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Biomedical subjects

R Hatz

Publications and source records attributed to R Hatz.

At least 19 recordsLinked to original sources
PubMed2001

Assessing the microcirculation in a burn wound by use of OPS imaging.

We report on the use of OPS imaging to visualize the microcirculation in a burn wound. This novel technique produces high quality images of the microcirculation and quantitative analysis of functional capillary density (FCD) was possible. FCD measured at day 3 following the injury was 11.2 +/- 4.6 (n/mm superset2; mean +/- SEM). During the initial phase of healing microcirculatory changes were characterized by a moderate but steady increase of FCD, which showed marked increase beginning from day 12 following the burn (16.6 +/- 6.9). Maximal FCD measured at day 23 (48.2 +/- 19.7) decreased from this point in time to finally reach 25.2 +/- 10.3 n/mm superset2 at the end of observation. OPS imaging allows for direct in vivo visualization and quantification of the microcirculation in burned skin. Our results of the use of OPS imaging in assessing the microcirculation in a burn wound appear promising, and we hope that this novel technique will allow to improve the knowledge of the dynamics of the microcirculation in the pathophysiology of thermal injury.

Adult↗
PubMed2000

Helicobacter pylori infections--are these diseases relevant for surgical treatment?

Helicobacter pylori infection and its strong association with gastroduodenal diseases has revolutionized our views and treatment options in these diseases. Surgery has always been considered a mainstay in their treatment. The development of potent eradication regimes has changed indications for operative treatment. With endoscopic procedures being increasingly performed by the surgeon himself, it has become necessary that he educate himself in the diagnosis and treatment of H. pylori infection in order to be able to cope with these diseases in every day surgical practice. Treatment of H. pylori infection may not only be seen as an alternative to operative therapy, but also as an adjunct following surgical treatment of gastroduodenal disease.

Duodenitis↗
PubMed1999

Effect of immunization on gastrin release in rat antrum mucosa.

Helicobacter pylori (H.P.) infection is the main cause of chronic active gastritis and is closely associated with peptic ulcer disease. Chronic hypergastrinaemia is known to be induced in patients infected with this pathogen. Gastrin is the most potent stimulator of gastric acid secretion. In animals infected with H.P. or H. felis vaccination against H.P.can eliminate the bacterium and alleviate associated gastritis. However little is known on the influence of immunization regimes on gastrin release. The aim of this study was to evaluate the effect of systemic immunization on gastrin release in a rat model, using a well defined but for the rat unknown protein. OVA-immunized and non immunized animals received OVA intragastrically in vivo, and serum gastrin was measured. Stimulation with bovine serum albumin (BSA) served as control. In vitro single cell suspensions of the antrum mucosa and mucosal fragments of immunized and non immunized animals were also incubated with OVA and BSA. The results show specific significant gastrin suppression after immunization and antigen feeding. The same results were obtained in the model of mucosa fragments but not in single cell suspensions. This hypothesized that gastric suppression could be mediated by mast cells or T-helper two cells (TH2) in the mucosal layer of the stomach. A single cell suspension is not suitable for studying immunologically mediated gastrin release because direct cell contact is necessary. Further studies with these animal models have to show whether effects seen by vaccination could be mediated by induction of gastrin suppression and studies on human tissues are necessary to show possible similar effects with H.P.

Animals↗
PubMed1999

Colonic mucosal proliferation is related to serum deoxycholic acid levels.

BACKGROUND: Hyperproliferation of the colorectal mucosa is regarded as an early step in colorectal carcinogenesis. Deoxycholic acid, a secondary bile acid, stimulates colorectal epithelial proliferation in animals and is considered a tumor promoter in human colorectal carcinogenesis. The aim of this study was to investigate the correlation between colorectal mucosal proliferation and the serum deoxycholic acid level. METHODS: From each of 19 patients (10 men and 9 women) with (n = 3) or without (n = 16) colorectal adenoma, 18 biopsy specimens were obtained by colonoscopy, 3 from each of the 6 colonic segments. A crude nuclei fraction was prepared, and DNA was stained by propidium iodide to determine the proliferative index (the percentage of cells in the S and G2/M phases of the cell cycle) by flow cytometry. Serum levels of deoxycholic acid were determined by gas-liquid chromatography. RESULTS: The colonic proliferation rates (median of the values obtained in all segments, 14.1%; range, 10.0-18.7%) and the fasting serum deoxycholic acid levels (median, 0.86 micromol/L; range, 0.28-1.58 micromol/L) showed a significant correlation (r = 0.51, P = 0.03). Serum lithocholic, cholic, chenodeoxycholic, and ursodeoxycholic acid levels were not correlated with the proliferation rates. CONCLUSIONS: Levels of deoxycholic acid in serum are correlated with the rates of the colorectal mucosa. These results are consistent with the concept that deoxycholic acid promotes colorectal carcinogenesis.

Adenoma↗
PubMed1998

Gastric carcinoma risk index in patients infected with Helicobacter pylori.

Epidemiological data show an association between Helicobacter pylori gastritis and gastric carcinoma. However, most people infected with H. pylori do not develop gastric cancer. We have therefore evaluated histological criteria indicating an increased risk for gastric cancer. H. pylori gastritis was investigated in 117 patients with small (O<2 cm) early gastric carcinomas and in 117 age-matched duodenal ulcer patients infected with H. pylori, who are known to have a low risk for developing gastric carcinoma. The results showed that infiltration with lymphocytes/plasma cells and infiltration with neutrophils predominating in the corpus, and intestinal metaplasia in antrum and corpus were associated with both types of gastric carcinoma (intestinal and diffuse, P<0.0001). If an index is computed by giving one point to each of these features, the predictive value for the presence of gastric carcinoma was 0.79 with a score of 2, and 0.94 with a score of 3 (all points on the index used). Application of this index might be a simple method of identifying patients infected with H. pylori and carrying a higher risk for gastric carcinoma.

Adult↗
PubMed1998

Severe expression of corpus gastritis is characteristic in gastric cancer patients infected with Helicobacter pylori.

In 50 Helicobacter pylori-infected gastric carcinoma patients the corpus gastritis was significantly higher than in matched H. pylori-positive control subjects (P < 0.01). Atrophy and intestinal metaplasia (IM) occurred significantly more often in the antrum of carcinoma patients (P < 0.01). The odds ratio for gastric carcinoma was 8.85 for high-grade corpus gastritis and 8.04 when atrophy in the antrum was present.

Female↗
PubMed1998

Double-blind trial of omeprazole and amoxicillin in the cure of Helicobacter pylori infection in gastric ulcer patients. The Ulcer Study Group, Germany.

BACKGROUND: Our aim was to investigate the efficacy of omeprazole and amoxicillin in curing Helicobacter pylori infection in gastric ulcer patients. METHODS: In a double-blind trial 185 H. pylori-positive gastric ulcer patients were prospectively randomized to receive 40 mg omeprazole twice daily and either 750 mg amoxicillin three times daily or 750 mg amoxicillin placebo three times daily on days 1-14, followed by 20 mg omeprazole daily on days 15-56. RESULTS: Twenty-seven patients were excluded because of lack of compliance or missed follow-up examinations; one patient receiving amoxicillin discontinued treatment owing to side effects. On an intention-to-treat basis, omeprazole/amoxicillin led to cure of H. pylori infection in 67.1% (47 of 70) of patients not using non-steroidal anti-inflammatory drugs (NSAIDs)/aspirin (ASA) and in 46.7% (14 of 30) of those taking NSAIDs/ASA (P < 0.05). With the omeprazole/placebo regimen, H. pylori infection was cured in 8.8% (no NSAIDs), and 0% (NSAIDs). CONCLUSIONS: The use of NSAIDs/ASA may limit the efficacy of omeprazole/amoxicillin in curing H. pylori infection in gastric ulcer patients.

Adolescent↗
PubMed1997

Differing degree and distribution of gastritis in Helicobacter pylori-associated diseases.

Infection with Helicobacter pylori (H. pylori) causes gastritis, and may be associated with gastric and duodenal ulcers and also with such malignant diseases as MALT lymphoma and gastric carcinoma. In order to determine whether there are differences in the degree and distribution of gastritis, each patient with H. pylori gastritis only (n = 50) was matched for sex and age with four patients, one each with H. pylori-associated duodenal ulcer, gastric ulcer, gastric carcinoma or MALT lymphoma. From each patient, two biopsies were taken from the antrum and two from the corpus for histopathological examination of H. pylori gastritis. The median summed gastritis score decreases in the following order: antrum: gastric ulcer > duodenal ulcer > gastritis alone > carcinoma > MALT lymphoma, and corpus: gastric ulcer > carcinoma > MALT lymphoma > gastritis alone and duodenal ulcer. We conclude that the degree and distribution of H. pylori gastritis differs significantly among H. pylori-associated diseases. These differences may explain some of the underlying pathomechanisms associated with H. pylori infection.

Adult↗
PubMed1997

Is the polymerase chain reaction or cure of Helicobacter pylori infection of help in the differential diagnosis of early gastric mucosa-associated lymphatic tissue lymphoma?

PURPOSE: The differential diagnosis of early gastric mucosa-associated lymphatic tissue (MALT) lymphoma based on Helicobacter pylori gastritis may be difficult when lymphoepithelial lesions are not detected. The aim of the present study was to investigate the question whether the polymerase chain reaction (PCR) or cure of H pylori infection may be of help in this respect. PATIENTS AND METHODS: Twenty patients with suspected low-grade gastric MALT lymphomas were treated in a double-blinded, randomized, crossover trial with 2,250 mg of either amoxicillin or placebo, both in combination with omeprazole, for 14 days with the aim to cure H pylori infection. PCR was performed using primers specific for the CDR3 region to detect monoclonal B cells. RESULTS: In five of 20 patients, MALT lymphomas were finally diagnosed. Three of these five patients went into complete remission, while two were referred to surgery. In the 15 patients with gastritis, complete regression was observed in all cases. With respect to PCR, monoclonal bands were detected in all four of the analyzed lymphoma patients before histology showed lymphoma. In addition, monoclonal bands were found in three patients with gastritis. In the patients with gastritis and monoclonal PCR, complete regression took longer as compared with the remaining 12 patients with polyclonal PCR and gastritis (P = .0209). Successful H pylori eradication was associated with earlier diagnosis of the MALT lymphoma (P = .0237). CONCLUSION: CDR3-PCR may be of help in the differential diagnosis of early gastric MALT lymphoma. Furthermore, H pylori eradication may lead to earlier diagnosis.

Adult↗
PubMed1997

[Surgical interventions in extracorporeal membrane oxygenation (ECMO)].

Extracorporeal membrane oxygenation is a suitable technique for short-term treatment of resistant respiratory failure with a comparably low mortality rate of 32%. However, pulmonary complications are quite often encountered during ECMO therapy making thoracic interventions necessary. The most frequent of these complications is hemorrhage followed by lung fistula, which remain resistant to conventional therapy. The indication for operative lung resection during ECMO treatment must remain restricted to selected cases, since these procedures have a high morbidity.

Adult↗
PubMed1996

Cure of gastric ulcer disease after cure of Helicobacter pylori infection--German Gastric Ulcer Study.

BACKGROUND: Helicobacter pylori infection is associated with gastric ulcer disease in about 75% of cases. OBJECTIVE: The aim of this study was to determine whether H. pylori eradication reduces gastric ulcer relapse rates. DESIGN: The study was randomized, controlled, multicentric and investigator blinded, and was conducted at three university hospitals, two teaching hospitals, and by six practising gastroenterologists. METHODS: During a period of 1 year 152 patients with gastric ulcers were randomly assigned to one of two treatment regimens: omeprazole 20 mg daily in the morning for 8 weeks (74 patients), or bismuth subsalicylate 600 mg three times daily for 8 weeks combined with 500 mg amoxicillin twice daily and 1000 mg tinidazole twice daily for the first 10 days (triple therapy) (78 patients). Follow-up examinations were performed 6, 12 and 18 months after treatment and whenever ulcer symptoms occurred. RESULTS: Of the 152 randomized patients five were excluded because of gastric cancer, 10 missed follow-up examinations and seven receiving triple therapy terminated treatment because of side effects. Of the remaining 130 patients, five of 69 (7.2%) in the omeprazole and six of 61 (9.8%) in the triple group were H. pylori negative. After 8 weeks' therapy, the gastric ulcer was healed in 85.9% (omeprazole) and in 81.8% triple) in H. pylori-positive patients, and in 80% (omeprazole) and 16.7% (triple) in H. pylori-negatives. H. pylori was eradicated in 8.1% of the patients who received omeprazole monotherapy and in 78.2% receiving triple therapy, and in 8.1% and 69.4% in an intention-to-treat analysis. The subsequent relapse rates during a follow-up period of 12 months were 50% in the omeprazole group and 4% in the triple group. Gastric ulcer relapse was observed in 49% of patients who were H. pylori positive and in 2% who were H. pylori negative after treatment. CONCLUSION: The data show that the presence of H. pylori is an important predictor of gastric ulcer relapse and that eradication of H. pylori may heal gastric ulcer disease.

Adult↗
PubMed1996

Severity of Helicobacter pylori gastritis predicts duodenal ulcer recurrence.

BACKGROUND: Helicobacter pylori gastritis is suggested to be the underlying condition leading to duodenal ulcer disease. The aim of the study was to investigate the relationship between chronic active H. pylori gastritis and the risk of duodenal ulcer (DU) recurrence. METHODS: One hundred and eighty-eight patients were followed up with regard to the evolution of their H. pylori gastritis after they had received antibacterial or acid-suppressing treatment for their DU. Four weeks, 1 year, and 2 years after treatment and in the case of DU recurrence several morphologic indicators of gastritis were studied histologically in the antrum and corpus. RESULTS: In patients who were cured of H. pylori infection a significant and long-lasting regression of all gastritis variables were observed. patients with persistent H. pylori infection after antibacterial treatment showed only a temporary regression of all gastritis variables. In the overall group of patients who received acid-suppressive therapy there was no change in gastritis. However, in the subgroup of patients who received omeprazole monotherapy, no change in the antrum but a statistically significant increase of gastritis in the corpus was observed. The grade of antral gastritis at the end of treatment was significantly and positively correlated with the risk of DU recurrence and was independent of the kind of pretreatment (18.5% recurrences in grade-2 versus 86% in grade-4 gastritis). CONCLUSIONS: The data show that the grade of gastritis is an important risk factor for duodenal ulcer recurrence. Cure of H. pylori infection is associated with healing of chronic H. pylori-associated gastritis. These data lend considerable support to the hypothesis that H. pylori gastritis is the most important factor among those leading to duodenal ulcer disease.

Chronic Disease↗
PubMed1995

Osteosynthetic reconstruction in a patient with Gardner-Diamond syndrome.

Based on clinical observations in one female patient who suffered from Gardner-Diamond syndrome, we noticed that surgery can be performed without any bleeding complications, although operations normally are contraindicated in persons with this condition. Additionally, a correlation seems to exist between ASS and sexual and hormonal maturity.

Autoimmune Diseases↗
PubMed1995

Expression of adhesion molecules on human granulocytes after stimulation with Helicobacter pylori membrane proteins: comparison with membrane proteins from other bacteria.

Type B gastritis in its active form is characterized by a dense infiltration of the lamina propria with granulocytes. Since the bacterium Helicobacter pylori does not invade the epithelial barrier, a signaling pathway chemoattractive for granulocytes must exist across this mucosal boarder. One possible mechanism tested was whether granulocytes are directly activated by water-soluble membrane proteins (WSP) from H. pylori. These findings were compared with the effects of WSP from other bacteria (Helicobacter felis, Campylobacter jejuni, Escherichia coli, and Staphylococcus aureus). A unique activation pattern by H. pylori WSP was found. Like all other WSP tested, they induced an upregulation of CD11b but had no influence on CD11c and, most strikingly, CD62L expression. In contrast, E. coli WSP, e.g., not only induce a strong CD11b and CD11c expression but also lead to a loss in surface CD62L. The lack of CD62L shedding conserves rolling of granulocytes along the endothelium, creating a favorable precondition for granulocytes to stick more readily to activated endothelium after H. pylori stimulation via CD11b-CD54 receptor-counterreceptor interaction. This may explain why H. pylori infection is a very strong stimulus for granulocyte infiltration. The active fraction for the induction of CD11b on granulocytes is a heat- and protease-sensitive protein with a molecular mass between 30 and 100 kDa. One activation step involved may be the binding of WSP to CD15 determinants on granulocytes with subsequent induction of CD11b.

Antigens, Bacterial↗
PubMed1995

Two-year follow-up of duodenal ulcer patients treated with omeprazole and amoxicillin.

The present study evaluated the time in remission during a 2-year follow-up after eradication of Helicobacter pylori (HP) in patients with an HP-associated duodenal ulcer (DU). HP was eradicated by combined treatment with high-dose omeprazole (2 x 40 mg) and amoxicillin (2 x 1,000 mg; n = 27) administered for 10 days (OME + AMX); alternatively, patients were treated with omeprazole monotherapy (OME) using the same dosage (n = 25). During the 2-year follow-up period endoscopy including histological examination was performed after 1 and 2 years or whenever symptoms compatible with ulcer relapse occurred. HP eradication was achieved in 82% of the OME + AMX group, but in 0% of the OME group. The cumulative DU relapse rates were 0% after 1 year and 7% after 2 years in 22 patients who became HP-negative. Both HP-negative patients who relapsed in the 2nd year of follow-up were HP-positive again at the time of relapse. Of the 5 patients who were not eradicated after OME + AMX therapy, 2 relapsed within the 1st year (40%) and another 2 within the 2nd year (80%). In the OME group the cumulative relapse rates within 1 and 2 years of follow-up were 52 and 76%, respectively. The results further confirm that eradication of HP with combined OME + AMX treatment leads to a distinct decrease in DU relapse rates and thus may cure DU disease. Long-term eradication with combined OME + AMX treatment is possible, and the rate of reinfection with HP is low (4.5%/year).

Amoxicillin↗
PubMed1994

Healing of protein losing hypertrophic gastropathy by eradication of Helicobacter pylori--is Helicobacter pylori a pathogenic factor in Ménétrier's disease?

Hypertrophic gastropathy--that is, Ménétrier's disease--was found, in a retrospective analysis, to be associated with Helicobacter pylori in more than 90% of patients. It is proposed that hypertrophic gastropathy represents a special form of H pylori gastritis in these patients. A case is described of a 28 year old woman with Ménétrier's disease associated with proved protein loss from the stomach. Treatment with cimetidine for more than three years had little benefit when colonisation by H pylori was detected. Density of H pylori colonisation and activity of gastritis, which was also present in the first biopsy specimens taken five years ago, were more pronounced in the body than in the antrum, which is in agreement with the characteristics of H pylori gastritis found in other cases with Ménétrier's disease. A 14 day antibacterial treatment course with 750 mg amoxicillin three times a day combined with 40 mg omeprazole three times a day was started in April 1991. This resulted in eradication of H pylori and the return to normal of giant folds and the mucosal histology. Serum protein concentrations returned to normal within six weeks and remained normal at two endoscopies during a two year follow up. This case report suggests that a subgroup of the patients with Ménétrier's disease may be healed by the eradication of H pylori.

Adult↗