Electronic data base in gastroenterological endoscopy.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Classen.
Explore the source record for details and available documents.
When a submucosal impression of the stomach fundus is seen during upper GI endoscopy, a true submucosal tumor can reliably be differentiated from an extragastric impression by endoscopic ultrasound (EUS). We report on 15 patients in whom EUS identified splenic vessels near the splenic hilum causing an impression of the posterior wall of the gastric fundus. Neither by EUS nor conventional ultrasound, computed tomography or clinical follow-up, was a tumor in the stomach or upper abdomen that could have been the cause of the gastric wall impression, identified. Two of the 15 patients had portal hypertension with multiple intra-/paramural venous collateral vessels. Twenty patients examined for other reasons and 10 patients with portal hypertension but without fundic impressions, served as controls: In these cases the splenic vessels were shown by EUS to follow a course more distant to the gastric wall. Thus, normal vascular structures should be included in the differential diagnosis of gastric fundus impression detected by endoscopy.
Explore the source record for details and available documents.
The majority of physicians consider the use of free dictation for medical reports to be essential in many domains. One of the main criticisms of structured data entry is the possible lack of flexibility and completeness. Electronic documentation systems exist for endoscopy and ultrasonography examinations which are based on structured input as well as on free dictation. Endoscopy and ultrasonography reports based on free dictation were evaluated for omissive errors. The data evaluated was drawn from a database of 18,239 gastroscopy and 3,340 colonoscopy reports dictated by 28 physicians over 74 months, and 18,834 ultrasonography reports dictated by 37 physicians over 42 months. The error rates varied from 0% to 41.8% depending upon the particular feature and the particular examination, but were usually below 15%. The results were independent of the experience of the examiner. This study provides baseline measurements of omissive error rates for selected findings in gastrointestinal endoscopy and abdominal ultrasonography which can be used as standards for the development and evaluation of systems for collection of clinical data.
A case is reported of a 56-year-old woman of Libyan origin presenting with dysphagia, retrosternal pain and weight loss. Oesophago-gastroduodenoscopy revealed an ulcerated tumor in the upper oesophagus strongly suggesting a malignancy. A positive Mendel-Mantoux test along with histological evidence of epitheloid cell granulomas and clinical findings consistent with pulmonary and lymph node tuberculosis led to the presumptive diagnosis of oesophageal tuberculosis. The diagnosis was later confirmed by positive bacteriological cultures of oesophageal biopsies and gastric washings. It is very unusual for dysphagia to be the presenting symptom of active adult tuberculosis. Oesophageal tuberculosis is extremely rare and must be distinguished predominantly from oesophageal carcinoma.
A pull-through trocar is described which establishes a percutaneous access to the stomach and may immediately be used for endoscopy. The trocar is placed in a similar fashion to PEG probes. The technique was evaluated in animals. Using rigid endoscopes and instruments introduced through the trocar operative manipulations of the gastric wall were carried out. There were no severe complications. The new method extends the scope of percutaneous therapeutic endoscopy (minimal invasive surgery) by permitting direct access to the interior of the stomach.
Eight healthy volunteers were studied before and after 3 weeks of dietary supplementation with fish oil (10.5 g day-1, 18% (1.9 g) eicosapentaenoic acid). Duodenal mucosal lesions were induced by instillation of 40 ml ethanol (40%). Mean endoscopic lesion score was lower after fish oil treatment (1.62 +/- 0.32; mean +/- SEM) than before (3.25 +/- 0.31; P less than 0.01). Histologic lesion score fell from 22.75 +/- 1.98 before treatment to 13.50 +/- 1.51 after fish oil (P less than 0.01). Basal and pentagastrin-stimulated gastric acid output remained unaffected. Release of prostaglandin E2, 6-keto-prostaglandin F1 alpha, and thromboxane B2 from biopsy specimens of the duodenal mucosa in vitro was not significantly altered after fish oil ingestion. In the same in vitro system calcium ionophore A23187-induced release of total leukotriene C (LTC) increased from 10.6 +/- 1.5 ng g-1 mucosa 20 min before treatment to 30.4 +/- 3.2 ng after fish oil. High pressure liquid chromatography analysis showed that this increase was partly due to formation of LTC5 as after fish oil 28% of total LTC were identified as LTC5 whereas 72% were LTC4. We conclude that in humans fish oil reduces ethanol-induced damage of the duodenal mucosa without inhibiting gastric acid secretion or stimulating prostaglandin formation. It remains to be clarified if the changes in leukotriene formation are relevant for the mucosaprotective fish oil effect.
We investigated the effect of glucagon-like peptide 1 (GLP-1)-(7-36) amide and its molecular variants GLP-1-(1-37) and GLP-1-(1-36) amide on enzymatically dispersed enriched rat parietal cells using [14C]aminopyrine accumulation as a measure of H+ production. GLP-1-(7-36) amide was 100 times more potent than GLP-1-(1-37) and GLP-1-(1-36) amide in stimulating [14C]aminopyrine accumulation. At their maximally effective concentrations, GLP-1-(7-36) amide (10(-8) M), GLP-1-(1-37) (10(-6) M), and GLP-1-(1-36) amide (10(-6) M) reached 80-90% of the response to 10(-4) M histamine. However, the peptides were 100-10,000 times more potent than histamine, which induced maximal [14C]aminopyrine accumulation at 10(-4) M. Stimulation by GLP-1 was dependent on the presence of a phosphodiesterase inhibitor and was not altered by pertussis toxin. Ranitidine failed to affect the response to the GLP-1 variants. Stimulation of H+ production by GLP-1 was accompanied by an increase in the formation of adenosine 3',5'-cyclic monophosphate (cAMP) but not by changes in phosphoinositol breakdown. In stimulating [14C]aminopyrine accumulation, the GLP-1 variants acted additively to threshold but not to maximal concentrations of histamine, suggesting that histamine and GLP-1 activate the same cAMP pool. In contrast, in anesthetized rats GLP-1-(7-36) amide (10-500 ng.kg-1.h-1) had no effect on basal and pentagastrin-stimulated acid secretion in vivo. We conclude that GLP-1 exerts a direct stimulatory effect on rat parietal cells. This potent effect is mediated by cAMP and is independent of H2 receptors. In vivo direct stimulation by GLP-1 of the parietal cells might be counterbalanced by indirect inhibitory mechanisms that are excluded in the in vitro cell system.
Intact segments of rat ileum were stimulated in vitro by either electrical field stimulation (EFS) or cholinergic stimulation with carbachol, in the presence of absence of varying insulin concentrations (50, 100 and 200 microU/ml), and the contraction in the longitudinal axis was recorded. Insulin had no significant influence on the carbachol contractile dose-response curve nor did it affect the cholinergically mediated 'on-contraction' at onset of the electrical stimulus. The 'off-contraction' occurring at cessation of the electrical stimulus was partly mediated by a cholinergic and partly by a noncholinergic and nonadrenergic mechanism, and decreased over time with repeated stimulation. This decay with time was significantly attenuated by insulin. In the presence of insulin, release of bombesin-like immunoreactivity induced by carbachol or EFS significantly increased. On the other hand, the release of somatostatin-like immunoreactivity was suppressed by 50-70% in the presence of insulin. These results demonstrate that in vitro insulin can modify both the motility responses of isolated segments of rat ileum and the neuropeptide release from such segments.
Three patients with ulcerative colitis in the active stage demonstrated reduced levels of F XIII activity and F XIII subunit A (61 and 80.3%, respectively). Because of the lack of clinical improvement during conservative therapy, the patients were treated additionally with F XIII concentrate (Fibrogammin HS, Behring, FRG) for 10 days. The substitution resulted in an increase in F XIII activity (144.3%) and F XIII subunit A (238%) as well as in a marked improvement in symptoms.
OBJECTIVES: Because disturbances of gastric emptying are a serious complication in insulin-dependent diabetic subjects with regard to the maintenance of good metabolic control, we wanted to assess the effectiveness of motilin as a potential treatment for gastric emptying disturbances. RESEARCH DESIGN AND METHODS: The intestinal hormone motilin has been shown to accelerate gastric emptying in healthy subjects. Therefore, we examined the effect of intravenous motilin on gastric emptying of a 99mTc colloid-labeled semisolid test meal in 9 insulin-dependent diabetic patients with diabetic gastroparesis. All patients had a significantly delayed gastric emptying rate compared with a group of 11 healthy control subjects. RESULTS: During the infusion of motilin, gastric emptying was accelerated, and it was no longer significantly different from control values. CONCLUSIONS: These data demonstrate that motilin and related compounds such as erythromycin derivatives could be useful for the treatment of disturbed gastric emptying in diabetic subjects.
Explore the source record for details and available documents.
The present study was designed to determine in humans the dose of CCK which suppresses food intake. 18 male subjects received in randomized order either i.v. saline or Thr28 Nle31 CCK 25-33 (CCK-9) at 100 or 500 pmol/kgh, respectively. In addition, 7 subjects received CCK together with the opiate receptor antagonist naloxone to examine if activation of endogenous opioids might interfere with the potential satiating effect of CCK. Food intake during saline was 32 +/- 2 sandwiches (mean +/- SEM), during CCK-9 100 pmol/kgh 28 +/- 2 (n.s.) and only 12 +/- 3 during CCK-9 500 pmol/kgh (p less than 0.01). The respective water intake was 730 +/- 70 ml, 590 +/- 60 ml (n.s.) and 320 +/- 50 ml (p less than 0.01). Naloxone further reduced food and water intake during high but not low dose CCK or saline. During saline postprandial insulin levels rose by 49 +/- 6 microU/ml within 45 min which was attenuated during low dose (23 +/- 6 microU/ml; p less than 0.01) and high dose CCK-9 (1 +/- 1 microU/ml; p less than 0.001). Plasma glucagon did not change in control or CCK experiments. The postprandial rise of pancreatic polypeptide was attenuated during high dose CCK. Naloxone had no effect on the hormonal response except for a prolonged reduction of insulin and glucose levels following high dose CCK + naloxone. Plasma CCK levels rose by 5.4 pmol/l in controls but by 55 and 255 pmol/l during the low and high dose CCK infusion, respectively. These data demonstrate that suppression of food intake in man by i.v. CCK is a pharmacological rather than a physiological effect.(ABSTRACT TRUNCATED AT 250 WORDS)
The main problem of conventional endoscopic or percutaneous biliary drainage is the clogging of plastic endoprostheses. Therapeutic advances may be achieved by self-expanding or balloon-expandable braided or slit metal stents due to their large lumen and small surface area. Preliminary clinical studies show excellent early results but a divergent long-term clinical outcome depending on the selection of patients, the implantation technique or the type of the stent. If a long-distance overlap of biliary stenoses is achieved the metal stents may be superior to plastic prostheses due to a reduction of the risk of bile encrustation.
Endoscopic ultrasound (EUS) has been used in the diagnosis and staging of gastroenterologic tumors for about ten years. High accuracy rates of EUS in staging of esophageal, gastric and pancreatic carcinoma (T-stage: 80-95%, N-stage: 75-85%) have been reported. EUS is therefore a valuable diagnostic tool für assessment of prognosis as well as for planning of therapy of these tumors. Its value in benign gastroenterologic disease is unclear. EUS seems to be much less reliable in the differentiation between benign and malignant changes (e.g. esophageal stenoses, gastric ulcers, pancreatic mass lesions).
Late diabetic effects are the sequelae of for a long time super elevated blood sugar levels. The diabetic nephropathy is the cause of the secondary arterial hypertension. The investigation seeks for the connections between the diabetes mellitus and the essential, that is primary hypertension. The two diseases frequently appear and clearly increase in the second half of life. Moreover, they are above average frequently associated with each other. Among brothers and sisters of diabetic hypertensives in comparison to normal cohorts clearly increased high blood pressure prevalences were found. The insulin resistance which could be proved in a great number of hypertensive and which has been known since more than two decades might be the connecting link between hypertension and diabetes mellitus. Like the obesity the essential hypertension can be associated with all degrees of an insulin hyposensitiveness. The sodium-retaining effect of the insulin might explain the increased sodium content of the body in hypertensives. The differential diagnostics of the essential hypertension should therefore seek for conditions of an insulin resistance. The type II diabetic lacks a release of bradykinin during muscle work. Thus the glucose uptake into the cell is unfavourable influenced and demands an increased insulin excretion. This genetically (?) fixed defect is found also in essential hypertensives. It could be the connecting link between the two diseases. ACE-inhibitors have via a kininase II inhibition an effect also on the bradykinin decomposition and can favourable influence the glucose uptake into the muscle. An improved insulin effect among the ACE-inhibitors was described. Therefore, they should be preferred in the treatment of hypertensive diabetics.
In man, only little is known about the site of origin of satiety signals within the gastrointestinal tract. Therefore, it was the aim of this study to examine the role of the stomach and the small intestine as a source of satiety signals. 8 overnight fasted healthy volunteers received intraduodenal (100 or 200 ml/h) or intragastric (100 ml/h) infusions of a mixed liquid diet (Biosorb) or iso-osmolar saline, respectively. 20 minutes after start of the infusion, standardized mini-sandwiches and water were presented and food intake was recorded for the ensuing 90 minutes. During both rates of intraduodenal nutrient infusion, cumulative food intake was identical to that during saline infusion. However, during intragastric nutrient infusion, cumulative food intake was significantly reduced compared to saline infusion (30 +/- 1 vs. 36 +/- 2 sandwiches; p less than 0.05). These data indicate that food consumption in man is reduced, if initiation of eating is preceded by nutrient administration into the stomach, but not into the duodenum. This effect does not appear to be mediated by gastrin, since plasma gastrin levels were not different during gastric and duodenal nutrient administration. In conclusion, the results of this study suggest that the generation of satiety signals in man is dependent on the presence of food in the stomach. Food only in the duodenum has no effect, although synergistic gastric and intestinal mechanisms can as yet not be excluded.
Explore the source record for details and available documents.