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H Friess

Publications and source records attributed to H Friess.

At least 235 records · Page 13Linked to original sources
PubMed1997

[Fundus rotation gastroplasty: fewer cervical suture failures after esophagectomy?].

Cervical leakage, occurring on average in 20-50% of the patients, is one of the major causes of morbidity following oesophagectomy for cancer. We report on a new technique of gastroplasty, namely fundus rotation gastroplasty which was used in 53 patients. There were 49 patients with oesophageal cancer and 4 with benign lesions. Hospital mortality was 5.7% (3/53) and the leakage rate 7.5% (4/53). The advantages of fundus rotation gastroplasty over conventional gastroplasty are the better blood supply and the greater length of the gastric tube. Controlled clinical trials will be necessary to confirm the advantages of fundus rotation gastroplasty versus conventional gastroplasty.

Adult↗
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

Absence of K-ras mutations in the pancreatic parenchyma of patients with chronic pancreatitis.

BACKGROUND: Human pancreatic cancers exhibit a high frequency of K-ras mutations. METHODS: In this study we used oligonucleotide specific hybridization to compare the frequency of K-ras mutations in genomic DNA samples prepared from 21 normal pancreatic tissues, 26 chronic pancreatitis tissues, and 24 pancreatic cancers. RESULTS: None of the DNA samples from normal or chronic pancreatitis tissues exhibited a K-ras mutation at codons 12 or 13 of K-ras. In contrast, 17 of 24 DNA pancreatic cancers harbored a K-ras mutation. Validity of the methodology was confirmed by genotyping 7 human pancreatic cancer cell lines. Analysis of focal areas of proliferation from 5 chronic pancreatitis and 5 pancreatic cancer samples processed by selective ultraviolet radiation fractionation (SURF), a procedure used to enrich DNA isolation from foci of proliferating cells, revealed complete concordance with total genomic DNA analysis. CONCLUSIONS: These findings indicate that the pancreatic parenchyma in patients with chronic pancreatitis most frequently does not possess a K-ras mutation.

Adolescent↗
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

Cytotoxic cells are activated in cellular infiltrates of alcoholic chronic pancreatitis.

BACKGROUND & AIMS: Perforin messenger RNA (mRNA) expression has been shown to be a specific in vivo activation marker for cytotoxic cells. In this study, the contribution of cell-mediated cytotoxicity in the pathogenesis of alcoholic chronic pancreatitis is assessed. METHODS: Tissue sections of patients with alcoholic chronic pancreatitis were analyzed for perforin mRNA expression by in situ hybridization. In a further step, the phenotype and the relative frequency of perforin mRNA-expressing cells were determined. RESULTS: In the normal pancreas, perforin mRNA-expressing cells are rarely present (mean, 0.3 cells/mm2). In contrast, the frequency of perforin mRNA-expressing cells is increased severalfold in diseased tissue specimens (mean, 6.6 cells/mm2). The frequency of perforin mRNA-expressing cells is high in the CD56+ (18%) and CD8+ cell population (12%) but low in the CD4+ cell population (1%). CONCLUSIONS: The significantly elevated frequencies of perforin mRNA-expressing cells in the pancreas of patients with alcoholic chronic pancreatitis suggest an involvement of cell-mediated cytotoxicity in the pathogenesis of this disease. The preferential localization of these activated cells close to areas with parenchyma provides circumstantial evidence that autoreactive cytotoxic cells may contribute to tissue destruction in alcoholic chronic pancreatitis.

Cell Separation↗
PubMed1997

Localization of cholecystokinin A and cholecystokinin B-gastrin receptors in the human stomach.

BACKGROUND & AIMS: Gastrin and cholecystokinin (CCK) are gut-brain peptides, with multiple functions in the gastrointestinal tract mediated through CCK-B-gastrin and CCK-A receptors. The receptor localization is, however, not well established in humans. The aim of this study was to investigate the distribution and pharmacological characteristics of CCK-A and CCK-B receptors in the human upper gastrointestinal tract and compare them with those in the rat and dog. METHODS: CCK receptors were localized by in vitro receptor autoradiography with 125I-[Leu15]gastrin-I and 125I-[D-Tyr-Gly, Nle(28,31)]-CCK 26-33 in stomach and gallbladder. RESULTS: High concentrations of CCK-B-gastrin receptors were detected in the midglandular region of the human fundic mucosa. CCK-A receptors were found in the basal region of the antral and fundic mucosa. CCK-A receptors were also located in the muscularis propria of antrum, fundus, and gallbladder, whereas CCK-B-gastrin receptors were only detected in gastric fundic circular muscle. Two nonpeptide CCK receptor antagonists distinguish both receptor subtypes. Comparisons among humans, dogs, and rats suggest that localization and density of CCK receptor subtypes in the upper gastrointestinal tract are species-dependent. CONCLUSIONS: Localization of CCK receptor subtypes in human upper gastrointestinal tract provides a biochemical and morphological basis for the separate regulatory roles of gastrin and CCK.

Animals↗
PubMed1997

Enhanced urokinase plasminogen activation in chronic pancreatitis suggests a role in its pathogenesis.

BACKGROUND & AIMS: Urokinase plasminogen activator (uPA) regulates plasmin generation from plasminogen. The aim of this study was to analyze the role of the plasminogen activator/plasmin system in chronic pancreatitis (CP). METHODS: Using Northern blot analysis, in situ hybridization, and immunohistochemistry, the expression of uPA, its receptor (uPAR), plasminogen activator inhibitor 1 (PAI-1), and transforming growth factor beta 1 (TGF-beta 1) was studied in 14 patients undergoing pancreatic resection for CP. Normal control pancreatic tissue was obtained through an organ donor program. RESULTS: Eight of 14 CP samples showed concomitant increased expression (P < 0.001) of uPA (5.2-fold), uPAR (5.9-fold), and TGF-beta 1 (8.8-fold) messenger RNA (mRNA) compared with normal controls. PAI-1 mRNA expression was increased (6.5-fold; P < 0.001) in all CP samples. By in situ hybridization, moderate to strong mRNA staining of all four factors was present in acinar cells, some ductal cells, and areas with ductal metaplasia in CP samples. A similar staining pattern was found by immunohistochemistry. Intense mRNA and immunostaining for all of these factors in CP samples was associated with a higher degree of pancreatic damage. CONCLUSIONS: uPA and its receptor may contribute to the lytic damage observed in CP by plasmin generation. Similarly, increased amounts of plasmin may activate latent TGF-beta, thereby leading to the accumulation of fibrotic tissue.

Adolescent↗
PubMed1997

Presence of two signaling TGF-beta receptors in human pancreatic cancer correlates with advanced tumor stage.

Transforming growth factor-beta (TGF-beta) signal transduction is mediated via specific cell surface signaling TGF-beta receptors, most notably the type I ALK5 (TbetaR-I[ALK5]) and the type II (TbetaR-II). We evaluated TbetaR-I(ALK5) and TbetaR-II expression in 41 human pancreatic cancer tissue samples and correlated these findings with clinical data of the patients. Northern blot analysis indicated that, in comparison with the normal pancreas, pancreatic adenocarcinomas exhibited 8.0-fold and 4.5-fold increases (P < 0.01), respectively, in mRNA levels encoding TbetaR-I(ALK5) and TbetaR-II. In situ hybridization showed that both TbetaR-I(ALK5) and TbetaR-II mRNA were highly expressed in the majority of pancreatic cancer cells. Immunohistochemical analysis of TbetaR-I(ALK5) and TbetaR-II revealed positive immunostaining in 73% and 56% of the tumors, respectively. Both receptors were concomitantly present in 54% of the pancreatic cancer samples. The presence of TbetaR-I(ALK5) or TbetaR-II and the concomitant presence of TbetaR-I(ALK5) and TbetaR-II in the cancer cells was associated with advanced tumor stage (P < 0.01). These findings show that in many human pancreatic cancers, increased levels of the two signaling TbetaRs are present. The presence of the signaling TbetaRs in advanced tumor stages indicates a role in disease progression.

Adenocarcinoma↗
PubMed1997

Enhanced expression of urokinase plasminogen activator and its receptor in pancreatic carcinoma.

Urokinase plasminogen activator (uPA) is a serine proteinase that has been suggested to play an important role in cancer invasion and metastasis. It binds to a specific membrane receptor denominated uPA receptor (uPAR). uPA activates plasminogen to form plasmin, which participates in tissue degradation and proteolysis. Binding of uPA to its receptor accelerates UPA's own activation from pro-uPA, enhancing the activity of the uPA/uPAR cascade. Using immunohistochemistry and Northern blot analysis, we analysed the role of uPA and uPAR in 30 human pancreatic cancers. Immunohistochemical analysis demonstrated moderate to strong immunostaining of both factors in most pancreatic cancers. Cancer lesions with signs of invasion exhibited the strongest immunohistochemical signals for both factors. In addition, in desmoplastic areas adjacent to the cancer cells, moderate uPA and uPAR immunoreactivity was detectable. Northern blot analysis revealed a sixfold and a fourfold increase in uPA and uPAR mRNA levels in pancreatic cancer, respectively, in comparison with normal controls (P<0.01). Correlation of the Northern blot data with the clinical parameters of the patients indicated that patients with concomitant overexpression of uPA and uPAR had a shorter post-operative survival (median 9 months; mean+/-s.d. 10.2+/-3.6 months) than patients in whom only one or none of these factors were overexpressed (median 18 months; mean+/-s.d. 20.3+/-8.7 months) (P<0.002). Our data suggest that uPA and uPAR may serve as prognostic markers in human pancreatic cancer and that the marked overexpression of both factors may create an environment that enables pancreatic cancer cells to invade surrounding tissues.

Adolescent↗
PubMed1997

Increased expression of transforming growth factor beta s after acute oedematous pancreatitis in rats suggests a role in pancreatic repair.

BACKGROUND: Transforming growth factor beta isoforms (TGF beta s) belong to a family of multifunctional regulators of cellular growth and differentiation. They are mitogenic and chemotactic for fibroblasts and are potent stimulators of extracellular matrix production (collagen) and deposition. Upregulation of TGF beta transcription has been reported for several in vivo systems during repair after injury. AIMS: To study the expression of the three mammalian isoforms of TGF beta (TGF beta 1-3) and their relation to collagen expression as a marker for fibroblast response in acute oedematous pancreatitis in rats. METHODS: Using northern blot analysis and immunohistochemistry, the expression and localisation of TGF beta isoforms, collagen, and amylase were analysed during the course of acute oedematous pancreatitis in rats, experimentally induced by intravenous caerulein infusion. RESULTS: Induction of acute pancreatitis resulted in a biphasic peak pattern of expression of TGF beta 1, beta 2, and beta 3 mRNA, with a pronounced increase from day 1 to day 3 (sixfold, 2.5-fold, fivefold, respectively) and again from day 5 to day 7 (three-fold, 2.3-fold, 3.5-fold, respectively). The temporal changes in TGF beta mRNA identically paralleled the expression in collagen mRNA. In contrast, amylase mRNA expression, used as a general indicator of acinar cell integrity, was slightly decreased after induction of acute pancreatitis. Immunohistochemical analysis of pancreatitis tissue showed that increased expression of TGF beta s was mainly present in the pancreatic acinar and ductal cells; this was evident within one day after pancreatitis induction. CONCLUSION: Overexpression of TGF beta s after induction of acute pancreatitis suggests a role for these proteins in pancreatic repair and remodelling. The increased levels of TGF beta s may help suppress immune activation, and may contribute to the increase in the extracellular matrix including collagen and to the repair of the pancreatic parenchyma.

Acute Disease↗
PubMed1997

Molecular versus conventional markers in pancreatic cancer.

Diagnosing and monitoring pancreatic cancer is an ongoing challenge. Conventional markers such as tumor-associated antigens might be supplemented by molecular markers such as gene mutations and growth factor/growth factor receptor alterations in the future. Tumor-associated antigens can easily be measured by different EIA/ELISA systems, but the analysis of gene mutations, growth factors and their receptors requires advanced molecular techniques. CA 19-9 is the most widely used conventional marker for pancreatic cancer and is a useful tool in the diagnosis and follow-up of patients after tumor resection. Nonetheless, its role in detecting early pancreatic cancer is limited. The detection of K-ras and p53 mutations, which occur in about 90 and 50% of pancreatic cancers, respectively, in blood, stool, or bile samples, seems to be a promising approach in the diagnosis. Growth factor and growth factor receptor alterations are often associated with increased tumor aggressiveness and shorter survival following tumor resection. To date the analysis of growth factors/growth factor receptors in pancreatic cancer has not entered clinical use, but further molecular characterization of pancreatic cancer is necessary for earlier and more accurate diagnosis and it may result in new treatment options.

Biomarkers, Tumor↗
PubMed1997

ESPAC-1 trial progress report: the European randomized adjuvant study comparing radiochemotherapy, 6 months chemotherapy and combination therapy versus observation in pancreatic cancer.

At the joint International Association of Pancreatology and European Pancreatic Club meeting at King's College, London (July 9-12, 1997), a satellite meeting of the European Study Group for Pancreatic Cancer (ESPAC) met to discuss the progress of the ESPAC-1 trial. This study will address which, if any, of the following adjuvant treatments are of benefit in patients with resectable pancreatic cancer: radiotherapy (40 Gy with 5-fluorouracil as a sensitising agent); 6 months chemotherapy (5-fluorouracil and folinic acid), or a combination of these treatments. The study, which commenced in 1994, had already recruited 348 patients into the 3 treatment arms and 1 control arm of the study by May 31, 1997. This is the largest study of its kind in pancreatic cancer and should definitively address the question of the role of conventional methods of adjuvant treatment in pancreatic cancer.

Chemotherapy, Adjuvant↗
PubMed1997

First clinical experience with fundus rotation gastroplasty as a substitute for the oesophagus.

BACKGROUND: Leakage of oesophagogastric anastomosis has been associated with poor perfusion of the gastric tube. The authors recently developed a new form of gastroplasty, preserving not only the arterial arcade along the greater curvature, but also the lesser curvature. In this study their first clinical experience with that gastric tube is reported. METHODS: Thirty-five patients undergoing either oesophagectomy or laryngopharyngo-oesophagectomy for malignant lesions and substitution of the oesophagus with a funds rotation gastroplasty were included. Patient outcome, including anastomotic leak, hospital mortality and morbidity rates, were studied prospectively. RESULTS: Hospital mortality rate was one of 35 and anastomotic leak (one minor, one moderate) was found in two patients with no subsequent mortality. Further major morbidity included pulmonary dysfunction in the form of acute respiratory distress syndrome (ARDS) in seven patients. Mean (s.e.m.) hospital stay was 27(19) days, and 21(9) days in patients who did not develop ARDS. CONCLUSION: Fundus rotation is a new method of gastroplasty that allows safe anastomosis of the tube with the remaining oesophagus or pharynx and is associated with a low leak rate even at high cervical levels.

Adenocarcinoma↗
PubMed1997

[Efficacy and economic aspects of preoperative diagnosis: laparoscopy is useful in only 13% of patients with pancreatic carcinoma].

The value of diagnostic laparoscopy to improve tumor staging in patients with pancreatic and periampullary cancer is still a matter of controversial discussion, especially with regard to whether diagnostic laparoscopy can identify patients in whom a laparotomy can be avoided due to metastases. To answer this question, all patients who underwent operations for pancreatic cancer (n = 97) or periampullary cancer (n = 30) between 11/1993 and 12/1995 were evaluated. Only 10% of the patients with periampullary/pancreatic cancer and 13% with pancreatic cancer could avoid laparotomy through diagnostic laparoscopy. Due to these low numbers, a diagnostic laparotomy cannot be recommended in general in patients with pancreatic and/or periampullary cancer on economic grounds and because of the risk of trocar metastases.

Adult↗
PubMed1997

[Duodenum preserving resection of the head of the pancreas: a new standard operation in chronic pancreatitis].

Between 1972 and 1993, 298 patients with chronic pancreatitis underwent a duodenum-preserving pancreatic head resection (DPPHR). The early and late outcomes were prospectively analyzed. An operative mortality rate of 1%, a postoperative morbidity rate of 28.5% and a relaparotomy rate of 5.7% for the DPPHR were competitive with the rates for Whipple resection. After a median late follow-up of 6 years (range: 1 to 22 years), late mortality was 9%; 88% of the patients had no or infrequent episodes of pain and 63% were completely rehabilitated professionally. Only 6 patients developed diabetes mellitus early postoperatively. Our study proves that the duodenum-preserving pancreatic head resection provides better results than the Whipple resection. Therefore, this operation should be adopted as a new standard operation in patients with chronic pancreatitis.

Adult↗
PubMed1997

Enhanced expression of vascular endothelial growth factor in human pancreatic cancer correlates with local disease progression.

Vascular endothelial growth factor (VEGF) is an angiogenic polypeptide that has been implicated in cancer growth. In the present study, we characterized VEGF expression in cultured human pancreatic cancer cell lines and determined whether the presence VEGF in human pancreatic cancers is associated with enhanced neovascularization or altered clinicopathological characteristics. VEGF mRNA transcripts were present in all six tested cell lines (ASPC-1, CAPAN-1, MIA-PaCa-2, PANC-1, COLO-357, and T3M4). Immunoblotting with a highly specific anti-VEGF antibody revealed the presence of VEGF protein in all of the cell lines. Northern blot analysis of total RNA revealed a 5.2-fold increase in VEGF mRNA transcript in the cancer samples in comparison with the normal pancreas. Immunohistochemical and in situ hybridization analysis confirmed the expression of VEGF in the cancer cells within the tumor mass. Immunohistochemical analysis of 75 pancreatic cancer tissues revealed the presence of strong VEGF immunoreactivity in the cancer cells in 64% of the cancer tissues. The presence of VEGF in these cells was associated with increased blood vessel number, larger tumor size, and enhanced local spread but not with decreased patient survival. These findings indicate that VEGF is commonly overexpressed in human pancreatic cancers and that this factor may contribute to the angiogenic process and tumor growth in this disorder.

Adenocarcinoma↗
PubMed1996

KAI1 expression is up-regulated in early pancreatic cancer and decreased in the presence of metastases.

KAI1 is a metastasis suppressor gene for prostate cancer that is located on chromosome 11p11.2-13. Using Northern blot analysis and in situ hybridization, we studied expression of KAI1 mRNA in specimens from 14 normal pancreases and 27 primary pancreatic cancers, and then correlated the findings with the clinical and histopathological parameters of the patients. Northern blot analysis showed increased steady-state levels of KAI1 mRNA expression in 24 of 27 (89%) pancreatic cancer samples. In situ hybridization showed enhanced KAI1 mRNA levels in the pancreatic cancer cells in 82% cancer tissues. The stroma surrounding the cancer mass and normal pancreatic tissue adjacent to the cancer cells exhibited very low levels of KAI1 mRNA expression. Correlation of the mRNA levels obtained by Northern blot analysis with clinical parameters of the patients revealed that KAI1 mRNA levels were significantly higher (P < 0.01) in earlier tumor stages (I, II), compared with advanced tumor stages (III, IV) in which lymph node or distant metastases were present. Furthermore, poorly differentiated tumors had significantly higher KAI1 mRNA levels than those that were moderately or well differentiated (P < 0.05). No association between KAI1 expression and survival was found. Our results indicate that KAI1 mRNA expression is reduced in patients with advanced tumor stages. This suggests that reduction of KAI1 expression might enable pancreatic cancer cells to spread in lymph nodes and to distant organs.

Adult↗