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Biomedical subjects

L Olbe

Publications and source records attributed to L Olbe.

At least 19 recordsLinked to original sources
PubMed2001

Intragastric nitric oxide/nitrite in Helicobacter pylori-infected subjects.

BACKGROUND: Nitrite (NO2-) in swallowed saliva is reduced to nitric oxide (NO) and other nitrogen oxides by the intragastric acidity. This mechanism is probably important for the intragastric clearance of ingested micro-organisms and nitrosating compounds. The study examines the balance between intragastric NO and NO2- in relation to endogenous acid production and infection with Helicobacter pylori. METHODS: Six healthy H. pylori-negative and six H. pylori-positive volunteers with no known gastroduodenal pathology were examined after an overnight fast. Gastric NO was measured using a chemiluminescence technique and pH as well as NO2- were analysed in gastric aspirates. RESULTS: Gastric NO was slightly lower in H. pylori-positive subjects (1560 +/- 211 ppb) than in uninfected controls (2112 +/- 430 ppb; P > 0.05) during basal conditions, whereas both pH and NO2- concentration were similar in the two groups. During inhibition of acid secretion (omeprazole 20 mg b.i.d. over 5 days) median pH and mean NO2- concentration in gastric aspirates were significantly higher in H. pylori positives than in the controls. Furthermore, during omeprazole treatment the intragastric NO levels were almost absent in H. pylori positives, whereas approximately 50% remained in H. pylori-negative individuals. CONCLUSION: Proton-pump inhibition in H. pylori-infected individuals abolishes the intragastric chemical reduction of swallowed NO2- in the fasting stomach.

Adult↗
PubMed2000

[When is H pylori a cause of duoenal ulcer? Hypersecretion of gastric acid, active duodenitis and reduced bicarbonate secretion are links in the chain].

Helicobacter pylori infection engaging mainly the gastric antrum causes hypersecretion of gastric acid. The increased duodenal acid load gives rise to islands of gastric mucosa in the proximal duodenum. As these bacteria thrive only on gastric mucosa it presents an opportunity for Helicobacter pylori to colonize the duodenum. A much higher density of virulent Helicobacter pylori has been found in the duodenum of duodenal ulcer patients in comparison to infected subjects without duodenal ulcer. The high density of virulent Helicobacter pylori in the proximal duodenum results in a strong inflammatory reaction with active duodenitis and impaired bicarbonate secretion. These characteristics of duodenal ulcer patients, together with the acid hypersecretion, seem to be the key factors in evoking a duodenal ulcer.

Bicarbonates↗
PubMed2000

Conceivable mechanisms by which Helicobacter pylori provokes duodenal ulcer disease.

A conceivable concept for the development of duodenal ulcers in Helicobacter pylori (H. pylori) infected subjects is presented in this chapter. The concept includes an explanation of the fact that only a minority of all H. pylori-infected subjects will develop a duodenal ulcer. Helicobacter pylori infection of the antrum induces a hypersecretion of gastric acid secretion, giving rise to gastric metaplasia in the duodenal bulb. This gastric metaplasia is a prerequisite for H. pylori colonization of the bulb. These events are common to all H. pylori-infected subjects. However, a much higher density of H. pylori bacteria and colonization with virulent organisms has been found in the bulb of duodenal ulcer patients, resulting in a much stronger inflammatory reaction with active duodenitis and an impaired bicarbonate secretion. These characteristics, together with acid hypersecretion, seem to be the important factors in evoking a duodenal ulcer.

Antigens, Bacterial↗
PubMed2000

Intragastric CO2 and nitric oxide participate in the regulation of peptone-induced gastrin release in humans.

BACKGROUND: Moderate acidification of the gastric lumen inhibits peptone-induced gastrin release. The aim of the present study was to investigate if the gastric acid neutralization products CO2 (from secreted HCO3) and NO (from reduced salivary nitrite) could act as intermediate messengers between luminal acidity and the inhibition of peptone-induced gastrin release. METHODS: Fourteen healthy volunteers (mean age, 27 years; range, 20-39 years; 3 women) participated in the study. Intragastric perfusion with saline or peptone was performed on the healthy volunteers. Venous blood samples were analyzed for serum gastrin concentrations. Intragastric NO was measured by chemiluminescence. RESULTS: Basal serum gastrin ranged between 11 and 23 pmol/l. Peptone in Sörensen's phosphated buffer (pH 6.9, PCO2 0 mmHg) increased serum gastrin by 83% +/- 23%, whereas acidified peptone (pH 2.0) did not stimulate gastrin release. Acidified peptone buffered with NaHCO3 to neutrality (pH 6.9, PCO2 approximately 600 mmHg) increased serum gastrin by 166% +/- 29%. Low intragastric NO levels were obtained by deviation of saliva. During such salivary depletion, acidified peptone (pH 2.0) stimulated gastrin release to a level of about 40% of the control response (pH 6.9). This peptone-induced gastrin response during salivary deviation was inhibited by addition of nitrite to the perfusate. CONCLUSIONS: Acid-induced inhibition of peptone-stimulated gastrin release is partly dependent on intraluminal NO formed in the reaction between salivary nitrite and gastric acid. In addition, the gastric acid neutralization product CO2 seems to potentiate the effect of peptone on gastrin release.

Adult↗
PubMed2000

Detection of colorectal tumor and inflammatory bowel disease during follow-up of patients with initial diagnosis of irritable bowel syndrome.

BACKGROUND: We wanted to estimate the incidence of irritable bowel syndrome (IBS) and functional dyspepsia (FD) in the general population, and the detection of colorectal tumor (CRT) and inflammatory bowel disease (IBD) after the diagnosis of IBS and FD. METHODS: Patients aged 20-79 years newly diagnosed with IBS (N = 2956) or FD (N = 9900), together with a comparison cohort randomly sampled from the general source population, were followed-up during a mean time of 3 years. RESULTS: We found an overall incidence of 10.3 per 1000 person-years for FD and 2.6 per 1000 person-years for IBS. There was a greater prevalence of depression, stress, fatigue, and pain disorders among IBS and FD patients than in the general population. During the 1st year after a diagnosis of IBS the cumulative risk of detecting CRT was close to 1% in IBS patients. After the 1st year the risk of CRT in IBS patients was close to that in the general population. We found a significantly increased risk of detecting IBD among patients initially diagnosed as having IBS (relative risk (RR), 16.3; 95% confidence interval (CI), 6.6-40.7), which was constant during all the follow-up period. No association was found between dyspepsia and CRT, or IBD. CONCLUSION: IBS and FD shared some comorbidity features, yet demographics and incidence rates were different. Unlike the detection of colorectal tumor, the excess risk of IBD after an initial diagnosis of IBS was cumulatively increased during all the follow-up period. The continuously increased risk of IBD detection in IBS patients favors a true association between IBS and IBD.

Adult↗
PubMed2000

Differences in surface-exposed antigen expression between Helicobacter pylori strains isolated from duodenal ulcer patients and from asymptomatic subjects.

We have analyzed possible qualitative and quantitative differences in antigen expression between Helicobacter pylori strains isolated from the antrum and different locations in the duodenum of 21 duodenal ulcer (DU) patients and 20 asymptomatic subjects (AS) by enzyme-linked immunosorbent assay (ELISA) and inhibition ELISA. Almost all antral and duodenal strains grown in vitro expressed the N-acetyl-neuroaminyllactose-binding hemagglutinin, flagellins (subunits FlaA and FlaB), urease, a 26-kDa protein, and a neutrophil-activating protein. In 75% of both the DU patients and the AS, antral H. pylori strains expressed either the blood group antigen Lewis y (Le(y)) alone or together with the Le(x) antigen. However, duodenal H. pylori strains of DU patients expressed Le(y) antigen more frequently than corresponding strains of AS (P < 0.05). Presence of Le(y) on H. pylori was related to the degree of active duodenitis (P < 0.05). Duodenal H. pylori strains isolated from AS were significantly more often Lewis nontypeable than duodenal strains of DU patients (P < 0.01). Presence of H. pylori blood group antigen-binding adhesin (BabA) was significantly higher on both antral and duodenal strains isolated from DU patients than on corresponding strains isolated from AS (P < 0.05). BabA-positive duodenal H. pylori strains isolated from DU patients were associated with active duodenitis more frequently than corresponding strains isolated from AS (P < 0.01). Infection with H. pylori strains positive for Le(y) and BabA in the duodenum is associated with development of duodenal ulcer formation.

ABO Blood-Group System↗
PubMed1999

Duodenal Helicobacter pylori infection differs in cagA genotype between asymptomatic subjects and patients with duodenal ulcers.

BACKGROUND & AIMS: It is unclear why only a minority of subjects infected by Helicobacter pylori develop duodenal ulcers (DU). The aim of this study was to investigate whether the number and type of H. pylori strains in the duodenum of patients with DU may play a critical role. METHODS: Twenty-one patients with DU and 20 asymptomatic subjects with antral H. pylori infection were studied. Paired biopsy specimens were taken from the antrum and from each quadrant of the duodenal bulb. Analyses included extent of duodenal gastric metaplasia, severity of duodenitis, bacterial density, presence of the cagA gene, and vacuolating cytotoxin activity. RESULTS: H. pylori was cultured from duodenal biopsy specimens in 95% of patients with DU and 80% of asymptomatic subjects. Both groups had a similar bacterial density and proportion of cagA-positive strains in the antrum (86% vs. 75%), but patients with DU had a 20-fold higher density of H. pylori and a higher proportion of cagA-positive strains in the duodenal bulb (81% vs. 30%). Active duodenitis was present only in patients with DU infected by cagA positive strains in the duodenum. CONCLUSIONS: The results suggest that a high density of cagA-positive strains in the duodenum with severe duodenitis are important determinants of DU disease.

Adult↗
PubMed1999

Comparison of survival between malignant neuroendocrine tumours of midgut and pancreatic origin.

The survival of 64 consecutive patients with disseminated midgut carcinoid tumours was compared in a retrospective study with that of 25 consecutive patients with sporadic malignant endocrine pancreatic tumours treated according to similar surgical principles. The presence of hepatic metastases implied a worse prognosis in neuroendocrine tumours of pancreatic rather than midgut origin. This infers that these tumour types must be separated when treatments are evaluated.

Adolescent↗
PubMed1999

Splanchnic circulation and regional sympathetic outflow during peroperative PEEP ventilation in humans.

The splanchnic organs represent a major target for sympathetic outflow and an important region for haemodynamic effects on cardiovascular homeostasis. We have studied regional haemodynamic and sympathetic changes in the splanchnic bed during standardized circulatory stress from positive end-expiratory pressure ventilation (PEEP). We investigated eight patients undergoing major upper abdominal surgery using a radiotracer method to measure plasma spillover of norepinephrine as an index of sympathetic nerve activity using arterial, portal and hepatic venous blood sampling. Mesenteric and hepatic perfusion were measured by ultrasound transit time flowmetry and blood-gas analyses. Steady state measurements were performed before and during PEEP ventilation at 10 cm H2O. Plasma spillover of norepinephrine in the mesenteric and hepatic organs represented mean 49 (SEM 8)% and 7 (2)%, respectively, of systemic norepinephrine spillover at baseline, and PEEP ventilation did not cause any significant changes. However, PEEP ventilation significantly decreased portal venous blood flow while hepatic blood flow was preserved by a compensatory increase in hepatic arterial blood flow. Mesenteric and hepatic oxygen delivery changed according to blood flow, and there were no changes in regional oxygen consumption. Thus PEEP ventilation altered mesenteric and hepatic perfusion, independent of any change in corresponding sympathetic nerve activity. Regulation of hepatic blood supply, not related to sympathetic activity, maintained liver oxygenation during PEEP ventilation despite a simultaneous decrease in mesenteric perfusion.

Adult↗
PubMed1998

Aspirin-induced gastritis, like Helicobacter pylori-induced gastritis disinhibits acid secretion in humans: relation to cytokine expression.

BACKGROUND: Helicobacter pylori infection contributes to hypergastrinemia and hypersecretion of acid by blocking inhibitory reflex pathways to gastrin and parietal cells normally activated by antral distention. Our aim was to investigate whether a similar blockade of inhibitory responses could be provoked by inducing gastritis with aspirin, thus implicating a common inflammatory component, possibly a proinflammatory cytokine(s). METHODS: We studied the effects of antral distention on stimulated acid secretion and gastrin release in H. pylori-negative volunteers, before and after 3 days of aspirin therapy (2 g daily). Immediately before the examinations, the severity of gastric mucosal injury was evaluated macroscopically and histologically, and the production of interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma was determined by immunohistochemistry. RESULTS: Most subjects had severe gastric injury after aspirin therapy, resulting in a substantially increased production of IL-1beta, IL-6, and IL-8 but not of TNF-alpha and IFN-gamma in the antral mucosa. In these subjects the acid-inhibitory response was abolished or markedly reduced. Conversely, aspirin therapy failed to affect the gastrin release in all subjects studied. CONCLUSIONS: The disinhibition of acid secretion in response to antral distention is a joint feature of the gastritis induced by aspirin and H. pylori infection, possibly related to the increased production of IL-1beta, IL-6, and IL-8. The H. pylori-related hypergastrinemia apparently has a different background.

Adult↗
PubMed1998

Human duodenogastric reflux, retroperistalsis, and MMC.

The aim of this study was to determine to what extent human migrating motor complex (MMC)-related secretory phenomena are influenced by a recently discovered period of duodenal retroperistalsis during late phase III. A constant-flow perfusion technique was used to measure gastric appearance of acid, bicarbonate, pepsin, bilirubin, IgA, and duodenally infused [14C]polyethylene glycol (PEG) 4000 in 12 healthy volunteers. Interdigestive gastroduodenal motility was recorded by digital manometry. During late antral phase II and III, the gastric lumen was acidified (P < 0.005 phase III vs. phase I) together with a marked increase in luminal pepsin output (3.1 +/- 1.2 during phase III vs. 0.25 +/- 0.08 kU/5 min in phase I, P < 0.01), followed by a realkalinization due to a simultaneous reduction of acid secretion and a duodenogastric reflux, aided by retrograde peristalsis, of bicarbonate and IgA but not of bilirubin, at the end of antral phase III (P < 0.05 phase III vs. phase I values). This physiological duodenoantral reflux phenomenon may play an important role in the chemical and immunological restitution of the antral mucosal barrier function after the exposure to high acid and pepsin concentrations during antral phase III activity.

Adult↗
PubMed1997

Vertical banded gastroplasty or gastric banding for morbid obesity: effects on gastro-oesophageal reflux.

OBJECTIVE: To assess the effect of vertical banded gastroplasty and gastric banding on the development of gastro-oesophageal reflux using both subjective and objective methods. DESIGN: Prospective, randomised study. SETTING: Teaching hospital, Sweden. SUBJECTS: 50 consecutive, morbidly obese patients (mean (SD) body mass index (BMI) 42.5 (5), 27 women and 23 men; mean age 48 years, range 38-57 years). INTERVENTIONS: Vertical banded gastroplasty (n = 24) or gastric banding (n = 26). MAIN OUTCOME MEASURES: Results of evaluation by standardised questionnaire, 24-hour ambulatory pH-metry, and endoscopy. RESULTS: After six months the mean (SD) BMI had decreased to 34.4 (5.7), with no differences between the groups. Mild dysphagia was somewhat more common (13 compared with 1) but the incidence of heartburn (8 compared with 17), and acid regurgitation (12 compared with 14) were less after the operation; 3 patients developed erosive oesophagitis, two in the vertical banded group and one in the banding group. Ambulatory pH-metry readings did not change significantly from preoperatively and there were no differences between the two operations. One patient developed pathological reflux, and in three the values returned to the normal range. CONCLUSION: Gastric restriction operations including those with a narrow stoma that causes outflow obstruction do not seem to increase the incidence of reflux in patients with functioning antireflux barriers.

Adult↗
PubMed1996

Sympathetic discharge to mesenteric organs and the liver. Evidence for substantial mesenteric organ norepinephrine spillover.

This study using sampling of blood from the portal vein, in addition to arterial and hepatic sites, to estimate separately spillovers of norepinephrine from mesenteric organs and the liver in seven patients undergoing upper abdominal surgery. Conventional measurements in arterial and hepatic venous plasma provided a measure of net hepatomesenteric NE spillover (403 pmol/ml) that indicated a 13% contribution of these organs to total body spillover of NE into systemic plasma (3,071+/-518 pmol/min). The net hepatomesenteric spillover of NE into systemic plasma was much lower than the spillover of NE from mesenteric organs into portal venous plasma (1,684+/-418 pmol/min). This and the hepatic spillover of NE into systemic plasma (212+/-72 pmol/min) indicated a considerable combined spillover of NE from hepatomesenteric organs (1,896+/-455 pmol/min). The sum of the latter estimate with the difference between total body and net hepatomesenteric NE spillovers provided an adjusted total body spillover of NE into both systemic and portal venous plasma (4,564+/-902 pmol/min). Mesenteric organs made a 37% contribution, and the liver made a 5% contribution to the adjusted total body spillover of NE. Thus, a substantial proportion of total body sympathetic outflow is directed towards mesenteric organs; this is obscured by efficient hepatic extraction of NE (86+/-6%) when measurements are restricted to arterial and hepatic venous plasma.

Aged↗
PubMed1996

Long-term results of a prospective randomized comparison of total fundic wrap (Nissen-Rossetti) or semifundoplication (Toupet) for gastro-oesophageal reflux.

The importance of the extent of the fundic wrap that encircles the distal oesophagus for the establishment of long-term control of gastro-oesophageal reflux disease (GORD) and for the risk of symptoms after fundoplication was evaluated in a prospective, randomized clinical trial. Of 137 consecutive patients with GORD, 72 were allocated to a semifundoplication (180-200 degrees, Toupet) and 65 to a total fundoplication (360 degrees, Nissen-Rossetti). Dysphagia was more common in the early postoperative period after a total fundic wrap, a difference which disappeared with time. This corresponded to a higher resting tone in the lower oesophageal sphincter area. Seven patients (5 per cent) experienced relapse of GORD during follow-up of more than 3 years. Although no difference in the cumulative relapse rate (5 per cent for Nissen-Rossetti versus 6 per cent for Toupet) was found between the two study groups, the total failure rate was higher (P < 0.05) among patients who had a Nissen-Rossetti procedure because of a procedure-specific complication: intrathoracic herniation of the fundoplication in five patients caused obstructive symptoms without reflux (four had no posterior crural repair). In addition, symptoms in the form of flatulence were more frequently seen after Nissen-Rossetti fundoplication (P < 0.05 at 2 years and P < 0.01 at 3 years). Both Nissen-Rossetti and Toupet fundoplication equally well and durably controlled GORD. Fewer symptoms occurred in those having a semifundoplication, both in the early and late postoperative period.

Adult↗
PubMed1996

Food intake after gastrectomy for gastric carcinoma: the role of a gastric reservoir.

Patients with carcinoma of the stomach who underwent curative resection were randomized to total gastrectomy (n = 49), total gastrectomy and an S-shaped gastric substitute (n = 28) or subtotal gastrectomy (n = 12); all had a Roux-en-Y reconstruction. The gastric substitute and gastric remnant allowed a volume of 400-500 ml to be installed without increments in basal pressures. The corresponding volume in the Roux limb was 100 ml. Energy intake was approximately 120 kJ/kg preoperative weight per day 3 months after operation, and then remained constant. Patients who had subtotal gastrectomy ate less (91.7 kJ/kg preoperative weight) 3 months after operation, but thereafter increased their intake. Patients allocated to have a gastric pouch or subtotal gastrectomy complained more frequently of adverse postprandial symptoms (P < 0.03) as a major cause of reduced calorie intake. The construction of a gastric reservoir did not improve nutritional adaptation after surgery for gastric carcinoma.

Adult↗
PubMed1996

Monoclonal antibodies against fimbrial subunits of colonization factor antigen I (CFA/I) inhibit binding to human enterocytes and protect against enterotoxigenic Escherichia coli expressing heterologous colonization factors.

Enterotoxigenic Escherichia coli (ETEC) bind to enterocytes in the small intestine by means of antigenically distinct colonization factors (CFs). By immunizing with isolated subunits of CFA/I fimbriae we have previously produced monoclonal antibodies (MAbs) that cross-react immunologically in vitro with several CFs. Two of these MAbs [S(subunit)-CFA/ I 17:8 and S-CFA/I 5:6] were found to significantly inhibit the binding of ETEC strains expressing either homologous or heterologous CFs, i.e. CFA/I and CS4, to isolated human jejunal enterocytes. The two MAbs also conferred passive protection against fluid accumulation in rabbit ileal loops caused by CFA/I-as well as CS4-expressing ETEC strains. Immunoelectron microscopy studies showed that both MAbs bound specifically to CFA/I as well as to CS4 fimbriae expressed on bacteria. These results indicate the possibility to induce anti-CF antibodies that can protect against ETEC infection caused by bacteria expressing not only homologous but also heterologous CFs, by immunizing with fimbrial subunits.

Adhesins, Bacterial↗
PubMed1996

A mechanism by which Helicobacter pylori infection of the antrum contributes to the development of duodenal ulcer.

BACKGROUND & AIMS: Helicobacter pylori infection and duodenal ulcer disease are firmly correlated. However, the bacteria do mainly colonize the antrum, indicating an indirect pathogenic mechanism. The aim of this study was to test a concept claiming that H. pylori infection of the antrum selectively blocks normal inhibitory reflex pathways to gastrin and parietal cells. METHODS: The effect of antral distention was studied on gastric acid secretion stimulated by pentagastrin and on gastrin release stimulated by gastrin-releasing peptide in H. pylori-infected and noninfected patients with and without duodenal ulcer disease, as well as after eradication of the bacteria. RESULTS: The inhibitory effect on gastric acid secretion induced by antral distention was absent in H. pylori-infected patients irrespective of whether or not they had duodenal ulcer disease. The inhibitory mechanism was restituted in 8 of 10 patients within 9 months after successful eradication of H. pylori infection. Similar results were obtained in studies on gastrin release. CONCLUSIONS: H. pylori infection blocks normal, physiological inhibitory mechanisms from the antrum to both the gastrin cells and to the parietal cell region, resulting in increased gastrin release and impaired inhibition of gastric acid secretion, which will probably lead to an increased duodenal acid load as a general prerequisite for the development of duodenal ulcer disease.

Adult↗