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Biomedical subjects

A Schmassmann

Publications and source records attributed to A Schmassmann.

At least 37 records · Page 2Linked to original sources
PubMed1998

[Evaluation of various screening and surveillance methods in colorectal carcinoma].

Colorectal cancer is a common disease which is almost wholly preventable by early removal of adenomatous polyps. Screening should be offered to all persons without risk factors from the age of 50. Selection of the appropriate screening programme should take into account personal preference, local expertise and insurance coverage. Endoscopic screening and surveillance investigations should be strongly encouraged in all persons wit risk factors such as (1) previous treatment of colorectal adenomatous polyps or cancers, (2) ulcerative colitis, (3) patients with hereditary colorectal cancer syndromes and (4) first degree relatives of patients with colorectal cancer. The following four strategies are available for candidates > 50 years without risk factors: (1) faecal occult blood testing (annually), (2) flexible sigmoidoscopy (every 5 years), (3) a combination of both (1 + 2) strategies and (4) coloscopy (every 10 years). Coloscopy should be performed after a positive test result in strategy programs 1-3. Results from prospective randomized trials are available only for faecal occult blood testing, showing an approximately 15% reduction of mortality in the screening group. The potential for reduction of colorectal cancer mortality has been estimated at 30-70% and 60-90% for flexible sigmoidoscopy and coloscopy respectively. However, no results from prospective randomized trials are presently available. Cost-effectiveness analysis has not shown relevant differences between the four different screening strategies.

Aged↗
PubMed1998

Mechanisms of ulcer healing and effects of nonsteroidal anti-inflammatory drugs.

Ulceration of the gastroduodenal mucosa occurs frequently in humans, particularly in patients with a history of peptic ulcer disease. In order for healing to occur, mucosal damage stimulates secretion of growth factors in the adjacent mucosa and ulcer bed. Peptic ulcer healing is accomplished by the filling of the mucosal defect with cells that migrate from the ulcer margin and by connective tissue, including microvessels originating from granulation tissue. Peptic ulcer healing is accelerated both in humans and experimental models by gastric acid inhibition, which enhances cell migration and maturation of the granulation tissue. In experimental models, peptic ulcer healing can also be accelerated by oral administration of basic fibroblast growth factor, which increases angiogenesis in the ulcer bed, or by nitric oxide-releasing compounds, which improve gastric blood flow. Clinical and experimental data indicate that traditional nonsteroidal anti-inflammatory drugs (NSAIDs) delay the healing of peptic ulcers by interfering with the action of growth factors, decreasing epithelial cell proliferation in the ulcer margin, decreasing angiogenesis in the ulcer bed, and slowing maturation of the granulation tissue. In order to reduce the gastroduodenal side-effects of NSAIDs, selective cyclo-oxygenase (COX)-2 inhibitors have been developed, which inhibit the inducible COX-2 isoform in inflammatory tissue but have only limited effect on the constitutive COX-1 isoform in the stomach. It has been reported that the selective COX-2 inhibitor L-745,337 has a reduced liability for gastrointestinal ulceration. In our chronic experimental gastric ulcer model in rats, however, delay of gastric ulcer healing with L-745,337 was comparable to that with ordinary NSAIDs. It has also been reported that nitric oxide-releasing NSAIDs have a low relative risk of gastrointestinal ulceration but, again, in our chronic gastric ulcer model, nitric oxide did not reverse NSAID-induced deleterious effects on ulcer healing. In contrast, the proton pump inhibitor omeprazole has been shown to reverse NSAID-induced deleterious effects on gastric ulcer healing in our model. Comparable results have also been reported in humans. Histologic analysis has shown that omeprazole reverses the effects of NSAIDs on cell proliferation, angiogenesis, and maturation of the granulation tissue. In conclusion, only highly effective gastric acid inhibition reliably reverses NSAID-induced delay of gastric ulcer healing.

Animals↗
PubMed1998

Effects of inhibition of prostaglandin endoperoxide synthase-2 in chronic gastro-intestinal ulcer models in rats.

1. In the stomach, prostaglandins protect the gastric mucosa against injuries. One rate-limiting step in prostaglandin synthesis is mediated by prostaglandin endoperoxide synthase (PGHS), the target enzyme of non-steroidal anti-inflammatory drugs (NSAIDs). Two isoforms of PGHS exist: a constitutive (PGHS-1) and an inducible (PGHS-2) enzyme. PGHS-1 is the major source of gastric prostaglandins under physiological conditions. Inhibition of prostaglandin synthesis by traditional NSAIDs such as indomethacin and diclofenac which non-selectively inhibit both PGHS-1 and PGHS-2, causes gastric and intestinal ulceration and delays gastric ulcer healing in chronic models. It has been shown that selective PGHS-2 inhibitors such as L-745,337 (5-methanesulphonamide-6-(2,4-difluorothio-phenyl)-1-inda none) are not ulcerogenic and do not inhibit gastro-intestinal prostaglandin synthesis. However, minimal information is available on the long-term effects of PGHS-2 inhibitors on the healing of previously established gastric injuries. We assessed the cellular localization and expression of PGHS-1 and PGHS-2 during gastric ulcer healing and assessed the effects of L-745,337 on previously established cryoulcers in the rat gastric stomach. 2. PGHS-1 and PGHS-2 were located and quantified by immunohistochemistry during experimental gastric ulcer healing. PGHS-2 immunoreactivity was only negligible in the normal gastric wall, but after gastric ulcerations, it was strongly detected in monocytes, macrophages, fibroblasts and endothelial cells below and between the regenerative glands. PGHS-1 immunoreactivity detected in normal gastric mucosa, disappeared after gastric ulceration in the mucosa adjacent to the ulcer crater. However, it reappeared in the regenerative glands from day 5 onwards. Thus, PGHS-1 and PGHS-2 were located at different sites and their maximal expression followed a different time-sequence. 3. We assessed the effects of L-745,337, indomethacin and diclofenac on gastric ulcer healing and histological healing parameters in rats. L-745,337, indomethacin and diclofenac dose-dependently decreased the healing of gastric ulcers. L-745,337, indomethacin and diclofenac decreased epithelial cell proliferation in the ulcer margin and microvessel density in the ulcer bed on day 8 and increased the thickness of the granulation tissue below the ulcer crater and the gap between both edges of the muscularis mucosae on day 15. Indomethacin and diclofenac, but not L-745,337, decreased synthesis of 6-keto-PGF1alpha and PGE2 in tissue fragments from the stomach and terminal ileum and decreased platelet thromboxane B2 synthesis in clotting whole blood. 4. Dose-response curves for the inhibition of chronic gastric ulcer healing by L-745,337 (administered twice daily intragastrically) showed an ID50 value of 1.7 mg (4.3 micromol) kg(-1). Dose-response curves for the inhibition of PGE2 synthesis in inflammatory exudates in the acute carrageenin sponge rat model, showed ID50 values of 1.1 mg (3.1 micromol) kg(-1) and 1.3 (3.3 micromol) mg kg(-1) for indomethacin and L-745,337, respectively. Thus, inhibition of chronic gastric ulcer healing by L-745,337 occurs within a potentially therapeutic dose-range. 5. In summary, PGHS-2 is markedly accumulated after gastric ulceration in monocytes, macrophages, fibroblasts and endothelial cells in regions of maximal repair activity. Selective inhibition of PGHS-2 by L-745,337 delayed gastric ulcer healing though interference with epithelial cell proliferation, angiogenesis and maturation of granulation tissue in a potentially therapeutic dose range. PGHS-2-derived prostaglandins seem to have an important role in gastric ulcer healing.

Animals↗
PubMed1998

Detection and prevalence of Helicobacter infection in pet cats.

The presence of spiral bacteria in the feline stomach has been recognized for over a century, but the identities and degrees of prevalence of such organisms in privately owned cats are still poorly documented. The aims of this study were (i) to adapt different diagnostic tools and evaluate their practicality for diagnosing feline gastric Helicobacter colonization, (ii) to determine the prevalence of gastric Helicobacter-like organisms in pet cats, (iii) to identify the feline species, and (iv) to correlate the presence of a Helicobacter infection with gastritis. Biopsy samples were taken gastroscopically from the antra and the corpora of clinically healthy pet cats. Helicobacter-like organisms were detected by Gram staining, Warthin-Starry staining, and rapid urease testing in biopsy specimens and by [13C]urea breath testing in 79, 77, 78, and 85% of cases, respectively. PCR analysis revealed that 78% of the cats (38 of 49) were infected by Helicobacter heilmannii; however, none of them was harboring Helicobacter pylori or Helicobacter felis. Culture was positive for one cat; the organism was identified as Helicobacter pametensis by dot blot DNA hybridization. By a combination of the detection methods, 91% of the pet cats were found to be Helicobacter positive. For 46 cats (79%) diagnostic tests were concordant. All cats showed mild to moderate gastritis in either the antrum or the corpus, regardless of the presence or density of gastric bacteria. In summary, pet cats are frequently colonized by H. heilmannii without a significant correlation between infection and degree of gastritis.

Animals↗
PubMed1998

Risk factor assessment of endoscopically removed malignant colorectal polyps.

BACKGROUND: Malignant colorectal polyps are defined as endoscopically removed polyps with cancerous tissue which has invaded the submucosa. Various histological criteria exist for managing these patients. AIMS: To determine the significance of histological findings of patients with malignant polyps. METHODS: Five pathologists reviewed the specimens of 85 patients initially diagnosed with malignant polyps. High risk malignant polyps were defined as having one of the following: incomplete polypectomy, a margin not clearly cancer-free, lymphatic or venous invasion, or grade III carcinoma. Adverse outcome was defined as residual cancer in a resection specimen and local or metastatic recurrence in the follow up period (mean 67 months). RESULTS: Malignant polyps were confirmed in 70 cases. In the 32 low risk malignant polyps, no adverse outcomes occurred; 16 (42%) of the 38 patients with high risk polyps had adverse outcomes (p<0.001). Independent adverse risk factors were incomplete polypectomy and a resected margin not clearly cancer-free; all other risk factors were only associated with adverse outcome when in combination. CONCLUSION: As no patients with low risk malignant polyps had adverse outcomes, polypectomy alone seems sufficient for these cases. In the high risk group, surgery is recommended when either of the two independent risk factors, incomplete polypectomy or a resection margin not clearly cancer-free, is present or if there is a combination of other risk factors. As lymphatic or venous invasion or grade III cancer did not have an adverse outcome when the sole risk factor, operations in such cases should be individually assessed on the basis of surgical risk.

Adult↗
PubMed1998

[Staging of esophagus carcinoma].

Prognosis and therapy of esophageal cancer is strongly related to the results of staging. Accurate staging is therefore essential. After initial endoscopic diagnosis with bioptic confirmation of the diagnosis, CT-scan of the chest and upper abdomen should be performed to assess the TNM-stage. In a potentially curable situation without detection of metastases, the TN-stage should be verified by endosonography. The local TN-stage which is decisive for complete local tumour resectability, can only be assessed with sufficient accuracy by endoscopic ultrasonography.

Biopsy↗
PubMed1998

[A patient with choledocholithiasis--no therapy without risk].

A 73-year-old man was admitted to the hospital because of recurrent fever and intermittent cholestasis. A cholecystectomy with hepatico-duodenostomy was performed ten years ago because of acute cholecystitis and impacted bile duct stones. Recurrent episodes of cholangitis occurred postoperatively and ERCP showed shrinkage of the hepatico-duodenal anastomosis with sump syndrome and recurrent bile duct stones. Endoscopic sphincterotomy for the improvement of bile flow was considered too dangerous at this time-point because of unfavourable intraduodenal position of the papilla Vateri. The patient refused reoperation. During the present hospitalization, endoscopic sphincterotomy and gallstone removal were performed. Within hours after intervention, necrotizing pancreatitis developed which could be managed without operation. No further episodes of cholangitis reoccurred after discharge from hospital. This case report demonstrates the risks of bile duct surgery and endoscopic sphincterotomy.

Aged↗
PubMed1997

Roles of hepatocyte growth factor and its receptor Met during gastric ulcer healing in rats.

BACKGROUND & AIMS: It is unclear which growth factors are primarily responsible for stimulating gastric ulcer healing. The roles of hepatocyte growth factor (HGF) and Met/HGF receptor during gastric ulcer healing were studied in rats. METHODS: HGF and Met/HGF receptor were located and quantified by in situ hybridization and immunohistochemistry during experimental gastric ulcer healing. The in vivo effects of exogenous recombinant human HGF on cell proliferation and ulcer healing were assessed and compared with those of placebo and omeprazole treatment. RESULTS: Compared with intact oxyntic mucosa, messenger RNA (mRNA) of HGF and met was substantially greater in the ulcerated region on days 3 and 15. HGF mRNA was located in stromal cells between the regenerative glands and in the arterial vessels of submucosal tissue, whereas met mRNA was located in the epithelial cells of the regenerative glands. After cryoinjury, immunoreactivity for the Met/HGF receptor was absent on day 3, reappeared on day 8, and was overexpressed on day 15. Exogenous recombinant human HGF had no effect on the ulcer healing parameters over days 3-8, but it did increase epithelial cell proliferation in the ulcer margin over days 8-15. CONCLUSIONS: These data suggest that HGF mediates specific tissue interactions between mesenchyme and epithelia during gastric ulcer healing.

Actins↗
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

Significance of histologic criteria for the management of patients with malignant colorectal polyps and polypectomy.

BACKGROUND: The management of invasive cancer in colorectal polyps (malignant polyps) is controversial, particularly with regard to the different sets of histologic criteria for deciding whether malignant colorectal polyps should be treated by polypectomy alone or be followed by surgical resection. We report on the outcome of patients in accordance with the histologic assessment of their malignant polyps. METHODS: Malignant polyps were defined as having favourable histology (free margin, grade I or II, and no angiolymphatic invasion) or unfavorable histology (no free margin, grade III, or angiolymphatic invasion). Malignant polyps with favourable histology were treated by endoscopic polypectomy alone, whereas further therapy was recommended for malignant polyps with unfavourable histology. Residual cancer in a resection specimen and local or metastatic recurrence during the follow-up period (mean, 60 months; range, 12 - 120) were defined as adverse outcome. RESULTS: Thirty-seven malignant polyps were detected in 35 (0.5%) of 6605 patients. Five of these 35 patients were treated by primary bowel resection and analysed separately. In the other 30 patients the following unfavourable histologic signs were detected in 20 (62.5%) of 32 malignant polyps; no free margin in 16, grade III in 1, and angiolymphatic invasion in 3 polyps. Twelve polyps with favourable histology had no adverse outcome; in contrast, 5 of 20 polyps with unfavourable histology had an average outcome (P < 0.05). CONCLUSIONS: Locally excised malignant polyps without unfavourable histologic signs may not need further surgical treatment; for all other malignant polyps an ensuing bowel resection is recommended.

Adult↗
PubMed1997

[Possibilities and limitations in endosonography of the gastrointestinal tract].

In addition to the endoscopic assessment of the mucosa, endoscopic ultrasonography allows the characterization of the gastrointestinal tract wall and the neighbouring structures. Due to the high ultrasonic frequencies employed, endoscopic images have a high resolution. Malignant tumours of the esophagus, stomach, periampullary region, and rectum are usually investigated both by computer tomography and endoscopic ultrasonography. The local T-N tumour stage is predominantly assessed by endoscopic ultrasonography. In contrast, the M stage is assessed predominantly by computed tomography. The local T-N stage, which ist decisive for the local tumour resectability, can only be assessed with sufficient accuracy by endoscopic ultrasonography.

Endosonography↗
PubMed1997

Self-expanding metal stents in malignant esophageal obstruction: a comparison between two stent types.

OBJECTIVES: Self-expanding metal stents are a promising alternative in the palliation of malignant esophageal obstruction, but the relative value of different stent types is not well established. METHODS: During a 3-year enrollment period in four different centers, 82 consecutive patients with malignant dysphagia without tumor recurrence after surgery or esophagorespiratory fistulas received either an uncovered Wallstent (44 patients) or a knitted nitinol stent (38 patients). RESULTS: Age (median: 79 yr), sex (F:M = 33:67), dysphagia score (median: 3), Karnofsky score (median: 53), body mass index (median: 19), type of pretreatment, tumor stage, stricture length (median: 5.4 cm), and stricture location were comparable in both stent groups. After stent placement, median dysphagia score improved markedly in both groups by two points. Procedure-related mortality (16 vs 0%; p < 0.01), early complication rate (32 vs 8%; p < 0.01), and severe persistent pain after stent placement (23 vs 0%; p < 0.002) were higher in the Wallstent compared with the knitted nitinol stent group. In contrast, stent dysfunction (7 vs 32%; p < 0.005), reintervention rate (9 vs 34%; p < 0.005), and costs were lower in the Wallstent compared with the nitinol stent group. CONCLUSIONS: In malignant esophageal obstruction, both stents markedly improved dysphagia. Uncovered Wallstents seem to cause more early severe complications than knitted nitinol stents. In contrast, stent dysfunction, reintervention rate, and costs appear to be higher in the nitinol stent group.

Adult↗
PubMed1996

[15 years of endoscopic therapy in choledocholithiasis].

INTRODUCTION: The relevance of endoscopic retrograde cholangiopancreatography (ERCP) in the diagnosis and treatment of common bile duct stones has increased since the introduction of laparoscopic cholecystectomy in 1989-1990. METHODS: The number, indications, success and complication rate of ERCP were analyzed retrospectively in 1121 consecutive patients with bile duct stones treated at Berne University Hospital between 1980 and 1994. RESULTS: The number of patients undergoing endoscopic stone extraction increased slowly from 1980 to 1990, but has shown a 4-fold increase in the last 5 years parallel to the introduction of laparoscopic cholecystectomy. Failure to diagnose and remove bile duct stones decreased 5-fold from 23% (14 of 60 patients) in 1986 to 4.4% (10 of 225 patients) in 1994. Major complications occurred in 3.2% (30 of 617 patients) and consisted of acute pancreatitis (1.6%), hemorrhage of the papilla (1%), and cholangitis (0.6%). The severity but not the number of complications has decreased in the last 15 years. CONCLUSION: Gallbladder stones with common bile duct stones are usually treated by endoscopic stone extraction combined with laparoscopic cholecystectomy. Open operation with bile duct exploration is reserved for a small subgroup of patients with specific problems.

Adult↗
PubMed1996

Wallstents versus plastic stents in malignant biliary obstruction: effects of stent patency of the first and second stent on patient compliance and survival.

OBJECTIVES: In prospective trials in patients with malignant biliary obstruction, it has been reported that Wallstents prolong stent patency, but this does not translate into a significant survival benefit. Compared with prospective trials, however, survival may be different in clinical practice because of differences in patient compliance. We report on a retrospective, long term analysis comparing Wallstents versus plastic stents. METHODS: Plastic endoprostheses (70 patients) and endoscopic Wallstents (95 patients) were placed in 165 consecutive patients with irresectable, malignant biliary obstruction in a first (1990-91) and second (1992-93) time period. Stent occlusion was treated by plastic stent placement. RESULTS: Patient characteristics were quite comparable in both stent groups. Initial placement of a Wallstent resulted in an increase of median stent patency of the first (10 vs 4 months, p < 0.001) and second (8 vs 3 months, p < 0.05) stent, a decrease of additional endoscopic procedures (20 vs 58%, p < 0.005), an increase of patient compliance reflected by a decrease of patients dying with untreated stent occlusion (9 vs 30%, p < 0.001), and an increase of survival time (6.5 vs 4 months, p < 0.05). CONCLUSIONS: Initial placement of a Wallstent results in an increase of stent patency of the first and second stent. Duration of stent patency appears to have a determinant effect on patient compliance. Increased stent patency and patient compliance seem to improve survival in clinical practice.

Aged↗
PubMed1996

[Pancreatic carcinoma: conservative and adjuvant therapy].

Patient with pancreatic have a median age of 78 years and without treatment an average survival of only a few months. Tumor stage and patient will determine the therapy. Patients with metastases or a high surgical risk are treated symptomatically. Jaundice, nausea, pain, and anorexia are the most relevant symptoms. The main symptom requiring treatment are jaundice and pruritus due to extrahepatic biliary obstruction which can be relieved in most cases by endoscopic placement of a biliary endoprosthesis. Pancreatic cancer may be a highly painful disease. Therapeutic modalities include, in addition to antitumoral treatment, narcotic and nonnarcotic analgesics, neurolytic celiac blockage, psychological support, and the treatment of associated symptoms such as emesis and constipation. Although radio- or chemotherapy show positive responses in a subgroup of patients, average survival remains unchanged with monotherapy. In contrast, improved median survival following combined radio-and chemotherapy has been demonstrated both in patients with locally unresectable pancreatic cancer and in patients after curative tumor resection.

Aged↗
PubMed1995

Influence of acid and angiogenesis on kinetics of gastric ulcer healing in rats: interaction with indomethacin.

Indomethacin delays healing of experimental gastric ulcers. We investigated whether inhibition of gastric acid secretion by omeprazole or stimulation of angiogenesis by basic fibroblast growth factor (bFGF) may reverse this delay. Rats with gastric ulcers induced by cryoprobe were treated subcutaneously with either placebo, indomethacin (2 x 0.5 mg/kg), bFGF (2 x 100 micrograms/kg), omeprazole (1 x 40 mumol/kg), indomethacin plus omeprazole, or indomethacin plus bFGF given daily for 8, 10, 15, and 22 days. Ulcer size, epithelial cell proliferation, angiogenesis, and maturation of granulation tissue were sequentially quantified. Omeprazole significantly accelerated ulcer healing in an early phase (days 3-8). In contrast, bFGF accelerated healing in a late phase (days 10-15). Indomethacin significantly delayed ulcer healing in late phase and decreased prostaglandin generation, cell proliferation, angiogenesis, and maturation of granulation tissue. Despite stimulation of angiogenesis, bFGF did not reverse indomethacin-induced delay in ulcer healing. In contrast, omeprazole reversed indomethacin-induced effects on angiogenesis, cell proliferation, maturation of granulation tissue, and ulcer healing rate.

Animals↗
PubMed1995

Indomethacin interferes with epidermal growth factor binding and proliferative response of gastric KATO III cells.

Indomethacin induces gastric ulcerations and decreases cell proliferation in the gastric ulcer margin. Since epithelial cell proliferation is under control of epidermal growth factor (EGF), we studied whether indomethacin may affect specific binding of [125I]-EGF to its receptors in cultured human gastric KATO III cells. To assess effects of EGF, indomethacin and their combination on cell proliferation, KATO III cells were incubated for 24 h with either (a) vehicle (b) indomethacin (doses from 10(-5) to 10(-3) M), EGF (doses 0.01, 0.05 or 0.1 microgram/ml) or (d) a combination of b and c, and the bromodeoxyuridine labeling index was determined. Indomethacin in a dose which did not affect cell viability significantly (by 21.5%) decreased [125I]-EGF binding to the KATO III cells and decreased the bromodeoxyuridine labeling index. Epidermal growth factor significantly increased cell proliferation and increased the labeling index from 28.9 +/- 0.6% in the vehicle group to 36.2 +/- 0.5%. Co-treatment with indomethacin significantly reduced the proliferative response of KATO III cells to EGF. In conclusion, indomethacin, in a dose which does not affect cell viability, decreased binding of EGF to cultured gastric KATO III cells and decreased their proliferative response to EGF.

Anti-Inflammatory Agents, Non-Steroidal↗