Biomedical subjects

J B Jansen

Publications and source records attributed to J B Jansen.

At least 235 records · Page 13Linked to original sources

PubMed1989

Gastric emptying after partial gastrectomy without vagotomy with primary Roux-en-Y or Billroth II anastomosis.

Several clinical studies have indicated that gastric emptying is delayed in patients with Roux-en-Y biliary diversion with vagotomy. In order to determine whether Roux-en-Y diversion without vagotomy also induces delayed gastric emptying, we have compared the effect of gastrectomy without vagotomy with either Billroth II or Roux-en-Y anastomosis on gastric emptying of a liquid and solid meal in 22 peptic ulcer patients. The emptying half-times (t1/2) for solid food were not significantly different, 54; 24-122 min (median and range) in the 11 patients with Billroth II gastrectomy, 68; 44-189 min in the 11 patients with Roux-en-Y gastrectomy, and 83; 27-114 min in 11 normal control subjects. However, the lag phase was significantly (p less than 0.01) shorter in the patients with Billroth II gastrectomy (5; 0-43 min) and Roux-en-Y gastrectomy (4; 2-12 min) than in the control subjects (10; 4-22 min). The t1/2's for the fluid meal were similar, 7; 4-49 min after Billroth II gastrectomy, 8; 4-32 min after Roux-en-Y gastrectomy, and 9; 3-20 min in the control subjects. In all subjects the lag phase for the fluid meal was very short, ranging from 0 to 3 min. It is concluded that Roux-en-Y diversion per se does not delay gastric emptying in man.

Anastomosis, Roux-en-Y↗

PubMed1989

Role of the gastric phase in fat-induced gallbladder contraction and cholecystokinin secretion in humans.

The present study was undertaken to investigate the role of the gastric phase of fat-induced gallbladder contraction and endogenous cholecystokinin (CCK) secretion in humans. Gallbladder emptying, measured by cholescintigraphy, and endogenous CCK secretion, measured by radioimmunoassay, were studied in healthy subjects after both intragastric and intra-intestinal administration of corn oil. In addition, patients with partial gastrectomy were investigated to study the effect of accelerated gastric emptying. In the healthy subjects, intragastric administration of fat resulted in a significantly (P less than 0.05) later increase in plasma CCK levels (20 +/- 2 min) compared to intraintestinal fat (5 +/- 1 min). Similarly, the onset of gallbladder emptying was significantly (P less than 0.05) delayed after intragastric fat (20 +/- 2 min) compared to intestinal fat (10 +/- 1 min). In the healthy subjects the integrated plasma CCK response to intragastric fat was significantly (P less than 0.005-P less than 0.01) reduced from 10 to 30 min. In the patients with partial gastrectomy the rise in plasma CCK (10 +/- 1 min) and the onset of gallbladder emptying (15 +/- 2 min) were in the same range after intra-intestinal and intragastric fat. No significant differences in plasma CCK levels, integrated CCK response or gallbladder emptying were found in the patients according to the site of fat application. It is concluded that endogenous CCK secretion and gallbladder emptying in response to intragastric fat are significantly delayed in healthy subjects but not in patients with partial gastrectomy, in whom gastric emptying is accelerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Prospective comparative study of the influence of postoperative bile reflux on gastric mucosal histology and Campylobacter pylori infection.

Biopsies of 17 peptic ulcer patients, randomly treated by partial gastrectomy with either Billroth-II (n = 9) or Roux-en-Y (n = 8) anastomosis were studied before and six months after surgery to determine the role of bile reflux in the early postoperative histological alterations of the gastric mucosa. After BII-gastrectomy bile acid reflux (median 16.1 mumol/h) was significantly higher (p less than 0.0001) than after RY-gastrectomy (0.1 mumol/h). Campylobacter pylori was present in the preoperative biopsies of all 17 patients. After RY-gastrectomy biopsies of all eight patients were positive for Campylobacter pylori, but was detected in only five of the nine patients with BII-gastrectomy. Preoperative scores of gastritis grading were similar in both groups and no significant differences were found postoperatively. Gastritis scores of the anastomotic mucosa in patients with BII-gastrectomy were significantly higher (p less than 0.02) than in the RY-gastrectomy group. Moreover, the reflux gastritis score in the four BII-gastrectomy patients cleared from Campylobacter pylori was significantly higher (p less than 0.02) than in the postgastrectomy patients harbouring Campylobacter pylori. The results suggest that reflux gastritis and Campylobacter pylori related gastritis are distinct microscopic entities and that bile reflux may play a role in the eradication of Campylobacter pylori after gastrectomy.

Anastomosis, Roux-en-Y↗

PubMed1989

Reversible gall bladder dysfunction in severe pancreatic insufficiency.

The present study was undertaken to examine the intestinal phase of cholecystokinin (CCK) secretion and gall bladder contraction in patients with severe pancreatic insufficiency. Plasma CCK concentrations, measured by radioimmunoassay, and gall bladder contraction by cholescintigraphy were studied in response to intraduodenal fat with and without addition of pancreatic enzymes. Fasting plasma CCK concentrations were in the same range in six patients with pancreatic insufficiency with (2.6 (0.2) pmol/l) and without (2.6 (0.3) pmol/l) addition of pancreatic enzymes and in six healthy subjects (2.0 (0.4) pmol/l). The integrated plasma CCK secretion in response to intraduodenal fat was significantly (p less than 0.005) reduced in the patients without addition of enzymes (46 (13) pmol/1.90 min) compared with healthy subjects (199 (22) pmol/1.90 min), but increased significantly (p less than 0.01) by the addition of pancreatic enzymes (174 (25) pmol/1.90 min) to values not significantly different from healthy subjects. Similarly, gall bladder emptying in response to intraduodenal fat was significantly (p less than 0.01) reduced in patients with pancreatic insufficiency without addition of enzymes (at 90 min: 35 (11)%) compared with healthy subjects (at 90 min: 66 (7)%) but significantly (p less than 0.01) increased by addition of pancreatic enzymes (at 90 min: 70 (8)%) to values not significantly different from healthy subjects. These results indicate that patients with severe pancreatic insufficiency have impaired gall bladder emptying after intraduodenal fat, which can be normalised by the addition of pancreatic enzymes. This impaired gall bladder emptying appears to be the result of a reduced plasma CCK response. Thus, intra-intestinal pancreatic enzymes play an important role in the intestinal phase of CCK secretion and gall bladder emptying.

Adult↗

PubMed1989

Simultaneous measurement of gallbladder emptying with cholescintigraphy and US during infusion of physiologic doses of cholecystokinin: a comparison.

Both ultrasonography (US) and cholescintigraphy are used to study gallbladder dynamics. The present study was undertaken to determine whether the two methods provide the same or different information relating to gallbladder emptying. Emptying was simultaneously studied with both methods during infusion of graded physiologic doses of cholecystokinin (CCK) in six healthy subjects. Infusion of stepwise increasing doses of CCK, ranging from 0.03 to 0.5 Ivy dog units per kilogram of body weight per hour (IDU/kg.h), induced significant dose-related increases in plasma CCK, decreases in gallbladder volume assessed with US, and gallbladder emptying assessed with cholescintigraphy. The threshold dose for inducing significant gallbladder emptying was 0.13 IDU/kg.h, as determined with both techniques, indicating similar detection limits. There was a highly significant correlation between decreases in gallbladder volume and decreases in radioactive counts over the gallbladder region, with a tendency toward greater gallbladder responses at sonography during the early phase of gallbladder contraction and toward greater responses at cholescintigraphy during the later phase of gallbladder contraction. It is concluded that these methods can be used interchangeably for the quantitation of gallbladder emptying.

Adult↗

PubMed1989

Cholinergic regulation of PP release is mediated through muscarinic M1-receptors.

The effects of the selective muscarinic M1-receptor antagonist pirenzepine and the nonselective muscarinic antagonist atropine on bombesin- and peptone-stimulated release of pancreatic polypeptide (PP) were studied in healthy subjects. To exclude any effect of changes in intraduodenal pH continuous intragastric titration was performed during all tests. Both pirenzepine (i.v. bolus 0.6 mg/kg) and atropine (i.v. bolus 15 micrograms/kg, followed by an infusion of 5 micrograms/kg.h) significantly reduced peptone-induced integrated mean rise of plasma PP from 28 +/- 5 to 8 +/- 4 and -2 +/- 5 pmol/l, respectively (n = 4). Both drugs also reduced bombesin-induced rise of plasma PP in all 4 subjects, from 27 +/- 12 to 6 +/- 4 and 7 +/- 1 pmol/l (0.05 less than p less than 0.1). It is concluded that cholinergic regulation of PP release is mediated mainly through muscarinic M1-receptors.

Adult↗

PubMed1989

Prospective study of the effect of gastrectomy with and without bile reflux on serum pepsinogens.

In order to prospectively determine the effect of gastrectomy with or without enterogastric reflux on serum pepsinogen concentrations, serum pepsinogen A, serum pepsinogen C and the pepsinogen A:C ratio were measured before, and 10 days and 6, 15 and 24 months after 2/3-3/4 distal gastrectomy in peptic ulcer patients with primary Roux-en-Y diversion (n = 11) or Billroth II reconstruction (n = 11). Gastrectomy induced early decreases in serum pepsinogen A from 100 +/- 12 to 66 +/- 7 micrograms/l (p less than 0.05) and from 111 +/- 11 to 82 +/- 20 micrograms/l (p = 0.05), serum pepsinogen C from 49 +/- 6 to 29 +/- 5 micrograms/l (p less than 0.05) and from 54 +/- 9 to 40 +/- 11 micrograms/l (p = 0.10) in patients with Roux-en-Y and Billroth II gastrectomy, respectively, but did not influence the pepsinogen A:C ratios. Serum pepsinogen A and the pepsinogen A:C ratio continued to decrease 6 months after surgery but no further significant reductions were observed 15 and 24 months postoperatively. Serum pepsinogen C concentrations did not significantly change during postoperative follow-up. Analyses of variances of serum pepsinogen A and the pepsinogen A:C ratio showed that the type of operation had no significant effect on the postoperative course. It is concluded that gastrectomy leads to early decreases in serum pepsinogen A and pepsinogen C levels followed by progressive further reductions of serum pepsinogen A and the pepsinogen A:C ratio for a period of 6 months postoperatively. These postoperative changes of serum pepsinogens are not due to increased enterogastric biliary reflux.

Atrophy↗

PubMed1989

Omeprazole in the treatment of Zollinger-Ellison syndrome and histamine H2-antagonist refractory ulcers.

Omeprazole is a very potent and long-acting inhibitor of gastric acid secretion. These characteristics make the drug very suitable for the management of gastric acid hypersecretion and symptom relief in patients with the Zollinger-Ellison syndrome, and in the treatment of patients with ulcers resistant to histamine H2-receptor antagonists. Most patients require only a once-daily dose, whereas in about 30% of patients with Zollinger-Ellison syndrome the dose has to be split. During long-term treatment the required dose of omeprazole is usually rather stable. Up until now neither in patients with Zollinger-Ellison syndrome nor in those with resistant ulcers have convincing reports of resistance to omeprazole been published. However, a relative disadvantage of omeprazole is the observation that symptom-free Zollinger-Ellison syndrome patients are less inclined to undergo the work-up for surgery, which is the only possible curative treatment for these patients. Omeprazole therapy has been well tolerated and no side effects, significant changes in laboratory variables or toxicity have been noted.

Drug Administration Schedule↗

PubMed1989

Omeprazole in the short-term treatment of reflux oesophagitis.

Studies with short-term administration of omeprazole in patients with erosive or ulcerative reflux oesophagitis have demonstrated that strong inhibition of gastric acid secretion will become the therapy of choice for these patients. However, because reflux oesophagitis relapses rapidly when short-term treatment is discontinued, these patients are candidates for maintenance treatment. In most cases, long-term treatment will also require strong inhibition of gastric acidity. Until more information on the long-term safety of strong inhibition of gastric acid secretion is available, this therapeutic option should preferably be restricted to those patients who do not respond appropriately to other therapeutic regimens. Future studies are needed to determine whether higher doses of histamine H2-receptor antagonist are equally efficacious as omeprazole in ulcerative oesophagitis and whether profound acid inhibition is also needed to alleviate reflux symptoms in patients with an intact oesophageal mucosa.

Drug Administration Schedule↗

PubMed1989

Postprandial gallbladder motility during long term treatment with the long-acting somatostatin analog SMS 201-995 in acromegaly.

The effects on gallbladder motility of long term treatment with the somatostatin analog SMS 201-995 (SMS) were studied in five patients with acromegaly treated for 6-32 months with 200-300 micrograms SMS daily. SMS (100 micrograms) or placebo was injected sc 45 min before a standard breakfast. Gallbladder volume (ultrasonography), plasma cholecystokinin (CCK), and pancreatic polypeptide (PP) were measured until 120 min after the meal. SMS completely suppressed the postprandial gallbladder contraction, despite a blunted, though still statistically significant, increase in plasma CCK from 1.6 +/- 0.2 pmol/L to an average of 3.7 +/- 1.7 pmol/L (P less than 0.01). The postprandial plasma PP peak after placebo was replaced by a slight but statistically significant decrease after SMS (P less than 0.05). A statistically significant correlation between the plasma CCK values and corresponding gallbladder volumes was seen only after placebo injection, not in the SMS study. We conclude that during long term treatment of acromegalics with SMS, an injection of 100 micrograms, sc, completely abolishes gallbladder contraction for at least 2 h after a standard breakfast, despite blunted, but still significant, CCK release. The data suggest a decreased sensitivity of the gallbladder to endogenous CCK during long term treatment with SMS. Careful control of patients with respect to the formation of gallstones is recommended.

Acromegaly↗

PubMed1989

Radioimmunoassay of human pepsinogen A and pepsinogen C.

We describe the development of radioimmunoassays to measure both human pepsinogen A and pepsinogen C concentrations in serum. The antibodies were raised in goats by immunization with purified pepsinogen A or C. The affinity constants of the respective antibodies were 20.10(10) l/mol and 7.10(10) l/mol. Pepsinogens A and C were labeled with Na 125I by the chloramine T method. The binding between labels and antibodies was inhibited by 0.50 at 0.82 ng pepsinogen A per tube and 2.1 ng pepsinogen C per tube. The detection limits of the assay of pepsinogen A and C were 0.12 microgram/l and 1.8 micrograms/l, respectively. Pepsinogen A and C were purified and added to a patient serum, showing a good recovery in the radioimmunoassays. Serial dilution of another patient serum, which contained a high concentration of both antigens, showed curves parallel to the standard curves. The intra- and interassay variations of these radioimmunoassays were evaluated. The intra-assay coefficients of variation for pepsinogen A were found to vary from 0.03 to 0.102 at concentrations in serum in the normal range, while the inter-assay coefficient of variation ranged from 0.118 to 0.194 at the same concentrations in serum. For the pepsinogen C radioimmunoassay we found intra-assay coefficients of variation between 0.126 and 0.147 at concentrations in serum in the normal range, while the inter-assay coefficient of variation ranged from 0.174 to 0.325 for the same sera. In 201 blood donors we found a mean serum concentration of pepsinogen A of 59 micrograms/l and a mean serum concentration of pepsinogen C of 15 micrograms/l. There was a significant relationship between these values (r = 0.779, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Achlorhydria↗

PubMed1989

Crossover study on effects of duct obliteration, celiac denervation, and autotransplantation on glucose- and meal-stimulated insulin, glucagon, and pancreatic polypeptide levels.

In segmental-pancreas transplantation the body and tail of the pancreas are used. In an experimental study in dogs, the effects of sequentially conducted removal of the right pancreatic lobe (pancreatic head), duct obliteration, celiac denervation, and autotransplantation were studied according to a crossover design. Two groups of dogs were studied. In both groups the right lobe of the pancreas was removed at primary operation, and the duct of the transected left lobe (body and tail) was injected with fibrin sealant. The left lobe was completely freed from surrounding tissue (celiac denervation) in group 1 (n = 9), and the innervation of the left lobe was left intact in group 2 (n = 8). At 12 wk, two dogs in group 1 and four dogs in group 2 underwent successful autotransplantation of the left lobe. Pancreatic hormone secretion was stimulated by intravenous glucose injection and test-meal administration before primary operation and at 11 and 18 wk thereafter. The combination of removal of the right lobe and duct obliteration led to a decrease in glucose tolerance at both stimulation tests and a decrease in peripheral insulin release after intravenous glucose injection. At test-meal administration, no change in insulin and glucagon levels was demonstrated. If celiac denervation was added, similar results were obtained based on the understanding that the peripheral insulin release after the test meal was significantly elevated. Meal-stimulated pancreatic polypeptide response was abolished in both groups. Removal of the right lobe leads to parasympathic denervation of the left lobe, and celiac denervation mainly interferes with alpha-adrenergic innervation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Use of omeprazole in the management of reflux oesophagitis resistant to H2-receptor antagonists.

Severe reflux oesophagitis, which is resistant to treatment with high doses of H2-receptor antagonists, can be treated successfully with the H+,K+-ATPase inhibitor omeprazole. Experience from more than 3 years of continuous treatment with omeprazole, in doses adjusted to prevent recurrences, has demonstrated its high efficacy in the long-term management of the patients. The use of this drug emphasizes the importance of long-standing, effective, 24-hour acid inhibition for reflux oesophagitis. Fasting gastrin levels increase 2-fold during the initial treatment period but continued treatment does not induce any further elevation. Omeprazole does not induce pathological changes in the endocrine cell population of the gastric oxyntic mucosa, though in some patients an increase in the argyrophilic cell volume density during omeprazole treatment has been reported. Careful surveillance of the safety profile of this drug is continuing.

Esophagitis, Peptic↗

PubMed1989

Contribution of partial pancreatectomy, systemic hormone delivery, and duct obliteration to glucose regulation in canine pancreas. Importance in pancreas transplantation.

Our aim was to isolate and determine the contribution of partial pancreatectomy, systemic delivery of pancreatic hormones, and duct obliteration to glucose regulation after segmental pancreas transplantation in dogs. Fasting, postprandial, and intravenous glucose-stimulated glucose, insulin, glucagon, pancreatic polypeptide (PP), and cholecystokinin (CCK) and intravenous bombesin-stimulated PP levels were studied in beagles at three successive intervals in a crossover design. The first was 6 wk after partial (approximately 70%) pancreatectomy with intact regular enteric exocrine drainage from the duodenal pancreatic remnant, the next was 2 wk after venous transposition with systemic delivery of pancreatic hormones, and the third was 6 wk after in situ duct obliteration of the remnant. With partial pancreatectomy, K values were modestly diminished (30%), and a concomitant reduction of second-phase intravenous glucose-stimulated insulin release was observed. Other parameters were not significantly affected. Venous transposition doubled peripheral plasma levels of insulin under all conditions. Fasting glucose, PP, and CCK levels decreased slightly. Other parameters were not affected. Duct obliteration of the systemic draining pancreatic remnants seriously impaired glucose sensitivity, resulting in a 50% reduction of K values and fasting and sustained postprandial hyperglycemia (approximately 8 mM) and a 70-50% reduction (acute and overall responses, respectively) of intravenous glucose-stimulated insulin. Fasting hormone and postprandial insulin, glucagon, and CCK levels were not affected. The postprandial PP response was severely reduced, and bombesin-stimulated PP release was abolished by duct obliteration. We conclude that histological changes associated with duct obliteration are the major determinants of glucose regulation in segmental pancreas transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Delayed plasma cholecystokinin and gallbladder responses to intestinal fat in patients with Billroth I and II gastrectomy.

This study was undertaken to examine the intestinal phase of cholecystokinin (CCK) secretion and gallbladder contraction in patients who had undergone partial gastrectomy. Plasma CCK concentrations, measured by radioimmunoassay, and gallbladder contraction, measured by cholescintigraphy, were studied after intestinal administration of fat. Fasting plasma CCK concentrations were in the same range in nine patients who had undergone Billroth I gastrectomy (1.0 +/- 0.2 pmol/L), in nine patients who had undergone Billroth II gastrectomy (1.4 +/- 0.2 pmol/L), and in nine normal subjects (1.5 +/- 0.4 pmol/L). The peak increments in plasma CCK after intestinal fat were significantly (p less than 0.05) lower in patients with partial gastrectomy (5.4 +/- 0.6 pmol/L) compared with normal subjects (7.9 +/- 0.8 pmol/L). The integrated plasma CCK secretion was significantly (p less than 0.01 to p less than 0.05) reduced during the first 30 minutes in patients after Billroth I (74 +/- 11 pmol/1.30 min) and Billroth II gastrectomy (51 +/- 11 pmol/1.30 min) compared with normal subjects (122 +/- 18 pmol/1.30 min). Similarly, the start of gallbladder emptying was significantly (p less than 0.05) delayed in patients after partial gastrectomy. After 1 hour, however, the integrated plasma CCK response and gallbladder emptying were in the same range in Billroth I patients (186 +/- 34 pmol/1.60 min, 60% +/- 7%), Billroth II patients (175 +/- 17 pmol/1.60 min, 63% +/- 7%) and normal subjects (190 +/- 18 pmol/1.60 min, 55% +/- 6%). It is concluded that in patients who have undergone partial gastrectomy plasma CCK and gallbladder responses to intestinal fat are significantly delayed but reach normal levels beyond 30 minutes.

Adult↗

PubMed1989

Pancreatic secretory response to intravenous caerulein and intraduodenal tryptophan studies: before and after stepwise removal of the extrinsic nerves of the pancreas in dogs.

In two sets of 6 dogs with gastric and pancreatic fistulas, we studied the effect of atropine (14 nmol/kg.h i.v.) on the pancreatic secretory response to intravenous caerulein and to intraduodenal perfusion with tryptophan (both given with a secretin background) before and after stepwise removal of the extrinsic nerves of the pancreas, i.e., celiac and superior mesenteric ganglionectomy alone or truncal vagotomy alone and truncal vagotomy plus celiac and superior mesenteric ganglionectomy. Atropine significantly (p less than 0.05) depressed the protein output in the basal state and in response to secretin at each stage of innervation. The incremental protein response to caerulein was not altered by the various denervation operations nor by atropine. Truncal vagotomy alone significantly decreased the incremental protein response to low (0.12, 0.37, and 1.1 mmol/h) but not high loads of tryptophan. Ganglionectomy in combination with vagotomy did not further depress the incremental protein response to low loads of tryptophan. Atropine significantly reduced the incremental protein response to low loads of tryptophan only in intact innervated animals. Ganglionectomy alone did not alter the incremental protein response to any load of tryptophan. Ganglionectomy, truncal vagotomy, and atropine did not alter basal or tryptophan-stimulated levels of plasma cholecystokininlike immunoreactivity. We conclude that (a) neither the extrinsic nor the intrinsic cholinergic pancreatic nerves modulate the protein response to caerulein; (b) the sympathetic pancreatic nerves do not mediate the response to tryptophan; (c) the protein response to intraduodenal tryptophan is at least in part mediated by long, cholinergic, enteropancreatic reflexes with both afferent and efferent fibers running within the vagus nerves; and (d) release of cholecystokinin by intestinal tryptophan is not under cholinergic or splanchnic control.

Animals↗

PubMed1989

Prospective comparison of gastric secretory function after gastrectomy with either Billroth II or Roux-en-Y anastomosis.

In order to delineate the role of enterogastric reflux in changes of postoperative gastric secretory functions, 22 patients with peptic ulcers, who were randomly assigned to partial gastrectomy without vagotomy with either Billroth II or Roux-en-Y anastomosis, were prospectively studied before and 6 months after surgery. Preoperatively, there were no significant differences in gastric secretory functions between the two groups of 11 patients. Postoperatively, median fasting bile acids in the stomach increased in the Billroth II patients from 0.35 to 16.10 mumol/hr (p less than 0.01), but significantly decreased in the Roux-en-Y patients from 0.30 to 0.10 mumol/hr (p less than 0.05), which indicated adequate prevention of enterogastric reflux after the Roux-en-Y procedure. Gastrectomy resulted in significant reductions of median values of basal acid output (4.6 vs 0.6 mmol/hr, p less than 0.01, and 4.2 vs 0.4 mmol/hr, p = 0.02), peak acid output (31.6 vs 4.2 mmol/hr, p less than 0.01, and 38.7 vs 4.5 mmol/hr, p less than 0.01), serum pepsinogen A (121 vs 86 micrograms/L, p less than 0.01, and 92 vs 45 micrograms/L, p less than 0.01), meal-stimulated serum gastrin secretion (1472 vs 199 pM.60 min, p less than 0.0001, and 1017 vs 199 pM.60 min, p less than 0.0001) in the patients with Billroth II and Roux-en-Y anastomosis, respectively. There were, however, no significant differences in gastric secretory parameters between the two groups when studied 6 months after surgery. Therefore it is concluded that after gastrectomy, enterogastric reflux does not affect the secretory function of the gastric remnant within the first 6 months after surgery.

Anastomosis, Roux-en-Y↗

PubMed1988

Decreased gastrin secretion in patients with late-onset hypogammaglobulinemia.

We undertook this study to determine whether patients with late-onset hypogammaglobulinemia, who are at very high risk for gastric cancer, have a reduced secretion of gastrin after stimulation with food or bombesin, a potent gastrin-releasing stimulus. We compared the plasma gastrin responses to bombesin and to a standard test meal in 18 patients with late-onset hypogammaglobulinemia with those in patients with X-linked agammaglobulinemia, early-onset hypogammaglobulinemia, or hypogammaglobulinemia due to lymphoproliferative cancer, and in 30 normal control subjects. Thirteen of 18 patients with late-onset hypogammaglobulinemia (72 percent) had an abnormally low gastrin response to bombesin, as compared with none of 21 patients with other forms of hypogammaglobulinemia (P less than 0.05). After a test meal, abnormally low gastrin secretion was found in 6 of 14 patients with late-onset hypogammaglobulinemia (43 percent) and in 1 of 18 patients with other forms of the disease (6 percent) (P not significant). The plasma gastrin responses to stimulation with bombesin or food distinguished late-onset hypogammaglobulinemia from other forms, with sensitivities of 72 and 43 percent and specificities of 100 and 94 percent, respectively. Stimulated gastrin response can therefore be used as a marker for this type of immunodeficiency. The test responses also showed heterogeneity among patients with late-onset hypogammaglobulinemia and may help to identify patients with an increased risk for gastric cancer.

Adolescent↗