Biomedical subjects

H Friess

Publications and source records attributed to H Friess.

At least 217 records · Page 12Linked to original sources

PubMed1998

CD8+CD103+ T cells analogous to intestinal intraepithelial lymphocytes infiltrate the pancreas in chronic pancreatitis.

OBJECTIVE: Chronic pancreatitis is a painful chronic inflammatory disease of the exocrine pancreas that is associated with the replacement of functional parenchyma by extended fibrosis and with a massive infiltration of T lymphocytes. However, to date further characterization of infiltrating T cells in chronic pancreatitis has not been undertaken. METHODS: Using the novel method of multiepitope imaging with fluorochrome-tagged specific monoclonal antibodies, which allows the simultaneous localization and characterization of T cells in tissues, we analyzed the distribution and phenotypes of T cells infiltrating the pancreas in chronic pancreatitis. RESULTS: The mean CD4:CD8 ratio in 10 cases of chronic pancreatitis was 2.4:1. In order of decreasing frequency, the following markers were observed: CD45RO, CD18, TCRgammadelta, and CD103. The lymphocytes, especially of the CD4+ subset, were found mainly in the fibrous stroma, but T cells were also observed periductally. A T-cell subset bearing the phenotype CD8+CD103+, analogous to intestinal intraepithelial lymphocytes, was found intracalating between the cells of the ductal epithelium. CONCLUSIONS: Phenotyping of the T lymphocytes in chronic pancreatitis supports the concept of the involvement of cell-mediated cytotoxicity in the pathogenesis of this disease. In addition, intraepithelial lymphocytes were found interspersed between the ductal epithelial cells, pointing to a role of this T-cell subset as a first-line defense against deleterious epithelial events in chronic pancreatitis.

Adolescent↗

PubMed1998

Neurotensin receptors: a new marker for human ductal pancreatic adenocarcinoma.

BACKGROUND/AIMS: New imaging possibilities for early diagnosis of the devastating exocrine pancreatic adenocarcinomas would be highly welcome. Recently, pancreatic neuroendocrine tumours have been successfully visualised in vivo on the basis of their high density of receptors for the regulatory peptide somatostatin. Unfortunately, exocrine pancreatic tumours do not express sufficient amounts of somatostatin receptors. Therefore over-expression of other regulatory peptide receptors in these tumours needs to be found. METHODS: Receptors for the regulatory peptide neurotensin were evaluated in vitro by receptor autoradiography in 24 ductal pancreatic adenocarcinomas, 20 endocrine pancreatic cancers, 18 cases of chronic pancreatitis, and 10 normal pancreatic glands. RESULTS: Some 75% of all ductal pancreatic adenocarcinomas, most of them differentiated, were neurotensin receptor positive, whereas endocrine pancreatic cancers did not express neurotensin receptors. No neurotensin receptors were found in chronic pancreatitis or normal pancreatic tissues, including pancreatic acini, ducts, and islets. CONCLUSIONS: The selective and high expression of neurotensin receptors in ductal pancreatic adenocarcinomas could form the molecular basis for potential clinical applications, such as in vivo neurotensin receptor scintigraphy for early tumour diagnosis, radiotherapy with radiolabelled neurotensin analogues, and chemotherapy with neurotensin receptor antagonists.

Adenocarcinoma↗

PubMed1998

bax, but not bcl-2, influences the prognosis of human pancreatic cancer.

BACKGROUND: bcl-2 and bax belong to the bcl-2-related gene family, which marks a new class of genes that influence apoptosis. The bcl-2 oncogene acts as a broad antiapoptotic factor and extends both normal and tumour cell survival. In contrast, the bax gene is a promoter of apoptosis. AIMS: To analyse the expression of bcl-2 and bax in pancreatic cancer and correlate the results with clinical parameters. PATIENTS: Pancreatic cancer tissue samples were obtained from 28 female and 32 male patients (median age 63, range 43-79 years) having surgery for pancreatic cancer. Normal pancreatic tissues obtained from 18 previously healthy organ donors served as controls. METHODS: The levels of bcl-2 and bax mRNA expression were analysed by northern blot and the exact site of mRNA transcription was determined by in situ hybridisation. The presence of the corresponding proteins was determined by immunohistochemistry. RESULTS: Northern blot analysis indicated that, in comparison with the normal pancreas, bcl-2 mRNA was overexpressed in 30% and bax mRNA in 61% of the pancreatic cancer samples. Concomitant overexpression of bcl-2 and bax was present in 26% of the cancer samples. Pancreatic adenocarcinomas exhibited 3.7-fold and 5.4-fold increases (p < 0.001) in bcl-2 and bax mRNA levels respectively. In situ hybridisation showed that both bcl-2 and bax mRNA were expressed in the cancer cells. Immunohistochemical analysis showed positive Bcl-2 and Bax immunostaining in 28 and 83% of the cancer samples respectively. In multivariate analysis (Cox regression model), bax expression was found to be a strong indicator of survival (p < 0.001). Patients whose tumours exhibited Bax immunostaining lived significantly longer (12 months) than those whose tumours were Bax negative (five months) (p < 0.039). In contrast, no relation was found between Bcl-2 and survival time. CONCLUSIONS: The data indicate that genes that are involved in the regulation of apoptosis are upregulated in human pancreatic cancer cells. Prolonged survival times in patients in whom apoptosis promoting factors are upregulated indicate that apoptotic pathways are of biological significance in pancreatic cancer.

Adolescent↗

PubMed1998

Influence of high-dose pancreatic enzyme treatment on pancreatic function in healthy volunteers.

CONCLUSIONS: Adaptive changes in exocrine and endocrine pancreatic function, as well as changes in pancreas size and morphology, were not observed after 4-wk of oral pancreatic enzyme application. These findings suggest that the normal pancreas does not significantly adapt--either morphologically or functionally--to a 4-wk oral application of high-dose pancreatic enzymes. BACKGROUND: The control of exocrine pancreatic enzyme secretion is not completely understood. Although it has been established that exocrine pancreatic secretion is mainly regulated in the short-term by the amount of pancreatic enzymes in the proximal small intestine, it is not known whether long-term application of pancreatic enzymes causes changes in exocrine pancreatic secretion in humans. METHODS: Twelve healthy male volunteers (median age 27 yr) participated in a prospective, randomized, placebo-controlled, double-blind study. Six were placed in the treatment group and six in the placebo group. Over a 4-wk period, the six subjects in the treatment group took 18 capsules of Panzytrat (20,000 units of lipase, 18,000 units of amylase, and 1000 units of protease per capsule) daily. Before (wk 0), 4 wk following pancreatic enzyme application and 2 wk afterward, a secretin-cerulein test was carried out in all subjects to study exocrine pancreatic function (trypsin, chymotrypsin, bicarbonate content, and total pancreatic fluid secretion in the duodenum). One day following the secretin-cerulein test, a standard test meal was given to all subjects to analyze endocrine pancreatic function. Additionally, before starting the treatment, once per week during treatment and 2 wk afterward, an ultrasound examination of the pancreas was carried out to see whether there was any change in pancreas size and morphology. RESULTS: Trypsin content in the duodenal aspirates following simultaneous stimulation with secretin and cerulein after 4 wk of high-dose pancreatic enzyme application was 92% in the treatment group and 82% in the placebo group compared with the wk 0 test results (100%). Two weeks after enzyme application, the secretin/cerulein-stimulated trypsin content was 88% in the treatment group and 107% in the placebo group. None of these changes was statistically significant. The same results were seen for chymotrypsin content, amylase, and bicarbonate content as well as for total pancreatic fluid secretion. Additionally, no change in the endocrine pancreatic function could be observed after 4 wk of pancreatic enzyme treatment. Pancreas ultrasonography revealed no alteration in pancreas size or parenchymal structure during the 4 wk of treatment and the following 2 wk.

Adaptation, Physiological↗

PubMed1998

[Keratinocyte growth factor significantly improves healing of left-sided colon anastomoses].

Inadequate healing and consequent leakage from large bowel anastomoses are a significant cause of morbidity and mortality following large bowel surgery. Systemic application of KGF has been shown to promote mucosal healing in models of colitis in rats and mice. The aim of the present study was to evaluate the effect of systemic Keratinocyte Growth Factor (KGF) administration on healing of colonic anastomoses in rats. Sprague-Dawley rats underwent laparotomy, division of the left colon and sigmoideo-sigmoideostomy. KGF (5 mg/kg) or its vehicle were administered intra-peritoneally 12 hours prior to surgery, and then once daily until sacrifice (2, 4, 7, 12 and 21 days after surgery). Bursting pressure measurements, histologic evaluation, morphometric analysis, mucin and collagen staining and hydroxyproline measurements of the anastomotic site were performed. Administration of KGF significantly increased anastomotic bursting pressure on postoperative day 2, 4 and 7 by +34%, +49% and +19%, respectively but not on day 12 and day 21. Histology, mucin staining and measurements of the colonic crypt depth showed markedly less extended inflammation, increased acidic mucin content and a significantly thickened mucosal layer in the KGF treated group when compared to vehicle treated animals. Hydroxyproline content and collagen staining were not different between KGF and vehicle treated animals. We conclude that KGF promotes healing of colonic anastomoses in rats during a one week postoperative period. KGF may be acting to accelerate host reparative processes as well as to enhance protection of the anastomotic wound bed by increased epithelium proliferation, increased mucus production and reduction of the inflammatory activity at the anastomotic site.

Anastomosis, Surgical↗

PubMed1998

[A new pathophysiologic concept in chronic pancreatitis: tissue destruction induced via inflammatory mediators].

In the present study we analyzed the three phospholipase A2 isoforms phospholipase A2 type I (PLA2-I), phospholipase A2 type II (PLA2-II), phospholipase A2 type IV (PLA2-IV) in chronic pancreatitis in comparison with normal pancreas. PLA2-I also named pancreatic phospholipase is a digestive enzyme while PLA2-II and PLA2-IV play an important function in inflammatory reactions. In chronic pancreatitis PLA2-I mRNA expression was significantly reduced. In contrast, PLA2-II and PLA2-IV mRNA were increased in 73% of the chronic pancreatitis samples (PLA2-II; 5.7-fold overexpressed; PLA2-IV:5.1-fold overexpressed; p < 0.05). By in situ hybridization the highest expression signals were found in chronic pancreatitis samples in areas with ductal metaplasia. Immunohistochemistry of PLA2-II revealed also the strongest immunoreactivity in ductal metaplasia. Increased PLA2-II and PLA2-IV mRNA levels were associated with a higher degree of tissue destruction, ductal metaplasia and degree of fibrosis. Our findings indicate that PLA2-II and PLA2-IV seems to play a role in the pathobiological alterations in chronic pancreatitis and contribute to the morphological changes which occur in chronic pancreatitis.

Adult↗

PubMed1998

The plasminogen activator/plasmin system is up-regulated after acute necrotizing pancreatitis in human beings.

BACKGROUND: Proteolysis and formation of new extracellular matrix components are important mechanisms in tissue remodeling and repair. In this study we analyzed the expression and distribution of the urokinase plasminogen activator (uPA), its membrane receptor (urokinase plasminogen activator receptor [uPAR]), and its inhibitor (plasminogen activator inhibitor-1 [PAI-1]) in acute necrotizing pancreatitis in human beings. In addition, we studied the concomitant expression of transforming growth factor-beta-1 (TGF-beta 1), which is activated by uPA from its precursor and is a potent regulator and stimulator of formation of extracellular matrix. METHODS: With immunohistochemistry and Northern blot analysis, the expression and cellular distribution of uPA, uPAR, PAI-1, and TGF-beta 1 were determined in 12 normal pancreata obtained from organ donors and 12 pancreatic tissues obtained from patients undergoing operation because of complications of acute necrotizing pancreatitis. RESULTS: Northern blot analysis showed enhanced expression of uPA, uPAR, and PAI-1 in eight of 12, seven of 12, and nine of 12 necrotizing pancreatitis samples, respectively, compared with normal control samples. In addition, increased TGF-beta 1 mRNA expression was present in eight of 12 necrotizing pancreatitis samples. In contrast, amylase mRNA expression was markedly decreased in the samples of acute necrotizing pancreatitis. Immunohistochemistry revealed elevated uPA, uPAR, and PAI-1 immunoreactivity in the remaining acinar and ductal cells adjacent to the necrotic tissue areas. In contrast, acinar and ductal cells that were located farther from pancreatic necrosis exhibited less uPA and uPAR immunoreactivity. A similar staining pattern in samples of necrotizing pancreatitis was found for TGF-beta 1. CONCLUSIONS: Up-regulation of uPA and uPAR, which activate proteolysis, might create a milieu that enhances lysis and removal of pancreatic necrosis. The increase in TGF-beta 1 might result from the enhanced catalytic conversion of its precursors by uPA, which subsequently might stimulate formation of extracellular matrix, formation of granulation tissue, and fibrosis.

Adolescent↗

PubMed1998

[Pancreatic carcinoma: conclusive clinical consequences based on molecular biology knowledge for therapy].

Molecular research techniques developed in recent years have increased our knowledge of the pathophysiology of pancreatic cancer tremendously. We now know that the malignant phenotype of pancreatic cancer is defined by the expression of growth stimulatory factors, their receptors and gene alterations. To translate molecular knowledge into new clinical therapy will be the challenge of the future. Although we have not yet developed direct clinical applications for our molecular findings, new diagnostic and therapeutic approaches are in development. Gene therapies such as antisense technology, pro-drug activation and the transfer of non-functioning growth factor receptors are potential new therapeutic options for the future. Wider clinical use can be expected in upcoming years.

Cell Transformation, Neoplastic↗

PubMed1998

[Transforming growth factor-beta controls pathogenesis of Crohn disease].

The pathogenetic mechanisms which contribute to the progression of Crohn's disease are still not known. Transforming growth factor-beta (TGF-beta) and its subtypes are multifunctional polypeptides which regulate immunological processes as well as the synthesis of the extracellular matrix and fibrogenesis. In the present study, Crohn's disease tissue samples of 18 patients undergoing intestinal resection were analyzed by Northern blot analysis, in situ hybridization and immunostaining for TGF-beta 1-3 and the TGF-beta receptors type I-III (T beta R-I, T beta R-II, T beta R-III). There was a marked overexpression of TGF-beta 1, TGF-beta 3 and T beta R-II in 94% of the Crohn's disease tissue samples. TGF-beta 2 and T beta R-I ALK5 and T beta R-III were enhanced in 72%, 72% and 82% of the Crohn tissue samples, respectively. In situ hybridization and immunostaining revealed that there was frequent coexpression of TGF-beta with its signaling receptors. Our data indicate that TGF-beta and their receptors seem to be involved in the pathogenesis of Crohn's disease. Their enhanced expression might contribute to the increase in extracellular matrix resulting in fibrosis and subsequently in intestinal obstruction.

Adolescent↗

PubMed1997

Cloning of novel transcripts of the human guanine-nucleotide-exchange factor Mss4: in situ chromosomal mapping and expression in pancreatic cancer.

In a previous large-scale analysis of gene expression in pancreatic cancer using gridded arrays of cDNA libraries and differential hybridizations, a gene that was a homolog to human mss4 was identified. Mss4 is a guanine-nucleotide-exchange factor for the Sec4/ Ypt1/Rab family of small GTP-binding proteins involved in the regulation of intracellular vesicular transport. By fluorescence in situ hybridization the human mss4 gene was assigned to chromosome 1q32-q41. Northern blot analysis revealed that three mss4 mRNA species are transcribed in human tissues of 780, 1200, and 2800 bp in length, respectively. Cloning and sequencing of the human mss4 transcripts from a pancreatic cancer cDNA library revealed that these mRNA species differ in the length of the 3-untranslated region and are probably due to the alternate use of polyadenylation sites. All mRNA species were detected at moderate to high levels in pancreatic cancer cell lines and were overexpressed in pancreatic cancer tissue compared to both normal pancreas and chronic pancreatitis tissue. However, the 1200-bp transcript was the Mss4 mRNA species with the highest level of expression in more than 50% of tumor cells and tissues. High levels of expression were found as well in other human tumor tissues. Mss4 as guanine-exchange factor required in the regulation of intracellular transport may be of importance for the function and growth of human tumor cells. However, the precise role of mss4 in human tumor cells is unknown and remains to be elucidated.

Amino Acid Sequence↗

PubMed1997

Characterization of a high copy number amplification at 6q24 in pancreatic cancer identifies c-myb as a candidate oncogene.

In a recent study designed to identify chromosomal aberrations in pancreatic cancer tissues using comparative genomic hybridization, a high copy number amplification on 6q was detected. To identify the most likely candidate oncogene, the extension of the amplification in pancreatic cancer tissues and cell lines was determined by Southern blot analysis. Exon trapping was performed with DNA from a yeast artificial chromosome clone containing the complete minimally amplified region. Only fragments from two genes, namely, the c-myb oncogene and a novel gene, were shown to be amplified. The c-myb proto-oncogene was amplified in 10% of the pancreatic carcinoma tissues and in the pancreatic cancer cell line PC2. Interestingly, the c-myb oncogene was overexpressed not only in the amplified samples but also in the majority of the examined pancreatic cancer tissues and cell lines, suggesting that amplification is only one of the mechanisms leading to overexpression. In contrast, the novel gene, which was called human eRF3b (eukaryotic release factor 3b), seems to be only coamplified with c-myb. Genetic alterations of c-myb were mainly found in advanced tumors, indicating a possible correlation to tumor progression and aggressive tumor phenotypes.

Adenocarcinoma↗

PubMed1997

Cloning of a gene highly overexpressed in cancer coding for a novel KH-domain containing protein.

In a previous large scale screen for differentially expressed genes in pancreatic cancer, we identified a gene highly overexpressed in cancer encoding a novel protein with four K-homologous (KH) domains. KH-domains are found in a subset of RNA-binding proteins, including pre-mRNA-binding (hnRNP) K protein and the fragile X mental retardation gene product (FMR1). By fluorescence in situ hybridization (FISH) the identified gene named koc (KH domain containing protein overexpressed in cancer) was assigned to chromosome 7p11.5. Two pseudogenes were localised on chromosome 6 and 11. The cloned koc cDNA has a 250 bp 5'-UTR, a 1740 bp ORF and a 2168 bp 3'-UTR. The AU-rich 3'-untranslated region of koc contains eight AUUUA and four AUUUUUA reiterated motifs. The deduced koc protein with 580 amino-acids has a relative molecular mass (Mr) of approximately 65,000 (65 K). The koc transcript is highly overexpressed in pancreatic cancer cell lines and in pancreatic cancer tissue as compared to both, normal pancreas and chronic pancreatitis tissue. High levels of expression were as well found in tissue samples of other human tumours. As the KH domain has been shown to be involved in the regulation of RNA synthesis and metabolism, we speculate that koc may assume a role in the regulation of tumour cell proliferation by interfering with transcriptional and or posttranscriptional processes. However, the precise role of koc in human tumour cells is unknown and remains to be elucidated.

Amino Acid Sequence↗

PubMed1997

Differential localization of transforming growth factor-beta isoforms in human gastric mucosa and overexpression in gastric carcinoma.

Transforming growth factor beta (TGF-beta) isoforms comprise a family of multifunctional polypeptide growth factors that either inhibit or stimulate cell proliferation. We examined TGF-beta expression in normal human gastric mucosa and carcinoma. The distribution and expression of TGF-beta isoforms in 4 normal mucosa samples from organ donors, in 12 normal mucosa samples adjacent to gastric cancer and in 12 gastric carcinomas were examined using immunohistochemistry and Northern blot analysis. Because TGF-beta s regulate collagen expression, collagen type I alpha1 mRNA amounts were also examined. Immunohistochemical analysis of normal human gastric tissue samples indicated that TGF-beta1 localized principally in parietal cells but also in some surface mucus cells, TGF-beta2 was present exclusively in chief cells and TGF-beta3 was present in parietal, chief and mucus cells. In the gastric cancers, strong colocalization of TGF-beta1, -beta2 and -beta3 was evident in the cancer cells. Northern blot analysis indicated that, compared to normal gastric tissue, gastric cancers showed a 4.8- and 6-fold increase in mRNA amounts encoding TGF-beta1 and TGF-beta3, respectively. In contrast, TGF-beta2 mRNA amounts were comparable in both groups. Northern blot analysis showed a 10-fold increase in human collagen type I alpha1 mRNA amounts compared to normal gastric tissue. These findings imply a role forTGF-beta s in normal human gastric mucosa function, and raise the possibility that the aberrant colocalization and overexpression of all 3 TGF-beta isoforms in human gastric cancer cells in vivo may contribute to the pathobiology of gastric carcinoma.

Adenocarcinoma↗

PubMed1997

Identification of genes with specific expression in pancreatic cancer by cDNA representational difference analysis.

cDNA representational difference analysis (cDNA-RDA) is a polymerase-chain-reaction-coupled subtractive and kinetic enrichment procedure for the isolation of differentially expressed genes. In this study, the technique was used to isolate novel genes specifically expressed in pancreatic cancer. cDNA-RDA was done on cDNA reverse transcribed from a poly(A)+ mRNA pool made from 10 cancer tissues (tester) by using as a driver a cDNA from a poly(A)+ mRNA pool made from a combination of 10 tissues of chronic pancreatitis and 10 healthy pancreatic tissues. The use of chronic pancreatitis in addition to healthy pancreas mRNA in the driver preparation eliminated the influence of stromal tissue components present as contamination in the cancer-specific preparations. Such cDNA-RDA led to the isolation of 16 distinct, cancer-specific gene fragments. These were confirmed to be overexpressed in pancreatic cancer tissues by Northern blot analysis. Sequence analysis revealed homologies to five genes previously implicated in the carcinogenesis of the pancreas or other tissues. Eleven fragments had no significant homology to any known gene and thus represent novel candidate disease genes. The experiments demonstrate that cDNA-RDA is a reproducible and highly efficient method for the identification of novel genes with cancer-specific expression.

Annexin A3↗

PubMed1997

Adjuvant therapy of pancreatic cancer using monoclonal antibodies and immune response modifiers.

Pancreatic cancer is a devastating disease with poor survival. At present, no effective adjuvant or palliative therapies are available. Unresponsiveness to chemotherapy, radiotherapy, and antihormonal treatment is one of the reasons that pancreatic cancer patients have an overall median survival time of 4-6 mo. This article summarizes clinical trials on immunotherapy of pancreatic cancer using the murine monoclonal antibodies (MAbs) 17-1A and BW 494. In addition, the use of MAb treatment in combination with immune response modifiers is discussed. In four clinical trials, MAb 17-1A was given by iv infusion to 100 patients with pancreatic cancer. In 30 of the these patents, antibody treatment was accompanied by gamma-interferon, also given intravenously. Complete response, partial response, and stable disease were reported in 1,5, and 23 patients, respectively. Passive immunotherapy using the MAb BW 494 was carried out in 148 pancreatic cancer patients in two phase I and two phase II trials. In 1 out of 75 patients a partial response and in 25 out of 74 patients stable disease were reported. However, in a controlled randomized trial enrolling 61 patients following Whipple resection, comparable survival times in patients with and without MAb BW 494 treatment led to the termination of further clinical trials with this antibody. New clinical studies using humanized MAbs in combination with immune response modifiers should be initiated to further evaluate immunotherapy as a treatment option in pancreatic cancer.

Antibodies, Monoclonal↗

PubMed1997

Progress report. A randomized multicenter European study comparing adjuvant radiotherapy, 6-mo chemotherapy, and combination therapy vs no-adjuvant treatment in resectable pancreatic cancer (ESPAC-1).

CONCLUSION: The ESPAC-1 trial 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. BACKGROUND: At the joint International Association of Pancreatology and the European Pancreatic Club meeting in Mannheim, Germany (June 12-15, 1996) a satellite meeting of the European Study Group for Pancreatic Cancer (ESPAC) met to discuss the progress of the ESPAC-1 trial. METHODS: A randomized multicenter study to address which, if any, of the following adjuvant treatments are of benefit in patients with resectable pancreatic cancer: radiotherapy (40 Gy with 5-FU as a sensitizing agent), 6 mo of chemotherapy (5-FU and folinic acid), or a combination of these treatments. RESULTS: From February 1994 to June 1996 (the time of the Mannheim meeting) 221 patients so far have been recruited into the three treatment arms and one control arm.

Adenocarcinoma↗

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 pancreas: a standard procedure in chronic pancreatitis].

Duodenum-preserving resection of the head of the pancreas was developed 25 years ago by Beger. This procedure is indicated in patients suffering from chronic pain in combination with inflammation of the head of the pancreas, common bile duct obstruction, pancreatic duct obstruction and/or obstruction of the retropancreatic vessels. At the Inselspital in Berne, 74 patients underwent this operation between 1993 and 1996. The median length of the operation was 380 min, with the need for transfusion in a median of 0 units (0-6). There was no postoperative mortality. Total postoperative morbidity was 13%. One patient needed relaparotomy on day 17 for small bowel obstruction. Median length of hospital stay was 11 days. Postoperatively, two patients developed diabetes. Duodenum-preserving resection of the head of the pancreas represents an organ-preserving principle of surgery. This procedure treats the complications of chronic pancreatitis and provides long-term pain relief in more than 80% of patients.

Adolescent↗