Biomedical subjects

R Befrits

Publications and source records attributed to R Befrits.

43 records · Page 3Linked to original sources

PubMed1984

Effect of graded 15(R)15 methyl prostaglandin E2 and of indomethacin on the gastric secretory and plasma gastrin response to modified shamfeeding.

Vagal stimulation by modified shamfeeding in healthy subjects induced about fourfold increases of gastric outputs of acid, chloride, sodium and potassium. Prior oral 15(R)15 methyl prostaglandin E2 inhibited dose-dependently the peak and total gastric acid response to modified shamfeeding by lowering both the secreted volumes and the acidity. The inhibition by 15 micrograms of the analogue exceeded 50% and the suppression was submaximal by 140 micrograms. Gastric output of chlorides decreased in a dose-related way. The hydrogen ion output was proportionally more reduced than the chlorides. The analogue did not affect the gastric output of sodium. Potassium decreased in a dose-related way. Indomethacin was without effect on the gastric acid response to shamfeeding but reduced the sodium output compared to in controls and in series with the analogue. Plasma gastrin was slightly but significantly elevated by the shamfeeding procedure. This elevation was absent or even reversed by 15(R)15 Me PGE2. No effect was recorded by indomethacin pretreatment. Vagal stimulation augments both the parietal and non-parietal components of the gastric secretion. Low doses of oral 15(R)15 Me PGE2 were effective in suppressing the vagally stimulated acid secretion. Neutralization by the gastric non-parietal secretion can contribute to reduce the acid response. Blocking of the prostaglandin biosynthesis decreased gastric sodium output, suggesting indirectly that endogenous prostaglandins may be involved in modulating the gastric non-parietal secretion.

Adult↗

PubMed1984

Gastric acid inhibition by antral acidification mediated by endogenous prostaglandins.

The effects of indomethacin on the basal and stimulated gastric acid secretion at controlled intragastric pH were examined. Four tests with modified sham feeding were made in nine healthy volunteers on different occasions, twice with acid and twice with alkaline perfusion of the stomach. Blocking of the prostaglandin biosynthesis with indomethacin preceded one of the tests at each pH. Plasma levels of gastrin were measured. Antral acidification suppressed the basal and vagally stimulated gastric secretion rate of H+ and Cl-. The inhibition was associated with a decreased plasma gastrin response. Indomethacin reduced the inhibition of the peak acid output and plasma gastrin levels induced by antral acidification. During alkalinization of the stomach indomethacin had no effect on the acid secretion rate or plasma gastrin levels. The results suggest that the pH-dependent inhibitory regulation of the gastric acid secretion is mediated by locally produced prostaglandins. The mechanism functions at least partially through modifying the release of gastrin.

Adult↗

PubMedDate not supplied

Villous and serrated adenomatous growth bordering carcinomas in inflammatory bowel disease.

The histologic phenotype of the dysplastic lesion juxtaposing colorectal carcinomas was assessed in 100 consecutive colectomy specimens: in 50 patients with inflammatory bowel disease (IBD) and in 50 controls (non-IBD patients). Adenomatous growths (AG) were regarded both Dysplasia Associated Lesion or Mass (DALM) and sporadic adenomas. AGs juxtaposing carcinomas were found in 76% (n = 38) of the IBD cases: 52.3% (20 out of 38) were villous, 28.9% (11 out of 38) serrated, 5.3% (2 out of 38) tubular and the remaining 13.2% (5 out of 38) were mixed AGs. Juxtaposing AGs (sporadic adenomas) were also found in 58% (n = 29) of the control cases: 51.7% (15 out of 29) were villous, 6.9% (2 out of 29) tubular, 3.4% (1 out of 9) serrated and the remaining 37.9% (11 out of 29) were mixed. The majority or 81.2% (31 out of 38) of the dysplastic lesions juxtaposing IBD carcinomas were villous or serrated AGs, but only 55.1% (16 out of 29) in control cases. Serrated AGs in particular accounted for nearly 29% of the non-invasive dysplastic lesions abutting IBD carcinomas but only for 3% in control specimens. It would appear that villous and serrated AGs are the most common non-invasive neoplastic lesions from which IBD carcinomas originate.

Adenoma↗

PubMedDate not supplied

Colorectal carcinoma in ulcerative colitis is decreasing in Scandinavian countries.

A total of 31 cases with Ulcerative Colitis (UC) and colorectal carcinoma were retrieved from the files of the Karolinska Hospital, Stockholm between 1951 and 1998. Sections from 16 colectomy specimens (operable cases) and 15 biopsies obtained at laparotomy (inoperable cases), were available for the study. Of the 31 patients reported here, 22 (71%) were 49 years of age or younger at the time of surgery for carcinoma. In comparison only 47 (5.5 %) of the 855 colorectal carcinomas without UC reported in the Stockholm area in 1990 were 49years of age oryounger. When this hospital was a referral Center (1951 through 1969) 18 cases of carcinoma in UC were operated between 1951 and 1960 (1.8 patients/year), but only 4 between 1961 and 1969 (0.44 patients/year). During the surveillance period of 29 years (1970 to March 1998) only 9 patients (0.31 cases/year) were found to have carcinoma complicating UC. Notably, 8 of the 9 patients were operated on between 1970 and December 1989 (0.42 patients/year), but only one case between January 1990 and March 1998 (0.11 patients/year). The data presented indicate that the frequency of carcinoma cases in pancolitics has decreased at this hospital, not only during the referral period, from 1.8 patients/year during the 50's to 0.40 patients/year during the 60's, but also during the surveillance period (from 0.44 patients/year/during the 70's and 80's to 0.11 patients/year between 1990 and March 1998). This, despite the incidence of UC in the Stockholm County remained stable for the past 40 years (4.2 to 5 patients/10(5) inhabitants) and that the population in the Stockholm County has steady increased since 1950. A review of the present literature indicated that the ris for colorectal carcinoma in pancolitics is presently decreasing, not only in Sweden but also in other Scandinavian countries.

Adenocarcinoma, Mucinous↗

PubMedDate not supplied

Colorectal cancer in colonic Crohn's disease--high frequency of DNA-aneuploidy.

BACKGROUND: The risk of colorectal cancer (CRC) in colonic Crohn's disease (CCD) seems to be of the same magnitude as in extensive, longstanding ulcerative colitis (UC) and colonoscopic surveillance has been advocated. Mucosal dysplasia and DNA-aneuploidy are early warning markers of malignant transformation in UC. Data concerning the occurrence of such premalignant lesions in CCD are scarce. AIMS: The objective of this study was to investigate the DNA ploidy pattern in CCD-patients with manifest CRC, both in the tumour, as well as in the adjacent and distant colorectal mucosa. The results from DNA-flow cytometry analyses (FCM) prior to the development of a CRC in CCD were also investigated. MATERIALS AND METHODS: Biopsies obtained at colonoscopy and surgical specimens from 43 patients with colonic or ileocolonic CD developing CRC between 1988 and 1998 were reviewed. The CRC histological phenotype, and the occurrence of dysplasia were registered. CRC-tissue and tissue from areas with dysplasia adjacent to and/or distant from the tumour were obtained from paraffin-embedded blocks and were analysed by FCM after preparation. RESULTS: Twenty-four CRCs in 21 patients (14 men) were suitable for FCM-analyses. The median age at CRC-diagnosis was 53 years (21-73) and the median CCD-duration was 14.5 years (1-50). A predominance of CRC was found either in the cecum (9124) or in the rectum (7/24). DNA-aneuploidy was found in 62.5% (15/24) of the tumours, in 25% (2/8) in adjacent and/or distant mucosa, and in 50% (2/4) of the patients that had been subjected to colonoscopic surveillance prior to the CRC-diagnosis. In 7patients (29%), definite dysplasia was detected adjacent to andlor distant from the tumour. Of the 6 patients undergoing colonoscopic surveillance, 3 (50%) displayed definite dysplasia prior to the colectomy. CONCLUSION: Since DNA- aneuploidy is a' common feature in CRCs in CCD and precede the development of invasive carcinoma, inclusion of FCM-analyses of colorectal biopsies may enhance the sensitivity of identifying high-risk CCD-patients prone to develop CRC within the frame of colonoscopic surveillance programs.

Adult↗

PubMedDate not supplied

Atypical mitoses in colectomy specimens from patients with long standing ulcerative colitis.

About 1% of dividing epithelial cells in esophageal, gastric and duodenal mucosas with chronic inflammation have been found to be atypical. In the present work, the characteristics of the mitotic figures in the colorectal mucosa with ulcerative colitis (UC)--a disease characterized by chronic mucosal inflammation--were investigated. Feulgen-stained histologic sections (having > 30 mitoses in 3 large tissue sections) from 59 colectomy specimens with long standing total UC were scrutinized at high power microscopy (1000 x). A total of 2,104 mitoses were recorded in the 59 specimens with UC: 591 (28.1%) were atypical. Atypical mitoses were present in 19.2% (SE 4.7) of the 26 specimens having chronic active inflammation, in 16.9% (SE 5.6) of the 9 with UC in remission, in 34.6% (SE 7.7) in mucosas with dysplasia (n = 8) and in 49.1% (SE 10.2) in carcinoma (n = 16). Atypical mitoses were also found in 17.0% (SE 5.4) in the non-dysplastic mucosa from colitic patients having dysplasia or carcinoma elsewhere as well as in 0.96% (SE 0.3) in 14 "noncolitic" controls with chronic inflammation. The percentage of atypical mitoses was influenced-except in areas with dysplasia or carcinoma-by the duration of the disease (< 15 or > 16 years), but not by the age or the gender of the patients. Since the frequency of atypical mitoses in "noncolitic" controls with chronic inflammation was low, it is evident that factors other than chronic inflammation may be involved in the induction of atypical mitoses in colitics. Acquired nuclear aberrations detected during the mitotic phase, but not at interphase do occur in colorectal epithelial cells from long-standing UC patients, not only in areas with dysplasia or carcinoma but also in areas without those neoplastic changes.

Adult↗

PubMedDate not supplied

Blood and tissue dehydroepiandrosterone sulphate levels and their relationship to chronic inflammatory bowel disease.

OBJECTIVE: To evaluate the levels of dehydroepiandrosterone sulphate (DHEAS) in the blood and tissues of patients with inflammatory bowel disease (IBD). METHODS: DHEAS levels were measured by radioimmunoassay in blood from 112 patients with IBD: 46 with ulcerative colitis (UC) and 66 with Crohn's disease. The levels were compared with those in 80 healthy controls. In addition, DHEAS concentrations were measured in gut tissue from 40 patients (28 patients with IBD and 12 with other bowel disorders) who had undergone gut surgery. Correlation analyses were carried out between the blood and tissue levels of DHEAS. RESULTS: The mean levels of DHEAS in the blood were markedly lower in the two patient groups (1350 nmol/l in UC and 1850 nmol/l in Crohn's disease vs. 3300 nmol/l in controls; p < 0.001 and p < 0.01 respectively). A diminution below the confidence limits of the controls (< 2500 nmol/l) was found in 37 (79%) of the patients with UC and in 49 (74%) of those with Crohn's disease. The remainder had DHEAS levels within the normal range (> 2500 nmol/l). The overall mean DHEAS concentration in gut tissue was 226 nmol/kg. A significant correlation was found between levels in the blood and those in tissues (correlation coefficient = 0.469; p < 0.002). CONCLUSION: These data indicate that low blood DHEAS is a feature in a majority of patients with UC or Crohn's disease. The possibility that there is a functional relationship between low DHEAS levels and some of the pathophysiologic features of IBD needs to be investigated.

Adult↗