[Nephrotic syndrome and microhematuria in a patient with nutcracker syndrome: Report of a case and review of the literature]. / Nephrotisches Syndrom und Mikrohämaturie bei einer Patientin mit Nussknacker-Syndrom: Ein Fallbericht mit Literaturübersicht.

We report about a 43-year-old woman with polyvalent drug addiction (i.e. alcohol, nicotine, methadone maintenance program with parallel consumption of heroin) who presented to the emergency department with peripheral edema, generalized weakness, and arthralgia. Laboratory findings revealed, among others, proteinuria, hyperlipoproteinemia and hypoproteinemia defining nephrotic syndrome. Computed tomography of the abdomen and iliocavography further revealed compression of left renal vein between aorta and superior mesenteric artery with distention of left ovarian vein as a possible cause of nephrotic syndrome (i. e. nutcracker syndrome). After excluding other possible causes of nephrotic syndrome, we decided against an interventional procedure due to poor compliance of the patient and potential risk of secondary stent dislocation. Instead, we opted for a surgical approach (i. e. veno-venous bypass, meaning transposition of left vena ovarica on vena cava inferior). The operative and postoperative course was uneventful. Postoperatively, proteinuria, microhematuria, arthralgia and edema receded.

[Neuroendocrine tumors of the stomach (gastric carcinoids) are on the rise: good prognosis with early detection]. / (Neuro-)Endokrine Tumoren des Magens sind auf dem Vormarsch: Gute Prognose bei frühem Nachweis.

Neuroendocrine tumors (NET) of the stomach are on the rise. In the United States they have increased about tenfold in the last 35 years. Prognosis has been much improved over the last three to four decades. Nowadays most of such NETs are diagnosed at an early stage. Quite often gastric NETs are found incidentally during a gastroscopy, performed for other reasons. Most of the asymptomatic, well differentiated gastric NETs are less than 2 cm in diameter. Conservative management and endoscopic surveillance is adequate for well differentiated, multifocal type 1 or type 2 gastric NETs (gastric carcinoids) of 10-20 mm , unless they are angio-invasive, have infiltrated into the muscularis propria or have metastasized. Endoscopic ultrasound is the method of choice to determine tumor size and depth of infiltration. Surgery is, however, indicated for all NETs larger than 20 mm. For optimal management tumor biology, type and stage of the neoplasm as well as the individual situation of the patient have to be taken into account. Most of the patients can be treated conservatively and be followed up with endoscopic surveillance.

Endoscopy in Barrett's oesophagus: adherence to standards and neoplasia detection in the community practice versus hospital setting.

OBJECTIVE: Potential process differences between hospital and community-based endoscopy for Barrett's oesophagus have not been examined. We aimed at comparing adherence to guidelines and neoplasia detection rates in medical centres (MC) and community practices (CP). DESIGN: Retrospective analysis. SETTING: All histologically confirmed Barrett cases seen over a 3-year period in six MC and 19 CP covering a third of all upper gastrointestinal endoscopies (n = 126,000) performed annually in Berlin, Germany. MAIN OUTCOME MEASURE: Rate of relevant neoplasia (high-grade intraepithelial neoplasia or more) in both settings in relation to adherence to standards. RESULTS: Of 1317 Barrett cases, 66% were seen in CP. CP patients had a shorter mean Barrett length (2.6 cm vs. 3.8 cm; P < 0.001) with fewer biopsies taken during an examination (2.5 vs. 4.1 for Barrett length

Effect of the somatostatin analog octreotide on gastric mucosal function and histology during 3 months of preoperative treatment in patients with acromegaly.

OBJECTIVE: To study the effects of the somatostatin analog octreotide on gastric mucosal function and histology during short-term (3 months) preoperative treatment in patients with acromegaly. DESIGN: Open design clinical study. METHODS: 10 patients were studied before treatment with octreotide (pre-tx), on day 1 of 300 microg octreotide/day (d300), after 1 week on 300 (w300), 600 (w600) or 1500 (wl500) microg octreotide/day, and after an additional 2.5 months on 1500 microg octreotide/day (M3). An 8h gastrin profile was obtained and ambulatory intragastric 23h pH-metry carried out at the indicated time points. Gastroscopy was performed at pre-tx and M3 and multiple mucosal biopsy specimens taken. RESULTS: The mean serum gastrin concentration at first declined during octreotide therapy to a nadir at w1500, then recovered despite ongoing therapy (probably in response to reduced gastric acidity) and was similar to pre-tx values at M3 (mean+/-S.E.: 87+/-26, 50+/-11 and 98+/-46ng/l for pre-tx, w1500 and M3 respectively; P<0.05, pre-tx vs w1500). Gastric acidity had also declined at d300(P<0.05, d300 vs pre-tx), then recovered (despite the increase in the octreotide dose), but declined again at M3 (mean pH (95% confidence interval): 2.4 (1.7-3.2), 3.3 (2.4-4.3), 2.6 (1.8-:3.5, n=8) and 2.9 (1.6-4.2, n=7) at pre-tx, d300, w1500 and M3 respectively). The gastrin concentration at M3, although similar to pre-tx values, remained inadequately low for the reduced gastric acidity. The reduction in gastric acidity was marked during the daytime (0900-2200 h; P<0.01, d300 vs pre-tx and P=0.028, M3 vs pre-tx). However, while the stimulated postprandial gastric acid secretion was reduced at d300 (P<0.01, d300 vs pre-tx) and at M3 (n=7; P=0.027, M3 vs pre-tx), fasting and preprandial acidity was not affected. During the night, gastric acidity was reduced from 2200 to 0300 h, but the reduction was less marked than during the daytime. Paradoxically, the physiological intermittent late nocturnal reduction in acidity ('pH peaks' (0300-0800 h)) was abolished rather than enhanced. No patient acquired new Helicobacter pylori infection. The mean gastritis scores for antrum and body (n=8, Sidney classification) increased marginally from 1.7 to 1.9 (chronicity) and from 0.7 to 0.9 (atrophy), while the activity score was slightly reduced from 1.2 to 1.0. CONCLUSIONS: Three months of preoperative octreotide treatment profoundly and persistently altered gastric mucosal function (gastrin suppression, reduced acidity), but caused only minor variations in the pre-existing gastritis scores.

Endoscopic sclerotherapy with fibrin glue as compared with polidocanol to prevent early esophageal variceal rebleeding.

BACKGROUND/AIMS: Endoscopic sclerotherapy is of proven benefit for patients after esophageal variceal bleeding, but is associated with substantial local and systemic complications. Since fibrin glue is a promising agent for endoscopic sclerotherapy of esophageal varices, we compared its safety and efficacy in patients after esophageal variceal bleeding. PATIENTS AND METHODS: In a randomized, controlled trial, 36 patients with an acute episode of variceal bleeding were endoscopically treated with either polidocanol (18 patients) or fibrin glue (18 patients) by intravariceal injections within 12 h of admission. Tissue compatibility, incidence of various complications, episodes of rebleeding and overall survival rates were investigated. RESULTS: Rebleeding, especially from enrollment to day 28, was less common in the fibrin group (p=0.046), and all patients treated with fibrin glue survived for more than 28 days, whereas five patients treated with polidocanol died within this period. The incidence of sclerotherapy-induced ulcers was significantly lower in the fibrin group than in the polidocanol group (p=0.001), and major complications such as perforation or ulcer bleeding were observed only in the polidocanol group. There were no complications in any group due to activation of systemic coagulation, fibrinolysis or clinically relevant pulmonary embolization. CONCLUSIONS: We conclude that fibrin glue is an efficient and safe agent for endoscopic sclerotherapy of bleeding esophageal varices, especially in the immediate posthemorrhagic period.

[Endoscopic ultrasound of pathological mediastinal findings]. / Endoskopischer Ultraschall pathologischer Mediastinalbefunde.

INTRODUCTION: Mediastinal diseases are mostly diagnosed by CT and MRI. The applicability of ultrasound is limited by the surrounding air- and bone-containing thorax, which permits only restricted echo windows. Transesophageal endoscopic ultrasonography circumvents this problem and ensures visualization of parts of the mediastinum. PATIENTS AND METHODS: We report our results in 38 patients with pathological mediastinal findings who were examined by endoscopic ultrasound between 1988 and 1993. The diagnoses were established by imaging and/or histological procedures. RESULTS: The following mediastinal diseases were diagnosed in 38 patients: aberrant right subclavian artery (n = 3), right aortic arch (n = 1), aortic aneurysm (n = 6), cysts (n = 4), retrosternal struma (n = 3), mediastinal lymph node tuberculosis (n = 1), Hodgkin's/non-Hodgkin's lymphomas (n = 11), lymph node involvement in bronchogenic carcinoma (n = 8), mediastinal inflammatory fibrosarcoma (n = 1). Altogether, 37/38 pathological findings were demonstrated endosonographically. CONCLUSIONS: The results in this small group of patients with pathological mediastinal findings show that endoscopic ultrasound can give additional information to conventional imaging methods. A prospective comparative study is necessary to evaluate this procedure in comparison to the established imaging techniques.

[Intramural pseudodiverticulosis of the esophagus]. / Intramurale Pseudodivertikulose des Osophagus.

Esophageal intramural pseudodiverticulosis is a rare benign condition with the cardinal symptom of dysphagia mostly due to inflammatory strictures. The disease frequently develops in connection with alcohol abuse and esophageal reflux, candidiasis or motility disorders. Characteristic is the radiological visualization of intramural saccular contrast accumulations. We report on five patients with esophageal pseudodiverticulosis endoscopically diagnosed at our hospital within a period of five years. Four of these patients underwent extensive investigations for additional esophageal conditions: Histological/cytological examinations, manometry, pH-metry and endoscopic ultrasonography. These four patients had a pathological reflux with marked esophagitis and inflammatory strictures. We achieved long-lasting therapeutic results with complete relief by bougienage and reflux therapy with additional candidiasis treatment in two and motility treatment in one patient each. The detailed discussion deals with the clinical aspects, characteristics, therapy and pathogenesis.

Immunological and trophical effects of Saccharomyces boulardii on the small intestine in healthy human volunteers.

Saccharomyces boulardii (S.b.) is used for the prevention and treatment of diarrhea of different etiologies. We prospectively investigated the effects of S.b. on lymphocytes and duodenal mucosa. Before and after oral administration of S.b. for 3 weeks, circulating and intestinal lymphocytes were isolated and characterized by flow cytometry. Trophic effects on duodenal mucosa were investigated by morphometry and determination of brush border enzyme activity. Results were compared intraindividually before and after S.b. In intestinal lymphocytes no phenotypic changes were observed. CD4+ cells of the peripheral blood had a significantly increased expression of CD25 (p < 0.02). None of twelve volunteers had an increase in villous surface area (n.s.). Immunoglobulin A content in small intestine secretion was unaltered. An increase in brush border enzyme activity of lactase, alpha-glucosidase, and alkaline phosphatase was observed (p < 0.01). Our findings indicate that S.b. has a positive effect on the maturation of enterocytes and only a minor influence on lymphocytes.

Distinct receptors mediate gastrin-releasing peptide and neuromedin beta-induced delay of gastric of liquids in rats.

The present study was carried out to define which bombesin receptors are involved in the delay of gastric emptying induced by bombesin-like peptides. Adult male rats were fitted with gastric and jugular vein cannulas. Gastric emptying was determined 5 min after a 3-ml intragastric load of 0.9 M NaCl using phenol red as a marker. Mammalian bombesin-like peptides gastrin-releasing peptide-10 and neuromedin B both induced a delay of gastric emptying. When [Phe6]bombesin-(6-13)-methyl ester, a selective antagonist of the gastrin-releasing peptide-preferring subtype of bombesin receptors, was injected 5 min before the agonists, the effect of gastrin-releasing peptide-10 was competitively inhibited, whereas that of neuromedin B remained unaffected. Our results indicate that gastrin-releasing peptide-10 and neuromedin B delay gastric emptying by acting on distinct receptors in rats, in vivo.

[Somatostatin receptor scintigraphy and endoscopic ultrasound for the diagnosis of insulinoma and gastrinoma]. / Somatostatinrezeptor-Szintigraphie und endoskopischer Ultraschall zur Diagnostik von Insulinomen und Gastrinomen.

In a prospective study of 13 patients (three males and 10 females; mean age 53 [8-82] years) the value of somatostatin receptor scintigraphy (SRS) and endoscopic ultrasonography (EUS) was compared with transabdominal ultrasound (US), computed tomography (CT) and magnetic resonance imaging (MRI) in the diagnosis of insulinoma (six patients) or gastrinoma (seven patients). There were ten separate primary lesions of each tumour type, proven histologically. For insulinoma the sensitivity of EUS was 90%, SRS 10% and CT, US and MRI together 20%. For gastrinoma the sensitivity of EUS was 90%, SRS 100%, and 30% for the other three methods together. Thus EUS had a high diagnostic localizing sensitivity for both tumours, while SRS was highly sensitive only in the diagnosis of gastrinoma, not insulinoma. The value of CT, MRI and conventional ultrasonography lies in their ability to visualize distant metastases.

Cholecystokinin suppresses food intake by a nonendocrine mechanism in rats.

A cholecystokinin monoclonal antibody (CCK MAb) was used to immunoneutralize CCK to test the hypothesis that CCK produces satiety by an endocrine mechanism. We first characterized the effects of CCK MAb on pancreatic secretion. Conscious rats with jugular vein and bile-pancreatic duct cannulas received CCK MAb or control antibody intravenously 30 min before a 2-h maximal dose of CCK-8 (200 pmol.kg-1.h-1 i.v.) or access to food. CCK MAb caused dose-related inhibition of amylase secretion. CCK MAb (2 mg/kg) completely blocked the response to CCK-8 and inhibited the response to food by 89%. In feeding experiments, rats with free access to food received CCK MAb or control antibodies (2 mg/kg iv) 2 h after lights off. CCK MAb had no effect on 1.5- or 3.5-h food intake. Another group of rats received CCK MAb (4 mg/kg i.v.) or a combined injection of type A and type B CCK receptor antagonists devazepide and L-365,260 (1 mg/kg each i.v.). CCK MAb had no effect on feeding, whereas the receptor antagonists stimulated 1-, 2-, 3-, and 4-h intake by 62, 45, 43, and 29%. These results suggest that endogenous CCK stimulates pancreatic enzyme secretion at least partially by an endocrine mechanism and produces satiety by a nonendocrine mechanism.

Endosonography of neuroendocrine tumors of the stomach, duodenum, and pancreas.

Neuroendocrine tumors (NETs) of the foregut type are frequently smaller than 2 cm in diameter and mainly located in the pancreas or the gastric and duodenal wall. Conventional cross-sectional imaging techniques, such as transabdominal ultrasonography (US), computed tomography (CT), and magnetic resonance imaging (MRI) are limited by their inability to detect small tumors and especially those located within the gastrointestinal wall. Endoscopic ultrasonography (EUS) allows detailed visualization of the whole pancreas and almost all parts of the gastric and duodenal walls. Therefore, EUS is an important diagnostic tool for the preoperative localization of NETs of the foregut type. Several studies performed in a retrospective manner, as well as two studies performed in a prospective manner, indicate a clear superiority of EUS as compared to CT, US, MRI, and also angiography in detecting NETs of the foregut type. Somatostatin-receptor scintigraphy (SRS) also detects NETs of the foregut type in a very high percentage of cases, and the combination of EUS and SRS appears to increase the sensitivity even more. Thus EUS and also SRS should be employed early if NETs of the foregut type are suspected. Conventional imaging procedures such as US, CT, and MRI should be mainly used to exclude local and distant metastases.

Mechanism of bombesin-induced pancreatic secretion in unanesthetized rats.

It is unclear whether stimulation of pancreatic enzyme secretion by intravenously administered bombesin is a direct effect on acinar cells or is mediated by release of CCK; this distinction is important for defining the potential role of bombesin-like peptides as regulators of pancreatic secretion. The role of CCK in bombesin-induced pancreatic secretion was examined in rats using CCK radioimmunoassay and the CCK receptor antagonist L-364,718. A biphasic pancreatic response occurred to sequential doubling doses of bombesin (31 to 2000 pmol/kg/h, each for 30 min; n = 9 rats); amylase secretion increased to peak at 250 pmol/kg/h (11.5 +/- 1.7 kU/30 min; 4.2 +/- 0.6 kU/30 min, basal) and then declined to basal levels at 2000 pmol/kg/h. The ED50 dose of bombesin for stimulation was 31 pmol/kg/h, and the maximal response did not differ significantly from that to exogenous CCK-8 (10.6 +/- 1.5 kU/30 min) in the same rats. When single doses of bombesin were infused for 2 h (31, 62, 125, 250 pmol/kg/h; one dose per day; order randomized; n = 8), a similar dose-response relationship was seen, both for peak amylase response and cumulative output over basal. L-364,718 (0.5 mg/kg IV) had no effect on the pancreatic response to ED50 or maximal doses of bombesin. Neither dose of bombesin altered plasma CCK levels. In contrast, other stimulants of pancreatic secretion (food ingestion, soybean trypsin inhibitor) caused marked elevations in plasma CCK levels. These results indicate that the potent stimulation of pancreatic secretion by exogenous bombesin in rats is not mediated by CCK, similar to findings in humans.

Octreotide long term treatment of acromegaly: effect of drug withdrawal on serum growth hormone/insulin-like growth factor-I concentrations and on serum gastrin/24-hour intragastric pH values.

We studied a possible persistence of low GH concentrations after drug withdrawal in eight acromegalic patients who had been receiving octreotide treatment continuously for 42 months. Since octreotide induces chronic active gastritis, intragastric pH and serum gastrin were also determined before and during drug withdrawal. Results were compared to the respective pretreatment (pre-Tx) values. GH and insulin-like growth factor-I (IGF-I) increased after 4 weeks of octreotide withdrawal to pre-Tx values (GH, 12-h profile, 4.5 +/- 0.6, 2.6 +/- 0.7, and 5.6 +/- 1.1 micrograms/L; IGF-I, three samples, 3.4 +/- 0.4, 0.8 +/- 0.1, and 2.5 +/- 1.0 IU x 10(3)/L; means +/- SE, pre-Tx, on and off octreotide). A reduced insulin and augmented glucose response to oral glucose during therapy normalized after octreotide withdrawal (insulin, 527 +/- 84, 289 +/- 62, and 733 +/- 110 pmol/L; glucose, 6.2 +/- 0.3, 8.5 +/- 0.4, and 6.8 +/- 0.2 mmol/L; pre-Tx, on and off octreotide, means +/- SE). During octreotide treatment, the median 24-h intragastric pH value was 2.8 (pre-Tx pH not determined), and the median serum gastrin concentration (areas under the curve of 12-h profiles) was 1275 +/- 153 ng/L.12 h (n = 7). During octreotide withdrawal, pH decreased to 1.4, while serum gastrin increased to a median of 2937 +/- 472 ng/L.12 h. We conclude that GH and IGF-I suppression by long term octreotide therapy does not persist after drug withdrawal, indicating a need for life-long treatment. Octreotide-induced insulin suppression and glucose elevation are reversible. A high gastric pH during treatment may facilitate the development of octreotide-related gastritis. The gastrin increase during octreotide withdrawal probably reflects a response to chronic active gastritis after release from octreotide-induced gastrin inhibition.