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H G Beger

Publications and source records attributed to H G Beger.

At least 199 records · Page 11Linked to original sources
PubMed1997

Celiac artery adjuvant chemotherapy. Results of a prospective trial.

CONCLUSION: Celiac artery infusion (CAI) seems to be a qualified and successful method for adjuvant treatment of pancreatic cancer. To improve the dismal prognosis of resected pancreatic cancer patients, we performed postoperative regional chemotherapy via the celiac axis. BACKGROUND: From 1994-1995, 20 patients with pancreatic cancer (18 ductal adenocarcinoma, 2 cystadenocarcinoma) received adjuvant celiac axis intra-arterial infusions (CAI) after resection of their tumors. Sixteen patients had macroscopically complete tumor removal (R0/R1 resection, 80% of the patients), whereas four patients had gross residual disease remaining after resection (R2 resection, 20% of the patients). Postoperative tumor stages were UICC I in 1 patient, UICC II in 3 patients, and UICC III in 16 patients. METHODS: CAI was performed for six postoperative cycles via catheters placed into the celiac artery using Seldinger's technique. The chemotherapeutic protocol consisted of mitoxantrone (Novantron), Wyeth-Lederle (Münster, Germany) 10 mg/m2 (d 1), folinic acid (Leucovorin, Wyeth-Lederle, or Rescuvolin, Medac, Hamburg, Germany) 170 mg/m2 for 10 min, followed by 5-FU (Fluoroblastin, Farmitalia, Freiburg, Germany) 600 mg/m2 for 120 min (d 2-4), and Cisplatin (Cisplatin-medac, Medac) 60 mg/m2 (d 5). The cycles were repeated after a rest period of 4 wk. Cisplatin infusions were accompanied by supportive antiemetic (8 mg Tropisetrone i.v. [Navoban, Sandoz, Nürnberg, Germany] and 8 mg Dexametason i.v.) and diuretic measures. RESULTS: Toxicity WHO III occurred in 8% of 100 cycles, and no toxic side effects WHO IV were encountered. The median survival of 21 mo in the treated group was nearly twice as long as the 9.3 mo of a historical matched control group (p < 0.0003). CAI seems to be a qualified and successful method for adjuvant treatment of pancreatic cancer.

Adult↗
PubMed1997

Multimodal therapies in ductal pancreatic cancer. The future.

CONCLUSIONS: Intra-arterial infusion chemotherapy via the celiac axis combined with external beam radiotherapy might be an effective method for palliative and perioperative multimodal treatment in pancreatic cancer. To improve the dismal prognosis in resectable and nonresectable pancreatic cancer, the results of multimodal palliative, adjuvant, and neoadjuvant therapies were reviewed and put into perspective with the results of two intra-arterial palliative and adjuvant treatment studies conducted at our department. The benefits and pitfalls of each method were outweighed, resulting in a concept for performing intra-arterial chemotherapy with radiotherapy in nonresectable stage UICC-III pancreatic cancer that eventually will be developed as a combined neoadjuvant/adjuvant treatment of all potentially resectable ductal pancreatic carcinomas.

Carcinoma, Ductal, Breast↗
PubMed1997

Inferior pancreaticoduodenal artery aneurysm as a consequence of traumatic acute pancreatitis. A case report and review of the literature.

Inferior pancreaticoduodenal artery (PDA) aneurysms are rare: To date, only 88 cases have been reported in the English literature. Although atherosclerosis represents the most common histological finding (60%), the pathogenetic mechanism consists usually of vessel erosion owing to acute or chronic pancreatitis. Most of these lesions are undetectable until symptoms of rupture occur. Rupture occurs typically in association with an episode of pancreatitis (60%) and caries a high mortality rate (50%), making diagnosis and early treatment essential. Angiography and computed tomography (CT) readily confirm the diagnosis. Ligation or resection of the aneurysm represents the definitive and radical therapy, but in an emergency, entails a high mortality rate (50%). Transcatheter embolization is a valid alternative to control bleeding (80%) in order to stabilize the patient; in some cases, it represents a definitive treatment. We present a case of an aneurysm that developed in a patient who had had posttraumatic acute pancreatitis. A surgical procedure with proximal and distal ligation of the aneurysm was performed successfully.

Acute Disease↗
PubMed1997

Pathological changes in pancreatic ducts from patients with chronic pancreatitis.

CONCLUSION: Chronic pancreatitis and restricted pancreatic outflow are accompanied by pathological changes in the ducts, including inflammation and alterations in the microvasculature. These changes and loss of epithelium provide a likely explanation for increased release of serum proteins, immunoglobulins, and lactoferrin into the juice, and the possibility of luminal contents entering the extracellular space and bloodstream. BACKGROUND: Enlargement of pancreatic ducts is a well-known phenomenon accompanying chronic pancreatitis and conditions restricting outflow of pancreatic juice. However, the relationship between ductal pathology and concomitant changes in the pancreatic juice is incompletely understood. METHODS: Segments of pancreatic ducts removed at surgery from patients with chronic pancreatitis and conditions restricting outflow were studied by light and electron microscopy to assess the pathological changes. RESULTS: Pathological changes in ducts from patients with chronic pancreatitis include chronic inflammation in the wall, enlarged and numerous capillaries packed with erythrocytes and leukocytes close to the lumen, and loss of epithelium and sometimes basement membrane. Plasma cells provide a source for increased immunoglobulins. Ducts from patients with diseases restricting outflow show significant pathology.

Case-Control Studies↗
PubMed1997

[Duodenum preserving resection of the head of the pancrease in therapy of pancreas divisum].

In 1-6% of the patients who are investigated by endoscopic retrograde cholangio-pancreatography a pancreas divisum can be found. In some patients pancreas divisum can lead to an acute relapsing and finally chronic pancreatitis (CP). Surgical intervention in these cases seems to offer a good chance of recovery. We report our experience with the duodenum-preserving resection of the head of the pancreas in 12 patients with pancreas divisum and CP. In all patients the preoperative evaluation showed clinical, functional or radiological signs of CP. The duodenum-preserving resection of the head of the pancreas was carried out in all patients without perioperative mortality. Ten postoperative versus eight preoperative patients showed a pathological exocrine function of the pancreas. Endocrine function, measured by the oral glucose tolerance test (OGTT), improved postoperatively in two patients. Eleven patients who were investigated after a mean follow-up time of 31 months (3-75 months) were completely pain free. No late mortality occurred. OGTT revealed a diabetic endocrine function in two patients. Disturbed exocrine pancreatic function had to be substituted in nine patients. One patient had to be reoperated by duct incision and renewal of the pancreatico-jejunostomy 10 months after the first operation. In conclusion, the duodenum-preserving resection of the head of the pancreas reduced pain in all patients with pancreas divisum and CP and may lead to an improvement of endocrine pancreatic function. Other, nonresecting procedures or endoscopic interventional therapy should be avoided in these patients.

Adult↗
PubMed1997

[Duodenum-preserving pancreatic head resection--a standard method in chronic pancreatitis].

In patients with chronic pancreatitis the inflammatory process in the pancreatic head is frequently the pacemaker of the disease. In these cases an inflammatory tumor develops which leads to local complications in half of the patients. Duodenum-preserving pancreatic head resection, contrary to procedures used in the past, offers the possibility to preserve stomach, duodenum, biliary tree, and the insulin secretory capacity. Duodenum-preserving pancreatic head resection is a subtotal resection of the pancreatic head. In a series of 380 patients the hospital mortality rate was 0.8%, the frequency of reoperation 5.3%, and the median hospitalisation time 13.9 days. The early postoperative glucose metabolism was deteriorated in 2% and improved in 9% of cases. After a median follow-up time of 6 years, 88% of the patients were completely painfree or suffered pain rarely. Sixty-three percent were gainfully employed; the late mortality was 8.9%. Only 10% of the patients had further bouts of pancreatitis. The decisive advantage of duodenum-preserving pancreatic head resection over Kausch-Whipple resection is preservation of the endocrine pancreatic function and of neighbouring organs.

Blood Glucose↗
PubMed1997

[Phospholipase A2--from basic research to clinical reality].

Phospholipase A2 (PLA2) is a group of secretory as well as intracellular enzymes that release phospholipids as an early step in inflammation and play a physiologic role in digestion. In humans, the group of secretory, low-molecular-weight PLA2 (sPLA2) is differentiated from the cytosolic, high-molecular-weight PLA2 (cPLA2). The two known cPLA2 mediate the intracellular response to inflammation by releasing arachidonic acid from membrane phospholipids. Secretory pancreatic PLA2 (sPLA2-I) is a digestive zymogen secreted from pancreatic acinar cells in its inactive form. Activated by trypsin in the duodenum, it is an important digestive enzyme. In acute pancreatitis, circulating sPLA2-I indicates pancreatic injury but is mostly inactive. Synovial-type secretory PLA2 (sPLA2-II), first isolated from synovial fluid of arthritis patients, is increased in inflammation, after surgery or trauma, and in various inflammatory diseases. Unlike sPLA2-I, its catalytic activity is held responsible for mediating the systemic inflammatory reaction and its complications by regulating the synthesis of prostaglandins, leukotrienes and platelet activating factor. Clinically, sPLA2-II offers new possibilities as an early marker for severe inflammation and predicting systemic complications in severely ill patients.

Acute Disease↗
PubMed1997

[Dynamic interstitial laser application for therapy of secondary liver tumors. An animal experiment study].

Laser-induced interstitial thermotherapy (LITT) is a promising method of treating different types of tumors. To increase the effectiveness of LITT, a new thermo-controlled application system for minimal invasive intervention was designed. This laser system consists of a laser applicator 3 mm in diameter, insertion equipment and an Nd:YAG laser source. The power of the laser source is controlled dynamically by thermosensors in a water-cooling system of the laser applicator. In in vivo experiments in five pigs, within 10 min we found homogeneous coagulation regions in the liver that were of 3 cm and 5 cm in diameter. Via ultrasound we observed in real time the increasing coagulation zone that appeared as a hyperechogenic halo. However, due to perifocal edema, the real coagulation area was smaller than detected by ultrasound. Macroscopically and microscopically, the coagulation zones showed well-demarcated borders of the coagulation lesions, and the surrounding tissue appeared vital. The reparative reaction after irradiation was early fibrosis. In the course of 4 weeks, the surrounding scar capsule, containing fibrocytes, biliary ductules and collagen fibers enlarged. As a result, the coagulation necrosis became more and more fragmented between collagen fibers and was largely resorbed. The absence of complications in our animal experiments suggest that the technique of thermo-controlled laser light application is safe and useful in therapy for metastases that are not resectable.

Animals↗
PubMed1997

Natural course of acute pancreatitis.

Acute pancreatitis comprises, in terms of clinical, pathologic, biochemical, and bacteriologic data, four entities. Interstitial edematous pancreatitis and necrotizing pancreatitis are the most frequent clinical manifestations; pancreatic pseudocyst and pancreatic abscess are late complications after necrotizing pancreatitis, developing after 3 to 5 weeks. Determinants of the natural course of acute pancreatitis are pancreatic parenchymal necrosis, extrapancreatic retroperitoneal fatty tissue necrosis, biologically active compounds in pancreatic ascites, and infection of necrosis. Early in the course of acute pancreatitis multiple organ failure is the consequence of various inflammatory mediators that are released from the inflammatory process and from activated leukocytes attracted by pancreatic injury. During the late course, starting the second week, local and systemic septic complications are dominant. Around 80% of deaths in acute pancreatitis are caused by septic complications. The infection of pancreatic necrosis occurs in 8% to 12% of acute pancreatitis and in 30% to 40% of patients with necrotizing pancreatitis. Bacteriologic analysis of intraoperative smears and aspirates reveals predominantly gram-negative germs deriving from the intestine, most frequently Escherichia coli. It has been confirmed that after necrotizing pancreatitis a considerable large group of patients suffer long-lasting exocrine and endocrine insufficiency.

Abscess↗
PubMed1997

Surgical treatment of infected necrosis.

Over the years, experience has shown that the cornerstone for improved survival in patients with infected pancreatic necrosis is an early, precise diagnosis followed by adequate drainage combined with modern intensive care management. In experienced hands, this goal can be achieved with different surgical approaches, provided that all septic collections are thoroughly removed and that reexploration is performed promptly if there is evidence of ongoing sepsis. If there is any concept preferable, and under what conditions, future large-scale randomized trials with precise and comparable patient stratification will have to demonstrate it.

Debridement↗
PubMed1997

Gastric emptying following pylorus-preserving Whipple and duodenum-preserving pancreatic head resection in patients with chronic pancreatitis.

BACKGROUND: After pylorus-preserving Whipple (PPW), delayed gastric emptying (DGE) is reported in up to 50% of these patients. We analyzed gastric emptying and hormonal adaptation of cholecystokinin (CCK), pancreatic polypeptide (PP), and gastrin following two surgical procedures for chronic pancreatitis (CP): the PPW and the duodenum-preserving pancreatic head resection (DPPHR). METHODS: Ten patients underwent DPPHR and 10 underwent PPW for CP. Preoperatively and 10 days and 6 months postoperatively, gastric emptying (paracetamol absorption test) and CCK, gastrin, and PP were measured using a test meal stimulation. RESULTS: The area under the serum paracetamol time curve for 0 to 120 minutes (AUC) showed no preoperative difference. Ten days postoperatively, the AUC was significantly reduced (P <0.05) after PPW but not after DPPHR. Six months postoperatively, AUC was comparable with the preoperative findings in DPPHR and PPW. The integrated 180-minute PP release was significantly reduced 10 days and 6 months postoperatively in both groups. The integrated 180-minute CCK release was decreased 10 days after PPW, but failed to be significant (P = 0.053). Gastrin levels were postoperatively unchanged. CONCLUSION: Following DPPHR we found no delay in gastric emptying. In contrast, DGE occurs early after PPW. Our data may help explain the slower recovery in PPW patients with regard to weight gain and relief from pain, which may be due to the functional alteration of gastric emptying and motility after this type of surgery.

Acetaminophen↗
PubMed1997

Immune cell infiltration and growth-associated protein 43 expression correlate with pain in chronic pancreatitis.

BACKGROUND & AIMS: Changes in innervation pattern and neuropeptide content have been shown in chronic pancreatitis (CP), including increased neuronal expression of growth-associated protein 43 (GAP-43). We used GAP-43 as an established marker of neuronal plasticity and correlated histological findings with pain scores of patients with CP. METHODS: In tissue samples from 29 patients with CP, the parenchyma-fibrosis ratio, degree of perineural immune cell infiltration, and neuronal GAP-43 immunoreactivity were determined by digitized morphometry and correlated with individual pain scores. RESULTS: In CP, GAP-43 was significantly increased in pancreatic nerve fibers and intrinsic neurons. GAP-43 expression correlated with individual pain scores. The infiltration of pancreatic nerves by immune cells was significantly correlated with the intensity of pain. Pain scores correlated neither with the degree of pancreatic fibrosis nor with the duration of the disease. CONCLUSIONS: The results suggest that infiltration of pancreatic nerves by immune cells and neuronal plasticity are pathogenic factors for the generation of pain, whereas the degree of pancreatic fibrosis has no major impact on pain in CP.

Adolescent↗
PubMed1997

Palliative and adjuvant regional chemotherapy in pancreatic cancer.

To improve the dismal prognosis of patients (pts) with pancreatic cancer we treated 32 patients with non-resectable (UICC III, 17 pts; UICC IV, 15 pts--group 1) and 20 patients with resected (UICC I, 1 pt; UICC II, 3 pts; UICC III, 16 pts--group 2) pancreatic cancer with palliative (group I) and adjuvant post-operative (group II) coeliac axis intra-arterial cyclic infusions (CAI). CAI consisted of mitoxantrone 10 mg/m2 on day 1, folinic acid 170 mg/m2 and 5-FU 600 mg/m2 during days 2-4, and cis-platinum 60 mg/m2 on day 5 for up to 11 (group I) or six (group II) cycles. In a total of 211 cycles toxicities at the level of WHO III occurred in 0-6% and of WHO IV in 0%. The median survival times, compared with institutional historical controls (treated vs controls), were 12 vs 4.8 months in UICC III (P < 0.006) and 4 vs 2.9 months in UICC IV (P < 0.05) group I pts, and 21 vs 9.3 months in group II (P < 0.0003). Hepatic disease progression appeared to be suppressed with CAI, which also appears to be effective for palliative and adjuvant treatment in non-resectable and resected pancreatic cancer.

Adult↗
PubMed1997

Nuclear accumulation of p53 correlates significantly with clinical features and inversely with the expression of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) in pancreatic cancer.

Recent studies have suggested a p53-independent expression of p21(WAF1/CIP1). We investigated the correlation between p53 overexpression and the expression of p21(WAF1/CIP1) in 57 patients with pancreatic adenocarcinoma. By means of reverse transcription and polymerase chain reaction (RT-PCR), we examined the mRNA levels of WAF1/CIP1 and compared them with the p53 status in 20 patients and in a further six pancreatic tumour cell lines. In pancreatic cancer tissues, immunohistological evaluation revealed a significant correlation between active p53 and p21(WAF1/CIP1) (P < 0.005) as well as WAF1/CIP1 mRNA expression (P < 0.005). This coherence was also evident in human pancreatic carcinoma cell lines. The analysis of p53 and p21(WAF1/CIP1) expression in relation to clinicopathological features revealed a significant correlation between p53 overexpression and tumour stage, tumour size, grading and lymph node metastases, whereas p21(WAF1/CIP1) expression correlated only with tumour size. We conclude that the expression of p21(WAF1/CIP1) normally depends on active p53, but that there may also exist p53-independent pathways of induction that reduce the correlation of p21(WAF1/CIP1) to clinicopathological features.

Adult↗
PubMed1997

Similar morphological and intracellular biochemical changes in alcoholic acute pancreatitis and ischemic acute pancreatitis in rats.

Pancreatic hyperstimulation with simultaneous duct obstruction does not cause the typical features of acute pancreatitis, therefore the role of an additional challenge, such as either ethanol intoxication or short-term ischemia, was studied. Alcoholic pancreatitis was induced in 28 rats by acute ethanol intoxication (0.25 LD50) and an obstruction/hyperstimulation mechanism (clip of the biliopancreatic duct for 20 min and intravenous stimulation with 5 U of cholecystokinin and secretin each). Ischemic pancreatitis was performed by obstruction/hyperstimulation and subsequent pancreatic ischemia by clamping the supplying arteries for 40 min. The macro- and microscopic alterations were evaluated and graded by a scoring system. Additionally, the pancreas was removed in 50% of the animals and the pancreatic acini were prepared. From those acini the intracellular enzymes trypsinogen, kallikreinogen, amylase, lipase, glucuronidase, and acidic phosphatases were determined. While obstruction/hyperstimulation, 40 min of ischemia, or ethanol alone did not induce acute pancreatitis, a combination of obstruction/hyperstimulation with either ethanol or ischemia resulted in acute pancreatitis in 68 and 60% of treated rats, respectively. Similarly, both models were characterized by extrapancreatic fat necrosis and acinar necrosis at the periphery of the lobules. Almost all intracellular enzymes were elevated in both pancreatitis models compared to sham-operated controls. Both alcohol and ischemia were insults that sensitize the pancreas to develop acute pancreatitis after obstruction/hyperstimulation. Since the observed morphologic and enzymatic alterations in both models are very similar, alcohol and ischemia might have some common pathways by which they make the pancreas vulnerable to enzymatic attacks.

Acute Disease↗
PubMed1997

Overexpression of intercellular adhesion molecule-1 (ICAM-1) in pancreatic adenocarcinoma in comparison with normal pancreas.

To elucidate the role of intercellular adhesion molecules (ICAMs), which has not been well understood in pancreas, we investigated the localization and expression of ICAM-1 by immunohistochemistry and in situ hybridization (ISH) in pancreatic adenocarcinoma and in normal pancreas. The localizations of ICAM-2 and ICAM-3 were also investigated by immunohistochemistry. In normal pancreas, acinar cells, duct epithelial cells, and Langerhans islet cells failed to stain with anti-ICAM-1, anti-ICAM-2, and anti-ICAM-3 antibodies. These cells showed no expression of ICAM-1 mRNA. On the other hand, various percentages of carcinoma cells were stained with anti-ICAM-1 antibody, while no carcinoma cells were stained with anti-ICAM-2 and anti-ICAM-3 antibodies. ICAM-1 mRNA expression was also observed in carcinoma cells, and ICAM-1 mRNA expression was associated with localization of the ICAM-1 protein. These results suggest that ICAM-1 expression is up-regulated in pancreatic adenocarcinoma cells and that ICAM-1 is involved in malignant processes in pancreas.

Adenocarcinoma↗
PubMed1997

Different changes in high-energy phosphates in alcoholic acute pancreatitis and taurocholate acute pancreatitis in rats using NMR spectroscopy at 2.0 T.

We studied the pancreatic high-energy phosphates in two models of acute pancreatitis using 31P nuclear magnetic resonance (NMR) in rats for the first time in vivo. Alcoholic pancreatitis was induced by acute ethanol intoxication and an obstruction-hyperstimulation mechanism. Taurocholate pancreatitis was generated by intraparenchymal administration of 1 ml of 1-10% taurocholate-Na+. In addition to the obligate control groups, a simple ischemia experiment was performed. The high-energy phosphates were monitored by 31P NMR spectroscopy at 2.0 T. Additionally, by means of a scoring system, the quality and quantity of pathomorphologic parameters were quantified after 24 h. 31P spectra acquired after injection of taurocholate showed an increase in inorganic phosphate with a concomitant decrease in ATP levels, similar to pancreatic ischemia. This irreversible decrease was accompanied histologically by severe pancreatic hemorrhage. After induction of alcoholic acute pancreatitis a reversible decrease in ATP was occasionally seen. Even when alcoholic pancreatitis had been fully established at 24 h, the 31P NMR spectrum was normal in all animals. In conclusion, depletion of high-energy phosphates seems to occur as a result of pancreatic cell death rather than being a cause of pancreatic necrosis. For the first time we applied in vivo NMR in the rat pancreas to study the time course in acute pancreatitis.

Acute Disease↗