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Biomedical subjects

M Buset

Publications and source records attributed to M Buset.

At least 19 recordsLinked to original sources
PubMed1998

Evaluation of antiandrogen therapy in unresectable hepatocellular carcinoma: results of a European Organization for Research and Treatment of Cancer multicentric double-blind trial.

PURPOSE: The aim of the study was to evaluate the efficacy of antiandrogen therapy on overall survival and response in unresectable hepatocellular carcinoma (HCC). PATIENTS AND METHODS: A total of 244 patients with unresectable HCC were included in this multicentric double-blind trial. According to a two-by-two factorial design, patients were randomly assigned to receive one of the following treatments: pure antiandrogen plus placebo (A+P group, 60 patients); luteinizing hormone-releasing hormone (LHRH) agonist plus placebo (LHRH+P group, 62 patients); pure antiandrogen plus LHRH agonist (A+LHRH group, 62 patients); or placebo plus placebo (P+P group, 60 patients). Pure antiandrogen consisted of Anandron (Roussel-Uclaf Laboratory, Romainville, France) administered orally (300 mg daily for 1 month, then 150 mg daily). LHRH consisted of goseriline acetate (3.6 mg) or triptoreline (3.75 mg) administered monthly by subcutaneous injection. Treatment was given until death. Response was evaluated every 8 weeks according to World Health Organization (WHO) criteria. RESULTS: Six patients were considered ineligible. One patient had a complete response (A+P arm) and three had a partial response (two in the LHRH+P arm and one in the A+LHRH arm). An overall log-rank test did not demonstrate any significant difference in survival among the four arms. Taking the factorial design into account, comparison of survival showed no significant difference between Anandron-containing regimens and others, or between LHRH-containing regimens and others. No serious side effects occurred for any regimen. CONCLUSION: This controlled study shows clearly the lack of efficacy of androgen treatment in unresectable HCC.

Androgen Antagonists↗
PubMed1996

Modulation of high-dose infusional fluorouracil by low-dose methotrexate in patients with advanced or metastatic colorectal cancer: final results of a randomized European Organization for Research and Treatment of Cancer Study.

PURPOSE: Methotrexate (MTX) has been described to modulate the activity of fluorouracil (5-FU) in patients with metastatic colorectal cancer. The European Organization for Research and Treatment of Cancer (EORTC) Gastrointestinal Tract Cancer Cooperative Group (GITCCG) conducted a phase III trial to investigate the efficacy and tolarability of the addition of low-dose MTX (40 mg/m2) to high-dose infusional 5-FU (60 mg/kg over 48 hours) given weekly for 4 weeks and thereafter every 2 (for 4 weeks) and 3 weeks. PATIENTS AND METHODS: Three hundred ten patients were randomized between 1987 and 1992. Eligible patients had measurable advanced or metastatic colorectal cancer and had not been pretreated with antifolates or fluorodinated pyrimidines. All 297 eligible patients were evaluated for survival; toxicity was assessed in 292 patients who received at least one course of treatment. Patients with bidimensionally measurable disease (n = 230) were also evaluated for response according to standard criteria. RESULTS: The addition of low-dose MTX to high-dose infusional 5-FU led to a doubling of the response rate from 10% to 21% (P = .025). The median survival time also increased from 9.3 to 12.5 months, but this difference was not statistically significant (P = .12). High-dose infusional 5-FU with or without low-dose MTX was well tolerated, with grade 3 to 4 toxicity in greater than 10% of patients only occurring for stomatitis with the combination treatment. Performance status was the sole prognostic factor for survival in a multivariate analysis. CONCLUSION: Low-dose MTX effectively modulated high-dose infusional 5-FU in a large, randomized trial in which less than 5% of patients received leucovorin.

Aged↗
PubMed1995

Omeprazole-based antimicrobial therapies: results in 198 Helicobacter pylori-positive patients.

AIM: To compare the efficacies of omeprazole-based antimicrobial therapies in Helicobacter pylori-positive patients. PATIENTS AND METHODS: We report the results of seven therapeutic trials combining omeprazole, clarithromycin, amoxycillin, colloidal bismuth subcitrate and tinidazole in 198 patients (peptic ulcer disease/non-ulcerative dyspepsia, 137/61) to eradicate H. pylori infection. The diagnosis of infection was performed by Sydney system biopsies, compliance was checked after a pill count at the end of the treatment and eradication was assessed at least 4 weeks after the end of the treatment either by the Sydney system for peptic ulcer disease or the urease breath test for non-ulcerative dyspepsia. RESULTS: When results were analysed on a protocol basis, the only significant difference in eradication (P = 0.006) was found between the total population of patients treated with amoxycillin-based combinations (27 eradications out of 48 patients) and those given a treatment that included clarithromycin (84 eradications out of 108). Forty-two patients (21%) dropped out either because of side effects (10 among patients taking clarithromycin and two taking amoxycillin) or because they were lost to follow-up (27 patients). Out of 64 patients with active ulcers, 43 (67%) were both H. pylori-negative and ulcer-free 4-8 weeks after the end of therapy, 12 out of 64 (19%) were ulcer-free but remained H. pylori-positive and nine out of 64 (14%) were H. pylori-positive and had active ulceration.

Amoxicillin↗
PubMed1994

Helicobacter pylori: the link with gastric cancer.

Gastric cancer is the world's overall second most common cancer, and carries a bad prognosis. In the Correa model of gastric carcinogenesis, environmental factors (salt, nitrate, a lack of vitamin C and beta-carotene, bile reflux, bacterial overgrowth in atrophic gastritis with nitrosamine formation) are related to the evolution from normal gastric tissue through superficial gastritis, multifocal atrophic gastritis, intestinal metaplasia and dysplasia to carcinoma. The incidence of H. pylori decreases with progressing preneoplastic lesions. In several studies, the prevalence of H. pylori was elevated in patients with gastric cancer, with a trend for a higher prevalence in intestinal type gastric cancer vs diffuse type. Family members of patients with gastric adenocarcinoma have a higher H. pylori prevalence than controls; patients infected with H. pylori have more family members with gastric cancer. Several epidemiological studies showed a higher H. pylori prevalence in regions or populations with high gastric cancer risk vs low-risk populations. Large-scale studies in China and Europe showed a correlation between H. pylori seroprevalence and gastric cancer incidence and mortality. Three prospective nested case-control studies showed that infection with H. pylori increased the risk of further development of gastric adenocarcinoma, showing that H. pylori infection precedes the development of gastric cancer. Several pathways can be identified explaining the association between H. pylori and gastric adenocarcinoma. We showed that gastric cell proliferation is increased in parallel with inflammation. The ascorbic acid concentrating mechanism is abolished in gastritis. Ammonia, generated by H. pylori's urease, gives rise to gastric mucosal atrophy. We showed that salt increases the gastric cell proliferation only in H. pylori-infected individuals. The organism's toxin may play a role in gastric cancer. Besides H. pylori, other environmental factors are important in determining the gastric cancer risk. For instance, we showed that in Belgium, Maghreb immigrants have a high prevalence of H. pylori infection but a low prevalence of intestinal metaplasia and gastric cancer. Gastric lymphoma is rare (about 5% of all gastric tumours), but its incidence is steadily increasing. It was shown that H. pylori also increases the risk for low-grade as well as high-grade gastric lymphoma. Eradication of H. pylori has been shown to cure several cases of unequivocally proven gastric low-grade lymphoma.(ABSTRACT TRUNCATED AT 400 WORDS)

Helicobacter Infections↗
PubMed1993

Gastric screening prospects.

The incidence of gastric cancer is rapidly declining in the Western world, but it remains high in the Third World and in Japan. Systematic screening for gastric cancer has been undertaken in Japan, where barium X-ray is used in people over the age of 40. Evaluation data suggest a benefit in reduced mortality, but biases cannot be ruled out. A similar screening programme has been started in Venezuela. Currently, stomach cancer screening programmes cannot be recommended as public health policy, except in high-risk areas where they have already started. The Correa model of gastric carcinogenesis states that environmental influences cause a normal gastric mucosa to undergo successive stepwise changes, through superficial gastritis, atrophic gastritis, intestinal metaplasia, dysplasia, carcinoma and, finally, invasion. Incriminated environmental influences include irritant, antibodies, gastrectomy, nutritional deficits, intake of nitrogen compounds and Helicobacter pylori. These bacteria cause a chronic superficial gastritis, which may develop into atrophic gastritis. H. pylori is less frequently found in advancing preneoplastic lesions, and seldomly in gastric carcinoma tissue (it may, however, be identified more readily in the surrounding non-cancerous tissue). Several lines of evidence suggest that H. pylori may play an important role in human gastric carcinogenesis. We found that in some patients with H. pylori infection and without preneoplastic lesions, the gastric cell turnover was increased; this was correlated with the intensity of the inflammatory changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Helicobacter Infections↗
PubMed1991

Management of dysphagia in suspected esophageal motor disorders.

Fifty-three patients suffering from dysphagia because of suspected esophageal motor disorders were treated by pneumatic dilatation using the Rider-Moeller technique. Fifteen had achalasia demonstrated by manometric studies. Forty-nine of them had remarkable clinical improvement after the procedure. During the mean period of follow-up (average 5 years, range 1-11), 75% of the patients needed a new dilatation, with a delay of two years. The results of the dilatation were excellent or good in 80% of the cases. Early complications consisted in two esophageal perforations surgically treated. There was no mortality. We did not observe late complications of the procedure. We conclude that pneumatic dilatation should be the initial procedure in the treatment of dysphagia in suspected esophageal motor disorders.

Aged↗
PubMed1991

Endoscopic palliative intubation of inoperable malignant esophagogastric obstruction.

In patients with obstructive tumors of the esophagus and who cannot undergo curative surgery, endoscopic palliative intubation can provide a quick relief to dysphagia with subsequent improvement of nutritional status. The technical success rate is as high as 95%. Broncho-esophageal fistulas can be occluded by esophageal prosthesis. The most serious complication is perforation, which incidence is 6 to 8%. The other rare complications are bleeding or aspiration pneumonia. The overall survival rate is only 6 months, but with a significant improvement in the quality of life. Endoscopic intubation is now challenged by laser therapy; their specific indications and advantages are discussed.

Esophageal Neoplasms↗
PubMed1990

Injury induced by fatty acids or bile acid in isolated human colonocytes prevented by calcium.

Measurement of the modulation of the growth fraction of isolated normal colonocytes from adult subjects in primary monolayer culture was used as a sensitive quantitative assay to evaluate toxic effects of several endogenous compounds found within the colon. This assay was used to study the role of CaCl2 in blocking cell injury. When added simultaneously with the injurious agent, 5-10 mM CaCl2 blocked the toxicity of physiological concentrations of deoxycholic acid, oleic acid, palmitic acid and linoleic acid.

Calcium Chloride↗
PubMed1989

Heterogeneity in the response of familial polyposis epithelial cells and adenomas to increasing levels of calcium in vitro.

A biomarker of increased risk for colon cancer is abnormally high proliferation of colonic epithelial cells. The authors developed an in vitro assay that measures the ability of human colonic epithelial cells that are in progressive stages of abnormal development to respond to direct application of calcium as the chloride in tissue culture medium. Incorporation of 3H-thymidine and autoradiography in situ was employed to measure the number of proliferating cells cultured at 0.1 mM CaCl2, the optimum level for growth, and 2.2 to 5 mM, both levels achievable in the colonic lumen. Abnormal cell proliferation was reduced in biopsies from 13 of 14 patients without familial polyposis but at increased risk for colon cancer because of previous colonic neoplasms or familial association; in cells from three of four asymptomatic individuals in familial polyposis families at risk for that disease; and in cells of three of ten patients symptomatic with familial polyposis. Growth of tubular adenoma cells from two of seven familial polyposis patients was also inhibited by calcium. Growth inhibition was not observed in more advanced colon tumors including eight adenomas, either villotubular or villous, and five carcinomas. These findings indicate heterogeneity within the familial polyposis phenotype for the normal cellular response to growth inhibition by calcium, and a further loss of response to calcium as these cells progress toward malignancy.

Adenoma↗
PubMed1988

Vasoconstrictive effect of portal blood in isolated dog kidney.

Humoral vasoactive substances coming from portal blood have been considered as a possible cause of renal dysfunction in cirrhotic patients. We have thus investigated the effect of perfusion of portal blood from anesthetized dogs on the isolated kidney functions. Both kidneys of a dog were simultaneously perfused on 2 Nizet's pump oxygenators, one kidney serving as control for the other. Renal blood flow was decreased in kidneys perfused with portal blood, as compared to the paired control kidneys perfused with sus-hepatic blood (group A experiments). Addition of polymyxin B to the portal blood restored the renal blood flow to the control level (group B experiments). No significant changes appeared between experimental and control kidneys for glomerular filtration rate, urine output, sodium and water excretion, renin activity, angiotensin II levels, plasmatic PGE2 levels, in group A as well as in group B. We conclude that portal blood of dogs contains vasoactive substances reducing renal blood flow; their action is mediated neither by the renin-angiotensin system nor by changes in renal PGE2 production. The complete abolition of this effect by Polymyxin suggests that these substances may be endotoxins.

Animals↗
PubMed1988

Tumor-promoter-enhanced destruction of noninvasive human benign colon tumor cells by cocultivated carcinoma cells.

Colon carcinoma cells are first found as microscopic foci within benign tumors or adenomas. The carcinoma must invade the adenoma which protrudes into the colon lumen before it can infiltrate the bowel wall. A quantitative model for this process has been developed in tissue culture in which human colon carcinoma cells destroy cocultivated adenoma colonies. 43 adenoma colonies were assayed by cocultivation with carcinoma cells. Constitutive secretion of the urokinase form of plasminogen activator by carcinoma cells apparently plays some role in adenoma destruction as inhibition of this protease by the competitive inhibitor benzamidine reversibly inhibited adenoma destruction (p less than 0.01). Elevation of plasminogen activator secretion by addition of the tumor promoter 12-tetradecanoylphorbol-13-acetate significantly enhanced the destruction of colonies cultured from tubular adenomas with only mild dysplasia (p less than 0.025) and from villous, villotubular and tubular adenomas with moderate to severe dysplasia (p less than 0.0005).

Adenoma↗
PubMed1987

Defining conditions to promote the attachment of adult human colonic epithelial cells.

An improved method for the attachment and growth of normal human colonic epithelial cells from minute 1 to 3-mm3 biopsies has been developed. This yields four times as many cultured cells per biopsy than older methods, with a success rate of 97% in a series of 29 biopsies. Fetal bovine serum was eliminated from the medium, the medium pH was decreased to 6.7, the oxygen tension in the incubator was decreased to 3%, and the NCTC 168 medium was supplemented with ethanolamine, phosphoethanolamine, hydrocortisone, ascorbic acid, transferrin, glutamine, insulin, epidermal growth factor, pentagastrin, and deoxycholic acid. The best substrate for cell attachment was a mixture of ungelled collagen I and bovine serum albumin. This substrate was better than the identical mixture with fibronectin added, fibronectin alone, a thin gelatin film, collagen IV with or without fibronectin, and basement membrane preparations from four different cell lines.

Basement Membrane↗
PubMed1987

Palliative endoscopic management of obstructive esophagogastric cancer: laser or prosthesis?

One hundred forty-four patients with unresectable malignant strictures of the upper digestive tract were managed by palliative endoscopic methods: 116 by intubation and 28 by YAG laser phototherapy. The success rate was 95% for intubation and 100% for laser. The morbidity rate was 13.8% for intubation (perforation 7.8%, bleeding 3.4%, and aspiration pneumonia 2.2%) and 3.6% (one perforation) for laser. The mortality rate was 4.3% for intubation and 0% for laser. Specific indications for intubation were esobronchial fistulas, extensive strictures, and very long stenotic lesions. Very high cervical strictures and nonocclusive asymmetrical tumors were better treated with laser. In select cases, combined therapy can be useful. We conclude that both methods are highly efficient in restoring patency and relieving dysphagia. Further large scale randomized trials are necessary to compare functional results and survival rate.

Aged↗
PubMed1987

Bleeding esophagogastric varices: an endoscopic study.

Among 857 patients admitted from October 1977 to December 1984 with acute upper gastrointestinal hemorrhage, 165 (19.5%) had endoscopically proved esophageal or gastric varices. Among this group, varices were considered as the actual bleeding lesion in only 83 (9.7%). Stigmata of variceal bleeding were observed in 76 (92%) including 35 venous spurts, 12 venous oozes, 20 adherent clots, and 14 "platelet aggregates." In only seven cases, variceal rupture could only be presumed, because no other lesion was present. In the other 82 patients, a lesion other than varices was the bleeding source, mostly peptic ulcers (32 = 38%) and erosive gastritis (30 = 36%). One-third of the patients with bleeding varices required more than one endoscopy to provide evidence of variceal bleeding. The most frequent bleeding point was the cardia and a good correlation between variceal size and bleeding was observed. There was no relationship with evidence of gastroesophageal reflux.

Acute Disease↗
PubMed1986

Radioimmunoassay of erythropoietin in chronic uraemia or anephric patients.

The erythropoietin (Ep) plasma titre of 41 anaemic patients with normal renal function or with renal insufficiency (with or without kidney) was measured by RIA and compared to values observed with the polycythaemic mouse assay. A good correlation was found with both methods (r = 0.88). However, about 20% of samples gave higher values with the bioassay. 21 Ep titres measurable by the bioassay ranged from 40 to 4400 mU (mean 717.1 mU) compared to 14.8 to 3788 mU (mean 484.7 mU) measured by the RIA. Low levels of Ep plasma titre have been observed in patients with renal insufficiency and no difference was found between nephric uraemic patients and the anephric group. These results suggest that the increased blood requirements in anephrics are not due to a smaller production of Ep, but ultimately to the presence of an inhibitor of erythropoiesis. The well-known inverse relationship between haematocrit and Ep level was not found in renal insufficiency. However, some humoral regulation of erythropoiesis seems to persist in these patients since the elevation of red blood cells by transfusions was followed by a decrease of the Ep level.

Biological Assay↗