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Biomedical subjects

L Olbe

Publications and source records attributed to L Olbe.

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

The influence of Helicobacter pylori infection on postprandial duodenal acid load and duodenal bulb pH in humans.

BACKGROUND & AIMS: Recently, we postulated a new concept of duodenal ulcer pathogenesis suggesting that antral Helicobacter pylori infection blocks inhibitory pathways to the gastrin and parietal cells, resulting in an increased and prolonged postprandial acid secretion. the aim of this study was to examine duodenal acid load and duodenal bulb pH after a meal before and after eradication of H. pylori. METHODS: Using a marker-dilution method and a pH electrode in the duodenal bulb, gastric emptying, acid secretion, gastrin release, duodenal acid load, and duodenal bulb pH were studied during 2 hours after peptone meals of pH 7.0 and 2.0 in 8 H. pylori-negative controls and 8 H. pylori-infected subjects before and 6 months after eradication. RESULTS: The H. pylori-infected subjects had an increased gastric emptying, gastrin release, and acid secretion, higher duodenal acid load, and lower duodenal bulb pH after the meals. These responses were normalized after eradication. CONCLUSIONS: H. pylori-infected subjects have an increased and prolonged postprandial acid secretion, partly caused by an impaired low pH inhibition of acid secretion, gastrin release, and gastric emptying, resulting in an increased duodenal acid load and a prolongation of low pH in the duodenal bulb, as a general prerequisite for the development of duodenal ulcer disease.

Adult↗
PubMed1996

Mechanisms behind changes in gastric acid and bicarbonate outputs during the human interdigestive motility cycle.

Human gastric interdigestive acid and bicarbonate outputs vary cyclically in association with the migrating motor complex (MMC). These phenomena were studied in 26 healthy volunteers by constant-flow gastric perfusion, with continuous recording of pH and Pco2 in mixed gastric effluent and concomitant open-tip manometry of gastroduodenal motility. Stable acid and bicarbonate outputs were registered during less than 50% of the MMC cycle. Acid secretion started to increase 71 +/- 3% into the cycle, with maximum output during antral phase III. Bicarbonate output increased biphasically 1) 40 +/- 5% into the cycle, coinciding with reflux of bile, and 2) at the end of duodenal phase III when the aspirate was devoid of bile. The bicarbonate peak associated with phase III was abolished by atropine (0.01 mg/kg iv, n = 8) and by pyloric occlusion (n = 9) but remained unchanged after omeprazole (n = 10). The acid peak was abolished by both atropine and omeprazole. It is concluded that the MMC-related changes in acid and alkaline outputs represent two different and independent phenomena. Acid secretion cyclicity is due to periodical variations in cholinergic stimulation of the parietal cells. In contrast, the phase III-associated increase in bicarbonate output is due to duodenogastric reflux.

Adolescent↗
PubMed1996

Assimilation of triglycerides in subcutaneous and intraabdominal adipose tissues in vivo in men: effects of testosterone.

To determine the effects of testosterone (T) on lipid assimilation in different adipose tissue depots, T (250 mg, im) was given to 17 middle-aged men 5 days before abdominal surgery. Twenty-four hours before surgery, 10 microCi labeled oleic acid in 80 g milk fat were administered orally. Lipid radioactivity was measured in adipose tissue biopsies from abdominal ac, omental, and retroperitoneal adipose tissues. Subcutaneous, visceral (omental plus mesenteric), and retroperitoneal adipose tissue masses were determined using computerized tomography scans at 22 levels. Sixteen men who were not treated with T served as controls. T administration was followed by an increase in serum concentrations from 17.7 +/- 1.1 to 32.6 +/- 1.8 nmol/L (P < 0.001) and a marked (> 50%) reduction compared with controls in lipid radioactivity in omental and retroperitoneal adipose tissues, but not in sc adipose tissue. In controls, sc, visceral, and retroperitoneal adipose tissues assimilated 59.2 g (73.4%), 16.9 g (20.9%), and 4.6 g (5.7%), respectively, of the orally administered fat. In the T-treated men, this was changed to 73.5 g (88.8%), 6.4 g (7.7%), and 2.9 g (3.5%), respectively. It was concluded that T inhibits triglyceride assimilation in intra-abdominal depots and apparently directs this lipid to sc fat in men.

Abdomen↗
PubMed1996

Vertical banded gastroplasty by laparoscopic technique in the treatment of morbid obesity.

From October 1993 through May 1994, 38 consecutive morbidly obese patients underwent a laparoscopic vertical banded gastroplasty (VBG). During the operation a gastric window was made by a 25-mm circular stapler; and the vertical staple line, establishing the gastric pouch, was constructed by using a 60-mm, four-row linear stapler. The outflow stoma was reinforced by a Gore-Tex band and calibrated to have an internal diameter of 9 mm. Three patients had to be converted to open surgery during the initial laparoscopic procedure because of insufficient operative access. Another three patients had to be reoperated during subsequent postoperative courses, one laparoscopically to reinforce a vertical staple line defect caused by a transected nasogastric tube, another because of an open reoperation during the first postoperative day for a rupture in the vertical staple line, and, finally, a patient was reexplored because of the present of postoperative fever with a left-sided pleuropneumonia and subphrenic accumulation of fluid. However, during the operation no leakage or any other local complications were detected. The subsequent postoperative courses were uneventful in all these patients. Compared with the reference group comprising the latest consecutive 17 obese patients operated with open VBG before the introduction of the laparoscopic technique, the laparoscopy group had less postoperative pain and had mobilization sooner. In the latter group, we recorded an improved respiratory status during the early postoperative period, as reflected by increased oxygen saturation and peak exspiratory flow rates as well as a lower body temperature. In conclusion, laparoscopic VBG is technically feasible and can be safely performed. Our early postoperative experiences suggest that these patients have a shorter and less cumbersome postoperative recovery period compared with conventionally operated obese patients. The long-term follow-up of these patients will determine whether these initial advantages of the laparoscopic approach are corroborated by comparable effects on weight control.

Adult↗
PubMed1995

Effects of hypochlorhydria and hypergastrinemia on structure and function of gastrointestinal cells. A review and analysis.

Since hypochlorhydria can induce hypergastrinemia, and gastrin has a trophic effect on some gastrointestinal cells, states that cause elevated plasma gastrin levels are of interest in terms of effects on cell growth and function. This article reviews the relationship between gastric mucosal cells during periods of acid stimulation and inhibition and analyses the effects of hypochlorhydria and hypergastrinemia on gastric and colonic cells and tumors. Hypochlorhydria releases the inhibitory effect of antral gastrin cells, inducing them to release gastrin in the presence of peptides or amino acids in the gastric lumen or in response to antral distension. Gastrin stimulates the oxyntic mucosa, which may lead to hyperplasia of enterochromaffin-like cells, resulting in enterochromaffin-like carcinoid tumors in aged rats and, rarely, in patients with chronic atrophic gastritis or gastrinomas. In addition to hypergastrinemia, other factors appear to be required for the progression of enterochromaffin-like hyperplasia to carcinoids; genetic factors may be involved. Gastrin elevations due to antisecretory drug therapy are indirectly proportional to the degree of acid inhibition and are reversible upon cessation of therapy. The gastrin levels during omeprazole therapy are similar to those caused by gastric vagotomy. Available evidence does not support a relationship between hypergastrinemia and the occurrence or growth of gastric carcinoma or colonic tumors.

Achlorhydria↗
PubMed1995

Gastric output of IgA in man: relation to migrating motility complexes and sham feeding.

BACKGROUND/AIMS: The immunologic reactivity of the gastric mucosa is poorly understood. The origin and dynamics of immunoglobulin A (IgA) occurring in the gastric lumen were investigated in healthy, Helicobacter pylori-negative volunteers. METHODS: Gastroduodenal manometric motility recordings were combined with gastric luminal perfusion, enabling calculation of gastric acid output and analysis of the total IgA output. RESULTS: Acid output and total IgA correlated with the migrating motility complexes (MMC). The gastric IgA release showed maximal values in association with gastric motility phase III (maximal motor activity) and lowest values during phases I and II (none or irregular motor activity). The IgA output correlated with neither swallowed saliva (as indicated by amylase in the gastric perfusate) nor duodenogastric reflux (as indicated by gastric occurrence of bilirubin and/or duodenally infused PEG4000). Stimulation of gastric acid secretion by sham feeding during phase II-like motor activity (n = 6) induced a rapid and transient doubling of IgA output. There was no significant correlation between gastric acid secretion and gastric IgA release. CONCLUSION: Substantial amounts of IgA are released into the human stomach, most likely originating from the gastric mucosa. The up-regulation of IgA release in association with the activity front of the MMC and anticipatory to food intake suggests a neuroendocrine control of gastric mucosal immune responses.

Adult↗
PubMed1995

The pH/PCO2 method for continuous determination of human gastric acid and bicarbonate secretion. A validation study.

BACKGROUND: The present paper describes and evaluates a methodologic approach for registration of the fast, interdigestive, motility-related changes in gastric acid and bicarbonate outputs seen in man. METHODS: The technique is based on continuous gastric luminal perfusion and measurements of pH and PCO2 in gastric effluent and concomitant intragastric/duodenal manometry. Fourteen healthy volunteers participated. RESULTS: Direct acid secretory estimations from pH recordings, corrected for hydrogen ion activity, correlated closely with values obtained by conventional titration. After intragastric infusion of bicarbonate, 96 +/- 5% of the newly measured steady-state value was registered virtually instantaneously provided that corrections for the PCO2 electrode time constant and the perfusion/aspiration time were made. In the neutral pH range (pH 5-7), practically full quantitative recovery of intragastrically infused bicarbonate was obtained. In the acid pH interval (pH 2-5) the recovery was significantly lower (53 +/- 6%; p < 0.01). With an aspirate without air admixture and during high perfusion rates (31 and 46 ml/min), full recovery of bicarbonate was obtained also at an acid pH, whereas a reduced perfusion rate (16 ml/min) significantly (p < 0.05) reduced the recovery rate. CONCLUSIONS: With the pH/PCO2 technique both acid and bicarbonate assessments have a close to on-line time resolution. Acid output is measured accurately, but the method potentially underestimates actual bicarbonate levels in the acid pH range, a combined effect of diffusion of CO2 into air bubbles in the aspirate and into the gastric mucosa from the lumen. A high gastric perfusion rate minimizes this source of error. The pH/PCO2 technique is well suited for studies of the interaction between secretion and motility in the human stomach.

Adult↗
PubMed1995

A simple, rapid, and highly reliable capsule-based 14C urea breath test for diagnosis of Helicobacter pylori infection.

BACKGROUND: Since the urea breath test (UBT) indirectly detects gastric Helicobacter pylori infection by measuring urease activity, the possibility of false-positive results due to other urease-producing bacteria cannot be excluded. Previous studies have shown that increased 14CO2 activity in early breath samples could be attributed to urea hydrolysis in the oropharynx. For that reason, reliable assessment of H. pylori status is hampered for at least 20 min after administration of a 14C-urea drink. METHODS: To overcome this problem we have developed a modified breath test in which 111kBq 14C-urea is supplied in a gelatin capsule, which prevents release of 14C before reaching the stomach. Our modified 14C UBT was evaluated in 100 healthy volunteers, and results were compared with those from enzyme-linked immunosorbent assay serology. RESULTS: The study showed a 99% concordance between the two noninvasive tests. When a biometric method for determination of cut-off values between positive and negative UBT results with the smallest possible arbitrariness was used, the calculated statistical probability of a false diagnosis was lowest in the 10-min breath sample (0.20%), and 100% sensitivity and specificity was achieved. Our capsule method was also compared with the urea drink method and was found more reliable because no overlapping in 14CO2 activity occurred between H. pylori-positive and -negative subjects, whereas conventional breath testing showed overlapping during the whole 30-min test period. Our study also showed that a fatty test meal lowers the 14CO2 excretion the first 20 min and may adversely affect the accuracy of a rapid UBT. CONCLUSIONS: Supplying the 14C-urea in a capsule obviates the problem of false-positive results in early breath samples and makes it possible to diagnose H. pylori infection with 99.8% reliability from a single 10-min breath sample, without the use of a test meal of adjustments for assumed individual CO2 production.

Adolescent↗
PubMed1994

Role of acid secretory response to sham feeding in predicting recurrent ulceration after proximal gastric vagotomy.

The completeness of vagal denervation in determining the long-term outcome of patients with duodenal ulcer disease after proximal gastric vagotomy (PGV) was studied by examining the relationship between the postoperative acid secretory response to sham feeding ('chew and spit' technique) and the subsequent ulcer recurrence rate during a mean follow-up of 7.5 (range 5-15) years. The cumulative recurrence rate of 98 patients analysed prospectively was 11 per cent. Of 22 patients who had incomplete vagotomy as suggested by the sham feeding response, five had a later relapse. This compares with only an 8 per cent relapse rate among those with a secretory response suggesting complete vagotomy. Four patients suffered from a relapse more than 5 years after operation but none had undergone incomplete vagotomy. However, in seven patients with an early postoperative relapse (within 5 years) five had had incomplete vagal denervation (P < 0.05). In this latter group the median time elapsed from surgery until the first recurrence was only 1 year. It is concluded that the early postoperative acid secretory response to a sham feeding stimulus is clinically useful as it allows prediction of the risk of early relapse after PGV. This test may be helpful for the validation of new techniques of vagotomy.

Adult↗
PubMed1994

Clinical management of gastric carcinoid tumors.

Four types of gastric carcinoids have been identified: (1) multiple small body-fundus carcinoids associated with chronic atrophic gastritis type A (A-CAG); (2) sporadic solitary lesions without specific pathogenetic background (non-A-CAG); (3) carcinoidosis associated with Zollinger-Ellison/MEN 1 syndrome, and (4) rare tumors, e.g. gastrin cell tumors, neuroendocrine carcinomas and mixed endocrine-exocrine tumors. In a retrospective study of 15 patients with gastric carcinoids (11 A-CAG, 3 non-A-CAG and 1 gastrin cell tumor) over a 10-year period, the histopathological and clinical features were assessed. The A-CAG-type carcinoids were clinically silent with lymph node metastases in 2/11 cases but no hepatic metastases. The non-A-CAG-type carcinoids were malignant with disseminated disease, hormonal symptoms and increased urinary excretion of the main histamine metabolite, MeImAA. Five patients with A-CAG tumors were subjected to antrectomy to remove hypergastrinemia, which is thought to be of pathogenetic importance for these tumors. During the observation period (1.5-8 years) 1 patient developed recurrent tumors, while the other 4 showed persistent argyrophil cell hyperplasia. A prospective treatment protocol of these tumors is suggested with endoscopic removal of less numerous, small lesions as first-step therapy, followed by antrectomy at recurrence. Larger lesions should be excised in combination with antrectomy. Gastrectomy is reserved for the rare cases of invasive tumors with lymph node metastases. As evident from the outcome of patients with non-A-CAG tumors radical surgery should be performed whenever practicable.

Carcinoid Tumor↗
PubMed1994

Hypovolemia-induced cardiovascular effects on human gastric mucosal acid and HCO3- release.

BACKGROUND: The bicarbonate ion seems to play a crucial role in mucosal acid-base regulation by generating a pH gradient that is regarded as a 'first line of defense' against acid back-diffusion. The aim of this study was to determine the effects of hypovolemia on gastric mucosal buffering capacity, as reflected by luminal HCO3- release, in human volunteers. METHODS: Central hypovolemia was induced by lower-body negative pressure (LBNP), and HCO3- release was measured by using a perfusion system based on continuous recording of the pH and PCO2 of gastric aspirate. The response to LBNP was related to concomitant cardiovascular effects, to gastric pH, and to the current phase of the migrating motor complex (MMC). RESULTS: At an acid gastric pH, LBNP induced a slight but statistically significant reduction in luminal HCO3- release (-27 +/- 10%, p < 0.05). The magnitude of the response was significantly correlated with the degree of reflex tachycardia. A larger and less variable response (-78 +/- 4%, p < 0.01 versus control group) was seen when luminal pH was increased by ranitidine pretreatment. The effect of LBNP on HCO3- release was statistically significant only during the early and middle parts of the MMC cycle. CONCLUSIONS: The results indicate that hypotension may reduce gastric mucosal buffering capacity, probably by activation of a sympathetic reflex. The magnitude of this response seems to depend on: 1) the degree of baroreceptor unloading; 2) luminal pH; and 3) the current phase of the MMC.

Adult↗
PubMed1993

Effect of once daily intravenous and oral omeprazole on 24-hour intragastric acidity in healthy subjects.

The effect of repeated once daily administration of 20 mg omeprazole orally and 10 mg and 40 mg intravenously on 24-h intragastric acidity was studied in nine healthy subjects. On day 1, 20 mg orally and 10 mg intravenously reduced integrated intragastric acidity by 18% and 15%, respectively (NS). On day 5 the reduction had increased to 60% and 53%, respectively (p < 0.05). The first dose of 40 mg intravenously produced a reduction of 71% (p < 0.05) with no further increase during continued administration. An increase in plasma omeprazole concentrations by 56% (p < 0.05) was seen during repeated dosing with 40 mg intravenously, while no significant change occurred with the two other doses. Thus once daily administration of 10 mg omeprazole intravenously produced an effect on 24-h intragastric acidity comparable to that of once daily administration of 20 mg omeprazole orally. However, for both these dosage regimens it took a few days before their maximal effect was obtained. Parenteral administration of 40 mg omeprazole produced, already on the first day of treatment, an effect similar to that seen after 5 days of oral administration of 20 mg omeprazole or intravenous administration of 10 mg and can therefore overcome this initial delay in drug action. The reduction of 24-h intragastric acidity seen in the present study appeared to be lower than that seen in a similar study in duodenal ulcer patients, a finding not explained by differences in age or pharmacokinetics.

Administration, Oral↗
PubMed1993

Motility-related cyclic fluctuations of interdigestive gastric acid and bicarbonate secretion in man. A source of substantial variability in gastric secretion studies.

The relationship between interdigestive gastric motility and secretion was studied in eight healthy volunteers. Acid and bicarbonate output rates were measured with a high time resolution, using a perfusion system based on continuous registration of pH and PCO2 of gastric effluent. Antral pressure was measured by manometry. The total duration of the interdigestive motility cycle (time between two phase-III complexes) was 96 +/- 12 min (mean +/- SE). In late migrating motor complex phase II, acid output, bicarbonate output, and bile reflux increased significantly. Acid secretion reached a peak in association with motor phase III. The gastric lumen was then rapidly alkalinized; this phenomenon was due to a simultaneous decrease in acid secretion and a short-lasting (15 +/- 2 min, mean +/- SE) phasic increase in bicarbonate output, which was not associated with bile reflux (bilirubin). After these phase-III-related events both acid and bicarbonate output rates reached a relatively stable level during phase I and early phase II. This period of stability constituted 47 +/- 3% (acid) and 41 +/- 6% (bicarbonate, means +/- SE), respectively, of the cycle. The peak to base line output ratio was 6.6 +/- 1.2 (p < 0.001) for acid and 2.8 +/- 0.3 (p < 0.001) for bicarbonate (means +/- SE). The results show a marked variability in acid and bicarbonate output rates during the interdigestive motility cycle. The magnitude of this variability has previously been underestimated owing to poor time resolution of the secretion measurements. If not taken into account, these 'spontaneous' secretory variations may constitute a considerable source of error in gastric secretion studies.

Adult↗
PubMed1993

Does antral distension inhibit gastric acid secretion or stimulate bicarbonate secretion in 'healthy' subjects?

The effects of a 150-ml antral balloon distension on pentagastrin-stimulated gastric acid secretion and bicarbonate secretion were studied in nine healthy subjects and eight duodenal ulcer (DU) patients. The gastric secretions were simultaneously measured, using a luminal perfusion and pH/PCO2 measurements. Two of the healthy subjects and six of the DU patients were positive for Helicobacter pylori. When H. pylori-positive and -negative subjects were compared, basal gastric acid and bicarbonate outputs did not differ significantly. In H. pylori-infected subjects the bicarbonate transport increased by about 70% on pentagastrin stimulation. In the H. pylori-negative group pentagastrin had no effect on the bicarbonate secretion. Antral distension elicited a 30-35% inhibition of pentagastrin-stimulated gastric acid secretion in the group of H. pylori-negative subjects, whereas the acid secretory level remained essentially unchanged in the positive group. Bicarbonate secretion decreased transiently by the distension in the negative subjects, whereas a slight increase was observed in the infected group. We conclude that antral distension inhibits pentagastrin-stimulated gastric acid output in healthy H. pylori-negative subjects. Our results strongly suggest that the underlying mechanism is a direct inhibition of gastric parietal cell function and not an increased gastric bicarbonate secretion. Furthermore, the results indicate that this defective distension-induced acid inhibition may be correlated to H. pylori infection rather than to duodenal ulcer disease.

Adult↗
PubMed1992

The morphology and metabolism of intraabdominal adipose tissue in men.

Mass, morphology, and metabolism of total adipose tissue and its subcutaneous, visceral, and retroperitoneal subcompartments were examined in 16 men with a wide variation of total body fat. Computerized tomography (CT) scans showed that the intraabdominal fat mass comprised approximately 20% of total fat mass. Visceral and retroperitoneal fat masses were approximately 80% and 20% of total intraabdominal fat mass, respectively. Enlargement of intraabdominal fat depots was due to a parallel adipocyte enlargement only. Direct significant correlations were found between these adipose tissue masses and blood glucose and plasma insulin levels, blood pressure, and liver function tests, while glucose disposal rate during euglycemic glucose clamp measurements at submaximal insulin concentrations (GDR), plasma testosterone, and sex hormone-binding globulin concentrations correlated negatively. The correlations for glucose, insulin, and GDR were strongest with visceral fat mass. Adipose tissue lipid uptake, measured after oral administration of labeled oleic acid in triglyceride, was approximately 50% higher in omental than in subcutaneous adipose tissues. Adipocytes from omental fat also showed a higher lipolytic sensitivity and responsiveness to catecholamines. Furthermore, these adipocytes were less sensitive to the antilipolytic effects of insulin. Both lipid uptake and lipolytic sensitivity and responsiveness showed strong correlations (r = 0.8 to 0.9) to blood glucose and plasma insulin concentrations and also to the GDR (negative), while no such correlations were found with lipid uptake in subcutaneous or retroperitoneal abdominal adipose tissues. Taken together, these results suggest a higher turnover of lipids in visceral than in the other fat depots, which is closely correlated to systemic insulin resistance and glucose metabolism in men.

Abdomen↗