Spontaneous rupture of a biliary metal stent.
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Drainage↗
Biomedical subjects
M Classen
Publications and source records attributed to M Classen.
Microbiological examinations and in-vitro testing of different antibiotics in therapeutic endoscopy of the biliary system.
BACKGROUND AND STUDY AIMS: Prior to endoscopic therapeutic procedures, no antibiotic prophylaxis is administered routinely. Because of the reported incidence of infectious complications, which may reach up to 10%, a prospective study was undertaken to investigate the effects of a prophylactic dose of cefuroxime on the incidence of bacteremia and clinical signs of infection, but no significant effects could be demonstrated. In addition to this published work, blood and bile cultures obtained in this trial were also investigated, and the in-vitro susceptibility to several antibiotics was tested in order to recommend the appropriate substances. PATIENTS AND METHODS: Ninety-nine consecutive patients (51 men, 48 women; mean age 61.4 +/- 17 years) with biliary obstruction who underwent an endoscopic retrograde cholangiopancreatography (ERCP) or percutaneous transhepatic cholangiography with drainage (PTCD) were included. Sequential blood cultures were taken before and up to 60 minutes after the endoscopic intervention. Bile cultures were obtained in 56 patients with biliary drainage. Aerobic and anaerobic cultures were prepared from all obtained specimens and the isolated organisms were identified. In the case of positive cultures, an in-vitro resistance test for 15 different antibiotics was performed. RESULTS: The incidence of bacteremia was 11.1% (n = 11), and 16 bacteria were isolated. Twelve different microorganisms were detected, with Escherichia coli found in four cases. From 41 positive out of 56 prepared bile cultures (73.2%), 91 isolates were found with 25 different species. A single agent was detected in eight cases (19.5%), while a mixed growth, with pathogens ranging from two to six species, was found in 33 cases (80.5%). The seven most frequently isolated germs were E. coli and Enterococcus (each n = 19), Klebsiella (n = 10), Streptococcus viridans (n = 9), Staphylococcus epidermidis (n = 5), Morganella morganii (n = 4), and Bacteroides fragilis (n = 3), representing 76% of all agents. Examination for fungal infection revealed positive cultures of Candida albicans in 16.1% of bile cultures (nine of 56). Interestingly, the use of proton-pump inhibitors (PPIs), with a consequent rise in the gastric pH value, led to an increase in the rate of bacteremia to 26.2% (five of 19) compared to the other patients not on PPIs (n = 80), who developed bacteremia in only six cases (7.5%; p = 0.02). In-vitro testing of different antibiotics was carried out in 73 isolates. Imipenem showed the best antimicrobial activity (98.4%), followed by trimethoprim and sulfamethoxazole (90%), amoxicillin plus clavulanic acid (87.3%), vancomycin (82.4%), and ofloxacin (76.9%). CONCLUSIONS: Escherichia coli was found to be the pathogen most frequently detected in blood and bile following endoscopic interventions in the biliary tract. Enterococci, Klebsiella and Streptococcus viridans were found in bile cultures with an incidence exceeding 10%. In view of the in-vitro test results, possible side effects, and contraindications, amoxicillin plus beta-lactamase inhibitors or quinolones are considered to be suitable antibiotics for the prophylaxis of biliary infections.
Adult↗
Long-term results of percutaneous transhepatic biliary drainage for benign and malignant bile duct strictures.
BACKGROUND: Long-term percutaneous transhepatic biliary drainage (PTBD) is a valid alternative to surgery in patients with benign or malignant bile duct strictures in whom endoscopic drainage has failed. However, few data are available on the long-term outcome with percutaneous drainage, specially when the application of Yamakawa-type prostheses is considered. METHODS: During 1996, 48 patients who were either treated with primary PTBD insertion followed by PTBD exchanges (n = 15) or who presented only for exchange of an earlier PTBD (n = 33) were included in the study. Thirty-one patients had malignant strictures, and 17 had benign ones. The PTBD catheters were scheduled for exchange every 3 months or earlier if signs and symptoms of obstruction or other problems were present. The data were collected prospectively during each follow-up visit and included both symptoms and the status and function of the PTBD at the time of exchange. RESULTS: Although PTBD was highly effective in relieving jaundice (progression of cholestasis was observed in only 2 cases), 73 of the 157 PTBD exchanges (47%) had to be carried out earlier than scheduled. Premature exchange was needed for clinical reasons, such as fever indicating PTBD dysfunction, in only 19% of these cases. The other reasons were related to the PTBD catheter and consisted of bile leakage alongside the drain (33%), PTBD disconnection or complete dislocation (30%), or occlusion suspected during regular flushing of the drain (15%). In most cases exchanging the drain was sufficient to solve the problem; in cases of complete dislocation, dilation of the same tract (n = 6) or fresh puncture and establishment of a new drainage site (n = 2) were necessary. Reducing the PTBD exchange interval from 3 to 2 months would have decreased the number of premature stent exchanges by 26%. CONCLUSIONS: Although PTBD is an effective method of biliary drainage, there are frequently minor problems-mostly catheter-related-which require premature exchange of the drain in almost half of the cases, and this may affect the patients' quality of life. Improvements in PTBD materials and catheter design are therefore needed. The effectiveness of reducing the intervals between PTBD exchanges should also be examined.
Adult↗
Extensive hepatic infarction caused by thrombosis of right portal vein branches and arterial vasospasm in HELLP syndrome associated with homozygous factor V Leiden.
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Adult↗
Growth factor effects on apoptosis of rat gastric enterochromaffin-like cells.
Enterochromaffin-like (ECL) cells are histamine-containing endocrine cells in the gastric epithelium that show increased density during chronic atrophic gastritis. The current study determined cell number and apoptosis of isolated rat ECL cells in response to several growth factors. Isolated ECL cells from fundic mucosa (enrichment >90%) were grown in serum-free medium over 2-5 days. Cell number was determined by mitochondrial formazan production; apoptosis was measured by Tdt-mediated dUTP nick end labeling reaction and DNA fragmentation-based enzyme-linked immunosorbent assay. Immunocytochemistry and RT-PCR demonstrated the presence of epidermal growth factor receptor, neuronal growth factor receptor (type 1), and fibroblast growth factor (FGF) receptor (type 1). Gastrin (EC50, approximately 2 pM), transforming growth factor-alpha (TGF alpha; 10-30 ng/ml), and basic FGF (bFGF; 1-10 ng/ml) increased the total number of cultured ECL cells. bFGF augmented the gastrin (1 pM)-induced response. Beta-neuronal growth factor (10 ng/ml) and bFGF (2 ng/ml) decreased the programed death of ECL cells. Interleukin-1beta (100 pg/ml, 24 h) stimulated apoptosis 2- to 3-fold in ECL cells, and simultaneous incubation with TGF alpha (20 ng/ml) or bFGF (2 ng/ml) significantly inhibited this effect. ECL cells express specific receptors for gastrin, epidermal growth factor, neuronal growth factor, and FGF. bFGF prolonged ECL cell survival by inhibiting spontaneous apoptosis. Our data further indicate that TGF alpha and bFGF increase ECL cell number by inhibiting cytokine-induced programed cell death.
Animals↗
[Palliative therapy of carcinomas of the biliary system].
CARCINOMA OF THE GALLBLADDER: Only patients suffering from advanced disease have symptoms, that is pain, jaundice, weight loss. Mean 5-year survival rate tends to be lower than 5%. Tumors can be resected with negative margins in 15 to 25% of the patients. Obstructive jaundice can be managed with endoscopic biliary stent in 84% of the patients. After radiotherapy tumor regression is observed in 80% of the patients. Their mean survival time is 10 months. CHOLANGIOCARCINOMAS: More than 90% of the patients present with jaundice. At the time of presentation, 50% of the patients already have metastases to lymph nodes. Mean total survival time of all patients is 12 months. Surgical resection can successfully be performed in 30 to 40% of the patients suffering from proximal cholangiocarcinomas. Distal unresectable tumors are best palliated with an endoscopically placed stent in 97.5% of the patients. Patients having undergone radiotherapy will have a mean survival time of 9 to 12 months. There is a 12% response rate after chemotherapy with single agents and one of 23% after combined regimens. Intraarterial application of chemotherapy results in 44% response rate. CONCLUSION: Carcinomas of the biliary tract are often diagnosed at advanced inoperable stages. Patients quality of life can be ameliorated by palliative treatment, i.e. biliary stents, radio-, chemotherapy. Mean survival time does normally not exceed 1 year.
Bile Duct Neoplasms↗
Role of vagal fibers and bombesin/gastrin-releasing peptide-neurons in distention-induced gastrin release in rats.
In the rat the exact role of vagal fibers and the interaction between the extrinsic and intrinsic neural system in distention-induced gastrin release are still a matter of debate. Accordingly, the aim of the present study was to examine the contribution of afferent and efferent vagal fibers as well as intrinsic neurons on gastrin response to gastric distention. In anesthetized rats graded gastric distention by 5, 10 and 15 ml saline for 20 min caused a significant volume-dependent increase of plasma gastrin levels by 12+/-6 pg/ml (5 ml saline, n = 8, P =0.05), 26+/-7 pg/ml (10 ml saline, n = 10, P < 0.05) and 37+/-7 pg/ml (15 ml saline, n = 8, P < 0.01 ), respectively. To examine the role of the extrinsic vagal innervation, gastrin response to distention was studied in anesthetized rats after bilateral truncal vagotomy (n = 9) or selective afferent vagotomy following pretreatment with capsaicin (n = 6). Stimulation of gastrin release by 10 ml distention in sham-operated control rats was reversed to an inhibition after truncal vagotomy (26+/-7 vs. -11+/-4 pg/ml; P<0.05) and capsaicin-treatment (37+/-18 vs. -34+/-11 pg/ml; P<0.05). A contribution of cholinergic mechanisms to this vagovagal-mediated stimulation of distention-induced gastrin release was excluded, since atropine (100 microg/kg/h; n = 8) further augmented distention-stimulated gastrin release. Since bombesin/gastrin-releasing peptide (GRP)-neurons contribute to vagally stimulated gastrin secretion, we have examined gastrin response to distention in the presence of the specific bombesin-receptor antagonist D-Phe6-BN(6-13)OMe (400 microg/kg/h: n = 10). This bombesin-antagonist completely reduced distention-stimulated gastrin release in vivo. In contrast, distention of the isolated, extrinsically denervated stomach significantly decreased gastrin release by 13+/-5 pg/min (5 ml saline, n = 8, P < 0.05), 28+/-8 pg/min (10 ml saline, n = 11, P < 0.05) and 35+/-10 pg/min (15 ml saline, n = 8, P < 0.01), respectively, without changing the activity of bombesin/GRP-neurons. Distention-induced decrease of gastrin release was attenuated to 50 percent by atropine (10(-7) M: n = 10) or tetrodotoxin (TTX) (10(-6) M; n = 10), respectively. These data demonstrate, that in anesthetized rats distention-stimulated gastrin secretion depends on the activation of a vagovagal reflex and intrinsic bombesin/GRP-neurons. In contrast distention of the isolated rat stomach inhibits gastrin release in part via intrinsic cholinergic pathways and other as yet unknown mechanisms.
Animals↗
[Prevention of cancer of the upper gastrointestinal tract].
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Adenocarcinoma↗
[Toxic megacolon after Helicobacter pylori eradication therapy].
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Aged↗
Laparoscopic gastrojejunostomy and endoscopic biliary stent placement for palliation of incurable gastric outlet obstruction with cholestasis.
BACKGROUND: For patients with incurable malignant gastric outlet obstruction and cholestasis, laparoscopic gastrojejunostomy combined with endoscopic biliary stent placement seems to offer a minimally invasive palliation. METHODS: We retrospectively analyzed the data of 16 patients submitted to laparoscopic gastrojejunostomy. Laparoscopic gastroenterostomy was performed as an antecolic, side-to-side gastrojejunostomy with enteroenterostomy. In 12 patients cholestasis was relieved preoperatively by stent placement via endoscopy (n = 6, 37.5%), percutaneous access (n = 5, 31%) or bilioenteric anastomosis (n = 1, 6.25%). One patient needed a percutaneous Yamakawa prosthesis postoperatively. RESULTS: Mean operative time was 126 min. There were no intraoperative complications. In one patient conversion to open surgery became necessary because of extensive adhesions. The only postoperative complication was bleeding from a trocar site requiring reintervention; there was no mortality. Median postoperative hospital stay was 7 days. Delayed gastric emptying was observed in 3 (18.7%) patients. Median survival was 87 days after the operation. All patients died from their primary disease but could maintain oral intake during the remaining survival time. CONCLUSIONS: We conclude that laparoscopic gastrojejunostomy and endoscopic or percutaneous biliary stenting provide a good functional result while impairing the quality of life only to a minimal extent.
Adult↗
Functional impairment of rat enterochromaffin-like cells by interleukin 1 beta.
BACKGROUND & AIMS: Histamine-producing enterochromaffin-like (ECL) cells play an integrative role in the regulation of acid secretion. Decreased mucosal histamine concentrations and increased levels of interleukin (IL) 1 beta, IL-6, and IL-8 have been detected in the gastric mucosa inflamed with Helicobacter pylori. The aim of this study was to investigate the response of isolated ECL cells to these cytokines. METHODS: Enriched rat gastric ECL cells (85%-95%) were cultured for 2-4 days. RESULTS: Polymerase chain reaction showed IL-1 and IL-6, but not IL-8 receptors, in ECL cell complementary DNA. Positive receptor staining with biotinylated IL-1 beta corresponded to ECL cell enrichment (92%). IL-6 and IL-8 had no effect on histamine secretion. IL-1 beta (2 U/mL) stimulated basal histamine secretion and nitric oxide production within 60 minutes and cyclic guanosine monophosphate production within 20 minutes. Pretreatment for 20 minutes with IL-1 beta (2 U/mL) attenuated gastrin-stimulated histamine secretion by 40%-50%, reversed by the IL-1 receptor antagonist (10 U/ mL). Pretreatment for 20 minutes with IL-1 beta (2 U/mL) completely inhibited gastrin-stimulated (1 nmol/L) histidine decarboxylase activity. IL-1 beta (2 U/mL, 60 minutes) increased lactate dehydrogenase release to 25% of cell content. Cells pretreated with IL-1 beta did not respond to gastrin after a further 48-hour culture and showed decreased histamine content. CONCLUSIONS: ECL cells appear to express IL-1 receptors. IL-1 beta causes sustained functional impairment of ECL cells in vitro.
Animals↗
Bombesin-like peptides stimulate somatostatin release from rat fundic D cells in primary culture.
In several species, bombesin-like neuropeptides stimulate somatostatin release in in vitro preparations of gastric mucosa. We sought to determine if this response is due to a direct effect on fundic D cells. Rat fundic mucosal cells were isolated by pronase E (1% D cells). D cells were separated by counterflow elutriation and subsequent density-gradient centrifugation (Nycodenz) (15% D cells) and grown in primary culture for 48 h (46% D cells). Cultured cells were double stained with affinity-purified rabbit-anti-gastrin-releasing peptide (GRP) receptor antibody and mouse monoclonal antibody to human somatostatin. After incubation with rhodamine-labeled anti-rabbit and fluorescein isothiocyanate-labeled anti-mouse antibodies, reactions were visualized by fluorescence microscopy. All cells positive for somatostatin had GRP receptors, whereas all non-D cells showed no expression in this G cell-free culture system. Somatostatin release from cultured cells was stimulated by sulfated cholecystokinin octapeptide (CCK-8; EC50 3 X 10(-10) M) and epinephrine (EC50 4 X 10(-8) M), which are established stimuli for canine fundic D cells. Bombesin (EC50 6 X 10(-11) M), its mammalian analog GRP-27, and neuromedin C (GRP-10) (EC50 1 X 10(-10) M, for both) were almost equally potent stimuli of somatostatin release, eliciting maximal response at 10(-9) M (400-550% above basal). Neuromedin B was less potent and effective (maximal response at 10(-8) M, 230% above basal). [D-Phe6]bombesin-(6-13)-OMe, a specific bombesin receptor antagonist, inhibited bombesin-stimulated somatostatin release in a competitive manner (IC50 9 X 10(-8) M). Potentiating interactions were observed between bombesin and dibutyryladenosine 3',5'-cyclic monophosphate (DBcAMP) or epinephrine, but not between bombesin and CCK-8. We conclude that bombesin-like peptides directly stimulate somatostatin release by interacting with specific receptors on rat fundic D cells. Bombesin-like peptides appear to induce Ca(2+)-phospholipid-dependent signal-response transduction, as is indirectly suggested by potentiating interactions with DBcAMP or epinephrine.
Animals↗
[Occlusion of an esophagobronchial fistula by implantation of a Montgomery esophageal and a dynamic tracheal stent after failure of conventional endoprosthesis].
Esophagorespiratory fistulas were frequently caused by malignant tumors, bougienage, laser therapy or radiochemotherapy. We here report the case of a patient with inoperable bronchial cancer, who developed a symptomatic esophagorespiratory fistula during combined radiochemotherapy with Cisplatin. A sufficient occlusion of the fistula could not be achieved with conventional plastic tubes or novel self-expanding silicone-coated Gianturco Song stents. After extraction of two Gianturco Song stents we inserted a Montgomery Salivary Bypass Stent into the esophagus and Dynamic stent into the trachea. This resulted in a total occlusion of the fistula. This present case suggests that the Montgomery stent may have little tendency to migrate due to its characteristic configuration and fixation and further demonstrates that the novel self-expanding silicone-coated Gianturco Song stents can be removed, if necessary.
Adenocarcinoma↗
[Interdisciplinary guidelines: cholelithiasis].
Quality management in internal medicine and surgery is especially difficult because of the magnitude of these two subjects. Between the years 1994 and 1996, the German scientific societies of internal medicine developed the manual "Rationelle Diagnostik und Therapie in der Inneren Medizin". The cooperation of colleagues was most helpful when the interests of several internal branches were involved. An even greater challenge is the development of interdisciplinary internal and surgical guidelines, which are presented here for cholelithiasis.
Cholecystectomy↗
[Minimal invasive therapy of gallstones by laparoscopic cholecystostomy].
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Cholecystostomy↗
Guanylin strongly stimulates rat duodenal HCO3- secretion: proposed mechanism and comparison with other secretagogues.
BACKGROUND & AIMS: Guanylin and heat-stable enterotoxin (STa) stimulate intestinal Cl- secretion via activation of the cystic fibrosis transmembrane regulator (CFTR)-encoded Cl- channel. It was speculated that CFTR activation also regulates electrogenic duodenal HCO3- secretion. Therefore, the effect of guanylin/STa and other secretagogues on rat duodenal HCO3- secretion was studied. METHODS: The HCO3- secretory rate of in vitro rat proximal duodenum was determined by pH stat titration and paracellular permeability by 3H-mannitol fluxes, bidirectional 36Cl- fluxes were measured, and the short-circuit current (Isc) was recorded. RESULTS: Luminal guanylin and STa concentration dependently stimulated the HCO3- secretory rate and Isc. Guanylin-stimulated HCO3- secretion was independent of luminal Cl-, inhibited by the Cl- channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoate, and additive to the HCO3- secretory rate stimulated by glucagon and carbachol but not by the tested adenosine 3',5'-cyclic monophosphate (cAMP)-dependent agonists. The ratio of the HCO3- secretory rate/Isc stimulated by the tested guanosine 3',5'-cyclic monophosphate (cGMP)-dependent agonists was markedly higher than the cAMP-dependent agonists. Prostaglandin E2 and 8-bromo-cAMP but not STa/guanylin also transiently increased paracellular permeability. CONCLUSIONS: Guanylin and STa stimulate electrogenic HCO3- secretion in rat duodenum, most likely via CFTR Cl- channel activation, but the different relationship for HCO3- to Isc in cGMP-than in cAMP-stimulated anion secretion suggests a different cellular source and/or signaling pathways.
Animals↗
Role of endogenous bombesin-peptides during vagal stimulation of gastric acid secretion in the rat.
The stimulatory effect of exogenous bombesin and its related mammalian peptides on gastric acid secretion and gastrin release has been examined in detail, while the regulatory role of endogenously released bombesin-like peptides is largely unknown. Accordingly we have determined the effect of a specific bombesin receptor antagonist during vagal stimulation of gastric acid secretion and gastrin release. In anesthetized rats electrical stimulation of the vagal nerves (10 V, 10 Hz, 1 ms) significantly increased plasma gastrin levels by 82 +/- 11 pg/20 min (P < 0.01) and gastric acid output by 99.4 +/- 9.9 mueq/20 min (P < 0.01). Intravenous infusion of the specific bombesin receptor antagonist D-Phe6-BN(6-13)OMe (400 nmol/kg/h) significantly reduced vagally induced increase of plasma gastrin levels by 70% to 29 +/- 8 pg/20 min (P < 0.05 vs control) and vagally stimulated gastric acid output by 40% to 57.4 +/- 10.6 mueq/20 min (P < 0.05 vs control). To demonstrate that the residual gastrin and acid response is due to non-bombesinergic mechanisms and not to an inadequate dose of the receptor antagonist, the latter was tested against gastrin-releasing peptide (GRP) at the maximally effective concentration of 300 pmol/kg/h, which resulted in an even 50% higher increase of plasma gastrin levels compared to vagal stimulation. The dose of the antagonist employed (400 nmol/kg/h) was sufficient to abolish GRP-induced stimulation of gastrin and gastric acid secretion. Previously it has been postulated that endogenous bombesin-peptides can stimulate acid secretion via gastrin-independent mechanisms. To investigate this possibility further the effect of the antagonist was examined on vagally induced acid secretion while gastrin levels were restored to the range of the respective control experiments. In presence of the antagonist the infusion of gastrin-17 (15 pmol/kg/h) in addition to vagal stimulation elevated plasma gastrin to levels not different from those during vagal stimulation alone. With identical plasma gastrin levels the bombesin receptor antagonist had no effect on vagally stimulated acid secretion (86.3 +/- 10.7 mueq/20 min vs 99.4 +/- 9.9 mueq/20 min in the controls; n.s.). In conclusion, the present data demonstrate for the first time that in rats in vivo endogenous bombesin peptides contribute to vagal stimulation of gastrin release and gastric acid secretion. Furthermore, endogenous bombesin-peptides exert their action on parietal cell function via an increase of gastrin release, while non-gastrinergic mechanisms are unimportant under the experimental conditions employed.
Animals↗
Gastrin secretion from primary cultures of rabbit antral G cells: stimulation by inflammatory cytokines.
BACKGROUND & AIMS: In Helicobacter pylori-induced gastritis, local production of cytokines may favor hypergastrinemia as an endocrine link between H. pylori-induced gastritis and duodenal ulcer. The aim of this study was to characterize cytokine effects on cultured rabbit antral G cells. METHODS: Monolayers (14.2% +/- 2.9% G cells) were studied after 48 hours in primary culture. RESULTS: Interleukin (IL) 1 beta (50% effective concentration [EC50], 5.3 +/- 0.4 ng/mL) and tumor necrosis factor (TNF) alpha (EC50, 5.5 +/- 0.5 ng/mL) stimulated gastrin release to 50% of the maximal response to 10(-9) mol/L neuromedin C. Stimulation by the maximally effective concentration of IL-1 beta (10 ng/mL) was inhibited by the human IL-1 receptor antagonist (100 ng/mL; inhibitory constant, 23.0 ng/mL), which prefers type I over type II IL-1 receptors. The response to the maximally effective concentration of TNF-alpha (10 ng/mL) was markedly inhibited by monoclonal antibody H398, an antagonist at TNF P55 receptors (inhibitory constant, 1.7 micrograms/mL), whereas monoclonal antibody utr1, an antagonist at TNF P75 receptors, was ineffective. Stimulation by IL-1 beta and TNF-alpha was additive to the responses to neuromedin C and O2-dibutyryl adenosine 3',5'-cyclic monophosphate. IL-6 and IL-8 (0.1-50 ng/mL) were ineffective. CONCLUSIONS: IL-1 beta and TNF-alpha stimulate gastrin secretion via receptors potentially residing on rabbit antral G cells themselves. We speculate that G cells express type I IL-1 receptors and TNF P55 but not TNF P75 receptors.
Animals↗