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Biomedical subjects

R Befrits

Publications and source records attributed to R Befrits.

At least 37 records · Page 2Linked to original sources
PubMed1996

Small, flat colorectal neoplasias in long-standing ulcerative colitis detected by high-resolution electronic video endoscopy.

BACKGROUND: High-resolution video endoscopy complemented with chromoscopy allows for more detailed visualization of the colonic mucosal surface. METHODS: Using high-resolution video endoscopy and chromoscopy, we investigated 85 patients with extensive ulcerative colitis with a disease duration of at least 10 years who were taking part in a cancer surveillance program. RESULTS: In 38 of the 85 patients, 104 polyps were detected at endoscopy. Seventy-seven (74%) of the 104 polyps were endoscopically flat, 21 (20%) were sessile, 3 (3%) were pedunculated, and 3 (3%) had no recorded morphology. Twenty-three (22%) polyps were neoplastic (15 flat, 5 sessile, 2 pedunculated, 1 not recorded). Low-grade dysplasia was found in 21 of the 23 neoplastic polyps and high-grade dysplasia in the remaining 2 (1 flat tubular adenoma and 1 sessile villous adenoma with invasive growth). Flat polyps were small, with a diameter of 5 mm or less in 73% (n = 56) of cases. At histology flat polyps revealed either flat adenomas (n = 11; 14.3%), tubular or villous structures with dysplastic cells at the lower part of the crypts (n = 4; 5.2%), flat hyperplastic polyps (n = 26; 34%), inflammatory mucosa (n = 5; 6.5%), or mucosa in remission (n = 31; 40%). CONCLUSION: The use of high-resolution video endoscopy complemented with chromoscopy in ulcerative colitis enables the detection of flat neoplastic polyps. The existence of those hitherto undetected neoplasms in ulcerative colitis and their possible role in the histogenesis of colorectal cancer in ulcerative colitis deserve further investigation.

Adenoma↗
PubMed1996

Factors influencing the response to interferon therapy in chronic hepatitis C. Studies on viral genotype and induction of 2',5'-oligoadenylate synthetase in the liver and peripheral blood cells.

BACKGROUND: The mechanism behind the antiviral action of interferon (IFN) therapy in chronic hepatitis C virus (HCV) infection is not well understood, and, furthermore, few factors have been shown to be good predictors of a favourable response to IFN treatment in chronic HCV infection. METHODS: Freshly explanted liver cells and peripheral blood mononuclear cells (PBMC) from 80 patients with chronic HCV infection were used to study the capacity of IFN to induce the enzyme 2',5'-oligoadenylate synthetase (2'5'-AS) in vitro. The HCV genotype was determined in 53 patients. The induction of 2'5'-AS was correlated to the results of IFN-alpha treatment in 36 patients. RESULTS: Normalization of transaminases during IFN treatment was significantly associated with 2'5'-AS levels in liver cells cultured in the absence of IFN. A similar tendency, although not statistically significant, was found for IFN-induced levels of 2'5'-AS in liver cells. No such associations were found when PBMC were analysed. Six patients showed a sustained biochemical response. These six did not deviate significantly from the remaining patients with regard to base-line or IFN-induced levels of 2'5'-AS in liver cells or PBMC. Eradication of HCV RNA during IFN treatment did not correlate with 2'5'-AS levels in liver cells. Comparison of HCV genotype and clinical response showed that patients with genotype 3a had the most favourable outcome. No association was found between liver histology and treatment outcome. CONCLUSION: These data imply that direct effects of IFN on liver cells are of importance for the response to IFN treatment.

2',5'-Oligoadenylate Synthetase↗
PubMed1995

Kupffer cell iron overload induces intercellular adhesion molecule-1 expression on hepatocytes in genetic hemochromatosis.

The mechanisms underlying iron-induced liver fibrogenesis in patients with genetic hemochromatosis are poorly understood. We studied signs of Kupffer cell activation and inflammatory responses in liver biopsy specimens obtained from 15 patients with untreated and six patients with treated hemochromatosis. Immunohistochemistry was performed on 11 of the untreated and all treated patients. Three of the untreated patients (20%) had cirrhosis and eight (53%) had fibrosis. None had chronic active hepatitis (CAH). Immunohistochemistry indicated that 55% of the untreated patients had sparse intercellular adhesion molecule-1 (ICAM-1) expression by hepatocytes, and all of these had Kupffer cell iron overload. No ICAM-1 expression was seen by hepatocytes in treated patients or healthy controls. ICAM-1 was strongly expressed by hepatocytes from control patients with inflammatory liver disease. HLA-DR reactivity was seen on sinusoidal cells in all groups, but not on hepatocytes except for two of the control patients with CAH. Twenty-seven percent of the untreated hemochromatosis patients displayed moderate infiltration by CD3-positive lymphocytes. Electron microscopy of samples from untreated hemochromatosis patients showed hypertrophic Kupffer cells containing iron-rich remnants of phagocytosed hepatocytes. Fat-storing cells close to iron-laden hepatocytes contained multiple lipid droplets and adjacent collagen fibril bundles. Thus, in patients with untreated genetic hemochromatosis and Kupffer cell iron overload, hepatocytes occasionally express ICAM-1. In regions with heavy iron overload, Kupffer cell hypertrophy and transition of fat-storing cells are seen. Our findings indicate that release of factors from iron-loaded, activated Kupffer cells is of importance for the transformation of fat-storing cells and increased collagen deposition seen in genetic hemochromatosis.

Adult↗
PubMed1995

Increased PiZ gene frequency for alpha 1 antitrypsin in patients with genetic haemochromatosis.

The putative relationship between genetic haemochromatosis and PiZ alpha 1 antitrypsin deficiency was studied using a monoclonal antibody against the PiZ variant in 67 consecutive patients with genetic haemochromatosis seen at Karolinska Hospital and Huddinge University Hospital, Stockholm over a 10 year period. Three (4.5%) of the patients with haemochromatosis were found to be PiZ homozygotes (odds ratio = 82, confidence interval = 26, 256; p < 0.0001). The prevalence of the heterozygous (PiZ) phenotype was similar to that in the general population (p = 0.937). During the ascertainment period, liver biopsy was performed in 65 (97%) of the patients; 66% (2 of 3) of the PiZ homozygotes were found to have cirrhosis compared with 10% (6/59) of the non-carriers of the PiZ variant (p = 0.039). None of the homozygous or heterozygous alpha 1 antitrypsin deficient patients had developed hepatocellular carcinoma compared with 3.4% (2 of 59) of the non-PiZ gene carriers (p = 1.0). Two of those with the homozygous phenotype had developed severe emphysema. HLA typing was performed in 18 patients, 16 (89%) of whom manifested antigens known to be linked to haemochromatosis. There were no significant differences between the PiZ gene carriers and non-carriers in mean age at onset of disease, sex distribution, or HLA type. Two of the PiZ heterozygotes had plasma alpha 1 antitrypsin concentrations below the normal range, though the group mean was lower than that of the non-PiZ carriers (p = 0.0003). The data suggest that the presence of the PiZ allele for alpha1 antitrypsin deficiency, in a double dose, is associated with genetic haemochromatosis and may contribute to the earlier onset of cirrhosis in these patients, though it does not increase the risk of hepatocellular carcinoma.

Adult↗
PubMed1995

Chronic hepatitis C in alcoholic patients: prevalence, genotypes, and correlation to liver disease.

BACKGROUND: Only one-fifth of chronic alcoholic patients develop chronic liver disease in spite of continuous alcohol abuse. Hepatitis C has been proposed to be one of several suggested factors contributing to the development of liver disease. METHODS: In 201 consecutive chronic alcoholic patients admitted to the hospital for detoxification, antibodies to hepatitis C virus (HCV) were determined, using second-generation enzyme-linked immunosorbent assay (ELISA) and recombinant immunoblot assay (RIBA) tests. Sera from patients with antibodies were tested with polymerase chain reaction (PCR) to detect HCV RNA and subsequently genotyped. RESULTS: Twenty-nine patients (14%) were positive in the ELISA and RIBA tests. HCV RNA was detected in 23 of the 29 (79%); 21 could be genotyped. Previous intravenous drug abuse was present in 18 of 29 (58%) in the positive group versus 3 of 172 (2%) in the negative group (p < 0.001), whereas the prevalence of previous blood transfusions did not differ between the groups. In one-third of the positive cases no obvious route of transmission was found. On the basis of clinical and biochemical variables and, if available, histology, altogether 6 of 29 (21%) HCV-positive patients were classified as having severe liver disease as compared with 12 of 172 (7%) HCV-negative patients (p < 0.05). HCV-positive patients with liver disease were younger than HCV-negative patients with liver disease (p < 0.05). CONCLUSIONS: Hepatitis C virus infection is common among chronic alcoholic patients in Stockholm, especially among patients with a history of intravenous drug abuse. To confirm ongoing infection, detection of HCV RNA is necessary. This infection seems to be a factor contributing to the development of liver disease in alcoholic patients.

Adult↗
PubMed1995

[Upper gastrointestinal bleeding--diagnosis and treatment guidelines].

Upper gastrointestinal bleeding is often an emergency condition requiring immediate treatment. With the introduction of acute endoscopy, the efficacy of diagnosis and treatment in such cases has been greatly improved. General guidelines for the treatment of upper gastrointestinal bleeding are given in the article.

Aged↗
PubMed1994

DNA aneuploidy and histologic dysplasia in long-standing ulcerative colitis. A 10-year follow-up study.

PURPOSE: This study was designed to assess the presence of DNA aneuploidy and mucosal dysplasia, respectively, in 63 patients with long-standing ulcerative colitis. METHODS: The DNA content in colonic biopsies was investigated, using a flow cytometry method, and compared with conventional histology. Patients were subsequently followed each or every second year with colonoscopy and histology. A second flow cytometry examination to monitor the DNA pattern was performed after 10 years. RESULTS: Initially, abnormal DNA pattern (i.e., aneuploidy) was found in 13/63 (21 percent) patients. The colonic mucosa was flat in 10, polypoid in 1, and tumor infiltrated in 2. Eight of the 10 aneuploid cases with a flat mucosa showed no signs of histologic dysplasia. In one of two cases with simultaneous aneuploidy and low-grade dysplasia, a carcinoma Dukes B was found at subsequent colectomy. On the other hand, dysplasia (one low grade and one high grade) without aneuploidy was found in two patients at the initial investigation. After 10 years, 13 had been colectomized, 11 had died (7 noncolitis related), and 3 were lost to follow-up. In the remaining 36 living patients with intact colorectum, no case of histologic dysplasia, but 6 cases of DNA aneuploidy were discovered at the initial investigation. Of the six aneuploid cases, one was later reclassified as diploid and one consisted of an aneuploid adenomatous polyp (removed by polypectomy). At follow-up 10 years later, 3/4 of the other aneuploid cases showed repeated abnormal DNA pattern, now together with histologic low-grade dysplasia (in flat colon mucosa). The 30 patients with initially normal DNA patterns were all still diploid at re-examination 10 years later, but 2 now revealed low-grade dysplasia histologically. CONCLUSIONS: DNA aneuploidy in chronic ulcerative colitis seems to be stable and it may precede histologic dysplasia by many years. It appears to be an additional marker for detecting neoplastic transformation in ulcerative colitis.

Adenocarcinoma↗
PubMed1994

The costs of colonoscopy in patients with ulcerative pan-colitis in Sweden.

The costs of colonoscopy examinations at a hospital in Sweden were calculated in ten consecutive patients with ulcerative pan-colitis. Since colonoscopy in such patients is incomplete if not followed by microscopic study of the state of the colon mucosa, the costs of both the endoscopic and histological examinations were calculated together. The costs of the material used (disposable items, recycled items and durable items) and the wages for personnel involved (endoscopists, pathologists, nurses, laboratory technicians, secretaries and clerks) were calculated for each colonoscopic and histological examination. The mean cost per complete examination was US$223, which is moderate despite the high personnel costs in Sweden. Since the biopsy material obtained in an endoscopic examination is of value not only for conventional histological study but also for DNA analysis, periodic colonoscopy is still to be recommended in patients with long-standing ulcerative pan-colitis until new methods of cancer detection and prevention become available.

Adult↗
PubMed1993

Helicobacter pylori in 205 consecutive endoscopy patients.

The presence of Helicobacter pylori in the gastric, antral mucosa of 205 consecutive, unselected gastroscopy patients was investigated by 1-3 biopsies for urea broth test and culture, 1 biopsy for histological examination and 1 blood sample for serology by ELISA. Overall, 41% were positive for H. pylori by culture, 32% by urea broth test, 24% by histological staining and 67%, 56% and 49% for the 3 cut-off limits applied to serology. Culture and serology indicated the presence of H. pylori in 79-92% of the 14 cases with duodenal ulcer, in 59-82% of the 28 cases with gastric ulcers, in 45-71% of the 51 cases with endoscopic gastritis and in 33-69% of 13 cases with oesophagitis. In patients with histological antritis, H. pylori was identified by culture in 71% (60/84), by serology in 95%, 88% and 81% with the different cut-off limits. The sensitivity of serology ranged from 99-78% depending on the cut-off limits and the specificity from 78-100% against all parameters combined. These results suggest that serology is a useful screening method for the presence of H. pylori. Future antibiotic treatment studies are required to evaluate the clinical relevance of H. pylori in gastrointestinal disease and to investigate the possibility to monitor eradication by serology.

Adolescent↗
PubMed1992

The characteristics of mitotic figures in jejunal mucosa of patients with celiac disease.

The morphologic characteristics of the mitotic figures present in the jejunal mucosa of 23 pediatric patients having gluten enteropathy were recorded. Of the 851 mitoses found, 4.9% were in prophase, 39.9% in prometaphase, 29.5% in metaphase, 22.3% in anaphase, and 3.3% in telophase. Of the 851 mitoses found, 98.8% were considered to be morphologically normal and the remaining 1.2% were considered atypical. The occurrence of atypical mitoses in the jejunal mucosa of pediatric patients was unexpected. However, because jejunal adenocarcinomas in celiac patients are known to be rare, the plausible explanation for the present findings is that the occurrence of atypical mitoses may mirror morphologic variations from the normal mitotic pattern occurring in a rapidly proliferating mucosa, such as that of patients with gluten enteropathy.

Celiac Disease↗
PubMed1990

Interactions between antral peptides and prostaglandin biosynthesis in gastric acid regulation in man.

UNLABELLED: The role of endogenous prostaglandins as modulators of antral hormone release and gastric acid secretion was studied in the intact human stomach. The subjects (n = 9) received indomethacin prior to gastric perfusion at pH greater than 7 or less than 2 and subsequent vagal stimulation. Indomethacin was also tested against parenteral somatostatin (n = 10) and pentagastrin (n = 8). The release of somatostatin into the circulation was biphasic after vagal stimulation, and the plasma levels were inversely proportional to those of plasma gastrin. Acidification of the gastric antrum from pH greater than 7 to less than 2 increased twofold the basal plasma levels of somatostatin (p less than 0.05) and suppressed basal and vagally stimulated gastrin release (p less than 0.05) and gastric acid secretion (p less than 0.05). Indomethacin prior to acidification had little effect in the basal state. Following stimulation the release of somatostatin increased, as indicated by a twofold elevation of somatostatinlike immunoreactivity in the gastric lumen (p less than 0.05), but there was less inhibition of plasma gastrin (p less than 0.05) and gastric acid secretion (p less than 0.05) as compared to acidification alone. During alkaline gastric perfusion, indomethacin increased circulating somatostatin (p less than 0.05) levels without affecting plasma gastrin or gastric acid. Indomethacin given against intravenously infused somatostatin (0.1 microgram.kg-1.h-1) partially reversed the inhibited gastrin response to vagal stimulation without affecting somatostatin-suppressed gastric acid secretion. The effects of indomethacin against pentagastrin were marginal. IN CONCLUSION: Gastric acidification in man stimulates plasma release of somatostatin in parallel to suppressing gastrin release and gastric acid secretion. Endogenous prostanoids participate to regulate antral hormone interactions and may have dual actions on antral somatostatin, as negative modulators of release and as mediators of somatostatin effects on the gastrin cell. It is suggested that an unrestricted release of antral somatostatin is reflected in the gastric lumen rather than in the circulation.

Adult↗
PubMed1986

Decrease in helper (T4+) lymphocytes following cimetidine treatment for duodenal ulcer.

We studied the possible in vivo influence of cimetidine on peripheral blood lymphocyte (PBL) subpopulations defined with monoclonal antibodies (MoAb) in eight haematologically normal patients with uncomplicated duodenal ulcers before cimetidine treatment, 1 week after the start, and finally 1 week following cessation of therapy. After cimetidine had been given for 3-5 weeks there was a significant decrease, compared with pretreatment numbers, in the proportion of T3+ cells (64.6 +/- 8.1 (mean +/- s.d.) v 51.0 +/- 7.8%) and in T4+ cells (47.3 +/- 4.3 v 30.8 +/- 4.7%). The number of T8+ cells was not affected (20.3 +/- 4.3 v 20.1 +/- 6.7%). These changes resulted in a significant reduction in the T4/T8 ratio (2.46 +/- 0.8 v 1.67 +/- 0.6). The total numbers of lymphocytes and monocytes as well as the percentage of B1+ lymphocytes did not change significantly. The observed decrease in T4/T8 ratio after cimetidine treatment is explained by a reduction in the number of T4+ cells and the appearance of a new subpopulation of T3-, T4-, T8-, B1-lymphocytes. The underlying mechanism, however, is not clear. Cimetidine does not seem to have a direct receptor-modulating effect, since in vitro exposure of normal lymphocytes to the drug did not change the proportions of the T cell subsets.

Adult↗
PubMed1985

Oral PGE2 inhibits gastric acid secretion in man.

The effect of oral prostaglandin E2 (PGE2) on gastric acid secretion was examined in healthy subjects. The gastric secretion was stimulated by a modified shamfeeding procedure. Each subject underwent one control test and three tests with intragastrically administered graded doses of PGE2: 0.5, 1.0 and 2.0 mg. Oral PGE2 significantly suppressed the peak and total acid response to vagal stimulation. The total acid output in controls was 27.5 +/- 3.2 mmol/90 min and 20.8 +/- 2.8, 15.8 +/- 2.2 (p less than 0.01) and 15.9 +/- 3.8 (p less than 0.005) mmol/90 min in test series with 0.5, 1.0 and 2.0 mg PGE2 respectively. The two higher doses were equally inhibitory to an average 40%. Gastric outputs of sodium and potassium in response to modified shamfeeding were reduced by PGE2. In controls there was a significant release of plasma-gastrin in response to shamfeeding. Plasma-gastrin was apparently suppressed after the two lower doses of PGE2 but 2.0 mg PGE2 gave an elevation similar to controls. Thus the study demonstrates that oral natural PGE2 suppresses the gastric acid secretion in man. The absence of such an effect in prior studies has been one of the objections against an acid regulatory action of endogenously formed prostaglandins. The present results do not support this argument.

Administration, Oral↗
PubMed1985

Protection of the gastroduodenal mucosa by prostaglandins.

Like other nucleated cell populations in the body, the cells of the gastroduodenal mucosa are capable to metabolise arachidonic acid into prostaglandins, with prostaglandin E2 as the probable major metabolite. The production increases on demand and can be followed in the gastric lumen, where the output of prostaglandin E2 increases two to fourfold after exposure of the mucosa to hydrochloric acid. Exogenous prostaglandins, in particular of the E series, stimulate several identified mucosal defense factors in the upper gastrointestinal tract. Prostaglandins of the E series stimulate the transport of bicarbonate and the production and release of mucus glycoproteins from the gastroduodenal mucosa. They have trophic effects on gastrointestinal epithelia by increasing the survival time of mucosal cells and have cytoprotective properties. In addition, E2 prostaglandins suppress the gastric acid secretion and accelerate peptic ulcer healing. Non steroidal antiinflammatory drugs, which block the biosynthesis of prostaglandins, suppress the bicarbonate secretion, the production of mucus glycoproteins and cytoprotective properties. They interfere with the inhibitory feedback regulation of the gastric acid secretion and are ulcerogenic in experimental and clinical situations. These actions of PG biosynthesis blockers provide indirect information on the importance of local prostaglandin formation for maintenance of gastrointestinal mucosal integrity. It is hypothesised that biosynthesis of prostaglandins in the gastroduodenal mucosa is of importance and may be a key event in triggering the different components of the mucosal defense.

Animals↗