Search PubMed⌕ Search

Biomedical subjects

H Koop

Publications and source records attributed to H Koop.

At least 19 recordsLinked to original sources
PubMed2002

Gastroesophageal reflux disease and Barrett's esophagus.

Gastroesophageal reflux disease (GERD) is a common clinical problem. More frequent and extended acidic reflux episodes are characteristic of GERD, although substantial (nonacid) reflux per se is also observed in control individuals. Helicobacter pylori may protect some people from reflux disease, but others do not experience deterioration of GERD as a result of H. pylori eradication, for reasons so far unknown. Medical treatment, preferably with proton-pump inhibitors, is well established and is also recommended in endoscopy-negative forms of the disease, although the efficacy is less marked in comparison with erosive esophagitis. Surgery has emerged as an alternative to medical therapy, but the long-term results do not now appear to be as promising as was initially claimed. A number of new endoscopic techniques for the treatment of GERD have been developed, but the future for these is unclear. Barrett's esophagus develops in some patients with GERD for unknown reasons, and surveillance should be carried out in these patients due to the risk of subsequent malignant transformation. Several new approaches have been developed for detecting premalignant conditions, but these need to be investigated further. Ablative techniques are still under intensive investigation, and appear to be promising, at least in a subset of patients, although they are not devoid of major complications. Whether antireflux therapy, irrespective of the method used, can slow down the development of cancer is still an intriguing and clinically important question.

Barrett Esophagus↗
PubMed2000

Efficient transformation of Dictyostelium discoideum with a particle inflow gun.

We report experiments to transform Dictyostelium discoideum using a simple home-made particle gun. Stable transformants were obtained at frequencies of up to 2500 clones/microg DNA. This is five times more than we achieve with the same vector using electroporation protocols. We also show that the particle inflow gun can be used for analysis of developmentally regulated gene expression in a transient assay.

Animals↗
PubMed2000

Reflux disease and Barrett's esophagus.

Gastroesophageal reflux disease (GERD) is still an important clinical problem. Continuing efforts are being made to establish a classification of the condition that would allow improved communications for both clinical and research purposes. In medical treatment, the trends are toward proton-pump inhibitor therapy at all stages of GERD, calling into question the role of endoscopy for tailoring individual therapy. Arguments against the use of H. pylori eradication therapy in GERD have gained importance. Surgeons are continuing to report excellent results with fundoplication, but careful studies are needed to prove whether antireflux surgery is really capable of saving costs, as its proponents claim. Barrett's esophagus is still a topic of lively interest. Since there is no method of primary prevention, endoscopy has a crucial role in detecting affected patients and guiding them toward one of the various surveillance strategies--which are not yet clearly established. The debate over short-segment Barrett's esophagus, and especially over "microscopic" Barrett's esophagus (at the squamocolumnar junction), has not yet been resolved. However, there is now less doubt that GERD is a condition associated with a substantially higher risk for the development of esophageal adenocarcinoma. Given this risk of malignant transformation, there is continuing competition between different ablation techniques; however, careful data from much larger populations will be needed before ablation reaches the stage of broad clinical application. Until specific guidelines become available, patients with Barrett's esophagus should receive endoscopic follow-up until it can be ascertained which individuals are at risk for cancer and require ablation of Barrett's mucosa.

Adenocarcinoma↗
PubMed2000

Esophagobronchial fistula combined with a peptic esophageal stenosis.

Peptic strictures are a rare complication of severe gastroesophageal reflux disease. An esophagobronchial fistula as a complication of a severe long-term reflux esophagitis with peptic stenosis is here described for the first time: A 43-year-old mentally disabled patient suffered from recurrent bronchopneumonia. Endoscopy revealed an esophagobronchial fistula originating in a peptic stricture. Under short-term fasting, intravenous feeding and application of a proton pump inhibitor (PPI) closure of this fistula was achieved within 4 days. Subsequently, dilatation was carried out. The case demonstrates that pulmonary complications in patients with peptic esophageal strictures may not only be due to aspiration of refluxate but--rarely--also to fistulae between the esophagus and the bronchial tree.

Adult↗
PubMed2000

Rifabutin-based triple therapy after failure of Helicobacter pylori eradication treatment: preliminary experience.

Despite continuous improvement of Helicobacter pylori (Hp) eradication therapy, new treatment regimens are necessary if established first-line treatments fail. In the present pilot study, a recently described rifabutin-based triple therapy was evaluated after preceding failure of triple therapy. Rifabutin (150 mg), amoxicillin (1 g), and lansoprazole (30 mg) were administered twice daily for 1 week to 25 patients infected with Hp who had previously failed to respond to eradication treatment and/or who had developed resistance to macrolides and nitroimidazoles. Four patients were lost to follow-up. Eradication rate of rifabutin-based triple therapy was 86% (18/21; per protocol) and 72% (18/25; intention-to-treat). Side effects were minimal. It is concluded that this new drug combination is an effective therapy for Hp strains resistant to clarithromycin or metronidazole; however, rifabutin-based treatment regimens for Hp eradication should be restricted to patients infected with resistant strains.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2000

Detection of autoantibodies against tissue transglutaminase in patients with celiac disease and dermatitis herpetiformis.

OBJECTIVE: Endomysial autoantibodies (EmA) are specific for celiac disease. The target antigen has been identified as tissue tranglutaminase (tTG). Our aim was to study the accuracy of a newly developed enzyme-linked immunosorbent assay (ELISA) for easy detection of tTG autoantibodies. METHODS: Thirty-one sera from patients with histologically proven celiac disease and 23 healthy controls were examined for EmA using monkey esophagus and human umbilical cord as substrate. IgA-tTG autoantibodies were determined by newly developed ELISA. Additionally, sera from patients with dermatitis herpetiformis (n = 20), inflammatory bowel disease (IBD; n = 32), chronic liver disease (n = 36), and diabetes mellitus (n = 19) were tested. RESULTS: The sensitivity of the tTG autoantibody ELISA accounted for 90% detection in patients with untreated celiac disease. The specificity was 76% owing to positive values in the lower range in patients with IBD (15%), chronic liver disease (36%), and diabetes (22%), all of whom were negative for EmA. In dermatitis herpetiformis patients 90% were EmA-positive. Of these, only 47% showed elevated tTG autoantibodies. Preincubation of sera from dermatitis patients with tTG abolished immunofluorescent staining of endomysial structures. CONCLUSION: Detection of mid- to high-titer tTG autoantibodies is highly specific for celiac disease. However, in the low-titer range, overlap exists with liver disease, IBD, and diabetes. Tissue transglutaminase autoantibodies may evolve as a new screening and follow-up method for celiac disease. Although tTG seems to be a major autoantigen in dermatitis herpetiformis, the low sensitivity of both tTG ELISA and immunofluorescence using human umbilical cord suggests differential involvement of tTG in this disease.

Animals↗
PubMed1999

Eradication of Helicobacter pylori heals atrophic corpus gastritis caused by long-term treatment with omeprazole.

Long-term treatment with proton pump inhibitors in patients with Helicobacter pylori gastritis can lead to atrophic changes in the corpus mucosa. What is still unclear, however, is whether this atrophy can regress in response to Helicobacter pylori eradication. We report on a male patient with Helicobacter pylori gastritis receiving long-term treatment (4 years) with omeprazole for gastrooesophageal reflux disease, who developed autoaggressive gastritis with progressive atrophy, hypochlorhydria, hypergastrinaemia and nodular ECL-cell hyperplasia. To determine whether these changes might be induced to regress, Helicobacter pylori eradication therapy was administered. Ten months after Helicobacter pylori eradication autoaggressive lymphocytic infiltrates were no longer detectable, and the glands in the corpus mucosa had normalised despite continued treatment with omeprazole - a finding that was confirmed at two further follow-up surveys performed at 6-month intervals. This case report shows that atrophy of the corpus mucosa developing under long-term treatment with a proton pump inhibitor can be cured by eradicating Helicobacter pylori.

Adult↗
PubMed1998

[Prevention of gastric cancer: Helicobacter--eradication and immunization].

Adenocarcinoma of the stomach (excluding carcinoma of the cardia) has been established as a consequence of gastric infection with Helicobacter pylori (H.p.). The specific role of H.p. in the pathogenesis is unknown so far; yet, several other factors are involved in the development of the neoplasia. Since-in contrast to the wide prevalence of the infection-only very few persons will develop gastric carcinomas, prophylaxis by H.p. eradication is not advisable. This may change after a vaccination has become available; however, studies on the characterization of efficient vaccines are still under investigation. Thus, H.p. eradication treatment may, if at all, be used as prophylaxis for gastric carcinoma only in clinical studies and in subjects at a high risk for this tumour.

Adenocarcinoma↗
PubMed1997

Impairment of hepatic transport processes in perfused rat liver by the specific CCK receptor antagonist loxiglumide.

The specific cholecystokinin (CCK) receptor antagonist loxiglumide has been used in several human and animal studies to investigate the role of CCK in gastrointestinal physiology. In the present study, the interference of this CCK receptor antagonist with hepatic transport processes was characterized in the perfused rat liver. Indocyanine green, an organic dye which is secreted into bile without being metabolized, was taken up in control experiments at a rate of 68.1 +/- 7.7%. The CCK receptor antagonist lowered the extraction to 0.5 +/- 2.6% (P < 0.001). The compound diminished the hepatic extraction of CCK-8 from 90.95 +/- 2.60% to 4.90 +/- 1.95% (P < 0.001) and of gastrin from 22.2 +/- 1.1% to 8.2 +/- 1.9% (P < 0.001). The hepatic extraction of lidocaine, which is metabolized by the cytochrome P450 system, was only slightly altered. For leukotrienes and taurocholate, the rate-limiting step for transport into bile is secretion across the canalicular membrane; the hepatic extraction of leukotriene D4 was markedly diminished by loxiglumide whereas the transport of taurocholate was only slightly inhibited. The present study demonstrates that the specific CCK receptor antagonist loxiglumide diminished the hepatic extraction of various substances, including peptides and organic anions. It did not interfere with the cytochrome P450 system. The pronounced reduction of hepatic uptake of indocyanine green and leukotriene may be due to an interference with the transport system of these substances in the liver.

Animals↗
PubMed1997

One-year prophylactic efficacy and safety of pantoprazole in controlling gastro-oesophageal reflux symptoms in patients with healed reflux oesophagitis.

BACKGROUND: Pantoprazole is a benzimidazole derivative which selectively inhibits the proton pump H+. K+-ATPase necessary for the final step in gastric acid secretion. AIM: To investigate the tolerability and the prophylactic effect of pantoprazole 40 mg once daily on relapse in patients whose reflux oesophagitis had been healed. METHODS: The safety of pantoprazole 40 mg once daily was assessed in an open 1-year trial on 222 patients whose reflux oesophagitis had been healed with omeprazole or pantoprazole. Relapse was defined as endoscopically-confirmed reflux oesophagitis (at least Grade I), with endoscopies being performed for patients experiencing 3 consecutive days of disease-specific symptoms. RESULTS: Kaplan-Meier survival analysis at 6 and 12 months gave estimated treatment failure rates of 2% and 6% from confirmed relapses (per-protocol), and of 9% and 30% for a worst-case group (all withdrawals counted as failures). The only population shift in laboratory variables was a doubling of the median serum gastrin level over the first 6 months; thereafter it stabilized. Fifty-four (24%) patients experienced adverse events; 15 of these withdrew. Serious adverse events were reported for 12 patients. CONCLUSIONS: Pantoprazole appears to be highly effective and to have a good safety profile for long-term prophylaxis of reflux oesophagitis.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1997

Gastro-oesophageal reflux disease: medical or surgical treatment? Report of an interactive workshop.

Gastroesophageal reflux disease (GERD) is the most common disease of the upper gastrointestinal tract. With the introduction of proton pump inhibitors medical treatment of GERD has been significantly improved. However, the development of laparoscopic antireflux surgery resulted in an increasing interest of surgeons in this disease. An interactive meeting was organized in order to develop an agreement between gastoenterologists and surgeons regarding therapeutic decisions and this is the main topic of this paper.

Barrett Esophagus↗
PubMed1996

[Therapy of Helicobacter infection].

Infection with Helicobacter pylori (H.p.) leads to mostly asymptomatic chronic gastritis. However, H.p. plays a role in peptic ulcer, giant fold gastritis (Menetrier's disease), and possibly in gastric carcinoma and low-grade MALT lymphoma. Whether functional dyspepsia also represents a Helicobacter-induced entity is questionable. H.p. should be eradicated in patients with peptic ulcer disease, Menetrier+s disease and - but in controlled studies only - in MALT lymphomas. Triple therapy with low-dose proton pump inhibitors and two antibiotics is the most favourable treatment compared to dual therapy with omeprazole and amoxicillin/clarithromycin despite the unresolved question of the development of drug resistance.

Anti-Bacterial Agents↗
PubMed1996

Physiological control of cholecystokinin release and pancreatic enzyme secretion by intraduodenal bile acids.

BACKGROUND: The physiological relevance of duodenal bile acids in the control of cholecystokinin release and pancreatic enzyme secretion is still unknown. AIMS: To provide a near physiological situation by perfusing a bile acid mixture mimicking the individual endogenous bile acid composition of the person under investigation. For maximal reduction of endogenous bile output the CCK-A receptor antagonist loxiglumide was infused intravenously. SUBJECTS AND METHODS: Seven healthy volunteers were studied on four different days by a duodenal marker perfusion technique. The individual bile acid composition in duodenal juice and test meal stimulated bile acid output was assessed on day 1. Bile acids were perfused at an amount of 30 or 100% as determined on day 1 in combination with the test meal in the presence or absence of loxiglumide. Pancreatic enzymes, bilirubin, and bile acid output were determined in duodenal juice. Plasma cholecystokinin (CCK) and plasma pancreatic polypeptide (PP) were measured radioimmunologically. RESULTS: Bile acid perfusion did not significantly alter stimulated pancreatic enzyme, bilirubin or bile acid output or plasma CCK. Loxiglumide did not alter basal CCK release but increased test meal stimulated CCK output fourfold (p < 0.05). The addition of bile acids to the test meal at a dose resembling 30% of bile acid output as determined on day 1 prevented this increase. Plasma PP concentration remained unchanged by bile acids and were mostly undetectable during loxiglumide infusion. CONCLUSIONS: The CCK producing cell is under constant suppression by intraduodenal bile acids which cannot be further enhanced by a physiological bile acid mixture. However, removal of duodenal bile acids by inhibition of gall bladder contraction unmasks this suppression leading to a dramatic increase in plasma CCK levels. As little as one third of postprandially released bile acids completely reverse this effect. Bile acids are the most important luminal regulator of CCK release in humans.

Adult↗
PubMed1996

[Can pharmaco-DSA of the kidney replace intraoperative rapid biopsy diagnosis?].

QUESTION: Can primary nephrectomy be performed without preliminary sample excision of the tumor if pharmaco-angiography of the kidney has demonstrated the typical tumor vascularization? MATERIAL AND METHOD: To clarify this question in 32 patients with "displacing mass" of the kidney, verified in sonography and computer-tomography, or hematuria of unknown origin, we prospectively performed and additional pharmaco-angiography of the respective kidney. RESULTS: In 18 patients with tumor vascularization in the pharmaco-angiography, intraoperatively we found 15 malignant renal cell carcinomas, 1 patient with transitional cell carcinoma of the renal pelvis, 1 leiomyosarcoma, and 1 high-differentiated tumor of only 2 cm in diameter with unclear dignity, which was treated by enucleation. CONCLUSION: In case of an intrarenal lesion of more than 3 cm in diameter and additional tumor vascularization seen in selective pharmaco-angiography, the kidney undoubtedly can be removed by primary nephrectomy without a preliminary sample excision to confirm the diagnosis. For tumors with a diameter of less than 3 cm and additional tumor-vascularization, the option should be enucleation. If there is a "tumor" without typical malignant vascularization, the exploration by sample excision should be performed. Depending on the histological result the tumor should be removed by enucleation or nephrectomy.

Adult↗
PubMed1996

Intragastric pH and serum gastrin during administration of different doses of pantoprazole in healthy subjects.

OBJECTIVE AND DESIGN: The effect of increasing doses of pantoprazole, a newly developed proton pump inhibitor, given at once daily doses of 40, 80 and 120 mg, on intragastric pH and serum gastrin profiles was studied in 15 healthy subjects in a randomized, double-blind, crossover study and compared to recordings without therapy. Measurements of intragastric pH and serum gastrin were performed on the 7th day of treatment by continuous pH recording and radioimmunoassay in blood samples obtained in 1-h intervals, respectively. RESULTS: Pantoprazole significantly increased gastric pH above basal at all pantoprazole doses studied: median 24-h pH rose from 1.2 without therapy to 3.4, 3.3 and 3.6 at 40, 80 and 120 mg daily, respectively. The corresponding integrated 24-h gastrin output was 1632, 2338 and 2248 pg/ml x 24 h compared to 575 pg/ml x 24 h without pantoprazole. There was no interindividual correlation between values of 24-h median pH and 24-h gastrin output at any pantoprazole dose studied. However, fasting gastrin levels closely correlated with 24-h gastrin output (r = 0.789; P < 0.0001). The acid inhibitory effect was significantly (P < 0.01) augmented in Helicobacter pylori positive subjects. CONCLUSION: It is concluded that pantoprazole is an effective inhibitor of gastric acid secretion. Increasing a single pantoprazole dose above 40 mg does not lead to increased median pH elevation. The individual extent of acid inhibition does not predict the magnitude of gastrin elevation. Acid inhibition appears more efficient in Helicobacter pylori positive subjects.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1995

Comparative trial of pantoprazole and ranitidine in the treatment of reflux esophagitis. Results of a German multicenter study.

In 249 patients with acute symptomatic reflux esophagitis grade II and III (Savary-Miller classification), we compared the efficacy and safety of pantoprazole, a newly developed proton pump inhibitor given at a once-daily dose of 40 mg, with a standard dose of the H2 receptor antagonist ranitidine (150 mg b.i.d.) in a randomized, double-blind, multicenter study. Complete healing was achieved after 4 and 8 weeks of therapy (protocol-correct) in 69 and 82% (pantoprazole) and 57 and 67% (ranitidine), respectively (p = 0.054 at 4 weeks and p < 0.01 at 8 weeks). The predominant symptoms of gastroesophageal reflux, i.e., heartburn and acid eructation, were more effectively reduced in pantoprazole- than in ranitidine-treated patients. The frequency of adverse events was low and did not differ between the two treatment groups. We conclude that pantoprazole is superior to ranitidine in the acute treatment of reflux esophagitis.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1995

Autonomic dysfunction in patients with achalasia.

It has been previously shown that patients with achalasia may have motor abnormalities of the stomach, small bowel and biliary system. This study investigates whether a disturbance of extraintestinal autonomic function occurs. Autonomic function studies were performed in 15 patients with achalasia and 15 age- and sex-matched healthy controls. Pupillograms were obtained during darkness, light exposure and after pilocarpine administration. Cardiovascular function studies included determinations of heart rate variation during deep breathing and orthostasis. In addition, we determined blood pressure changes in response to sustained handgrip, cold exposure and orthostasis. Neurohormonal function was investigated by measuring serum pancreatic polypeptide (PP) levels prior to and following sham feeding. Pupillary function did not differ in patients as compared with controls. However, 9 of 15 patients (95% CI: 32-84%) and none of the controls showed at least one abnormal autonomic cardiovascular response. A significant difference between the two groups was observed in sympathetic function (P = 0.023). More patients than controls did not respond to sham feeding with a PP increase. It is concluded that some patients with achalasia exhibit an abnormality of the autonomic nervous system that extends beyond the gastrointestinal tract. These abnormalities mainly concern cardiovascular function but may also involve neurohormonal responses.

Adult↗