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Biomedical subjects

L A Christiansen

Publications and source records attributed to L A Christiansen.

At least 19 recordsLinked to original sources
PubMed1988

Peptic ulcer complications and how to treat them.

The main complications to peptic ulcer are perforation, stenosis and bleeding. Diagnosis and treatment are discussed with special reference to the principles of 1st Department, Kommunehospitalet, Copenhagen. The three main complications to peptic ulcer disease include perforation, stenosis and bleeding. The etiology to peptic ulcer disease and the pathogenesis of ulcer disease complications are still poorly understood, although an imbalance between mucosa-protecting and -destructing factors seems to be of major importance. However, the introduction of neither H2 receptor antagonists nor the so-called mucosaprotection agents during the seventies and eighties significantly have reduced the frequency of peptic ulcer disease or the frequency of its complications (perforation 10 per cent, stenosis 10 per cent and bleeding 20 per cent of patients with peptic ulcer disease. The unchanged frequency of operation for peptic ulcer complications was confirmed in a recent study by A. Christensen et al. 1987. Their data suggested unchanged frequency of operations for ulcer complications prior to and following the introduction of H2 receptor antagonists (Fig. I and II) in a well defined population in Copenhagen.

Humans↗
PubMed1987

Gastrin and partial gastrectomy in duodenal ulcer patients 25 years postoperatively.

Serum gastrin concentrations were measured in 26 patients (Group A) who underwent partial gastrectomy for duodenal ulcer disease at least 25 years previously. The basal serum gastrin level was 31.6 +/- 1.5 pg/ml, increasing significantly after food stimulation to 36.8 +/- 2.4 pg/ml (p less than 0.05). In 16 of these patients (Group B), endoscopic biopsy specimens were taken from the minor and major curvatures of the stomach, from the jejunal part of the gastrojejunostomy, and from the duodenum. Mucosal gastrin concentrations measured were 0, 20.4 +/- 3 ng/g, and 30 +/- 7.1 ng/g, respectively. Ten of these patients (Group C) had a repeated gastroscopy with food stimulation of the duodenal pouch, using a balloon catheter in the lower duodenum. Serum gastrin concentrations after pouch stimulation did not differ significantly compared with basal values. No changes in the mucosal gastrin concentrations during pouch stimulation were seen. In conclusion, since no gastrin could be detected in the gastric mucosa and the mucosal gastrin concentration in the duodenum was 50 times lower than reported in other studies, the gastrin release measured after food stimulation could have been of extragastric or extraduodenal origin.

Aged↗
PubMed1987

Parietal cell density in duodenal ulcer patients after short-term treatment with cimetidine and antacids.

In a prospective study, 20 patients with endoscopically proven duodenal ulcers were randomised to be treated with cimetidine 1 g daily or with antacids 350 mmol daily. The duration of treatment was 30 days, but this was extended to three months in 3 patients in the cimetidine group and 4 patients in the antacid group. A morphological study of biopsies taken via a gastroscope from the corpus mucosa showed no change in mucosal height, parietal cell density per unit volume or changes in cellular infiltration after 30 and 90 days treatment in the two groups. Neither H-2 receptor blockers nor antacids alter mucosal height or parietal cell density. Treatment was not found to induce gastritic changes in the mucosa.

Adult↗
PubMed1987

Effect of intragastric pH on antral gastrin and somatostatin release in anaesthetised, atropinised duodenal ulcer patients and controls.

The synchronous change in the antral release of gastrin and somatostatin into a vein draining the stomach was studied during acidic and alkaline intragastric pH in six anaesthetised duodenal ulcer patients and six controls after atropinisation. No differences in the basal secretion of gastrin and somatostatin were observed among the two groups. Alkaline as well as acidic intragastric pH had no effect on the antral release of somatostatin in duodenal ulcer patients and controls. In contrast, alkaline intragastric pH was associated with a significantly higher antral gastrin release in duodenal ulcer patients than in controls. Acidic intragastric pH was associated with a significantly smaller inhibition of antral gastrin release in duodenal ulcer patients than in controls. These results suggest that atropinised anaesthetised duodenal patients release gastrin abnormally in the presence of acidic or alkaline intragastric pH and that any inverse relationship between antral gastrin and somatostatin release is uncoupled under these conditions.

Adult↗
PubMed1985

Fibrin adhesive sealing of ureter after ureteral stone surgery. A controlled clinical trial.

In a prospective randomized study 8 patients were peroperatively allocated to closure of ureterotomies with a fibrin adhesive (Tisseel) and 8 patients to closure with Dexon sutures to evaluate whether the duration of postoperative urinary leakage could be diminished by the use of fibrin adhesive. The median drainage period was 6.5 days (range 3-15 days) and 5.5 days (2-16 days), respectively. Closure of ureterotomies with a fibrin adhesive cannot be recommended.

Adult↗
PubMed1984

The metabolism of gastrin-34, gastrin-17, and gastrin-14 in the isolated perfused pig liver.

The degradation of porcine and human gastrin-34, -17, and -14 in the isolated pig liver was investigated in 13 perfusion experiments. The concentrations of gastrins in the perfusate were measured by radioimmunoassay, and the molecular nature was determined by gel chromatography. Gastrin-34 was neither eliminated nor converted to other molecular forms, whereas gastrin-17 and -14 were both degraded in the liver, gastrin-17 being degraded to measurable smaller forms during the process. It is suggested that the liver plays an important part in the regulation of circulating gastrins.

Animals↗
PubMed1983

Causes and clinical significance of gastritis following Billroth II resection for duodenal ulcer.

Billroth II resection was carried out in 1000 duodenal ulcer patients in the period 1948-1956. Twenty-two to thirty years later, gastroscopy and biopsy was performed in 196 of 423 survivors. Chronic atrophic gastritis appeared in 93 per cent of the cases, 47 per cent showed slight and 46 per cent severe changes. Seven per cent had normal mucosa. The microscopic grade of gastritis proved to be independent of age, alcohol and tobacco consumption and serum gastrin. No correlation between clinical status, such as dumping, diarrhoea, vomiting and pain, haematological parameters and the microscopic grade of gastritis, could be found. It is suggested that gastritis might be caused by reflux of bile, pancreatic and intestinal juices, and that postgastrectomy symptoms and anaemia do not depend on the microscopic grade of gastritis.

Adult↗
PubMed1983

Hepatic elimination of femoxetine in pig.

Hepatic elimination of femoxetine was studied in seven anaesthetized 40 kg pigs by means of constant rate infusions of 3-41 mg/min. (8.6-118 mumol/min.) into the portal vein. The elimination followed saturation kinetics (Michaëlis-Menten constants: Vmax 12 mg . min.-1 . kg-1 liver; Km 1.3 mg . 1-1 blood) and was characterised by high hepatic extraction, due to metabolism. The hepatic output of the active metabolite, nor-femoxetine, was very low, indicating that other metabolic pathways than demethylation were more important in the pig. The high hepatic elimination in the pig corresponds to the high first pass effect, earlier found in man, and it depends upon the infusion rate as well as the total dose.

Animals↗
PubMed1983

Gastrin production following antrectomy. A study on the occurrence of gastrin-producing cells and the serum gastrin response to feeding.

Fifteen patients were studied 3 to 35 years after antrectomy, with a gastroduodenal (Billroth I (BI)) anastomosis in 8, and a gastrojejunal (Billroth II (BII)) anastomosis in 7. The investigations included gastric acid secretion, serum gastrin response to feeding and immunohistochemical search for gastrin-producing cells in gastric remnant mucosal biopsies. All of the patients had hypochlorhydria. The gastrin response to feeding was minimal. Apart from a significantly higher value of serum gastrin 3 hours post-prandial in BI operated as compared to BII operated patients, no greater differences were found in the gastrin production between the two groups of patients. No gastrin-producing cells could be identified in the gastric remnant, not even in areas of pseudopyloric metaplasia. It is concluded that the gastrin production following antrectomy is caused by extragastric G-cells; these cells are poorly stimulated by food, and do not respond to hypochlorhydria with hypergastrinaemia.

Aged↗
PubMed1982

N-Terminal sequences of pig intestinal sucrase-isomaltase and pro-sucrase--isomaltase. Implications for the biosynthesis and membrane insertion of pro-sucrase--isomaltase.

The hog sucrase-isomaltase complex is anchored to the small-intestinal brush border membrane, as in the rabbit, via a hydrophobic segment located in the N-terminal region of the isomaltase subunit. The immediate precursor of the 'final' sucrase-isomaltase (i.e., pro-sucrase-isomaltase as prepared from adult hogs whose pancreas had been disconnected from the duodenum) is an amphiphilic single polypeptide chain of Mr 260000-265000. Its N-terminal sequence is virtually identical with (not merely homologous to) the corresponding region of the isomaltase subunit of 'final' sucrase-isomaltase. This shows that the isomaltase portion of pro-sucrase-isomaltase is the N-terminal 'half' of the precursor polypeptide chain. Thus the succession of domains in pro-sucrase-isomaltase and its mode of anchoring in the membrane could be deduced. On this basis a likely mechanism of biosynthesis and insertion is proposed.

Amino Acid Sequence↗
PubMed1982

The antral gastrin-producing cells and tissue gastrin in duodenal ulcer patients.

Morphometric estimation of the antral G-cells, radioimmunoassay estimation of the antral tissue gastrin, estimation of the antral mucosal volume and gastric acid secretion have been carried out on 10 duodenal ulcer patients. The total antral tissue gastrin varied from 52.4 to 245.1 micrograms and the mean G-cell gastrin from 0.5 to 1.8 pg. No constant relationship was found between G-cell densities and antral gastrin concentration, suggesting that no constant relationship exists between G-cell numbers and G-cell function. Furthermore, no constant relationship was observed between total antral gastrin and acid secretion.

Adult↗
PubMed1982

Hepatic elimination of endogenous gastrin in pigs.

To assess hepatic elimination of gastrin, concentrations of gastrin were determined radioimmunochemically in plasma samples collected simultaneously in six pigs from the portal vein, hepatic vein, and a peripheral artery before and after stimulation of the antrum with meat extract. The portal plasma flow and the total plasma volume were measured. During meat extract stimulation the antral release of gastrin increased significantly (p less than 0.05), from 15.9 +/- 3.4 ng/min to 35.6 +/- 5.4 ng/min, and the hepatic elimination increased significantly (p less than 0.05), from 10.4 +/- 2.8 ng/min to 25.5 +/- 5.9 ng/min (mean +/- S.E.M., six pigs). The artery to mesenteric vein concentration ratio was 1.03 +/- 0.05 in the basal and 0.97 +/- 0.10 in the stimulated period, indicating neither release nor uptake of gastrin in the intestines of five pigs. Hepatic elimination of gastrin was roughly proportional to the gastrin concentrations in portal venous plasma. The mean hepatic plasma clearance of gastrin was 148 +/- 26 ml/min and the total body clearance 268 +/- 43 ml/min. Thus extrasplanchnic gastrin removal accounted for half of total body elimination. It is concluded that in anesthetized pigs the "first-pass" effect on portal gastrin content makes the liver one of the important sites for elimination of endogenous gastrin.

Animals↗
PubMed1981

Hypotension during and after operation in glucocorticoid-treated patients.

The frequency and likely aetiology of systemic arterial hypotension occurring either during or following operation, in patients receiving steroids was analysed retrospectively. Hypotension occurred during surgery in 29 of 250 operations. Although patients receiving steroids until shortly before operation appeared more likely to develop hypotension during operation the differences were eliminated when allowance was made for the severity of the disease. In almost half of the instances of hypotension during surgery there was no adequate explanation. Hypotension occurred after surgery on eight occasions; there was one case of acute adrenocortical insufficiency, six of various types of circulatory failure and in one the cause as uncertain.

Adolescent↗