Current state of treatment of carcinoma of the oesophagus and gastro-oesophageal junction. Clinical review.
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Adenocarcinoma↗
Biomedical subjects
L Olbe
Publications and source records attributed to L Olbe.
Evaluation of propranolol for prevention of recurrent bleeding from esophageal varices between sclerotherapy sessions.
Forty-one patients admitted with first episode of bleeding from esophageal varices were enrolled in a trial of the efficacy of oral propranolol to prevent rebleeding during the course of endoscopic sclerotherapy until obliteration. Single-blind randomization to sclerotherapy alone or with propranolol was used. At monthly endoscopy the varices were injected with 1% Aethoxysclerol until obliteration. If bleeding recurred, additional sclerotherapy was given. There was no intergroup difference in time to eradication of varices (8.1 vs. 7.7 months). The cumulative number of bleedings from varices and from distal esophageal ulcerations was identical in the two study groups. Five patients in the control group but only one in the propranolol group died of bleeding in the study period, a difference of only borderline significance (chi 2 = 4.08, df = 1). There were no specific side effects of propranolol. Thus propranolol did not significantly reduce the frequency of rebleeding until variceal obliteration, but could have had some influence on the gravity of rebleeding.
Esophageal and Gastric Varices↗
Alterations in body composition after gastroplasty for morbid obesity.
Body compositional changes during rapid weight loss and after weight stabilization were prospectively studied in morbidly obese patients undergoing gastroplasty operations. Body composition was studied preoperatively and 6 and 24 months postoperatively in 23 patients by use of a total body counter (40K) and an isotope dilution technique. The mean fat mass, cell mass, and intracellular water (ICW) decreased during the first 6 months (p less than 0.001) and remained unchanged at the 24-month test. However, the mean liters of extracellular water (ECW) did not change. Consequently, the ECW/ICW ratio, high in states of malnutrition, rose above postoperative levels. A strong correlation was found between decreases in cell mass and increases in the ECW/ICW ratio.
Adult↗
[Reflux esophagitis--new diagnostic and therapeutic methods].
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Esophagitis, Peptic↗
Metabolism of adipose tissue in intraabdominal depots of nonobese men and women.
Adipocyte size, lipoprotein lipase (LPL) activity, and the lipolytic response to noradrenaline and isoproterenol were studied in three intraabdominal depots (mesenteric, omental, retroperitoneal), as well as in subcutaneous abdominal adipose tissue, in nonobese groups of middle-aged men and in premenopausal and postmenopausal women. Subcutaneous adipocytes were larger than intraabdominal adipocytes in all groups. The men had large adipocytes in all intraabdominal depots as compared with the women. The premenopausal women seemed to have low LPL activity in intraabdominal depots. Two types of responses to catecholamine-stimulated lipolysis were observed: a similar response from mesenteric and omental (portal) fat depots and from retroperitoneal and subcutaneous abdominal (nonportal) fat depots. Young women had higher lipolysis in nonportal than in portal adipose tissues. In the men the reverse characteristics were found. These dissimilarities seem to be based on differences in beta-adrenergic responsiveness. Postmenopausal women showed no differences between depots. The differences in lipolytic responsiveness between these groups might be caused by sex steroid hormones.
Abdomen↗
Influence of age, fat cell weight, and obesity on O2 consumption of human adipose tissue.
The oxygen consumption of human adipose tissue (AT) was determined in 53 adults, lean and obese, and in nine lean boys. The oxygen consumption was positively related to fat cell weight and negatively to age and degree of obesity. Men and women did not differ with respect to oxygen consumption of AT. The positive relationship between oxygen consumption per cell and fat cell size was also demonstrated in size-separated cells from the same donors. Expressed per cell the oxygen consumption was higher in fat cells from obese than in cells from lean subjects, but expressed per gram of tissue the opposite result was found. The oxygen consumption of the total AT organ was higher in obese than in lean subjects. The energy expenditure of AT constituted approximately 4% of the estimated 24-h energy expenditure in both groups. It is concluded that obese subjects do not maintain their obesity because of a reduced energy expenditure of the total AT (or of the total body). After a partial weight reduction in five subjects, the energy metabolism tended to change in direction toward the conditions seen in lean subjects. However, it is still an open question whether the observed energy metabolic aberrations of obese human AT are only secondary to the obese state or partly primary and thus of etiological importance.
Adipose Tissue↗
Simultaneous measurement of gastric acid and bicarbonate secretion in man.
Experiments were performed to validate the computerized pH/PCO2 technique for measurement of HCO3 secretion at a physiologic pH in the human stomach. In bench-side experiments the system detected 103 +/- 2% (mean +/- SE, n = 66) of boluses or infusions of NaHCO3. The standard curve was linear in the physiologic concentration range, and in the pH interval from 1.8 to 6.9 the recovery rate of added HCO3 was independent of the pH of the aspirate. In vivo the recovery rate of an exogenous NaHCO3 infusion (240 mumol/15 min) was 95 +/- 5% (n = 9), and there was no significant correlation between basal gastric pH and recovery rate. The results support that our computerized gastric perfusion method can be used for quantification of gastric bicarbonate secretion also at a physiologic acid pH.
Bicarbonates↗
Effect of omeprazole on gastric acid secretion and plasma gastrin in man.
Single doses of omeprazole inhibit pentagastrin-stimulated gastric acid secretion and almost complete inhibition can be achieved for 4-6 hours with a single dose of 80 mg. Acid secretion then slowly returns and reaches normal levels after 3-4 days. Omeprazole also dose-dependently inhibits basal acid secretion as well as acid secretion stimulated with histamine, peptone and modified sham feeding, with similar efficiency. During repeated once-daily dosing with an enteric-coated granule capsule formulation, inhibition of acid secretion increased initially, and stabilized within about 4 days. Dose-response studies in patients with duodenal ulcers and healthy subjects have shown that 20-40 mg/day results in a peak reduction (80-100%) of pentagastrin-stimulated acid secretion 6 hours after dose. Studies of 24-hour intragastric acidity in duodenal ulcer patients have shown that 4 weeks of treatment with omeprazole, 20 mg once daily, resulted in a reduction of median intragastric acidity by 97%, which was superior to the 57% median reduction achieved with ranitidine, 150 mg b.d., for 4 weeks in the same patients. During omeprazole treatment, fasting plasma gastrin increased in relation to the degree of inhibition of acid secretion. After discontinuation of treatment, plasma gastrin normalized. Treatment with omeprazole, 20 mg, increased 24-hour plasma gastrin to the same extent as after highly selective vagotomy. Long-term treatment with omeprazole, 20-40 mg, for up to 2 years has not been associated with any progressive rise in fasting plasma gastrin.
Dose-Response Relationship, Drug↗
Studies of the release of gastrin from the human duodenum induced by gastrin-releasing peptide.
In the present study the influence of duodenal exclusion and vagotomy on basal release of gastrin from extra-antral stores has been investigated in addition to the consequences of these procedures on the gastrin response to gastrin-releasing peptide (GRP) infusion. Basal gastrin concentrations and the response to GRP were measured in seven patients after a Whipple operation, in seven patients after antrectomy combined with selective gastric vagotomy and B I reconstruction, in seven patients operated on with antrectomy, selective gastric vagotomy, and Roux-en-Y reconstruction, and finally in seven patients after antrectomy, truncal vagotomy, and Roux-en-Y reconstruction. Gastrin was measured by a highly specific radioimmunoassay. Very low concentrations were obtained after a Whipple operation, and no increase followed GRP infusion. The basal gastrin concentrations were slightly higher in antrectomized patients, irrespective of whether a selective gastric vagotomy had been added. However, in these patients a significant gastrin response followed GRP infusion. Duodenal exclusion seemed not to influence the response to GRP. On the other hand, extragastric vagotomy was followed by low gastrin concentrations in the basal state and only a marginal response to GRP administration. These results strongly suggest that GRP releases gastrin from the human duodenal mucosa and that duodenal exclusion does not alter the response of the duodenal gastrin cells to GRP stimulation. Vagal denervation of the duodenal mucosa seems to suppress the gastrin response to GRP, indicating an excitatory influence of the vagus nerve.
Adult↗
Palliative endoscopic dilatation in carcinoma of the esophagus and esophagogastric junction.
The palliative effect of repeated endoscopic dilatation of malignant strictures of the esophagus and esophagogastric junction was prospectively evaluated in 41 patients. Dilatation was performed with Eder-Puestow technique in brief general anesthesia. Substantial improvement in swallowing ability was experienced after each treatment. The dysphagia recurred, however, and the dilatations were repeated at intervals of about 4 weeks. Most patients required less than or equal to three treatments during their remaining lifespan. There were few complications, the most prominent being perforation (in 5% of 128 sessions). Only short hospital stay was required, and 18 patients remained at home during the periods between dilatations. Endoscopic dilation of the esophagus and esophagogastric junction gives good palliation. The technique is simple, cheap and safe. It is suitable for lesions at any site, not time-consuming, available at almost all endoscopy units, and consequently to be recommended in this clinical setting.
Adenocarcinoma↗
Effect of omeprazole on gastric acid secretion and plasma gastrin.
Omeprazole represents a new class of gastric acid inhibitors, which inhibits the H+, K(+)-ATPase in the secretory membrane of the parietal cell. Single oral doses inhibited pentagastrin stimulated acid secretion with an ED50 of 27 mg. Almost complete inhibition could be achieved with a single dose of 80 mg. Acid secretion then slowly returned and reached normal levels after 3-4 days. Omeprazole also inhibited basal, histamine peptone and vagally stimulated acid secretion with similar potency. For clinical use omeprazole has been formulated as enteric coated granules. During repeated once daily dosing with this formulation the degree of acid suppression increased over the first days after the start of treatment but stabilized within about 4 days. Dose-response studies in both DU-patients and healthy subjects have shown that daily doses of 20-40 mg result in 80-100% reduction of stimulated acid secretion when measured 6 h after dose. Due to the long duration of action the inhibition was still 50-80% when measured 24 h after dose. Studies of 24 h intragastric acidity in DU-patients have shown that once daily treatment with 20 mg omeprazole results in a reduction of intragastric acidity by 97% which in the same study was superior to the 57% reduction caused by treatment with ranitidine, 150 mg twice daily. During omeprazole treatment, plasma gastrin increased in relation to the degree of acid suppression. The level of increase of 24 h plasma gastrin during once daily treatment with 20 mg omeprazole was slightly higher than for ranitidine, 150 mg twice daily, but similar to that seen after highly selective vagotomy.
Dose-Response Relationship, Drug↗
Long-term follow up of patients with Zollinger-Ellison syndrome (ZES).
We have followed 14 patients with the Zollinger-Ellison syndrome for a median period of 9 years. All patients have suffered from peptic ulcer disease and six of the 14 have had complications such as bleeding or perforated ulcer. Almost half the patients have had diarrhoea as a dominant symptom and 4 patients suffered from multiple endocrine neoplasia. Before 1978, the year when the H2-receptor antagonists were introduced, the majority of the patients were operated with total gastrectomy. After that year there has been no need for gastrectomies, but all but two patients have undergone an explorative laparotomy. We have been able to localize the gastrinoma in 9 of 12 operated patients; in 7 cases it was localized within the gastrinoma triangle. Three of the patients are considered to have been cured after surgery. Eight patients have needed adjuvant acid-reducing medical therapy. Five of these have been failures to high doses of H2-receptor antagonists and have been successfully treated with omeprazole. Five patients have died during the follow-up period and death in two of these cases was related to tumor progression.
Aged↗
Comparative potency of carbachol, sham feeding, fundic distension and 16,16-dimethyl prostaglandin E2 as stimulants of human gastric bicarbonate secretion.
Six healthy subjects in random order underwent gastric bicarbonate secretion investigations, including stimulation with increasing doses of the cholinergic agonist carbachol, sham feeding, fundic distension and gastric instillation of 16,16-dimethyl prostaglandin E2. Bicarbonate secretion was measured by a computer-based system which continuously recorded pH and PCO2 of the effluent in a high-volume gastric perfusion system. The peak 30 min gastric bicarbonate output in response to carbachol, 150 mg subcutaneously, was 114% (P less than 0.05). Vagal stimulation by sham feeding resulted in a corresponding increase of 112% (P less than 0.05), while fundic distension to a volume of 600 ml gave an increase of 114% (P less than 0.05). In comparison, the response to 80 micrograms 16,16-dimethyl prostaglandin E2 was much greater, the peak bicarbonate output being increased by 245% (P less than 0.05). Both sham feeding and fundic distension appear to be either submaximal stimuli of gastric bicarbonate secretion in man or may possess both stimulatory and inhibitory actions.
16,16-Dimethylprostaglandin E2↗
Reflex sympathetic activation in humans is accompanied by inhibition of gastric HCO3- secretion.
The study was performed to determine whether the sympathetic nervous system contributes to the reflex control of gastric HCO3- secretion in humans. Gastric HCO3- secretion was registered by a computerized technique based on measurements of pH and PCO2 in gastric effluent. To minimize formation of CO2 in the stomach, subjects were pretreated with the H2-receptor blocker ranitidine. Compensations were made for HCO3- of nongastric origin. As indicators of cardiovascular sympathetic activity, we measured heart rate, forearm vascular resistance, and plasma catecholamine concentrations. In one series of experiments, peripheral sympathetic activity was enhanced by the application of a negative pressure around the lower part of the body (lower body negative pressure, LBNP), at a rate sufficient to induce a slight decrease in systemic arterial pressure. In another series of experiments, peripheral sympathetic activity was inhibited by elevation of the legs, a procedure that simulates volume loading by redistributing blood volume toward the central circulation. LBNP at -20 mmHg decreased systolic pressure and pulse pressure and significantly increased heart rate, forearm vascular resistance, and plasma catecholamine levels. All these effects were observed in the first 15-min period of LBNP and were well maintained throughout the 45-min observation period. LBNP also inhibited basal gastric HCO3- secretion rate in seven of eight individuals, but this response was slower in onset with a latency of at least 15 min. Elevation of the legs increased pulse pressure and decreased forearm vascular resistance. Catecholamines were not measured in these experiments. Gastric HCO3- secretion tended to increase, but the magnitude of the response was highly variable.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Relationship between reduction of gastric acid secretion and plasma gastrin concentration during omeprazole treatment.
We have studied the relationship between reduction of gastric acid secretion and fasting plasma gastrin concentrations during once daily omeprazole treatment. Healthy subjects were given omeprazole for 5 days in daily doses of 5, 10, 20, 40, or 80 mg. Acid secretion and fasting gastrin concentration were measured 6 h (maximal omeprazole effect) and 24 h (minimal omeprazole effect) after the fifth omeprazole dose. Omeprazole in doses lower than 20 mg daily did not suppress pentagastrin-stimulated acid secretion in all subjects 6 h after dosing on the 5th day. Doses of 20-80 mg omeprazole, however, significantly reduced acid secretion 24 h after the fifth dose, the range being 36-76%. A relationship between degree of acid inhibition and fasting gastrin concentration was observed. However, acid secretion needed to be reduced by more than 80% before gastrin levels were clearly affected. This degree of acid inhibition was only achieved 6 h after administration of omeprazole in doses of 20 mg and higher. The inhibitory effect of omeprazole on acid secretion decreased 24 h after dosing. Thus, fasting gastrin concentrations were moderately increased in the beginning and normalized at the end of each 24-h period during treatment with daily doses of 20-80 mg omeprazole.
Adult↗
A criterion for completeness of vagotomy based on basal and vagally stimulated gastric acid secretion after esophagectomy or proximal gastric vagotomy.
The variation in basal acid secretion was determined in 10 patients after resection of the esophagus, an operation resulting in a total transection of all vagal nerves to the abdomen. After recording basal acid secretion over a 3-h period, a 15-min modified sham feeding procedure was performed, and the acid output was studied for an additional hour. The mean basal acid output +2 SD was 0.27 mmol/15 min. The difference between the highest and lowest recorded 15-min output--that is, the oscillation of basal acid output--was calculated for each patient. The mean oscillation of basal acid output +2 SD was 0.58 mmol/15 min. Vagal stimulation accomplished by sham feeding produced no significant increase in acid output above this level. The variation in basal acid secretion was also investigated in 20 duodenal ulcer patients after proximal gastric vagotomy. These patients were insulin-negative and remained asymptomatic during a 7- to 10-year follow-up study. Shortly after the vagotomy, measurement of basal acid secretion over 3 h showed a mean basal acid output +2 SD of 0.58 mmol/15 min. The mean oscillation of basal acid output +2 SD was 0.66 mmol/15 min. On the basis of the oscillation in basal acid secretion after complete vagotomy we propose a new criterion for completeness of vagotomy, namely a response to physiologic vagal stimulation which does not exceed the lowest basal level by more than 0.6 mmol/15 min.
Adult↗
The pentagastrin-induced gastric acid response in humans.
The pentagastrin-induced acid response, alone and versus different doses of cimetidine, was studied in humans. The inhibitory effect of the histamine H2-receptor antagonist cimetidine could only in part be counteracted by increasing doses of pentagastrin. The maximal gastric acid response was significantly decreased by cimetidine, and the ED50 values for pentagastrin showed a minor but still statistically significant increase, indicating both a competitive and a non-competitive inhibition by cimetidine of pentagastrin-induced gastric acid secretion. The pA2 characterization of the receptor mediating the pentagastrin-induced gastric acid response gave a value of 6.2, compared with the pA2 value of the human H2 receptor of 6.1. This suggests that the pentagastrin-induced gastric acid response in humans is mediated via the histamine H2-receptor.
Adult↗
Intestinal function after total gastrectomy and possible consequences of gastric replacement.
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Aged↗