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O Fausa

Publications and source records attributed to O Fausa.

At least 19 recordsLinked to original sources
PubMed1995

[Immunological research and diagnosis in gastroenterology--a review on occasion of two jubilees].

Norwegian immunological research in gastroenterology is well recognized internationally, and the European Medical Research Council Clinical Network for Gastroenterological Immunology is organized from Oslo. This development can be explained mainly by successful cooperation between clinical gastroenterology and laboratory-based research. A current jubilee in each of these fields may justify this review. It is now well documented that the gut is the largest antibody-producing organ. A unique molecular integration exists between the local B cells and the secretory epithelium to facilitate external transport of dimeric IgA and pentameric IgM. The mucosal immune system is subjected to T-cell regulation and significant local alterations are observed in T- and B-cell populations, and in the macrophage subsets associated with several diseases of the gut. Subsequent functional immune deviation may largely explain mucosal pathology and indicates potential targets for future immunotherapeutic measures. Observations made in the gut mucosa of HIV/AIDS patients have contributed to greater understanding of the complex cellular and molecular interactions involved in mucosal immunity.

Fluorescent Antibody Technique↗
PubMed1995

Duodenal adenomatosis in familial adenomatous polyposis. DAF Project Group.

In order to evaluate the prevalence of duodenal adenomas in familial adenomatous polyposis (FAP) and the risk of carcinoma development, a multicenter study was initiated in Denmark, Finland, Holland, Norway and Sweden, which have national polyposis registers with an almost complete registration. Patients aged 20 years or more are being examined with biennial gastroduodenoscopy during 1990-2000. Multiple duodenal biopsies are examined by one pathologist from each country, and the endoscopic and histological criteria of Spigelman have been adopted. At the end of August 1992, 312 patients with a median age of 37 years (range 20-86) had completed their first endoscopy. The duodenum was examined in 310 patients, of whom 199 (64%) had duodenal adenomas. Twenty-two patients (11% of all patients with duodenal adenomas) had no endoscopically visible polyps. One patient had an asymptomatic adenocarcinoma. The Spigelman stage worsened significantly (P < 0.05) with time from the diagnosis of FAP, which may suggest an increasing risk of carcinoma by time.

Adenomatous Polyposis Coli↗
PubMed1995

Intestinal B-cell isotype response in relation to local bacterial load: evidence for immunoglobulin A subclass adaptation.

BACKGROUND & AIMS: In experimental animals, the indigenous microbiota modulates mucosal immunity. In humans, such direct evidence is scarce. The aim of this study was to examine the effect of intestinal bacteria on the local immunoglobulin (Ig) response. METHODS: The numbers of IgA-, IgM-, and IgG-producing immunocytes per defined mucosal length unit were determined, and the local IgA subclass response was studied using immunohistochemistry in jejunal segments from adults with bacterial overgrowth and in sterile ileal urinary conduits from children. RESULTS: The ileal bladder mucosa showed atrophy, but the number of immunocytes only tended to be decreased. The jejunal segments with bacterial overgrowth showed minor histological changes; the numbers of IgA and IgG immunocytes were fairly normal, whereas the number of IgM immunocytes was significantly reduced (P < 0.05) (12 cells/U) compared with control mucosa (24 cells/U). The number of IgA2 immunocytes was significantly decreased (P < 0.01) in ileal conduits (7 cells/U or 30% of total IgA) but increased (P < 0.05) in jejunal segments with bacterial overgrowth (42 cells/U or 43% of total IgA) compared with normal ileum (15 cells/U or 40% of total IgA) and jejunum (24 cells/U or 23% of total IgA). CONCLUSIONS: An association exists between bacterial load and IgA subclass production. An increase in IgA2 may enhance mucosal protection and probably reflects immunomodulation caused by lipopolysaccharides.

Adolescent↗
PubMed1995

Olsalazine versus sulphasalazine for relapse prevention in ulcerative colitis: a multicenter study.

OBJECTIVE: To compare the relapse-preventing effect and the frequency of adverse events of olsalazine and sulphasalazine in sulphasalazine-tolerant patients with ulcerative colitis. METHODS: Patients in remission, with at least two episodes of active disease during the last 5 yr, were randomized to 2 g of sulphasalazine or 1 g of olsalazine daily and were followed for 6-18 months. Relapse rates in the two groups were compared using frequency and life-table analysis. Sixty-nine patients with proctitis, 140 with left-sided colitis, and 113 with subtotal or total colitis were evaluated. RESULTS: In the intention-to-treat analysis, the failure rate (relapses plus withdrawals) was 54.7% in the olsalazine and 47.2% in the sulphasalazine group. In the per-protocol analysis excluding withdrawals, 44.7% relapsed in the olsalazine and 39.3% in the sulphasalazine group. Remission curves did not differ significantly, although at all time intervals the frequency of remission was slightly higher in the sulphasalazine group (p = 0.19 in the intention-to-treat analysis and p = 0.42 in the per-protocol analysis estimated by the log-rank test). Twelve patients (of whom five had diarrhea) in the olsalazine group versus eight patients in the sulphasalazine group discontinued the study because of side effects. CONCLUSION: The relapse-preventing effect of olsalazine and sulphasalazine in sulphasalazine-tolerant patients did not differ. Furthermore, the tolerability of olsalazine, particularly concerning diarrhea, appears to be better than previously reported.

Adult↗
PubMed1994

T cells from the small intestinal mucosa of a DR4, DQ7/DR4, DQ8 celiac disease patient preferentially recognize gliadin when presented by DQ8.

CD is an immunologic disease of the small intestine which is precipitated by ingestion of wheat gliadin. Most patients carry the HLA-DQ (alpha 1*0501, beta 1*0201) (DQ2) heterodimer. We recently reported that a preponderance of gliadin-specific T cells from the small intestinal mucosa of DQ2-positive CD patients were restricted by this DQ heterodimer. However, a small percentage of CD patients do not carry this DQ heterodimer, and most of them instead carry DQ (alpha 1*0301, beta 1*0302) (DQ8). Here we report that a majority of gliadin-specific T cells from the small intestinal mucosa of a DR4,DQ7/DR4,DQ8 heterozygous CD patient are restricted by DQ8. Thus, preferential presentation of gliadin-derived peptides to T cells by the CD-associated DQ2 and DQ8 molecules may be an initial and important immunopathogenic step in CD.

Antibodies, Monoclonal↗
PubMed1994

Risk factors in primary sclerosing cholangitis.

The increasing use of liver transplantation and new treatment regimens requires an accurate estimate of the prognosis in primary sclerosing cholangitis. To clarify the natural history and prognosis of this disease, we studied the clinical features at the time of presentation and the outcome in 77 consecutive patients admitted to our hospital. The median age at diagnosis of primary sclerosing cholangitis was 32.5 years; 66% of the patients were male; 76 had concomitant inflammatory bowel disease and two had celiac disease. Thirty-four patients were classified as asymptomatic at diagnosis of primary sclerosing cholangitis. The mean follow-up time was 6.2 years; 25 patients have died or been transplanted. Cholangiocarcinoma has been diagnosed in 11 patients (14%). Female patients have a significantly poorer survival rate than male patients. The bilirubin level was found to be an independent risk factor for both mortality/transplantation, and for the occurrence of cholangiocarcinoma. Age at diagnosis of primary sclerosing cholangitis was an additional risk factor of death/transplantation. As bilirubin is an important prognostic factor for the development of both cholangiocarcinoma and death/transplantation, the construction of prognostic indices seems to be of limited value in the timing of transplantation of the individual patient.

Adolescent↗
PubMed1994

Heterogeneity of M-cell-associated B and T cells in human Peyer's patches.

The specialized M cells in the follicle-associated epithelium (FAE) of Peyer's patches (PP) represent an intimate interphase between luminal antigens and gut-associated lymphoid tissue (GALT). M cells form pockets that contain clusters of leucocytes probably involved in the first encounter with antigens from the gut lumen. Three-colour immunofluorescence in situ phenotyping of these leucocytes in humans revealed about equal numbers of B (CD19/20+) and T(CD3+) lymphocytes, the latter mainly CD4+ (median 73%, range 40-90%), but relatively few macrophages (CD68+). Most B cells (90%) were positive for surface IgM (sIgM) and often co-expressed sIgD (median 34%, range 6-60%). Occasional B cells (median 2%) did not express CD45RA (range 0-15%) and 13% virtually lacked HLA-DR (range 0-40%). Some B and T lymphocytes expressed the nuclear proliferation marker Ki-67 (range 1-10%). The M-cell pockets also contained occasional cells with cytoplasmic IgA or IgM. These sites thus contained a heterogeneous B-cell population with features of both follicular mantle (sIgD+ sIgM+) and marginal zone (sIgD- sIgM+) B lymphocytes. Adjacent T lymphocytes were generally of the memory phenotype (CD45RO+). Our findings suggest that the M-cell-associated B lymphocytes represent local extensions of B-cell follicles towards the gut lumen, developed topically to facilitate antigen presentation and diversification of mucosal immune responses.

Adolescent↗
PubMed1992

Association of subepithelial deposition of activated complement and immunoglobulin G and M response to gluten in celiac disease.

Patients with celiac disease produce not only immunoglobulin A (IgA) but also immunoglobulin G (IgG) and M (IgM) antibodies to gluten. Intake of dietary gluten may hence induce local complement activation and mucosal damage. Jejunal tissue sections from adult patients with celiac disease were examined by immunofluorescence with monoclonal antibodies to activation neoepitopes in C3b and the terminal complement complex (TCC). Subepithelial deposition of TCC was observed in 93% of 28 untreated and in 57% of 23 partly treated study subjects. The immunofluorescence staining intensity was well correlated with the serum level of gluten-specific IgG and IgM (but not IgA), the number of mucosal IgG-producing cells, and the degree of villous atrophy. Similar immune deposits were not observed in 5 successfully treated patients with celiac disease, 5 patients with dermatitis herpetiformis without jejunal villous atrophy, and 90% of 21 control patients with histologically normal jejunal mucosa. Gluten challenge increased the amount of subepithelial TCC and produced additional C3b deposition, suggesting recent complement activation. Ingested gluten might thus, via Ig-mediated subepithelial complement activation, damage the surface epithelium in celiac disease and induce compensatory crypt hyperplasia.

Adolescent↗
PubMed1992

Subclass composition and J-chain expression of the 'compensatory' gastrointestinal IgG cell population in selective IgA deficiency.

The subclass distribution of IgG-producing immunocytes was examined by two-colour immunohistochemistry in gastrointestinal mucosa of 14 patients with selective serum IgA deficiency providing the following biopsy material: gastric (n = 1); jejunal (n = 12); colonic (n = 1); and rectal (n = 2). All except two patients suffered from various infections, and coeliac disease was observed in six of them. Control reference data were based on biopsies from immunologically intact subjects, including histologically normal jejunal (n = 10) and large bowel (n = 10) mucosa and stomach mucosa with slight chronic gastritis (n = 8). The total mucosal population of immunoglobulin-producing cells per 500 microns gut length unit was only slightly decreased in IgA deficiency because of an increased number of IgG (30%) and especially IgM (71%) immunocytes. The IgG1 immunocyte proportion in the proximal gut (median 87%) was higher than that in the comparable controls (gastric 69%, jejunal 66%). A similar trend was seen in the distal gut (69%) compared with controls from the large bowel mucosa (55%). Conversely, IgG2 and IgG3 cell proportions were significantly decreased compared with the respective controls from the proximal gut. The same was true for IgG4, which also was significantly reduced in jejunal mucosa. Paired staining for cytoplasmic J chain and immunoglobulin isotype showed 71% positivity for jejunal IgG-producing cells in IgA deficiency, which was somewhat reduced compared with comparable controls (89%). J chain appeared to be preferentially expressed by IgG1 cells (75%), but was also found in IgG2 (70%), IgG3 (32%) and IgG4 cells (33%). IgM-producing cells showed a J-chain positivity (99%) in IgA deficiency similar to normal (100%). Our results suggested that the block in mucosal B cell differentiation to IgA expression in the proximal gut is mainly located immediately upstream to the CH alpha 1 gene, giving excessive terminal maturation of J-chain-positive IgG1 immunocytes.

Adolescent↗
PubMed1992

Surface epithelium related activation of complement differs in Crohn's disease and ulcerative colitis.

IgG1 and activated complement are colocalised on the colonic epithelial brush border in active ulcerative colitis. To investigate whether such deposition is specific for ulcerative colitis, we examined ethanol fixed mucosal specimens from 18 patients with Crohn's colitis and 14 with terminal ileitis by indirect two colour immunofluorescence staining. Monoclonal antibodies to the IgG subclasses and to neoepitopes of activated complement C3b and the terminal complement complex were used in combination with rabbit antiserum to C1q, C4c or cytokeratin. Granular deposition of C3b and terminal complement complex were observed at the luminal face of the surface epithelium in 10 of 18 patients with Crohn's colitis. Specimens from eight of 14 patients with ileal involvement were intensely stained for activated complement (primarily C3b) within the surface mucus layer. No epithelial IgG, C1q or C4c deposition was observed. The results suggest that early and late phase complement activation takes place at the luminal face of the epithelium in Crohn's disease. The absence of colocalised IgG and complement components involved in the classical activation pathway (C1q and C4c), however, suggest that other immunopathological mechanisms (the alternative pathway?) are primarily involved in Crohn's disease in contrast with ulcerative colitis.

Adolescent↗
PubMed1991

[Cytomegalovirus disease in the upper gastrointestinal tract. Endoscopic findings].

Cytomegalovirus disease is seen mainly in immunocompromised patients. While gastrointestinal symptoms are difficult to interpret, the typical finding at endoscopy of the upper alimentary tract is ulcers. Diagnosis of cytomegalovirus disease is based on typical histological findings in biopsy specimens. Antiviral treatment should be started when cytomegalovirus disease is detected in transplant patients. If it is decided to treat patients suffering from AIDS, lifelong maintenance treatment is required. Early diagnosis by means of endoscopy and biopsies is very important, and will decide the outcome of instituted treatment.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Relationship of inflammatory bowel disease and primary sclerosing cholangitis.

There is a strong association between PSC and IBD. PSC is the most common hepatobiliary lesion seen in association with IBD. Whether there are two subsets of PSC, one associated with IBD and one unassociated, is controversial. A lower male to female ratio in patients without IBD supports this view. The demonstration of the haplotype DRw52a in 100% of patients with PSC, irrespective of the absence of IBD, speaks against this view. Patients with isolated PSC tend to present with jaundice, pruritus, and fatigue more frequently than those with combined PSC and IBD. There may also be a difference in bile duct involvement between patients with and without IBD combined with PSC. Apart from usually being a total colitis, either Crohn's colitis or UC, the IBD associated with PSC cannot be distinguished from IBD without PSC with respect to symptoms and clinical course. Patients with combined IBD and PSC may have somewhat worse prognosis than those with isolated PSC. The majority of patients developing BDC have concomitant IBD, suggesting that patients without IBD represent a different subgroup of PSC and run a different clinical course. Most studies have, however, found no differences in epidemiology, pathogenetic factors, clinical findings related to the hepatobiliary disease and prognosis between those who present with PSC alone and those who present with combined PSC and IBD. A major problem when discussing the relationship between IBD and PSC is that the bowel is inadequately examined in many of the studies relating to this question.(ABSTRACT TRUNCATED AT 250 WORDS)

Cholangitis, Sclerosing↗
PubMed1991

Sampling efficiency in the diagnosis of Helicobacter pylori infection and chronic active gastritis.

The methods and sampling procedures used in the diagnosis of Helicobacter pylori infection and chronic active gastritis were evaluated. Five biopsy specimens for bacteriological cultivation and three specimens for histological examination were obtained endoscopically from a defined area of the gastric antral mucosae of 83 patients. An increase in the number of biopsy specimens for cultivation from one to five revealed only one more H. pylori-infected patient. H. pylori was isolated from 31 of 83 patients. Three technically adequate samples for histological examination were obtained from each of 74 patients. Of these 74 patients, chronic active gastritis was diagnosed by demonstration of typical histological changes in all three specimens from each of 20 patients, in two of three specimens from each of 3 patients, and in one of three specimens from 1 patient. The results indicate that one biopsy specimen is sufficient for the isolation of H. pylori, whereas several specimens may be necessary for the histological diagnosis. Chronic active gastritis was found in four patients not infected with H. pylori; on the other hand, H. pylori was isolated from nine patients who showed no signs of chronic active gastritis in any of three samples.

Adolescent↗
PubMed1991

Prevention of relapse of reflux esophagitis after endoscopic healing: the efficacy and safety of omeprazole compared with ranitidine.

Ninety-eight patients with erosive and/or ulcerative esophagitis unhealed after at least 3 months' treatment with standard doses of cimetidine (greater than or equal to 1200 mg daily) or ranitidine (greater than or equal to 300 mg daily) were primarily included in an acute healing phase study, and 51 were allocated to 40 mg omeprazole once daily and 47 to 300 mg ranitidine twice daily. After 12 weeks of treatment, 46 (90%) patients given omeprazole were healed, compared with 22 (47%) allocated to ranitidine. Healed patients were then given maintenance treatment with either 20 mg omeprazole once daily or 150 mg ranitidine twice daily for 12 months. Plasma gastrin was determined and gastric mucosal biopsy specimens were obtained during the entire study to assess the structure of the exocrine and endocrine cell populations of the oxyntic mucosa. Sixty-seven per cent of the total number of patients randomized to omeprazole were maintained in clinical and endoscopic remission throughout the 12-month study period as compared with only 10% among those given ranitidine (p less than 0.0001). After 4 weeks of omeprazole treatment basal gastrin levels were slightly increased, with a 95% confidence interval for the change of from 8.6 to 16.9 pmol/l. No further increase in basal gastrin levels was observed during the ensuing study months. No significant histopathologic lesion was found in the oxyntic gland mucosa. In conclusion, omeprazole was far superior to ranitidine in preventing recurrence, a goal achieved without adverse events and significant abnormalities in the oxyntic mucosal exocrine or endocrine cells but with a moderate increase in basal gastrin levels.

Adult↗
PubMed1990

[Portal vein thrombosis. Etiology, complications and therapy].

In a retrospective study of 25 patients with portal vein thrombosis the etiology has been disclosed in 44%. The most common causes were infection, cirrhosis and a myeloproliferative syndrome. The most common mode of presentation was gastrointestinal bleeding (44%). 12 patients (48%) died, the majority after life-threatening variceal bleeding. Today we restrict ourselves to treating the complications of portal hypertension. The aim for the future must be to diagnose and dissolve the thrombi shortly after formation.

Adolescent↗
PubMed1990

[Dilatation of esophageal stenoses].

During the period 1979-88, 129 patients (49 women and 89 men) were dilated for oesophageal strictures. The total number of dilatations was 811. The main causes were gastro-oesophageal reflux (54 patients), achalasia (17 patients) and malignant stenosis (27 patients). Almost all strictures were successfully dilated, but with short duration of effect in the malignant group. During the ten-year period, the method of dilatation has changed from almost exclusively Eder-Puestow dilators to balloon dilators. Four perforations of the oesophagus were experienced with the use of Eder-Puestow dilators (448 dilatations), whereas no perforations were experienced with the use of balloon dilatation (363 dilatations). The article presents a follow-up study of 37 available patients from the 54 with gastro-oesophageal reflux. It is concluded that endoscopic dilatation is a safe and efficient treatment for oesophageal strictures.

Adolescent↗
PubMed1990

[Primary sclerosing cholangitis and inflammatory bowel disease].

Primary sclerosing cholangitis (PSC) is a syndrome of unknown etiology, characterized by fibrosis and inflammation of the intra- and extrahepatic bile ducts. PSC is usually seen in association with inflammatory bowel disease, particularly in younger patients with extensive ulcerative colitis. Crohn's disease is seen in more than 10% of all patients with PSC. The bowel disease may produce no symptoms in some patients, and the clinical course is usually silent. The development and widespread use of endoscopic retrograde cholangiopancreaticography (ERCP) have enabled us to diagnose the disease far more often than was possible only a decade ago, and also to recognize that PSC has a much wider clinical and pathologic spectrum than previously realized. Most patients with concomitant ulcerative colitis and persistently abnormal liver function tests are likely to have PSC. Patients with PSC usually have a cholestatic biochemical profile, whereas the histologic features of the liver biopsy are variable and often nonspecific. Cholangiography displaying strictures and beading is diagnostic of the disease. The prognosis is variable, with a benign clinical course in many patients. However, an increased rate of cholangiocarcinoma is found in PSC, as is an increased rate of colonic cancer in patients with PSC and ulcerative colitis.

Adolescent↗