Biomedical subjects

W Dekker

Publications and source records attributed to W Dekker.

At least 19 recordsLinked to original sources

PubMed2001

Long-term lansoprazole treatment for gastro-oesophageal reflux disease: clinical efficacy and influence on gastric mucosa.

BACKGROUND: Long-term acid suppression is believed to accelerate atrophic gastritis in Helicobacter pylori-positive patients. The influence of long-term therapy with lansoprazole has not been examined. AIM: To study the clinical and endoscopic efficacy and histological evolution of gastric mucosa during 5 years of maintenance treatment with lansoprazole, 30 mg. METHODS: Seventy-eight patients with endoscopically proven oesophagitis were followed for 5 years. Biopsies taken at the start of the study, during follow-up and after 5 years were available for 73 patients. RESULTS: The total endoscopic relapse rate was 14.1%. At the start of the study, 34 patients were Helicobacter pylori negative and 39 were Helicobacter pylori positive (two atrophy, 25 antral gastritis, 12 pangastritis). At 5 years, no histological changes had occurred in Helicobacter pylori-negative patients. In the Helicobacter pylori-positive group, 20 patients developed pangastritis, six had normal histology and one had antral gastritis. Ten of the 12 patients with pangastritis had reduced antral activity. There was no increase in intestinal metaplasia, but there was a tendency towards regression of atrophy in the antrum and towards increased atrophy in the body of the stomach. CONCLUSIONS: Maintenance treatment with lansoprazole, 30 mg, is efficacious. The development of glandular atrophy and intestinal metaplasia was not accelerated in Helicobacter pylori-positive patients. Helicobacter pylori eradication must be considered only because of the higher cancer risk associated with chronic Helicobacter pylori-related gastritis.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed2000

Lack of cyclin D1 overexpression in gastric carcinogenesis.

AIMS: Cyclin D1 overexpression was examined in early gastric carcinomas and precursor lesions with the following aims; (1) to assess the chronology of cyclin D1 overexpression in various stages of gastric carcinogenesis, (2) to correlate cyclin D1 overexpression with the Lauren type, the grade of differentiation and the type of growth pattern of the tumours and (3) to correlate cyclin D1 overexpression with clinical parameters, in particular lymph node metastasis and overall prognosis. METHODS AND RESULTS: Forty-five paraffin-embedded gastrectomy specimens from early carcinomas were examined for the presence of various precursor lesions. The Lauren type, the grade of differentiation and the type of growth pattern were reassessed for all early carcinomas. Cyclin D1 overexpression was examined using the monoclonal antibody DCS-6. Cyclin D1 overexpression was absent from all precursor lesions. Ten early carcinomas (22%) were cyclin D1 positive without significant differences when stratified according to Lauren type, grade of differentiation, type of growth pattern or lymph node status. Univariate analysis failed to show a significant difference in 5-year surival rate between cyclin D1 positive and negative early carcinomas (90% vs. 94%). CONCLUSIONS: Cyclin D1 protein overexpression does not play a role in the progression from normal to neoplastic gastric mucosa and does not discriminate between intestinal and diffuse type early gastric carcinomas of Caucasian origin. Moreover, mechanisms other than cyclin D1 protein overexpression underlie the reported difference in biological behaviour of early gastric carcinomas with different types of growth pattern. Finally, although it appears that cyclin D1 does not have prognostic significance, studies on larger numbers, including advanced carcinomas, are warranted.

Cyclin D1↗

PubMed2000

Acute pancreatitis in peritoneal dialysis and haemodialysis: risk, clinical course, outcome, and possible aetiology.

BACKGROUND: It has been suggested that the incidence of acute pancreatitis in patients with end stage renal failure is increased. AIMS: To assess the risk of acute pancreatitis in patients on long term peritoneal dialysis and long term haemodialysis compared with the general population, to evaluate its clinical course and outcome, and to identify possible aetiological factors. PATIENTS: All patients who were maintained on long term peritoneal dialysis and/or haemodialysis (total dialysis time more than six weeks) from January 1989 to March 1998 in a large general hospital in The Netherlands. METHODS: Retrospective cohort study. Standardised ratios (as an approximate relative risk) between the incidence of acute pancreatitis in haemodialysis or peritoneal dialysis and the general population were calculated. Possible risk factors were identified. Patients with and without acute pancreatitis were compared. RESULTS: In 269 patients on haemodialysis (total of 614 person years), one patient developed an attack of acute pancreatitis. Patients on haemodialysis did not show an increased risk for acute pancreatitis compared with the general population (standardised ratio 11; 95% confidence interval (CI) 0.275 to 60.5). In 128 patients on peritoneal dialysis (total of 241 person years), seven patients had nine attacks of acute pancreatitis. Patients on peritoneal dialysis had a significantly and highly increased risk for acute pancreatitis (standardised ratio 249; 95% CI 114 to 473). Mortality in this series of nine attacks was 11%. No single aetiological risk factor could be identified. CONCLUSIONS: The risk of acute pancreatitis in patients on long term peritoneal dialysis is significantly and highly increased compared with the general population. The underlying causal mechanisms remain to be elucidated.

Acute Disease↗

PubMed1999

[Whipple's disease in a man with weight loss and diarrhea].

In a 45-year-old man with diarrhoea, upper abdominal pain and malabsorption Whipple's disease was diagnosed by gastroduodenoscopy with small bowel biopsies. The disease is rare and can present with gastrointestinal problems but also with cardiac or neurological complaints. Tropheryma whippelii, the aetiological organism, can be demonstrated by pathological investigation of biopsies and with the polymerase chain reaction (PCR). Treatment with trimethoprim-sulfamethoxazole 160-800 mg twice daily is the therapy of choice: it must be continued for a year, otherwise there is a high possibility of relapse. Correct diagnosis, based mostly on gastroduodenoscopy, can lead to the right therapy and recovery of the patient.

Biopsy↗

PubMed1999

p21(Waf1/Cip1) expression and the p53/MDM2 feedback loop in gastric carcinogenesis.

Data are non-existent regarding coincidental alterations in the expression of p53 and its downstream target genes MDM2 and p21(Waf1/Cip1) in gastric carcinogenesis. An immunohistochemical study was therefore performed to examine the interrelationships of p53, MDM2, and p21(Waf1/Cip1) expression in a series of Caucasian early gastric carcinomas and precursor lesions. In normal gastric mucosa, chronic gastritis, and intestinal metaplasia, the surface cells expressed p21(Waf1/Cip1) in the absence of detectable nuclear p53 and MDM2 protein. Nuclear p53 protein accumulation was found in 60 per cent of the carcinomas, with significant differences in staining characteristics between the Lauren types in the absence of detectable MDM2 protein ( p< 0.005). Nearly 80 per cent of the carcinomas expressed p21(Waf1/Cip1), irrespective of Lauren type. Stratification of the carcinomas according to histological grade and growth pattern did not result in significant differences in p53 and p21(Waf1/Cip1) expression. Finally, no significant correlation was found between overall p53 and p21(Waf1/Cip1) expression in early gastric carcinomas. It is concluded that p21(Waf1/Cip1) expression in the non-neoplastic mucosa most likely relates to cell senescence and/or terminal differentiation, perhaps even in a p53-independent manner. In view of p53/MDM2 homeostasis, the differences in p53 staining characteristics between intestinal and diffuse-type carcinomas probably result, at least in part, from a difference in the prevalence of p53 gene mutations. Moreover, p53-independent induction of p21(Waf1/Cip1) expression apparently occurs in a considerable proportion of early carcinomas. Finally, in contrast to other carcinomas, p21(Waf1/Cip1) expression is not significantly correlated with histological grade in gastric carcinomas, suggesting possible defects downstream of p21(Waf1/Cip1) as an underlying cause for this apparent discrepancy.

Carcinoma↗

PubMed1999

Loss of E-cadherin expression in early gastric cancer.

AIMS: Reduction or loss of E-cadherin expression was examined in early gastric carcinomas and precursor lesions with the following aims: (1) to assess overall E-cadherin expression in various stages of gastric carcinogenesis; (2) to correlate E-cadherin expression with the Lauren type, the grade of differentiation and the type of growth pattern of the tumours; and (3) to correlate E-cadherin expression with lymph node metastasis and overall prognosis. METHODS AND RESULTS: Forty-five paraffin-embedded gastrectomy specimens from early carcinomas were examined for the presence of various precursor lesions. The Lauren type, the grade of differentiation and the type of growth pattern were reassessed for all early carcinomas. E-cadherin expression was examined using antibody HECD-1. Whereas E-cadherin was strongly and evenly expressed in the gastric foveolar epithelium, intestinal metaplasia and early gastric carcinomas showed a lower expression. A significant difference in E-cadherin expression was found between the Lauren types (P < 0.0001). Moreover, an inverse correlation was found between E-cadherin expression and histological grade (P < 0.0001). Neither a difference in E-cadherin expression between the various growth types nor an association with lymph node metastasis and overall prognosis was found. CONCLUSIONS: The Lauren types differ in E-cadherin expression, although reduced E-cadherin expression in all probability rather reflects poor differentiation than a diffuse growth pattern 'genotype'. Moreover, E-cadherin expression does not underlie the difference in biological behaviour of early carcinomas with different types of growth pattern. Finally, E-cadherin expression is not associated with lymph node status and 5-year survival rate, at least not in early gastric carcinomas.

Cadherins↗

PubMed1999

Molecular alterations in early gastric carcinomas. No apparent correlation with Helicobacter pylori status.

Data on the differences in molecular profile between H pylori-positive and H pylori-negative early gastric carcinomas, if any, are almost nonexistent. We therefore investigated whether molecular differences can be observed between H pylori-positive and H pylori-negative early gastric carcinomas. Forty-five early gastric carcinomas were analyzed for alterations in certain oncogenes (ras, MDM2, c-erbB-2, cyclin D1), the p53 tumor suppressor gene, and the e-cadherin gene. Of these 28 carcinomas were H pylori-positive, and 17 were H pylori-negative. No significant differences were found in the groups irrespective of Lauren type; ras (0% vs 0%), MDM2 (0% vs 0%), c-erbB-2 (0% vs 0%), cyclin D1 (18% vs 29%), p53 (68% vs 47%), and e-cadherin (46% vs 41%). Helicobacter pylori-positive and H pylori-negative early gastric carcinomas do not differ in molecular profile. Although they may prove different when tested for other abnormalities, our findings suggest that the acquisition of molecular alterations occurs via an H pylori independent pathway.

Cadherins↗

PubMed1999

Automated separation of whole blood in top and bottom bags into components using the Compomat G4.

BACKGROUND AND OBJECTIVES: Whole blood can be separated by hard spin centrifugation into layers of blood components according to their specific gravity. The aim was to develop a program for an automatic separator to subsequently express the various components into their respective satellite bags in top and bottom systems with the following requirements: a red cell concentrate with a low leukocyte and platelet contamination, a 'cell-free' plasma, and a buffy coat with a volume of about 50 ml with an acceptable loss of red cells. MATERIALS AND METHODS: The Compomat G4 possesses an independently moving upper and lower press, to automatically express plasma or red cells to satellite bags of top and bottom systems. The influence of the extension of the lower press was studied by pooling and dividing two units of whole blood, and separating these units after centrifugation (2,960 g, 10 min) either with a program where the lower press was completely extended (program C), or with a program that left approximately 1 mm between the door and the lower press (program D). RESULTS: The program (program D), where the lower press was not completely extended, yielded a buffy coat with a volume of 52+/-1 ml (mean +/- SD, n = 36), which contained >75% leukocytes and >90% platelets of the original whole blood unit, with a red cell loss in the buffy coat of 21+/-1 ml (10.8+/-0.8% of the original volume). The leukocyte content of the red cell concentrates was 775+/-379x10(6) per unit, whereas the plasma contained 3+/-3x10(6) leukocytes and 4+/-3x10(9) platelets per unit. The pooling experiment indicated that complete extension of the lower press (program C) resulted in a significantly higher leukocyte contamination of the red cell concentrate (788+/-431x10(6 ) vs. 658+/-419x10(6); n = 12; p = 0.03), while there was no difference in the yield of red cells or plasma. The buffy coat produced with program D contained significantly more leukocytes (2,242 +/-396x10(6) vs. 2,065+/-327x10(6), p = 0.005) and more platelets (96+/-14x10(9) vs. 92+/-17x10(9), p = 0.02) per unit than with program C, probably because buffy coat cells sticking to the container wall are not expressed to the red cell concentrate, and thus remain in the buffy coat bag. Therefore, program D met our specifications for blood products. CONCLUSIONS: The Compomat G4 warrants reproducible separation of whole blood in top and bottom bags into red cells, buffy coat and plasma meeting our specifications.

Automation↗

PubMed1998

No evidence for functional inactivation of wild-type p53 protein by MDM2 overexpression in gastric carcinogenesis.

Inactivation of wild-type p53 during gastric carcinogenesis is usually caused by mutations within exons 5-8 of the p53 gene leading to mutated, usually immunohistochemically detectable p53 proteins. However, functional inactivation of wild-type p53, mimicking mutational inactivation, may also result from binding to overexpressed MDM2 protein. While these two mechanisms of p53 inactivation are considered to be mutually exclusive, no data exist as to whether MDM2 overexpression occurs during gastric carcinogenesis. MDM2 protein overexpression was therefore studied in relation to p53 protein accumulation in gastric carcinogenesis. Forty-five paraffin-embedded gastrectomy specimens from early gastric carcinomas were examined for the presence of chronic active gastritis, chronic atrophic gastritis, subtypes of intestinal metaplasia, and dysplasia. The Lauren type was reassessed for all early carcinomas. p53 protein accumulation was examined using the monoclonal antibody DO-7. MDM2 protein overexpression was assessed with the monoclonal antibody SMP-14. Complete absence of nuclear p53 protein accumulation was observed in chronic active gastritis, chronic atrophic gastritis, and intestinal metaplasia, irrespective of the subtype. In gastric dysplasia (one mild, two moderate, one severe), only severe dysplasia was p53-positive. Intestinal-type (n = 20) and diffuse-type early gastric carcinoma (n = 25) were p53-positive in 70 and 52 per cent of the cases, respectively. MDM2 protein overexpression was not observed during gastric carcinogenesis, either in the p53-positive or in the p53-negative cases. In conclusion, it appears that functional inactivation of wild-type p53 by MDM2 protein overexpression plays no role in (early) gastric carcinogenesis.

Chronic Disease↗

PubMed1998

No evidence for c-erbB-2 overexpression in gastric carcinogenesis.

AIMS: Conflicting data on c-erbB-2 overexpression in gastric carcinomas can be found in the literature with regard to overall prevalence, prognostic significance and the histological type according to Lauren. The majority of these studies have focused on advanced gastric carcinomas whereas data on c-erbB-2 overexpression in early gastric carcinomas, especially of Caucasian origin, are relatively sparse. We therefore examined a series of Caucasian early gastric carcinomas to assess overall c-erbB-2 overexpression and to correlate c-erbB-2 overexpression, if any, with the type of growth pattern and the Lauren type. METHODS AND RESULTS: Forty-five paraffin-embedded gastrectomy specimens from early carcinomas were examined for the presence of chronic active gastritis, chronic atrophic gastritis, subtypes of intestinal metaplasia and dysplasia. The Lauren type and the type of growth pattern were reassessed for all early carcinomas. c-erbB-2 overexpression was assessed with monoclonal antibody 3B5 and polyclonal antibody A485. Complete absence of c-erbB-2 overexpression was observed in chronic active gastritis, chronic atrophic gastritis, subtypes of intestinal metaplasia, and dysplasia. Moreover, c-erbB-2 overexpression was found absent in both intestinal-type (n = 20) and diffuse-type early gastric carcinomas (n = 25), irrespective of growth type. CONCLUSIONS: c-erbB-2 overexpression does not play a role in the progression from normal to neoplastic gastric mucosa and should be considered as a late event in gastric carcinogenesis. Moreover, c-erbB-2 overexpression does not discriminate between intestinal and diffuse type early gastric carcinomas of Caucasian origin. Finally, it appears that mechanisms other than c-erbB-2 overexpression underlie the reported differences in biological behaviour of early gastric carcinomas with different types of growth pattern.

Gastric Mucosa↗

PubMed1998

Colonic pseudo-obstruction due to beta2-microglobulin amyloidosis after long-term haemodialysis.

Beta2-microglobulin (A beta2M) amyloidosis is a relatively new secondary amyloidosis associated with renal failure and haemo- and peritoneal dialysis. Although beta2-microglobulin depositions are systemic, clinical manifestations are limited to articular and para-articular disease in most cases. A very limited number of patients have been reported with extra-articular manifestations including those of the gastrointestinal tract. We report on a patient who was treated with haemodialysis for 23 years and developed colonic pseudo-obstruction due to A beta2M amyloidosis.

Aged↗

PubMed1997

CT before and after ERCP: detection of pancreatic pseudotumor, asymptomatic retroperitoneal perforation, and duodenal diverticulum.

BACKGROUND: A prospective study was done to investigate the occurrence of morphologic changes after ERCP that present as pancreatic pseudotumor on CT scan. Fifty-eight patients underwent CT before and after ERCP. In addition, post-ERCP complications and the value of routinely obtained CT before ERCP were assessed. RESULTS: Thirty-nine patients could be fully analyzed; 12 underwent a papillotomy (group 1). Pseudotumor of the pancreatic head was demonstrated on CT after ERCP in them (17%). No changes were seen in the 27 patients who underwent diagnostic ERCP (group 2) (p = 0.048). Asymptomatic retroperitoneal perforation after papillotomy was diagnosed in 3 patients (13%). Routinely obtained CT scans before ERCP defined a specific etiology of the biliary obstruction in 12% of patients not suggested by ultrasound. Duodenal diverticulum was found in 4 patients, resulting in a sensitivity of 36% and a specificity of 100% for CT. Oral contrast (600 ml) administered a few hours before endoscopy never hampered the endoscopist. CONCLUSION: Pancreatic pseudotumor on CT after ERCP occurred only when papillotomy was performed. CT remains a valuable diagnostic tool after diagnostic ERCP. Asymptomatic perforation may occur following ERCP with papillotomy. Routinely obtained CT before ERCP was not profitable for the endoscopist in more than 80% of our patients.

Cholangiopancreatography, Endoscopic Retrograde↗

PubMed1997

Preliminary experience with a new ultraviolet-cured expandable plastic endoprosthesis in the management of malignant esophageal strictures.

BACKGROUND AND STUDY AIMS: Different types of expandable metal stent are currently available for the palliative treatment of malignant esophageal strictures. To overcome some of the disadvantages involved in the design of metal mesh stents, we designed a balloon-expanded plastic endoprosthesis, which is hardened by irradiation with ultraviolet light after deployment. We present here our preliminary results. PATIENTS AND METHODS: From April 1995 to January 1996, four patients with unresectable esophageal malignancies were treated with this stent. Insertion of the stent was the only palliative procedure carried out. The patients were followed up until death. RESULTS: Stent placement was successful in all patients, and no procedure-related complications occurred. Dysphagia was reduced from an average score of 2.6 to 1.0. Early complications included retrosternal pain of limited duration in one patient. One patient died 72 hours after uncomplicated stent placement, due to cardiac arrhythmia. Late complications were limited to tumor overgrowth in two patients, after a mean of 104 days. The stent patency rate averaged 92 days. CONCLUSIONS: In patients with a malignant esophageal stricture, this newly developed expandable endoprosthesis is effective in relieving dysphagia. The deployment of the stent is easy and safe. The endoprosthesis has potential advantage over current expandable metal mesh stents.

Aged↗

PubMed1996

Lansoprazole 30 mg versus omeprazole 40 mg in the treatment of reflux oesophagitis grade II, III and IVa (a Dutch multicentre trial). Dutch Study Group.

OBJECTIVES: To compare the efficacy and safety of lansoprazole 30 mg daily (LAN30) and omeprazole 40 mg daily (OME40) in the treatment of moderate (Savary-Miller grade II) as well as severe reflux oesophagitis (grade III/IVa). DESIGN: A double-blind, randomized, multicentre study, involving 211 patients at 29 Dutch hospitals. METHODS: Healing was assessed by endoscopy, performed on admission, after 4 weeks and after 8 weeks if the patient was not healed after 4 weeks. Symptom relief was determined by symptom assessments at the same time points. Safety was evaluated by determining the incidence of adverse events. RESULTS: There was no significant difference in intention-to-treat (ITT) healing rates after 4 weeks (LAN30 87.5%, OME40 80.6%; 95% CI (-4.0; +17.8)) and in the ITT overall healing (LAN30 96.1%, OME40 93.1%; 95% CI (-4.2; +10.2)) rates between the LAN30 and the OME40 group. Relief of reflux-related symptoms at 4 weeks as well as 8 weeks did not differ significantly between the treatment groups. No difference in the incidence of adverse events was observed between the groups. CONCLUSION: Treatment of patients with reflux oesophagitis grade II, III or IVa with LAN30 was as effective as with OME40 with respect to healing as well as symptom relief.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1995

Comparison of the efficacy and safety of 1.5 compared with 3.0 g oral slow-release mesalazine (Pentasa) in the maintenance treatment of ulcerative colitis. Dutch Pentasa Study Group.

OBJECTIVE: To investigate a possible dose-effect relationship with two dosages of oral slow-release mesalazine in patients with quiescent ulcerative colitis. METHOD: One hundred and sixty-nine patients with ulcerative colitis in remission were treated with either 1.5 or 3.0 g/day mesalazine for 1 year or until relapse into active colitis. RESULTS: Fewer of the 3.0 g dose group relapsed than of the 1.5 g dose group (33 compared with 46%). This difference failed to reach statistical significance (P = 0.057). A significant relationship between age and relapse rate was established. No dose-related adverse events were found. Three serious drug-related adverse events were, however, reported. All of the serious adverse reactions resolved after the medication was discontinued. CONCLUSION: There is a trend for high doses of oral mesalazine to be more effective in prevention of relapse of ulcerative colitis. These higher doses are not associated with a higher incidence of adverse reactions.

Administration, Oral↗

PubMed1995

Chronology of p53 protein accumulation in gastric carcinogenesis.

p53 Protein accumulation in early gastric carcinoma was studied in relation to the histological type (Lauren classification) and the type of growth pattern, including the chronology of p53 protein accumulation during carcinogenesis. Forty five, paraffin embedded gastrectomy specimens from early carcinomas were examined for the presence of chronic atrophic gastritis, subtypes of intestinal metaplasia, and dysplasia. The Lauren type and the type of growth pattern were reassessed for all early carcinomas. p53 Protein accumulation was examined using the monoclonal antibody DO-7. Complete absence of p53 protein accumulation was observed in normal gastric mucosa, chronic atrophic gastritis, and intestinal metaplasia, irrespective of subtype. In gastric dysplasia (one mild, two moderate, and one severe), only severe dysplasia was p53 positive. Intestinal type (n = 20) and diffuse type early gastric carcinomas (n = 25) were p53 positive in 70% and 52% of cases, respectively. Both tumour types differed significantly in the percentage of p53 positive tumour cells per tumour (p < 0.01) and in staining intensity (p < 0.05). No significant difference in p53 protein accumulation was found between early carcinomas with different types of growth pattern. It is concluded that p53 protein accumulation--usually reflecting missense p53 gene mutation--seems to be a late event in gastric carcinogenesis. Moreover, it is suggested that missense p53 gene mutation occurs in a final pathway common to both intestinal and diffuse type of early gastric carcinoma. Finally, the types of growth pattern do not seem to differ in p53 protein accumulation.

Cell Transformation, Neoplastic↗

PubMed1995

Absence of ras gene mutations in early gastric carcinomas.

The aims of this study were to assess the prevalence and type of activating point mutations at codons 12, 13, and 61 of the Ki-, Ha-, and N-ras genes in a series of early gastric carcinomas in white patients and to correlate these ras gene mutations, if any, with the histological type (Lauren classification), the type of growth pattern, and with the Helicobacter pylori status. Haematoxylin and eosin and Giemsa stained sections from 45 formalin fixed, paraffin wax embedded early gastric carcinomas were used to assess the Lauren type, the type of growth pattern, and the antral H pylori status. DNA was extracted according to standard procedures. Mutations at codon 12 of the Ki-ras gene were examined with a polymerase chain reaction based restriction fragment length polymorphism (PCR-RFLP) method and dot blot hybridisation with allele-specific 32P-labelled oligodeoxynucleotide (ASO) probes. All other ras genes were analysed with specific PCR amplification and dot blot hybridisation with ASO probes. Mutations were detected by overnight autoradiography at -70 degrees C. Some 20 intestinal-type and 25 diffuse-type early gastric carcinomas were seen. According to growth pattern, there were 24 small mucosal type early gastric carcinomas, five superficial spreading type early gastric carcinomas, and 16 penetrating type early gastric carcinomas (four penetrating A type, 12 penetrating B type). H pylori was found in the antral mucosa of 28 early gastric carcinomas (62%). Activating ras gene mutations were not found. It was discovered that activating point mutations at codons 12, 13, and 61 of the Ki-, Ha-, and N-ras genes do not play a part in the development of early gastric carcinomas in white subjects, irrespective of Lauren type. Moreover, differences in biological behaviour between early carcinomas with different types of growth pattern are not related to these ras gene mutations. Finally, H pylori positive and H pylori negative gastric carcinomas cannot be discriminated on the basis of ras gene mutational analysis.

Base Sequence↗

PubMed1994

Esophageal dysfunction as a cause of angina pectoris ("linked angina"): does it exist?

PURPOSE: The differentiation between cardiac and esophageal causes of retrosternal chest pain is notoriously difficult. Theoretically, cardiac and esophageal causes may coexist. It has also been reported that gastroesophageal reflux and esophageal motor abnormalities may elicit myocardial ischemia and chest pain, a phenomenon called linked angina pectoris. The aim of this study was to assess the incidence of esophageal abnormalities as a cause of retrosternal chest pain in patients with previously documented coronary artery disease. PATIENTS AND METHODS: Thirty consecutive patients were studied, all of whom had undergone coronary arteriography. The patients were studied after they were admitted to the coronary care unit with an attack of typical chest pain. On electrocardiograms (ECGs) taken during pain, 15 patients (group I) had new signs of ischemia; the other 15 patients (group II) did not. In none of the patients were cardiac enzymes elevated. As soon as possible, but within 2 hours after admission, combined 24-hour recording of esophageal pressure and pH was performed. During chest pain, 12-lead ECG recording was carried out. RESULTS: In group I, all 15 patients experienced one or more pain episodes during admission, 25 of which were associated with ischemic electrocardiographic changes. The other two episodes were reflux-related. Only one of the 25 ischemia-associated pain episodes was also reflux-related, ie, it was preceded by a reflux episode. In group II, 19 chest pain episodes occurred in 11 patients. None of these was associated with electrocardiographic changes, but 8 were associated with reflux (42%) and 8 with abnormal esophageal motility (42%). CONCLUSION: Linked angina is a rare phenomenon.

Aged↗