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Biomedical subjects

O Fausa

Publications and source records attributed to O Fausa.

At least 109 records · Page 6Linked to original sources

The effect of gastric bypass operation on glucose tolerance in obesity.

A series of variables involved in glucose handling were monitored before and after gastric bypass operation for morbid obesity. Blood glucose, insulin, C-peptide, gastric inhibitory polypeptide (GIP), pancreatic polypeptide (PP), and gastrin were measured basally and after an oral glucose load. Blood glucose, insulin, C-peptide, and PP were also measured after an intravenous glucose load. Adrenocortical function was evaluated by measuring plasma cortisol and urinary excretion of 17-hydroxy-corticosteroids and 17-ketosteroids. Nine subjects were examined before and 3 and 12 months after operation. Glucose tolerance improved postoperatively concomitant with decreased basal levels of C-peptide and insulin, increased hepatic insulin extraction, and evidence of reduced adrenocortical function. Parallel with reduced insulin resistance, support for an increase in both insulin secretion and removal was obtained postoperatively. It is concluded that the considerable endocrine abnormalities seen in morbid obesity can be normalized after gastric bypass operation and weight reduction.

Adult↗

The pancreatic ducts in primary biliary cirrhosis and sclerosing cholangitis.

Endoscopic retrograde pancreatograms were examined in a consecutive series of patients with cholestatic disease caused either by primary biliary cirrhosis (PBC) (35 patients) or by sclerosing cholangitis (SC) (38 patients). The pancreatic ducts were abnormal in three of the patients with PBC but in none with SC. Gallstone disease occurred concomitantly in the two patients with most advanced pancreatic involvement. The liver disease was classified as advanced PBC in 11 of the 35 patients. Symptoms of hepatobiliary disease were scarce in most SC patients. Eight of the 38 patients had histologically verified biliary cirrhosis. SC was associated with extensive, but most often inactive or mild, colitis in 97% (ulcerative colitis in 34 and Crohn's disease in 3 patients). Three of these patients had concomitant cholangiocarcinoma.

Adolescent↗

Injection sclerotherapy of bleeding oesophageal and gastric varices in children.

During a 4-year period (1980-1984) nine children aged 11/2 to 13 years with acute or recent bleeding from gastro-oesophageal varices were treated by injection sclerotherapy. Chronic liver disease was the cause of portal hypertension in three and extrahepatic portal venous obstruction in six. Seven had experienced recurrent bleeding episodes, and massive haemorrhage initiated treatment in two children. Seven patients rebled before eradication of all critical varices and two after, both from ulcers at the site of injection. All critical varices were eradicated in the nine children within a median of 11/2 months, after a median of five courses of injections. No further variceal bleeding occurred during the follow-up period of up to 57 months (mean, 20.9 months). Complications included oesophageal and gastric ulcers in four patients. One patient with congenital hepatic fibrosis and aortic insufficiency died of septicaemia 19 months after entering the treatment.

Adolescent↗

Short-chain fatty acids in the proximal gastrointestinal tract of healthy subjects.

The total concentration of short-chain fatty acids (SCFAs) in healthy subjects, measured by gas chromatography, was in saliva and jejunal aspirates (n = 6) (median (range] 4480 (2780-9940) mumol/l and 265 (185-1470) mumol/l and in gastric and duodenal aspirates (n = 7) 719 (425-1770) mumol/l and 480 (137-778) mumol/l, respectively. Acetic and propionic acid accounted for 85% and 11%, respectively, and i-butyric, n-butyric, and i-valeric for less than 2% each in jejunal aspirates. A very similar relative distribution was present also in saliva and gastric and duodenal aspirates, essentially different from that of feces. Through anaerobic culturing from jejunum, 10(3) to 10(8) bacteria/ml was obtained; there was no correlation between the log number of bacteria and the SCFAs concentration before and after ingestion of sucrose. Swallowed exogenous radiolabeled propionate was partly recovered in the jejunum. The findings indicate that the SCFAs recovered from the jejunum in healthy subjects are mainly produced in the mouth and swallowed with the saliva.

Adult↗

Nonoperative treatment of subcervical oesophageal perforations after forced dilatation for nonmalignant disease.

Eight patients with perforation of the oesophagus following forced dilatation because of nonmalignant disease were treated conservatively with antibiotics and parenteral nutrition. None had primary leakage to the pleural cavities. Nasogastric suction was employed in three patients, and one had a feeding gastrostomy prior to perforation. Recovery was uneventful in six cases. A single thoracocentesis was required in one case. In the eighth patient there was leakage to the right pleural cavity with massive pleural effusion after two weeks of treatment and thoracotomy was necessary. All the patients survived. The authors conclude that subcervical oesophageal perforation following forced dilatation because of nonmalignant disease should be managed conservatively when there is no leakage to the pleural or peritoneal cavities.

Aged↗

Short-chain fatty acids in the normal human feces.

The short-chain fatty acids ( SCFAs ) have been studied in the feces of 20 healthy subjects--10 methane excretors and 10 non-methane excretors. The analytical procedure included homogenization of fecal samples followed by vacuum distillation and subsequent gas chromatography. This method for analysis of fecal SCFAs showed recoveries of the individual acids from 90% to 109% and coefficients of variation for the inter-assay reproducibility from 6.0% to 19.7%, highest for those acids present in the smallest concentrations. There was no difference in the concentrations or relative compositions of SCFAs between methane-excreting subjects and non-methane-excreting subjects. The concentrations of SCFAs , given as mmol/kg feces (wet weight), were (median and range): total, 76.8 (27.9-187.7); acetic acid, 37.4 (12.8-103.4); propionic acid, 12.5 (4.5-27.8); i-butyric acid, 2.2 (0.7-3.8); n-butyric acid, 12.4 (4.0-53.0); i-valeric acid, 3.2 (0.8-5.9); n-valeric acid, 2.4 (0.6-3.8) and n-caproic acid, 0.5 (0.0-3.6). The study shows that the SCFAs are quantitatively the most important anions in the feces of healthy subjects. The pronounced individual variations in the concentrations of SCFAs are real biological variations and cannot be explained by methodological variations.

Adult↗

Immune response patterns in coeliac disease. Serum antibodies to dietary antigens measured by an enzyme linked immunosorbent assay (ELISA).

Serum IgG, IgA and IgM activities to wheat, egg and cow's milk antigens were measured by an ELISA method in children and adults with coeliac disease (CD). In untreated patients, the IgA activity was characteristically raised to gluten antigens but often also to proteins from egg or cow's milk. Setting the upper reference range for gluten antibodies as the highest IgA reading obtained in healthy controls and patients with other intestinal disorders, IgA measurements afforded virtually 100% diagnostic sensitivity and specificity and detected 94% of children and 80% of adults with untreated CD. Such measurements, therefore, represent a valuable adjunct in the diagnosis of this disease. IgA activity to beta-lactoglobulin, casein or ovalbumin higher than the normal 95 percentile was found in 44-89% of untreated patients. Reduction of these antibody titres seemed to reflect relatively well the response to treatment with a gluten free diet, particularly the activity to beta-lactoglobulin. Monitoring of IgA antibodies to dietary antigens other than gluten may therefore be of particular importance in the follow-up of CD patients.

Adolescent↗

Basal hyperchlorhydria and its relation to the plasma concentrations of secretin, vasoactive intestinal polypeptide (VIP) and gastrin during prolonged strain.

Twenty young men divided into two groups participated in a five day training course with prolonged and heavy physical exercise, calorie supply deficiency and severe sleep deprivation. Basal acid output (BAO) was measured immediately after the course in seven of ten subjects who were given placebo tablets (placebo group) and in four of ten subjects who had a daily intake of 1 g cimetidine (cimetidine-group) during the course. Median BAO increased 3-fold in the placebo subjects (from 2.7 mmol/h to 8.2 mmol/h) but showed no increase in the cimetidine treated subjects. The median fasting plasma concentrations of secretin increased 2-8-fold during the course. Gastric suction for 1 h or ingestion of cimetidine reduced the plasma concentration of secretin by approx. 50%. Vasoactive intestinal polypeptide (VIP) increased 2-fold and was not influenced by reduction of gastric acid. The placebo group showed a small increase (P less than 0.05) in plasma concentration of gastrin on day two during the course. The study shows a marked hyperchlorhydria which partly explains the fasting hypersecretinemia found during prolonged strain. This strain-induced hyperchlorhydria could be abolished by treatment with the selective H2-receptor antagonist cimetidine.

Acid-Base Equilibrium↗

T-lymphocyte activation by a gluten fraction, glyc-gli. Studies of adult coeliac patients and healthy controls.

A gluten fraction (glyc-gli) induced proliferation of T lymphocytes obtained from coeliac patients or healthy controls. Glyc-gli acted as an antigen, and T-cell activation was strongly dependent on antigen-presenting monocytes in the cultures. The lymphocyte response was similar for HLA-B8/DR3-positive and HLA-B8/DR3-negative healthy controls, and coeliac patients in remission on a gluten-free diet could not be distinguished from the controls by the degree of proliferative activity in this test. Conversely, untreated coeliac patients showed a significantly lower lymphocyte response to glyc-gli than both coeliac patients in remission and controls. This result may reflect sequestration of gluten-specific cells into the mucosal lesion or mesenteric lymph nodes in patients with active coeliac disease.

Adolescent↗

Role of the 26-hydroxylase in the biosynthesis of bile acids in the normal state and in cerebrotendinous xanthomatosis. An in vivo study.

On the basis of different in vitro studies, we have previously suggested that the basic metabolic defect in the rare inherited disease cerebrotendinous xanthomatosis (CTX) is a lack of a hepatic mitochondrial C27-steroid 26-hydroxylase, involved in the normal biosynthesis of bile acids (1980. J. Clin. Invest. 65: 1418-1430; 1981. J. Lipid Res. 22: 191-200; 22: 632-640). In the present work, this hypothesis was tested in vivo. One patient with CTX and two control subjects received intravenously a mixture of [4-14C]7 alpha-hydroxy-4-cholesten-3-one and [6 beta-3H]7 alpha,26-dihydroxy-4-cholesten-3-one, steroids believed to be important precursors of chenodeoxycholic acid. The ratio between 14C and 3H in cholic acid and chenodeoxycholic acid isolated from bile of the CTX-patient was approximately 1/40 and 1/60 of those of the control subjects, respectively. Another patient with CTX and one control subject received a mixture of [4-14C]5 beta-cholestane-3 alpha,7 alpha-diol and [1,2-3H]5 beta-cholestane-3 alpha,7 alpha,26-triol, both possible precursors to chenodeoxycholic acid. In this case the 14C/3H ratio in cholic acid and chenodeoxycholic acid from the patient with CTX was 1/10 and 1/15, respectively, compared with that of the control subject. The most likely explanation for these findings is that very little of the 14C-precursors, i.e. without a 26-hydroxyl group, can be converted into cholic acid and chenodeoxycholic acid because of a defect of the 26-hydroxylase step. The results obtained are in accord with our previous findings in vitro. The results further underline the importance of the 26-hydroxylase pathway in the normal biosynthesis of cholic acid and chenodeoxycholic acid in man.

Adult↗

The release of human pancreatic polypeptide, gastrin, gastric inhibitory polypeptide, and somatostatin in celiac disease related to the histological appearance of jejunal mucosa before and 1 year after gluten withdrawal.

Jejunal biopsies and the postprandial response of pancreatic polypeptide (PP), gastrin, gastric inhibitory polypeptide (GIP), and somatostatin have been examined in nine patients with celiac disease before and 1 year after gluten withdrawal. All presented initially with total villous atrophy of the jejunal mucosa. After gluten withdrawal five showed marked mucosal regeneration on light microscopy examination (responders) and four only moderate or no regeneration (nonresponders). Before treatment the celiac patients had enhanced gastrin response and normal PP response compared with normal controls. After gluten withdrawal the integrated gastrin release was reduced to normal in the responders (275 versus 114; p less than 0.05) but remained elevated in the nonresponders (231 versus 204). Postprandial PP release was similar before and after treatment regardless of the degree of mucosal regeneration. In the responders the integrated release of GIP was increased (180 versus 241; p less than 0.05), and the somatostatin release was enhanced (-2.6 versus 8.4; p less than 0.05) after gluten withdrawal. We conclude that the postprandial release of GIP and somatostatin increases and that the release of gastrin decreases when the intestinal mucosa is regenerated in celiacs on a gluten-free diet. The release of PP after food is not influenced by mucosal regeneration.

Adult↗

Small-bowel bacterial overgrowth in the postgastrectomy syndrome.

Jejunal flora, bile acid deconjugation, and breath hydrogen (H2) and methane (CH4) excretion were studied in 22 Billroth II (BII)-operated patients with chronic postprandial symptoms, dumping (9), vomiting (7), pain (10), and diarrhoea (14). Sixteen were below 90% of desirable weight. Two control groups were included, one comprising 5 symptom-free, BII-operated volunteers and another comprising 12 healthy, unoperated volunteers. The numbers of bacteria recovered from jejunal secretions in the postgastrectomy patients did not differ significantly from those recovered in the symptom-free BII-operated controls but were significantly lower in the unoperated controls. Production of fermentation gas in anaerobic media supplemented with carbohydrates occurred in 17 of 22 postgastrectomy patients and in 4 of 5 BII-operated controls but in none of the unoperated controls. Bacterial bile acid deconjugating activity did not differ significantly between the postgastrectomy patients and the BII-operated controls but was significantly lower in the unoperated controls. Breath H2 excretion after glucose ingestion was significantly higher in the postgastrectomy patients than in both the BII-operated and the unoperated controls. The addition of pectin or guar gum to the glucose meal largely prevented postprandial symptoms and breath hydrogen excretion. Six out of 12 postgastrectomy patients treated with metronidazole recorded symptomatic effects, mainly on diarrhoea. Our findings indicate that jejunal bacterial overgrowth may be a major cause of the symptoms in some postgastrectomy patients. The tests available for demonstration of small-bowel bacterial overgrowth, perhaps with the exception of the glucose H2 breath test, did not differentiate satisfactorily between symptom-producing and non-symptom-producing abnormal jejunal flora. Thus these tests may seem to have a limited practical diagnostic value in such patients.

Adult↗

Bacterial overgrowth in jejunal and ileal disease.

The number of bacteria recovered in anaerobic cultures of jejunal secretions was significantly higher in a group of 10 patients with jejunal disease and stagnation of gut content in the proximal small bowel than in a group of 10 patients with similar conditions in the distal ileum. Some overlap in bacterial numbers occurred between patients with jejunal disease, ileal disease, and healthy controls, whereas production of fermentation gas in anaerobic media supplemented with glucose occurred only in cultures from the patients with jejunal disease. The 14C-glycocholic acid test showed increased output of breath 14CO2 in both patient groups, whereas faecal 14C was significantly increased only in patients with ileal disease. Increased breath hydrogen excretion after glucose ingestion was recorded in 8 of 10 patients with jejunal disease only. Breath methane excretion, previously found in 44% of healthy subjects, was absent in all of 28 patients with Crohn's disease of the small, indicating that these patients have a gut flora that is different from that of the healthy population.

Adolescent↗

Immunohistochemical evaluation of carcinoembryonic antigen, secretory component, and epithelial IgA in ulcerative colitis with dysplasia.

Immunofluorescence staining for carcinoembryonic antigen, secretory component, and epithelial IgA was evaluated semiquantitatively in routine formalin-fixed mucosal biopsy samples from five patients with ulcerative colitis who had undergone colectomy because of carcinomas. Selected areas were given fluorescence intensity scores without knowledge of whether dysplasia or reactive hyperplasia was present as judged by another observer from conventional histopathological features in adjacent sections. The two types of lesion did not differ significantly with regard to the expression of the three marker antigens. In a prospective study based on cold ethanol-fixed mucosal biopsy samples, lesions from 11 ulcerative colitis patients with dysplasia were compared blindly with lesions from six patients with reactive hyperplasia and with samples obtained endoscopically from eight normal controls. The range of disease-associated fluorescence intensity scores was wide, but staining for all markers tended to be brighter in reactive hyperplasia than in dysplasia (P less than 0.01). In the controls, the fluorescence intensity score tended to be lower for carcinoembryonic antigen but was significantly (P less than 0.01) higher for secretory component and epithelial IgA than in both types of lesion. Moreover, staining for secretory component and epithelial IgA in the lesions seemed to be inversely related to the grade of dysplasia and the degree of inflammation. No such trend was seen for carcinoembryonic antigen. The wide ranges of individual fluorescence scores precluded the possibility of applying carcinoembryonic antigen, secretory component, and epithelial IgA as immunohistochemical markers to differentiate between dysplasia and reactive hyperplasia in routine diagnostic work.

Adolescent↗

Sclerosing cholangitis in ulcerative colitis. A follow-up study.

In the 5-year period 1974-78, 48 (14%) of 336 patients with ulcerative colitis were found to have hepatobiliary disease. Endoscopic retrograde cholangiography (ERC) was successfully performed in 39 of these 48 patients, and sclerosing cholangitis was demonstrated in 19. One is excluded from this series because Crohn's disease was diagnosed at reclassification of the bowel disease. Two of the 18 patients with ulcerative colitis and sclerosing cholangitis have died, one of cholangiocarcinoma and one of an unrelated cause. The remaining 16 patients have been observed for a median period of 6 years (3-13 years) since the diagnosis of hepatobiliary disease. Ten have remained symptom-free, four have had intermittent or non-progressive symptoms, and two have developed symptoms of advanced chronic liver disease. The bilirubin level, which was initially raised in one of the patients, was elevated in four at the follow-up examination. Otherwise the laboratory values have remained stationary. Evidence of a progression of the hepatobiliary disease was found in most patients by repeated liver biopsy and particularly ERC. It is concluded that sclerosing cholangitis may remain asymptomatic for several years. Since progressive cholangiographic changes were often seen without concomitant worsening of symptoms, laboratory data, and liver biopsy findings, it is concluded that these criteria are of limited use in evaluating the progression of this disease.

Adult↗

HLA antigens and immunoregulatory T cells in ulcerative colitis associated with hepatobiliary disease.

Serologic HLA typing was carried out in 20 patients with ulcerative colitis (UC) combined with hepatobiliary disease, in 34 UC patients without hepatobiliary disease, and in control subjects. Association with HLA-B8 and -DR3 was found in both groups of patients. HLA-B8 was found in 80% of patients with combined disease (p less than 0.0005 vs. controls; relative risk (RR), 12.0), whereas 32% of the patients with UC without hepatobiliary disease were HLA-B8-positive (not significant vs. controls). Concomitantly, HLA-DR3 was found in 70% of patients with combined UC and hepatobiliary disease (p less than 0.0005 vs. controls; RR 9.95) and in 35% of UC patients without hepatobiliary disease (p less than 0.05 vs. controls; RR, 2.33). HLA-B8 was found more frequently in UC patients with than without hepatobiliary disease (p less than 0.001; RR, 8.36), as was the case with HLA-DR3 (p less than 0.025; RR, 4.28). No indications of defects in immunoregulatory lymphocytes (T gamma and T mu cells) which could explain hyperactivity in the immune system were observed in the patients with combined UC and hepatobiliary disease. The present study gives support to the theory that UC and, particularly, UC combined with hepatobiliary lesion may be autoimmune diseases with a genetic predisposition.

Adult↗