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Biomedical subjects

E Aadland

Publications and source records attributed to E Aadland.

At least 19 recordsLinked to original sources
PubMed1992

[Indications for surgery in ulcerative colitis. Some aspects of a hospital case load].

From 1.1.1985 to 1.1.1992, 233 patients with ulcerative colitis were treated in the Medical Department, Aker Hospital. 30 patients (12.9%) were referred for surgery. The main indications for surgery were severe colitis and chronic persisting symptoms. The increased risk of developing colorectal carcinoma in cases of long-standing extensive ulcerative colitis is generally accepted. Many of our unoperated patients belong to this risk group. In the present sample the resection rate was lower than recently reported from Sweden and Denmark. Symptomatic patients in the risk group for developing colorectal carcinoma should be offered surgery more liberally, and asymptomatic patients in this group should be offered colonoscopic surveillance.

Adolescent↗
PubMed1992

Free protein S deficiency in patients with chronic inflammatory bowel disease.

Free protein S, protein C, and C4b-binding protein (C4b-BP) were measured in randomly selected outpatients: 22 with Crohn's disease (CD) and 16 with ulcerative colitis (UC). Active disease was recorded in 10 patients with CD and 4 with UC. Fourteen patients (63.6%) with CD and 4 (25%) with UC had free protein S values below the normal range, with mean values of 62% and 78% of that found in healthy control subjects (p < 0.01). The C4b-BP level was 127% in patients with CD as compared with 89% in both healthy subjects and UC patients (p < 0.01). The protein C levels were similar in the three groups. The present results add to the factors already known favouring thromboembolic complications in inflammatory bowel disease and which might play a major role both for the pathogenesis and for the increased tendency to venous thromboembolism in these diseases.

Adult↗
PubMed1992

Assessment of the neutrophil dominating protein calprotectin in feces. A methodologic study.

This study describes methods for extraction and quantification of calprotectin (L1 protein) in feces by enzyme immunoassay. This protein is a prominent antimicrobial component of neutrophils, monocytes, macrophages, and squamous epithelia. Calprotectin was stable in feces during storage for 7 days at room temperature. Small fecal samples taken from a 24-h feces collection gave a reliable estimate of calprotectin. Within-assay precision was 1.9%, and between-assay precision 14.8%. In healthy subjects (n = 33) median fecal calprotectin was 2025 micrograms/l and in hospital controls (n = 40) 10,500 micrograms/l. Median values in patients with Crohn's disease (n = 21) was 43,000 micrograms/l and in ulcerative colitis (n = 17) 40,000 micrograms/l. Fecal calprotectin was significantly correlated to fecal alpha 1-antitrypsin in the patients with Crohn's disease. Ten of 11 patients with gastrointestinal carcinomas had calprotectin level above the suggested reference limit of 6740 micrograms/l.

Adolescent↗
PubMed1990

[Severe ulcerative colitis].

In a hospital material concerning 162 patients with ulcerative colitis, 20 patients (12.3%) had attacks of severe colitis. Nine of the patients with severe colitis went into remission on medical therapy and 11 were operated on by colectomy. It is concluded that no real progress has taken place in the treatment of severe attacks of ulcerative colitis in the last 15-20 years. We discuss possible prognostic factors. Active medical treatment and surveillance and early colectomy in this serious disease is still recommended.

Adult↗
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↗
PubMed1990

The determination of copper in human liver biopsy specimens by cup-in-tube ETAAS.

A method for the direct determination of copper in human liver biopsy specimens is described. The addition of a mixed Mg-Pd nitrate modifier is shown effectively to delay the volatilization of copper both from aqueous standards and the powered NISTBovine Liver to an appearance time comparable with the solid biopsy specimens. Calibration against solid liver reference materials is preferable compared with aqueous copper standard solutions. A number of copper absorption lines provide a wide range of sensitivities; the less sensitive Cu-line 222.6 nm was found optimal in the determination of copper concentrations in the range of 20-200 mg/kg in liver biopsy specimens. The copper concentrations measured in liver biopsy specimens from patients suffering from sclerosing cholangitis were considerably higher than those reported for a group of healthy persons.

Animals↗
PubMed1987

Protection by misoprostol against naproxen-induced gastric mucosal damage.

The protective effect of misoprostol against naproxen-induced gastric mucosal damage was the subject of a double-blind, randomized, parallel-group study. Thirty-two healthy subjects were treated with naproxen 500 mg twice daily and either misoprostol 200 micrograms or matching placebo twice daily for seven days. Gastroscopy was performed before and after the treatment period and the mucosa was assessed for erosive and petechial lesions according to a predetermined scoring scheme. Of 25 evaluable subjects, 12 were treated with misoprostol and 13 were treated with placebo. The mean overall endoscopic score was 1.24 +/- 0.09 with placebo and 0.26 +/- 0.07 with misoprostol. The difference, 0.98, was highly significant (p less than 0.001), with 95 percent confidence limits of 0.74 to 1.22. All subjects in the placebo group had higher mean scores than any in the misoprostol group. The scores for erosive and bleeding lesions in the antrum and corpus/fundus of the stomach were all reduced by administration of misoprostol. In conclusion, the results clearly demonstrate that misoprostol protects the gastric mucosa of humans against naproxen-induced damage.

Adolescent↗
PubMed1987

An autoantibody profile in primary sclerosing cholangitis.

A high frequency of a variety of autoantibodies has been found in sera from patients with primary sclerosing cholangitis (PSC). The prevalence of all types of autoantibodies in PSC was significantly higher than that in healthy controls and patients with isolated inflammatory bowel disease. The titres of the antibodies were rather elevated, particularly in females, and most of them were IgM. The most frequent type of antinuclear antibody was the 'homogenous' type, which is a marker of many autoimmune diseases. The overall prevalence of the antibody was 35%, whereas in female patients it reached 67%. No correlation was found between autoantibody positivity and any clinical parameter. The present findings support the hypothesis that immunological factors may be relevant in PSC.

Antibodies, Antinuclear↗
PubMed1987

The effect of omeprazole on gastric acidity and the absorption of liver cobalamins.

The effect of gastric anacidity on the absorption of food-bound cobalamins is uncertain. Omeprazole, an inhibitor of the enzyme H-K-ATPase in the parietal cell, is the most potent inhibitor of gastric acidity known so far. In 17 healthy male volunteers the absorption of liver-bound cobalamins was assessed after a single intravenous dose of omeprazole (80 mg) or placebo in a double-blind, crossover manner. The effect of omeprazole on pH, gastric acidity, and intrinsic factor (IF) concentration was measured in aspirates of gastric juice 5 min before and 30 and 60 min after the administration of liver homogenate containing 0.74 nmol of 57Co-labelled cobalamins. Omeprazole treatment resulted in anacidity (pH values above 6.0) in 14 individuals 30 min after the liver dose and in 15 individuals after 60 min. The IF concentration was unchanged in the omeprazole experiment as compared with the placebo experiment. The absorption of liver-bound cobalamins was 310 pmol (189-501 pmol) in the omeprazole experiment as compared with 415 pmol (150-549 pmol) in the placebo experiment (median values and range, p = 0.5228). We suggest that anacidity induced by omeprazole does not reduce the absorption of liver-bound cobalamins.

Absorption↗
PubMed1987

Primary sclerosing cholangitis: a long-term follow-up study.

During the 10-year period from 1 January 1975 to 31 December 1984, primary sclerosing cholangitis (PSC) was diagnosed in 45 patients. Twelve of the patients have died (26.7%), 10 of them of causes related to PSC. Inflammatory bowel disease was found in all patients; ulcerative colitis was found in 37, Crohn's disease in 6, and unclassified colitis in 2 patients. Of the patients alive, 27 were submitted to a follow-up study in 1985. At the follow-up examination no general progression of the liver disease, as measured on the basis of clinical examination and levels of transaminases, alkaline phosphatases, and bilirubin, was found. Cholangiographic evaluation in 24 patients showed that the stage of ductal changes progressed from mild to moderate in 3 patients; in the other patients the stage was not altered. Morphologic examination of liver biopsy specimens in patients with a benign clinical course usually showed portal inflammation, fibrosis, and minor signs of piecemeal necrosis, whereas widespread piecemeal necrosis was found in patients who deteriorated and died. The 50% survival since diagnosis of liver disease was calculated to be 17 years in patients with PSC and 50 years in a comparable group among the general population. The estimated survival curve in PSC was displaced to the left, indicating a reduced life expectancy of about 30 years.

Adolescent↗
PubMed1986

Augmented postprandial gastric acid secretion due to exposure to ranitidine in healthy subjects.

In 10 healthy volunteers gastric acid output in response to a meal was significantly increased 60-64 h after cessation of 4 weeks of ranitidine treatment as compared with the response before treatment. Four to 6 weeks after discontinuation of treatment the acid secretory response to the meal had returned to values not significantly different from those seen before treatment. There was no change in pepsin output owing to ranitidine treatment.

Adult↗
PubMed1985

Effect of omeprazole on the secretion of intrinsic factor, gastric acid and pepsin in man.

The effect of an intravenous infusion of omeprazole (0.35 mg/kg) and placebo on basal and stimulated (pentagastrin 1.0 microgram/kg/h) secretion of gastric acid, intrinsic factor and pepsin was studied in 10 healthy male subjects. Omeprazole caused a marked inhibition of basal and stimulated acid output. The inhibition of pepsin output was less marked, but also significant. The output of intrinsic factor, however, showed no significant change. The results indicate that acid and intrinsic factor might have different secretory mechanisms within the parietal cell.

Adult↗
PubMed1985

Gastroscopic findings after treatment with enteric-coated and plain naproxen tablets in healthy subjects.

The damaging effect of enteric-coated and plain naproxen tablets on the gastric mucosa was studied in 12 healthy subjects before and after 7 days' treatment in a randomized, double-blind, double-dummy, cross-over trial. Both formulations of the drug caused mucosal lesions, but the extent of the damage was significantly decreased after enteric-coated naproxen as compared with plain tablets. The subjects' preference was significantly in favour of the enteric-coated naproxen tablets. The plasma naproxen concentration was significantly higher after treatment with enteric-coated naproxen than after treatment with plain tablets. In conclusion, the results of the study indicate that naproxen might damage the gastric mucosa by local and systemic effects and that the local effect might be prevented by enteric coating of the tablets.

Adult↗