-proliferative effects of gemcitabine were determined in MIA PaCa-2 and PMH2/89 pancreatic and HT29 and NMG64/84 colon cancer cell lines and in fresh tumours from patients with liver metastases of colon, rectal and pancreatic cancer in vitro using the human tumour colony forming assay. RESULTS: Gemcitabine showed concentration and time-dependent cytotoxic effects in all tested cell lines. The IC(50)of gemcitabine in MIA PaCa-2, PMH2/89, HT29 and NMG64/84 cells at 2 h exposure time were >100, 18, 100 and 2.5 microg/ml, respectively, at 4 h 15, 1.2, 45 and 0.5 microg/ml, respectively, and at 24 h 0.2, 0.1, 1.8 and 0.1 microg/ml, respectively. All tumours displayed concentration dependent inhibition of colony formation after exposure to gemcitabine for 2 h. The IC(50)values of gemcitabine in six of the 10 metastases were </=100 microg/ml. CONCLUSIONS: Based on our results and theoretical considerations regarding hepatic arterial infusion therapy gemcitabine seems to be suitable for HAI therapy phase II studies. Moreover, patients with colorectal or pancreatic tumours that demonstrated in vivo sensitivity may benefit from regional chemotherapy with gemcitabine.

Aged↗

[Stenting in chronic pancreatitis--the mistakes and limitations].

Endoscopic treatment of chronic pancreatitis using pancreatic duct stents was first described 15 years ago. Considering our own experience and the data of the literature we describe indications, contraindications, risks and limitations of the procedure and on the other hand its therapeutic effects. According to the actual experience an indication for pancreatic duct stenting can be seen in patients with a solitary prepapillary stenosis without stenosis of side branches or as success control for a planned surgical intervention. Contraindications are suspected malignancy, multiple pancreatic duct stenosis in the main duct or stenosis in small ducts and chronic calcifying pancreatitis with pancreatic duct stones. From 6/92 until 5/97 189 patients were operated for chronic pancreatitis in the Ulm University Hospital. Of these patients 35 (18.7%) were unsuccessfully treated preoperatively in other hospitals by pancreatic duct stent. Because of frequent complications like stent dislocation and stent occlusion repeated ERCPs (4.5/patient) and stent exchanges (3.7/patient) were performed. A therapeutical long-term benefit of pancreatic duct stenting is questionable, a definitive therapy can only be achieved in a small group of patients. However stent-induced changes of the pancreatic duct similar to chronic pancreatitis can be observed in up to 80% of all patients. Long-term observations of the reversibility of these stent-induced changes are missing, persisting chronic pancreatitis in the stented region is reported in animal models and in humans. The rates in the literature for stent dislocation and stent occlusion rate are 10-18% and 39-100% respectively. Induction of acute pancreatitis (up to 10%), duodenal reflux into the pancreatic duct, and bacterial infection with abscess formation are further severe and frequent complications of pancreatic duct stenting (1, 2). Lethal courses are reported (3, 4). Endoscopic pancreatic duct stenting in chronic pancreatitis at present is not indicated because of low success rate and a substantial risk of complications.

Animals↗

Frequency and time course of pancreatic and extrapancreatic bacterial infection in experimental acute pancreatitis in rats.

BACKGROUND: Infectious complications in severe pancreatitis are the main factors determining clinical course and outcome. The taurocholate model for acute necrotizing pancreatitis was evaluated for frequency and time course of pancreatic and extrapancreatic bacterial infection. METHODS: Sixty-five male Wistar rats were divided into 5 groups of 13 animals each. Specimens for bacteriologic examination were taken, and pancreatitis was induced by intraductal infusion of 3% taurocholate under sterile conditions. Animals were killed 8, 16, 24, or 32 hours thereafter, and bacteriologic examination was performed. A control group of animals with intraductal infusion of 0.9% saline solution were killed after 32 hours. RESULTS: There was no significant pancreatic infection in the control group and in the 8-hour group (1 of 13 rats). Sixteen and 24 hours after induction of pancreatitis, infection and inflammation of the pancreas were found in 77% (10 of 13 rats), and after 32 hours pancreatic infection occurred in 69% (9 of 13 rats). Extrapancreatic bacterial infection after 16 hours occurred in the liver (62%), spleen (62%), and mesenteric lymph nodes (46%). Bacteria infecting the pancreas reflected the bacterial spectrum of the large bowel and terminal ileum before induction of pancreatitis (Escherichia coli [77%], Proteus [43%], Enterococcus [37%], and Staphylococcus [23%]). CONCLUSIONS: Pancreatic infection is an early and frequent finding in the taurocholate model of acute necrotizing pancreatitis. Infection occurs between 8 and 16 hours after induction of pancreatitis. The source of infecting bacteria seems to be the large bowel or the terminal ileum. We present a useful model of severe pancreatitis in which to study bacterial translocation, the further route of spread, and therapeutic approaches.

Acute Disease↗

Single doses of FK506 and OKT3 reduce severity in early experimental acute pancreatitis.

OBJECTIVE: To find out if two immunomodulatory drugs used in organ transplantation (FK506 (tacrolimus) and OKT3 (Orthoclone) would reduce early inflammatory complications in experimental acute pancreatitis. DESIGN: Laboratory study. SETTING: University hospital, Germany. ANIMALS: 36 Balb/c mice. INTERVENTIONS: Pancreatitis induced by 7 intraperitoneal injections of cerulein 50 microg/kg at hourly intervals followed by FK506 0.32 mg/kg, OKT3 0.6 mg/kg, or 0.9% sodium chloride (controls) (n = 12 in each group). 12 hours after induction of pancreatitis the animals were killed. MAIN OUTCOME MEASURES: Serum amylase activity and interleukin-6 (IL-6) concentrations; histological damage to pancreas and lungs, apoptotic cells in pancreas; and myeloperoxidase activity in lungs. RESULTS: No animal died during the experiment. At 12h serum amylase activity and IL-6 concentrations were increased in all 3 groups, but highest in the OKT3 group. The pancreatic histological score, apoptosis, and inflammatory infiltration were lower in the two experimental groups than controls, but the degree of vacuolisation of acinar cells was similar. Packed cell volume was higher in the control than the experimental groups, and pulmonary damage and myeloperoxidase activity were less in the experimental groups than the controls. CONCLUSION: Single therapeutic doses of FK506 and OKT3 reduced the early severity of pancreatitis, pulmonary damage, and haemoconcentration in mice. Single doses of FK506 or OKT3 may therefore be effective in preventing the early complications of pancreatitis.

Acute Disease↗

Endotoxin and antiendotoxin antibodies in patients with acute pancreatitis.

OBJECTIVE: To elucidate the time course of endotoxaemia and antiendotoxin antibodies in patients with acute pancreatitis. DESIGN: Prospective clinical study. SETTING: University hospital, Germany. SUBJECTS: 25 patients with oedematous (n = 9) or necrotising (n = 16) pancreatitis, and 20 healthy controls. MAIN OUTCOME MEASURES: Concentrations of endotoxin and immunoglobulins (classes G, M, and A) directed at two lipid A molecules, four lipopolysaccharides, and alpha-haemolysin of Staphylococcus aureus measurements in plasma during a 12 day period. RESULTS: There were no differences in the degree of endotoxaemia between patients with oedematous and necrotising pancreatitis on admission. However, from the day after admission and throughout the observation period patients with necrotising pancreatitis had significantly higher concentrations of endotoxin than those with oedematous pancreatitis. Concentrations of IgM specific for endotoxin peaked at day 4, and then decreased in patients with oedematous pancreatitis while remaining high for those with necrotising pancreatitis. There was only a slight increase in IgA specific for endotoxin, and IgG and immunoglobulins to gamma-haemolysin remained steady throughout the observation period. There was strong cross-reactivity (r > 0.7) between IgM specific for endotoxin (70%), but this was less with IgA (52%), and IgG (20%). CONCLUSIONS: Necrotising pancreatitis is accompanied by persistent endotoxaemia with an extended rise in antiendotoxin antibodies. Patients with oedematous pancreatitis have a transient endotoxaemia with a temporary increase of Ig specific for endotoxin. Endotoxin stimulates the synthesis of specific antibodies (IgM) despite general immunosuppression.

Acute Disease↗

Pathophysiologic role of oxygen free radicals in acute pancreatitis: initiating event or mediator of tissue damage?

BACKGROUND AND OBJECTIVE: Oxidative stress is an important factor in the pathogenesis of acute pancreatitis, as shown in vivo by the beneficial effects of scavenger treatment and in vitro by the potential of free radicals to induce acinar cell damage. However, it is still unclear whether oxygen free radicals (OFR) act only as mediators of tissue damage or represent the initiating event in acute pancreatitis in vivo as well. In the present study the authors aimed to address this issue in an experimental set-up. MATERIALS AND METHODS: Two hundred male Wistar rats were randomly assigned to one of the following experimental groups. In two groups, acute necrotizing pancreatitis was induced by retrograde intraductal infusion of 3% sodium taurocholate. Through the abdominal aorta, a catheter was advanced to the origin of the celiac artery for continuous regional arterial (CRA) pretreatment with isotonic saline (NP-S group) or superoxide dismutase/catalase (NP-SOD/CAT group). In another group, oxidative stress was generated by CRA administration of xanthine oxidase and intravenous administration of hypoxanthine (HX/XOD group). Sham-operated rats received isotonic saline both arterially and intraductally. After observation periods of 5 and 30 minutes and 3 and 6 hours, the pancreas was removed for light microscopy and determination of reduced glutathione (GSH), oxidized glutathione (GSSG), conjugated dienes (CD), and malondialdehyde as a marker for OFR-induced lipid peroxidation as well as myeloperoxidase as a parameter for polymorphonuclear leukocyte accumulation. RESULTS: A significant decrease of GSH was paralleled by an increased ratio of GSSG per total glutathione and elevated CD levels after 5 minutes in the NP-S group versus the sham-operated group. Thereafter, the percentage of GSSG and GSH returned to normal levels until the 6-hour time point. After a temporary decrease after 30 minutes, CD levels increased again at 3 hours and were significantly higher at 6 hours in contrast to sham-operated rats. Myeloperoxidase levels were significantly elevated at 3 and 6 hours after pancreatitis induction. In contrast to NP-S rats, treatment with SOD/CAT significantly attenuated the changes in glutathione metabolism within the first 30 minutes and the increase of CDs after 6 hours. HX/XOD administration lead to changes in levels of GSH, GSSG, and CDs at 5 minutes as well as to increased myeloperoxidase levels at 3 hours; these changes were similar to those observed in NP-S rats. Acinar cell damage including necrosis was present after 5 minutes in both NP groups, but did not develop in HX/XOD rats. In addition, serum amylase and lipase levels did not increase in the latter group. SOD/CAT treatment significantly attenuated acinar cell damage and inflammatory infiltrate compared with NP-S animals during the later time intervals. CONCLUSION: OFRs are important mediators of tissue damage. However, extracellular OFR generation alone does not induce the typical enzymatic and morphologic changes of acute pancreatitis. Factors other than OFRs must be involved for triggering acute pancreatitis in vivo.

Animals↗

Fas and Fas-ligand expression in human pancreatic cancer.

OBJECTIVE: To investigate Fas and FasL expression in pancreatic tissues and cultured pancreatic cancer cell lines, and to assess the ability of anti-Fas antibodies to induce apoptosis. SUMMARY BACKGROUND DATA: Activation of the Fas receptor by Fas-ligand (FasL) results in apoptosis, and dysregulation of this pathway may contribute to abnormal cell proliferation. METHODS: Northern blotting and immunohistochemistry were used to compare Fas and FasL expression in normal and cancerous tissues. DNA 3'-OH end labeling was used to detect apoptotic cells. The effects of Fas activation on cell growth and signaling pathways were investigated in culture. RESULTS: Pancreatic cancers exhibited increased Fas RNA levels, whereas FasL mRNA levels were similar in both groups. Despite the colocalization of Fas and FasL in the cancer cells, an apoptotic signal was present in approximately 10% of these cells in only 2 of 16 cancer samples. Fas and FasL were coexpressed in all four cell lines, whereas Fas-associated phosphatase 1 was below the level of detection in all cell lines. Only COLO-357 cells underwent apoptosis after Fas activation. Apoptosis was associated with enhanced activation of jun kinase (JNK) and p38 mitogen-activated protein kinase (MAPK). In the presence of actinomycin D, Fas antibody also induced apoptosis in the other three cell lines. CONCLUSIONS: These results suggest that pancreatic cancer cells are resistant to Fas-mediated apoptosis by mechanisms excluding receptor downregulation or Fas-associated phosphatase upregulation and raise the possibility that Fas-mediated apoptosis may be dependent on the activation of the JNK/p38 MAPK pathway in these cells.

Adenocarcinoma↗

Serum amyloid A versus C-reactive protein in acute pancreatitis: clinical value of an alternative acute-phase reactant.

OBJECTIVES: The acute-phase reactant C-reactive protein (CRP) is currently the serum variable of choice for an early, accurate, and cost-effective severity assessment of acute pancreatitis in the daily clinical routine. Serum amyloid A (SAA) proteins comprise a family of apolipoproteins that constitute another major acute-phase reactant and thus could be a potential alternative to CRP assessment. In the present study we investigated the clinical usefulness of SAA determinations in acute pancreatitis using an automated immunoassay technique. DESIGN: Cohort study, comparing patients with complicated and mild acute pancreatitis; control groups included individuals with further abdominal disorders and healthy volunteers. SETTING: A collaborative study between the department of general surgery and the routine laboratory of the department of clinical chemistry/pathobiochemistry. PATIENTS: We enrolled 66 patients with acute pancreatitis in the present study. Control groups consisted of healthy subjects (n = 30), patients with chronic pancreatitis (n = 20), patients with pancreatic carcinoma (n = 20), and patients with acute appendicitis (n = 20). INTERVENTIONS: Blood samples were collected during 14 consecutive days in patients with acute pancreatitis. A single blood specimen was taken in all control groups after the diagnosis was established. MEASUREMENTS AND MAIN RESULTS: SAA concentrations were 3 mg/L (median; range, 3-93) in healthy subjects. Although SAA and CRP both reached their maximum within 4 days after onset of symptoms in patients with acute pancreatitis, SAA concentrations rose faster above normal ranges and reached 676 mg/L (median; range, 12-1880), higher than CRP, which reached 313 mg/L (median; range, 29-613). As observed for CRP, SAA was significantly higher in patients who developed complications such as necrosis, infection of necrosis, or multiple organ dysfunction syndrome or in patients who died. SAA achieved best results in discriminating between necrotizing pancreatitis and interstitial edematous pancreatitis. However, CRP provided an earlier differentiation between both entities and a significantly better overall accuracy, as shown by receiver operating characteristics analysis. SAA concentrations in patients with chronic pancreatitis were 6 mg/L (median; range, 3-756). In patients with pancreatic carcinoma, SAA concentrations were 7 mg/L (median; range, 3-492), and in patients with acute appendicitis, they were 50 mg/L (median; range, 3-2140). CONCLUSION: SAA is a nonspecific and rapidly produced variable in inflammatory abdominal disorders with a wider dynamic range than CRP. The current assay technique renders SAA an applicable and readily available variable under clinical routine conditions. In cases of acute pancreatitis, however, CRP is still superior to SAA for early and accurate stratification of patients with a complicated course.

Acute Disease↗

Association of endotoxemia and production of antibodies against endotoxins after multiple injuries.

BACKGROUND: Endotoxemia after injury has been a controversial issue. Endotoxins stimulate the innate and adaptive immune system. OBJECTIVE: To investigate endotoxemia and its effects on the production of antiendotoxin antibodies of cultured mononuclear cells of patients with multiple injuries. METHODS: Blood samples of 20 patients with multiple injuries were collected up to 12 days after trauma. The endotoxin concentration was measured in the plasma, and mononuclear cells were isolated and cultured. Specific antibodies against two lipopolysaccharides, one lipid A preparation, and alpha-hemolysin of Staphylococcus aureus were measured in the cell culture supernatant by an enzyme-linked immunosorbent assay. RESULTS: Endotoxemia peaked at admission of the patients, decreasing thereafter to almost normal values within 5 days. Isolated mononuclear cells synthesized antibodies against all tested antigens with a peak at or between day 5 and day 7. The increase was significant for immunoglobulin (Ig)A and IgM specific to all endotoxins tested and for IgA specific to alpha-hemolysin. However, there were no significant changes of the concentrations of total IgM, IgA, and IgG. All specific IgG remained unaffected. CONCLUSION: Patients with multiple injuries initially have temporary endotoxemia. Endotoxin may be suggested as a stimulator of the synthesis of antiendotoxin antibodies, in particular of the IgA and IgM class in patients with multiple injuries.

Adult↗

Values and limitations of 18F-fluorodeoxyglucose-positron-emission tomography with preoperative evaluation of patients with pancreatic masses.

The aim of this study was to determine the value and limitations of 18F-fluorodeoxyglucose (FDG)-position-emission tomography (PET) for differentiating benign and malignant pancreatic disease and for staging malignant disease. One hundred fifty-nine patients with 89 malignant and 70 benign pancreatic lesions all received PET, computed tomography (CT), and endoscopic retrograde cholangiopancreatography (ERCP) before pancreatic surgery. The original reports were compared for all patients (group I; N = 159), for a subgroup that neither had fasting plasma glucose levels > or =130 mg/dL or known elevated levels of C-reactive protein ([CRP], group II; n = 123), and for the remaining patients (group III; n = 36). For group I, accuracy values (areas under receiver operating characteristic [ROC] curves) for differentiation of benign/malignant masses were 0.86 (PET), 0.93 (ERCP), 0.82 (CT), and 0.95 for ERCP + PET (N = 159). For group II, ROC areas increased to 0.92 (PET), 0.94 (p < 0.05; n = 123) (ERCP), 0.82 (CT), 0.97 (p < 0.05; n = 123) (ERCP + PET). The results for group III were 0.71 (PET), 0.81 (CT), and 0.93 (ERCP); (n = 36). With 54 patients of group II that either had contradictory or indeterminate/technically unsuccessful CT/ERCP, PET was correct in 43 patients (84%). Sensitivity/specificity for lymph node staging was 49%/63%, respectively. For patients with hepatic metastasis, PET was 70% sensitive and 95% specific, missing some metastasis that were <1 cm. PET detected peritoneal metastasis in 25% of patients, missing poorly localized microscopic spread. For selected patients who have indeterminate pancreatic masses but no hyperglycemia or serologic evidence of active inflammation, FDG-PET is an independent functional assay that significantly adds to the diagnostic accuracy of ERCP and CT in the differentiation of benign and malignant pancreatic disease. PET can reliably detect hepatic, peritoneal, and other distant metastases that are > or =1 cm.

Area Under Curve↗