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The objective of this study was to gain insight into the hormonal responses to enteral nutrition in critically ill newborns requiring venoarterial extracorporeal membrane oxygenation (ECMO) by analyzing plasma gut hormone levels of gastrin, cholecystokinin and peptide‐YY in relation to enteral nutrition. In 24 consecutive neonates treated with venoarterial ECMO intestinal hormone secretions were determined by radioimmunoassay at 2‐day intervals. Twelve received parenteral nutrition only. In 12 enteral nutrition was introduced later. The findings in these patients were compared with those of 16 measurements in eight non‐ECMO treated age‐matched controls. Mixed model analysis of variance was used for statistical analysis. Concentrations of gastrin, cholecystokinin and peptide‐YY were significantly higher in ECMO patients receiving enteral nutrition compared with ECMO patients who received parenteral nutrition (62, 3.8 and 59.4 pmol/L versus 46, 3.1 and 34.7 pmol/L, respectively). Overall, plasma hormone levels did not differ from those in age‐matched controls. Intestinal hormone levels showed normal responses after introduction of enteral feeding, comparable with those in age‐matched controls without ECMO. These results do not provide an argument for withholding enteral nutrition even in the most severely ill neonates on venoarterial ECMO.

The objective of this study was to gain insight into the hormonal responses to enteral nutrition in critically ill newborns requiring venoarterial extracorporeal membrane oxygenation (ECMO) by analyzing plasma gut hormone levels of gastrin, cholecystokinin and peptide-YY in relation to enteral nutrition.

Gallbladder volume, determined by ultrasonography (US) using the sum-of-cylinders (SOC) method, is tedious and time-consuming. We therefore examined whether ellipsoid (ELL) or area-length (A-L) methods, which are easier to perform, could reliably replace the SOC method. Fasting gallbladder volume and emptying were determined according to these 3 methods in 20 normal subjects and 20 gallstone patients. Excellent correlations were found but the ELL method yielded significantly larger mean volumes and the A-L method revealed significantly smaller volumes than the SOC method. Analysis of differences between methods revealed a considerable lack of consistency. Volumes according to the ELL method were 35 percent larger to 46 percent smaller for normal subjects and 34 percent larger to 41 percent smaller for gallstone patients than volumes according to the SOC method. Volumes according to the A-L method were 35 percent larger to 15 percent smaller for normal subjects and 51 percent larger to 17 percent smaller for gallstone patients. Maximal decrement of gallbladder volume in ml and in percentage according to the 3 different methods did not differ. Regardless of the method used, both fasting and minimal gallbladder volumes were significantly larger in gallstone patients than in normal subjects, whereas maximal decrement of gallbladder volume in ml and percentage was not different. The present study indicates that the SOC method remains the method of choice for US determination of gallbladder volume for scientific purposes.

The increased risk of gallstone formation in acromegalics treated with the somatostatin analog octreotide has been related to an impaired gallbladder emptying. To determine the duration of these inhibitory effects, meal-stimulated gallbladder motility, plasma cholecystokinin (CCK), and pancreatic polypeptide (PP) were measured in five acromegalics treated for 6–32 months with 200–300 µg octreotide daily. Meal tests were performed 45 min, 8 hr and two weeks after the last 100-µg subcutaneous dose. Results were compared with those in normal subjects. Integrated postprandial gallbladder contraction (-125±194 cm3/120 min) and integrated PP secretion (-0.1±0.2 nmol/liter/120 min) were completely suppressed in the 45-min study, but significantly improved (P<0.05) when measured 8 hr (1376±322 cm3/120 min and 3.0±1.0 nmol/liter/120 min) and two weeks (1437±263 cm3/120 min and 10.6±1.6 nmol/liter/120 min) after the last dose of octreotide. The integrated gallbladder contraction in acromegalics at 8 hr was comparable to that at two weeks and to that in normal subjects, but the integrated PP response at 8 hr was significantly smaller (P<0.05 vs two weeks and vs normals). Integrated plasma CCK secretion at 45 min (0.13±0.06 nmol/liter/120 min) was not statistically significantly different from the response at 8 hr (0.15±0.02 nmol/liter/120 min) and from that in normal subjects, but it was significantly increased at two weeks after cessation of octreotide (P<0.05 vs 45 min and 8 hr). In conclusion, during long-term octreotide treatment in acromegalics, initial abolishment of postprandial gallbladder emptying is completely reverted to normal values 8 hr after the last subcutaneous dose. No major differences in postprandial plasma CCK at 45 min and at 8 hr were observed when compared with normal subjects, whereas plasma PP responses were diminished.

A pharmaco-epidemiologic study in hospitalized patients was carried out in order to establish the place and use of omeprazole (Losec®), a new and promising drug in the treatment of acid-related diseases. A comparison is made with cimetidine and ranitidine use. It appeared that prescribed omeprazole doses were high in relation to the established defined daily doses and that substitution of H2 receptor antagonists by omeprazole led to tremendously increased drug costs. From the clinical indication data it could be established that the drug was prescribed appropriately.

Background: This study evaluates the effect of eradicating Helicobacter pylori on basal and bombesin-stimulated gastric acid secretion and serum gastrin in non-ulcer dyspepsia. Methods: Before and 1 month after an attempt to eradicate H. pylori basal and bombesin-stimulated gastric acid outputs were measured in 23 patients. H. pylori was eradicated in 15 patients (group A) but not in the other 8 (group B). Incremental gastric acid output was calculated by subtracting basal from bombesin-stimulated values. Results: Basal acid output increased significantly (p = 0.01) after therapy in group A (Δ 1.6 ± 0.6 mmol/h) but not in group B (Δ0.2 ± 0.5 mmon). Incremental gastric acid output decreased distinctly (Δ-3.9 ± 1.4mmol/h) after therapy in group A (p = 0.02) but not in group B (Δ-2.2 ± 1.7mmol/h). Basal serum gastrin decreased significantly (p < 0.005) after therapy in group A (Δ -9 ± 4 pM) but not in group B (Δ-1 ± 2pM). Integrated serum gastrin responses to bombesin decreased markedly (p < 0.001) after therapy in group A (Δ-5.0 ± 1.6 nM60min) but slightly in group B (Δ-0.9 ± 1.3nM60min) (p < 0.05). Conclusions: In patients with non-ulcer dyspepsia basal serum gastrin concentrations decrease but basal gastric acid outputs increase after eradication of H. pylori. Bombesin-induced increments in gastric acid output, however, decrease in parallel with gastrin release.

To determine the relation between pancreatic morphology and pancreatic exocrine and endocrine function, we have studied 8 adult cystic fibrosis patients and 14 normal control subjects by ultrasonography and pancreatic function testing. In the patients with cystic fibrosis the maximum anteroposterior diameter of the pancreatic head was significantly increased over that in control subjects (p < 0.01), whereas the maximum diameter of the body was significantly decreased (p = 0.05). Increased echogenicity of the pancreatic body was observed in most patients. In the cystic fibrosis patients postprandial insulin secretion was reduced in the 1st h (p < 0.005 versus control), whereas pancreatic polypeptide secretion was virtually abolished for at least 3 h (p < 0.01 versus control). All cystic fibrosis patients had evidence of exocrine pancreatic dysfunction as reflected by a diminished urinary para-aminobenzoic acid excretion. Intraduodenal enzyme and bicarbonate output in response to secretin-cholecystokinin was reduced in all of three patients studied. It is concluded that loss of endocrine and exocrine pancreatic function in adult cystic fibrosis patients is accompanied by a small and echo-dense pancreatic body relative to a large pancreatic head.

1. In patients with cystic fibrosis, abnormalities in plasma cholecystokinin level and gall-bladder emptying may contribute to the development of maldigestion and gall-stones. 2. Therefore, we have measured plasma cholecystokinin levels and gall-bladder volumes before and after ingestion of a standard breakfast in eight adult patients with cystic fibrosis and in eight normal control subjects. 3. In the patients with cystic fibrosis basal (2.8 ± 0.4 pmol/l; P < 0.05, t-test) and maximum post-prandial (5.7 ± 0.5 pmol/l; P < 0.05, t-test) plasma cholecystokinin levels were significantly higher than those in the control subjects (1.9 ± 0.1 pmol/l, and 4.5 ± 0.2 pmol/l, respectively). On the other hand, integrated plasma cholecystokinin secretion in response to the meal was similar (t-test, P = 0.4 versus control subjects). The increased plasma cholecystokinin levels in the patients with cystic fibrosis were accompanied by reduced gallbladder volumes in both the basal (7.8 ± 2.1 cm3 versus 20.9 ± 2.3 cm3 in control subjects; P < 0.005, t-test) and the post-prandial state (2.2 ± 1.0 cm3 versus 4.8 ± 0.8 cm3 in control subjects; P = 0.06, t-test). Gall-bladder emptying in the patients with cystic fibrosis was well preserved (70 ± 7% versus 78 ± 9% in control subjects; P = 0.4, t-test). 4. In comparison with normal control subjects, patients with cystic fibrosis have an increased basal plasma cholecystokinin level and a reduced gall-bladder volume, whereas post-prandial gall-bladder emptying and plasma cholecystokinin secretion are not significantly different. In cystic fibrosis, neither impaired cholecystokinin release nor impaired gall-bladder emptying appear to play a role in the pathogenesis of either gall-stones or maldigestion.

This study compared a severity of illness system (APACHE II) and a 10% random sample of charts in terms of their ability to identify cases with quality problems. Using condition-specific data bases of 337 pneumonia, 363 acute myocardial infarction and 266 hip fracture charts, severity of illness information was used to separate cases into those with a high and a low likelihood of a poor outcome. Cases with low admission severity of illness combined with subsequent death were flagged as potential quality problems. Physician evaluation was used as the gold standard to measure flag performance. Flags were tested against a 10% random sample drawn from within the three condition-specific data bases. Analyses focused on a combination of sensitivity and positive predictive value. The low severity plus death flag performed much better than a 10% random sample approach, suggesting that outcomes monitoring flags based on severity of illness could play an important role in screening cases for potential quality problems.

On the basis of the observation that patients occasionally develop symptoms suggesting vagal damage after surgery for gastro-oesophageal reflux disease (GORD), we have studied the pancreatic polypeptide (PP) secretion in response to hypoglycaemia, as indicator of vagus nerve function, in 24 patients with Nissen fundoplication, in 9 non-operated patients with severe GORD, in 6 patients with truncal vagotomy, and in 20 normal control subjects. All subjects had a plasma glucose trough of less than 2.5 mmol/l after intravenous injection of 0.1 U/kg insulin. In the normal subjects plasma PP increments ranged from 94 to 730 pM. Seven of 24 (29%) patients with Nissen fundoplication (p < 0.05), all 6 patients with truncal vagotomy (p< 0.001), but none of the non-operated patients with GORD had plasma PP responses to insulin hypoglycaemia below the lowest value in the control subjects. It is concluded that patients with Nissen fundoplication often have an abnormal plasma PP response to insulin hypoglycaemia. Although this abnormality is most likely due to vagal damage during surgery, prospective studies are needed to elucidate the exact mechanism and to establish the clinical significance of this finding.

The radioimmunologic determination of cholecystokinin (CCK) has proved to be notoriously difficult. This is due to the specificity of antibodies, preparation of radiolabeled CCK and low CCK concentrations in human plasma. About 10 years ago we succeeded in developing two highly sensitive region-specific radioimmunoassays for CCK. Antibody T2M binds to the sulfated tyrosine region of CCK, while antibody 1703 reacts with biologically active molecular forms of CCK containing at least 14 amino acid residues. Both antibodies are devoid of significant cross-reaction with gastrin. By means of these two radioimmunoassays CCK concentrations were measured in both tissue and plasma of various species, including man. In addition, the molecular forms of CCK in tissue and plasma were characterized. These CCK assays were used to study the mechanism of CCK secretion. It appeared that digested rather than intact protein and fat stimulated CCK release from the small intestine. The physiologic and pathophysiologic role of CCK in humans was studied using CCK radioimmunoassays and specific CCK-receptor antagonists. CCK was found to play an important role in pancreatic enzyme secretion, gallbladder contraction, and gastrointestinal motility but possibly also in pancreatic carcinogenesis and regulation of satiety and satiation.

The effect of intragastric dextrose on albumin-stimulated cholecystokinin (CCK) release was studied in five healthy subjects and was related to gastric emptying and pancreatobiliary secretions. When combined with low concentrations of dextrose (4 g/100 ml), a 500-ml solution of albumin (7 g/100 ml) was rapidly emptied from the stomach into the duodenum (T1/2: 35 min). This rapid gastric emptying resulted in an only transient stimulation of pancreatobiliary secretion and an integrated CCK release of 278±45 pM × 180 min. When the concentration of dextrose in the albumin solution was increased from 4 g/100 ml to 21 g/100 ml, gastric emptying rate was distinctly slower (T1/2: 78 min;P<0.01) and pancreatobiliary secretions became sustained (P<0.01). CCK release was markedly higher (900±421 pM × 180 min;P<0.05) after ingestion of the solution containing a high dextrose concentration. Intraduodenal infusion of 21 g/100 ml dextrose (3.1 ml/min) failed to significantly stimulate plasma CCK levels (119±38 pM × 120 min). We suggest that the higher CCK release in response to intragastrically administered albumin solution containing high concentrations of dextrose may have been induced by augmented peptic digestion of albumin due to delayed gastric emptying and by increased enteral digestion of albumin due to increased pancreatobilary outputs.

Background: Cholestyramine enhances gallbladder emptying and plasma cholecystokinin responses to oral ingestion of a mixed meal. It is not known whether this effect occurs independently of alterations in gastric emptying or maldigestion of nutrients. Methods: We perfused 15 g of an amino acid meal intraduodenally for 60min in seven healthy volunteers, once with and once without cholestyramine. Intraduodenal perfusion of saline with or without cholestyramine (6 g/h) was started 60 min before the amino acid meal and continued for 2 h. Results: Cholestyramine markedly enhanced the incremental plasma cholecystokinin response to the meal from 36 ±12 to 139 ± 25 pmol/1 60 min (P < 0.005), incremental amylase output from 2.4 ± 0.7 to 5.7 ± 0.7 kU/h (P < 0.05), and incremental integrated gallbladder contraction from1948 ± 235 to 2840 ± 189% 60 min (P < 0.05). Conclusion: The enhancing effect of cholestyramine on postprandial gallbladder contraction, pancreatic enzyme secretion, and plasma cholecystokinin release is not dependent on gastric emptying rates or appropriate digestion of nutrients.

Gallbladder volume, determined by ultrasonography (US) using the sum-of-cylinders (SOC) method, is tedious and time-consuming. We therefore examined whether ellipsoid (ELL) or area-length (A-L) methods, which are easier to perform, could reliably replace the SOC method. Fasting gallbladder volume and emptying were determined according to these 3 methods in 20 normal subjects and 20 gallstone patients. Excellent correlations were found but the ELL method yielded significantly larger mean volumes and the A-L method revealed significantly smaller volumes than the SOC method. Analysis of differences between methods revealed a considerable lack of consistency. Volumes according to the ELL method were 35 percent larger to 46 percent smaller for normal subjects and 34 percent larger to 41 percent smaller for gallstone patients than volumes according to the SOC method. Volumes according to the A-L method were 35 percent larger to 15 percent smaller for normal subjects and 51 percent larger to 17 percent smaller for gallstone patients. Maximal decrement of gallbladder volume in ml and in percentage according to the 3 different methods did not differ. Regardless of the method used, both fasting and minimal gallbladder volumes were significantly larger in gallstone patients than in normal subjects, whereas maximal decrement of gallbladder volume in ml and percentage was not different. The present study indicates that the SOC method remains the method of choice for US determination of gallbladder volume for scientific purposes.

The effect of ingestion of 50 g fat, 50 g protein, and 50 g starch on plasma cholecystokinin (CCK) concentrations was studied in eight healthy volunteers. Plasma CCK concentrations were measured by radioimmunoassay with Bolton-Hunterlabelled CCK 33, CCK 33 standard, and antibody T204. Antibody T204 was directed to the sulphated tyrosine region of CCK. Ingestion of fat and protein induced significant increases in plasma CCK, whereas ingestion of starch did not significantly influence plasma CCK levels. Peak increments in plasma CCK after fat (4.8 ± 0.9 pmol/l) and protein (3.4 ± 0.5 pmol/l) were significantly greater than that after starch (0.9 ± 0.3 pmol/1). Similarly, the integrated plasma CCK secretion after fat (213 ± 49 pmol/1.120 min) and after protein (178 ± 53 pmol/1.120 min) was significantly greater than that found after ingestion of starch (9 ± 23 pmol/1.120 min). It is concluded that, in contrast to starch, fat and protein are potent stimuli for the release of CCK.