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Biomedical subjects

G Dorta

Publications and source records attributed to G Dorta.

At least 37 records · Page 2Linked to original sources
PubMed2000

The effects of omeprazole on healing and appearance of small gastric and duodenal lesions during dosing with diclofenac in healthy subjects.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) are associated with gastrointestinal mucosal damage. Omeprazole prevents the formation, and accelerates the healing, of NSAID-induced ulcers. AIM: To test whether omeprazole accelerates healing of standardized gastroduodenal lesions in the presence of diclofenac. METHODS: In a double-blind, double-dummy, placebo-controlled, crossover study, 12 healthy volunteers received consecutive, 2-week courses of omeprazole (40 mg o.d.) and placebo, in random order, with an intervening, 4-week washout period; diclofenac (50 mg t.d.s.), was given for the second week of each course. Five endoscopies were performed, one at the outset and the others before and after each course of diclofenac. Biopsies were taken from the endoscopically normal mucosa of the corpus, antrum and duodenum and also from any new mucosal lesion that developed after diclofenac. The sites of biopsies taken before each course of diclofenac were evaluated endoscopically after each course to assess the extent of healing according to a predetermined healing score scale. RESULTS: The healing scores observed after administration of placebo/diclofenac (median=0; range 0-6) and after omeprazole/diclofenac (median=0; range 0-6; P=0.17) did not differ. Small gastroduodenal lesions developed de novo in six subjects during placebo/diclofenac and in seven during omeprazole/diclofenac. Focal chemical gastropathy was observed only in close proximity to macroscopic lesions. CONCLUSIONS: In healthy subjects, omeprazole does not accelerate the healing of pre-existing mucosal lesions or prevent the development of small diclofenac-induced mucosal lesions.

Adult↗
PubMed2000

Cushing's syndrome in an 81-year-old patient treated with budesonide and amiodarone.

This is the first report of Cushing's syndrome under oral budesonide treatment. An 81-year-old man known for paroxysmal atrial fibrillation and chronic renal insufficiency, treated with 6 mg budesonide for collagenous colitis, developed Cushing's syndrome under co-administration of amiodarone. The Cushing's syndrome disappeared after discontinuation of the amiodarone treatment. Metabolism of the two medications by hepatic cytochrome P 450 3A may explain the development of Cushing's syndrome.

Aged↗
PubMed2000

Diagnostic accuracy and interobserver agreement of CT colonography (virtual colonoscopy).

BACKGROUND AND AIMS: Computed tomographic (CT) colonography or virtual colonoscopy (VC) is a non-invasive imaging method proposed for screening patients with colorectal neoplasias. Our aims were to study the diagnostic accuracy and interobserver agreement of VC for correct patient identification compared with conventional colonoscopy (CC). METHODS: This was a prospective study of 50 patients successively undergoing VC and CC. Multiplanar two dimensional CT images and three dimensional VC were constructed using surface rendering software and interpreted by two independent investigator teams. VC findings were compared with those of CC. Interobserver agreement was determined using kappa statistics. RESULTS: CC found 65 polyps in 24 patients. For identification of patients with polyps > or =10 mm, the sensitivity of VC was 38% and 63%, and specificity was 74% and 74% for teams 1 and team 2. Interobserver agreement was good (kappa 0.72). For patients with polyps of any size, the sensitivity of VC was 75% and 71%, and specificity was 62% and 69% for teams 1 and 2. Interobserver agreement was fair (kappa 0.56). Accuracy improved when comparing the results of the first 24 with the last 26 patients. CONCLUSIONS: In our experience, VC had a low diagnostic value for identification of patients with colorectal neoplasias. Interobserver agreement for VC interpretation was fair. These results may be explained by software imperfections and a learning curve effect.

Aged↗
PubMed1999

Effects of pumaprazole (BY841), a novel reversible proton pump antagonist, and of omeprazole, on intragastric acidity before and after cure of Helicobacter pylori infection.

BACKGROUND: Omeprazole produces a higher intragastric pH in the presence of Helicobacter pylori infection than after cure. AIM: To investigate whether this effect also occurs with pumaprazole (BY841), a reversible proton pump antagonist which, in contrast to omeprazole, does not require activation in the acid compartment of the parietal cell. METHODS: In a randomized, crossover, double-blind study, 24-h intragastric pH was measured in 13 H. pylori-positive subjects before and after a 1-week course of omeprazole (20 mg o.d.) or of pumaprazole (100 mg b.d.). The studies were repeated after the infection was cured. RESULTS: In the absence of drug administration, the median 24-h pH values before cure (median 2.0, 90% CI: 1.2-3.2) did not differ from those after cure (median 1.5, 90% CI: 1.3-2.2; P = 0.115). The 24-h pH values were higher before cure of the infection than after during both pumaprazole (6.0, 4.8-6.7 vs. 4.3, 2.6-5.7; P = 0.002) and omeprazole (5.8, 4.0-6.2 vs. 3.6, 2.8-5; P = 0.004). Both before and after cure, there were no significant differences between the two drugs with respect to acid inhibition over the 24-h period. The median decrease in acid inhibition after cure of the infection (calculated as the difference in H+ activity in mmol/L) during pumaprazole (median 0.05, 90% CI: 6 x 10-4- 2.3) was no different from that during omeprazole (median 0.2, 90% CI: 3 x 10-3-1.5; P = 0.6). CONCLUSIONS: Both before and after cure of H. pylori infection, pumaprazole raised the intragastric pH over a 24-h period to a similar degree as omeprazole. H. pylori infection similarly augments the pH-increasing effect of both drugs. This effect is related to H. pylori infection and not to an increased activation of acid inhibitory agents in the parietal cell compartment.

Adult↗
PubMed1999

Effect of whey-based culture supernatant of Lactobacillus acidophilus (johnsonii) La1 on Helicobacter pylori infection in humans.

BACKGROUND: Specific strains of Lactobacillus acidophilus are known to inhibit intestinal cell adhesion and invasion by enterovirulent bacteria. As L. acidophilus can survive transiently in the human stomach, it may downregulate Helicobacter pylori infection. METHODS: The ability of L. acidophilus (johnsonii) La1 supernatant to interfere with H. pylori bacterial growth, urease activity, and adhesion to epithelial cells was tested in vitro. Its effect on H. pylori infection in volunteers was monitored in a randomized, double-blind, controlled clinical trial, using a drinkable, whey-based, La1 culture supernatant. H. pylori infected volunteers were treated 14 days with 50 ml of La1 supernatant four times a day combined with either omeprazole 20 mg four times a day or with placebo. Infection was assessed by breath test, endoscopy, and biopsy sampling, performed at inclusion, immediately at the end of the treatment (breath test only), and 4 weeks after the end of the treatment. RESULTS: La1 supernatant inhibited H. pylori growth in vitro, regardless of previous binding of H. pylori to epithelial cells. In 20 subjects (8 females, 12 males, mean age 33.1 years) a marked decrease in breath test values was observed immediately after treatment with La1 supernatant, both in the omeprazole and in the placebo group (median 12.3 vs. 28.8 and 9.4 vs. 20.4, respectively; p < 0.03). In both treatment groups, breath test values remained low 6 weeks after treatment (omeprazole treated 19.2, placebo treated 8. 3; p < 0.03 vs. pretreatment), but the persistence of H. pylori infection was confirmed in gastric biopsies. CONCLUSION: La1 culture supernatant shown to be effective in vitro has a partial, acid-independent long-term suppressive effect on H. pylori in humans.

Adolescent↗
PubMed1999

Role of octreotide and somatostatin in the treatment of intestinal fistulae.

Intestinal fistulae usually arise as a complication of abdominal surgery. Its treatment is complex and intestinal fistula-related morbidity and mortality is high. Fistula closure rates under conservative medical treatment vary between 24 and 72%. Octreotide and somatostatin reduce gastrointestinal, biliary and pancreatic secretion and increase intestinal water and electrolyte absorption. In recent years, octreotide and somatostatin have been associated with conservative medical treatment for patients with intestinal fistulae. Four placebo-controlled studies have been published within the past 6 years. The interpretation of their results is difficult because patient collectives were small and heterogeneous. In one study, somatostatin decreased fistula-related complications when compared to placebo, and in another study, octreotide decreased the healing time of intestinal fistulae and the time patients required total parenteral nutrition when compared to placebo. In contrast, the fistula closure rate, hospitalization time and mortality were not influenced by the use of octreotide or somatostatin in conservative medical treatment. In conclusion, octreotide and somatostatin actually cannot be recommended in the treatment of intestinal fistulae in settings outside of controlled trials.

Gastrointestinal Agents↗
PubMed1998

Differential expression of laminin-5 subunits and integrin receptors in human colorectal neoplasia.

Cell-matrix interactions contribute to regulating the adhesion, growth, migration, and differentiation of epithelial intestinal cells. Alterations in matrix components and their cellular receptors have been found in tumours but their specific roles remain unclear. The tissue patterns of laminin-5 and alpha 3, beta 3 and gamma 2 subunits, as well as those of the alpha 3, alpha 6, beta 1, and beta 4 integrin chains, were determined by immunofluorescence on frozen sections of 12 colorectal mucosal samples from four patients, 15 adenomas, 29 adenocarcinomas, and eight metastases. Distinct patterns of laminin-5 and integrin expression were found along the mucosa-adenoma, and adenoma-carcinoma transitions. Expression of basement membrane laminin-5 and subunits was continuous and gradient-like in normal mucosa, enhanced at the periphery of adenomas, and discontinuous in places in carcinomas and metastases. Decrease of the alpha 3 integrin chain was found in adenomas, together with that of alpha 6 and beta 4 chains in carcinomas. A subpopulation of carcinoma cells dissociating (budding) from neoplastic tubules was found to accumulate the laminin-5 beta 3 gamma 2 heterodimer in the cytoplasm, with progressive loss of surface integrin expression. These results suggest that in colorectal cancer, an abnormal expression of laminin-5 subunits and integrin chains may identify a subset of carcinoma cells prone to invade focally and to contribute to disease aggressiveness.

Adenocarcinoma↗
PubMed1998

Alterations in plasminogen activation correlate with epithelial cell dysplasia grading in colorectal adenomas.

Proteases are important for neoplastic invasion but a specific role for the plasminogen activator system in the progression of colorectal epithelial dysplasia to adenomatous lesions remains unclear. Consecutive tissue cryosections of 51 adenomas, 49 distant mucosa samples and five mucosa samples from control subjects were histopathologically analysed for dysplasia grade and tissue type, urokinase plasminogen activator levels and plasminogen activator inhibitor type 1 (PAI-1) using immunosorbent methods. Plasminogen activation and urokinase-mediated proteolytic activity levels were assessed using in situ zymography. Plasminogen activation and tissue-type activator levels were lower in adenomas than in mucosae (P < 0.001). PAI-1 concentration and urokinase levels were higher in adenomas than in mucosae (P < 0.001 and P < 0.001 respectively). In adenomas, urokinase concentration increased in parallel with PAI-1, but only the urokinase levels correlated with the dysplasia grade (P < 0.01). Thus, the alterations in plasminogen activation correlated with epithelial cell dysplasia grading. In the mucosa to adenoma transition, a marked decrease in tissue-type plasminogen activator occurred. In adenomas, this decrease was accompanied by a concomitant increase in urokinase and PAI-1. The urokinase level only continued to rise in parallel with the dysplasia grade. Resulting protease-antiprotease imbalance in high-grade dysplasia may represent the phenotypic change associated with malignant transformation and invasive behaviour.

Adenoma↗
PubMed1997

Genetic heterogeneity in sporadic colorectal adenomas.

The majority of colorectal cancers develop from adenomatous polyps under the influence of factors that are still poorly understood. Tumourigenesis is generally considered a multistep process in which multiple genetic alterations occur, eventually reflected in abnormalities of the cellular DNA content. Macroscopical features such as tumour size and tumour architecture (tubular, tubulovillous, or villous) are correlated wit the chance of malignancy in the lesion. Grade of dysplasia can be considered an indicator for the level of progression of the adenoma towards invasive carcinoma. These characteristics were correlated with the presence or absence of K-ras mutations and the DNA ploidy in a prospective study performed on 46 large sporadic colorectal adenomas resected by endoscopy. DNA ploidy and K-ras mutations were analysed in two samples taken at distant sites in the adenomas. Aneuploidy was present in 12 adenomas (26 per cent) and K-ras mutations occurred in 26 (57 per cent). A highly significant correlation was found between aneuploidy and adenoma size, architecture, and grade of dysplasia. The presence of K-ras mutations was significantly correlated only with the size of the adenomas. The proportion of adenomas with aneuploidy and/or a K-ras mutation increased when two samples were analysed instead of one. This observation suggests that the prevalence of genetic mutations and of aneuploidy is probably underestimated, as generally only one sample is investigated. No correlation was observed between K-ras mutations and ploidy. This study demonstrates the presence of genetic heterogeneity in colorectal adenomas and supports the notion that K-ras mutation is an early event, while aneuploidy is a late event in the adenoma-carcinoma sequence.

Adenoma↗
PubMed1997

Comparison between esophageal Wallstent and Ultraflex stents in the treatment of malignant stenoses of the esophagus and cardia.

BACKGROUND AND STUDY AIMS: Several published studies have examined various self-expanding metal esophageal stents for use in the palliative treatment of esophageal or cardiac neoplasia, but few have compared different self-expanding metal stents. The aim of this study was to evaluate non-covered Wallstent and Ultraflex prostheses in the treatment of malignancies in the esophagus and the cardiac region. MATERIALS AND METHODS: In a retrospective study, the effectiveness of non-covered Wallstents (46 patients) and Ultraflex stents (36 patients) was compared in the treatment of malignancies in the esophageal and cardiac regions. RESULTS: Reintervention procedures were necessary in 16 of the 46 Wallstent patients (six patients during an early phase) and in 22 of the 36 Ultraflex patients (13 during an early phase) (overall P = 0.022; early P = 0.018). The major complication in the Wallstent group was tumor ingrowth (12 of 35 complications), while in the Ultraflex group, it was incomplete deployment (18 of 49 complications). Incomplete stent deployment occurred more often in patients treated with Ultraflex (P = 0.01), and food impaction was more often observed in the Wallstent group (P = 0.001). In addition, in patients with Ultraflex stents, more complex reinterventions were necessary than those required with Wallstents (four vs. 13 complex reinterventions, P = 0.0046). Wallstents tended to improve dysphagia better than Ultraflex stents. CONCLUSION: Compared to Ultraflex stents, Wallstents have several significant short-term and long-term advantages in the palliative treatment of malignancy of the esophagus and cardia.

Adult↗
PubMed1997

Meglumine gadoterate: a new safe radiocontrast medium for endoscopic retrograde cholangiopancreatography?

The radiocontrast substance meglumine gadoterate (MG) is used in magnetic resonance imaging. It is characterized by its low rate of adverse drug reactions. In an open study we tested whether MG is useful in endoscopic retrograde cholangiopancreatography. The patients received in sequence MG and ioxotalamate. MG, in contrast to ioxotalamate, failed to visualize the proximal pancreatic and peripheral intrahepatic ducts. Thus, MG is not useful in routine endoscopic retrograde cholangiopancreatography. However, in patients with a history of severe allergic reactions to conventional contrast media, MG may be recommended when pathological findings of the extrahepatic bile duct or the area of the pancreatic head are suspected.

Adolescent↗
PubMed1997

In situ stromal expression of the urokinase/plasmin system correlates with epithelial dysplasia in colorectal adenomas.

An increase of urokinase-type plasminogen activator (uPA) and a decrease of tissue-type PA (tPA) have been associated with the transition from normal to adenomatous colorectal mucosa. Serial sections from 25 adenomas were used to identify PA-related caseinolytic activities by in situ zymography, blocking selectively uPA or tPA. The distribution of uPA, tPA, and type 1 PA inhibitor mRNAs was investigated by nonradioactive in situ hybridization, and the receptor for uPA was detected by immunostaining. Low- and high-grade epithelial cell dysplasia was mapped histologically. Results show that 23 of 25 adenomas expressed uPA-related lytic activity located predominantly in the periphery whereas tPA-related activity was mainly in central areas of adenomas. In 15 of 25 adenomas, uPA mRNA was expressed in stromal cells clustered in foci that coincided with areas of uPA lytic activity. The probability of finding uPA mRNA-reactive cells was significantly higher in areas with high-grade epithelial dysplasia. uPA receptor was mainly stromal and expressed at the periphery. Type 1 PA inhibitor mRNA cellular expression was diffuse in the stroma, in endothelial cells, and in a subpopulation of alpha-smooth muscle cell actin-reactive cells. These results show that a stromal up-regulation of the uPA/plasmin system is associated with foci of severe dysplasia in a subset of colorectal adenomas.

Adenoma↗
PubMed1996

Effects of misoprostol on healing and prevention of biopsy-induced gastroduodenal lesions occurring during the administration of diclofenac to volunteers.

AIM: To determine whether misoprostol promotes the healing of non-steroidal anti-inflammatory drug-induced gastroduodenal lesions in a human experimental model. METHODS: Mucosal damage and healing of mucosal biopsy sites were assessed endoscopically in 10 healthy, Helicobacter pylori-negative volunteers with a normal initial endoscopy: they were enrolled in a double-blind, double-dummy, placebo-controlled cross-over study. They received 2-week courses of misoprostol (200 micrograms b.d.) or placebo; a water-soluble non-steroidal antiinflammatory drug diclofenac 50 mg t.d.s., was given during the second week of each dosage regimen after three endoscopic biopsies had been taken from each of the duodenum, antrum and corpus. RESULTS: The number of unhealed biopsy sites was not different after misoprostol or placebo, although the number of healed biopsy sites was greater in the corpus and duodenum than in the antrum. Misoprostol did not prevent the appearance of diclofenac-induced erosions and petechiae. Epigastric discomfort was related to the intake of diclofenac and was reduced by misoprostol. Bloating and flatulence occurred more frequently with misoprostol alone and with misoprostol plus diclofenac, than with placebo alone or placebo plus diclofenac. CONCLUSION: Misoprostol does not prevent new mucosal lesions induced by diclofenac in healthy volunteers and it does not accelerate the healing of the biopsy sites. Misoprostol decreases the frequency of diclofenac-induced epigastric discomfort, but it increases gas bloating and flatulence.

Adult↗
PubMed1995

Effect of cisapride on gallbladder motility after extracorporeal shock-wave lithotripsy.

BACKGROUND/AIMS: Altered gallbladder motility is regarded as one of the important factors involved in the formation and recurrence of gallstones. Previous studies have suggested that cisapride increases postprandial gallbladder contraction and may therefore be theoretically useful in preventing stone recurrence. The aim of our study was therefore to investigate the effect of cisapride on gallbladder motility in stone-free patients after extracorporeal shock-wave lithotripsy, as compared to healthy volunteers pair-matched for age and sex. METHODS: Each subject received cisapride or placebo in a double-blind, cross-over, random order. Gallbladder volumes were measured by ultrasonography in the fasting state and after intake of a standard liquid meal. Plasma cholecystokinin levels were determined by radioimmunoassay. RESULTS: Fasting gallbladder volumes were smaller in patients as compared to volunteers (20.7 +/- 1.3 ml vs. 46.0 +/- 9.2 ml; p < 0.05) but were not modified by cisapride (21.1 +/- 1.7 ml vs. 58.6 +/- 11.3 ml). The maximal postprandial decrease in gallbladder volume was similar in patients and volunteers (64.5 +/- 12% vs. 62 +/- 10%; NS) and was not significantly altered by cisapride (59 +/- 9.4% vs. 54 +/- 9%; NS). In patients, cisapride increased integrated postprandial gallbladder volume by accelerating gallbladder refilling as compared to placebo by 37 +/- 15% (p < 0.05). Integrated cholecystokinin plasma levels were similar in patients and volunteers and were 13.4 +/- 4.7% higher after cisapride as compared to placebo (p < 0.05). CONCLUSIONS: The results of this study suggest that cisapride does not alter postprandial gallbladder contraction but accelerates gallbladder refilling in patients free from gallstones after extracorporeal shock-wave lithotripsy. This effect of cisapride is probably due to an acceleration of gastric emptying also causing a secondary enhanced cholecystokinin release.

Adult↗
PubMed1995

Endoscopic features of Helicobacter pylori-related gastritis.

BACKGROUND AND STUDY AIMS: It is still controversial whether certain endoscopic features can be used to diagnose Helicobacter pylori (Hp)-related gastritis. To clarify this issue, we performed two consecutive prospective studies. PATIENTS AND METHODS: In the first study, we tried to identify endoscopic criteria associated with Hp-related gastritis from a total of 66 predefined gastric features on endoscopy. These features were selected by a stepwise logistic regression analysis in 101 patients. The validity of these features gained from this first study was then evaluated in a second study in 86 patients (40 with Hp gastritis, 8 with Hp-unrelated gastritis and 38 with normal gastric mucosa). RESULTS: Three features, namely an abnormal antral surface texture, a mammillated corpus surface, and white antral erosions, were identified in the first study as independent predictors of Hp-related gastritis. However, the sensitivity and specificity of these three criteria, as assessed in the second study, were only 75% and 63% respectively. CONCLUSIONS: We conclude that it is not possible to diagnose Hp-related gastritis on the basis of the endoscopic appearance alone. The diagnosis should be based on other criteria, such as a rapid urease test, or a histological examination of gastric biopsies, or both.

Adult↗