gastrins and Pyloric-Stenosis

Pyloric stenosis (PS) has no known cause. A testable theory of cause is proposed, based on the inheritance of a parietal cell mass (PCM) at the upper end of the normal range. It is proposed that, until 3-4 wk of age, the obligatory high fasting gastrins are at maximal levels and not able to be diminished by increasing antral acidity. Hence, rising acidity is not reduced by a lowered gastrin during this time, and very high acidity occurs.. Persisting duodenal hyperacidity is created by an inherited high PCM and loss of gastrin control. These two factors produce pyloric stenosis through work hypertrophy from repeated pyloric contraction in response to hyperacidity.

Topics: Gastric Acid; Gastric Acidity Determination; Gastrins; Histamine H2 Antagonists; Humans; Infant; Parietal Cells, Gastric; Pyloric Stenosis

A theory is advanced about the cause of pyloric stenosis of infancy (PS). Developmental changes will conspire to produce pathogenetic gastric hyperacidity within the first 4 weeks of life in babies who develop PS. The prime cause will be an increased gastric acidity due to a genetically determined supernormal parietal cell mass. This theory satisfactorily explains many known clinical features.

Topics: Age Factors; Female; Gastric Acid; Gastrins; Humans; Infant; Infant, Newborn; Male; Parietal Cells, Gastric; Pyloric Stenosis; Risk Factors; Time Factors

Topics: Bombesin; Calcium; Eating; Gastric Emptying; Gastrins; Gastrointestinal Hormones; Histamine H2 Antagonists; Humans; Kidney Failure, Chronic; Peptic Ulcer; Pyloric Stenosis; Secretin; Vagotomy; Zollinger-Ellison Syndrome

A review of the publications on mediators of pyloric contraction, together with experimental lesions in animals, suggest that the lesions characteristic of hypertrophic pyloric stenosis in infants (hypertrophy of Torgersen's circular muscle and degenerative changes in Auerbach's myenteric plexus) are probably functional in nature. The hypothesis of a double mechanism is discussed. The primary defect would be an excess of pyloric contraction agonists, such as duodenal hormones and acetylcholine. This would be followed by self-maintenance of the lesions, where pyloric spasm and subsequent distension of the antrum would induce gastrin release with secondary stimulation of duodenal hormone release by oxyntic secretion and acidification of the duodenum.

Topics: Gastrins; Humans; Hypertrophy; Infant; Pyloric Stenosis

After reviewing the more recent acquisitions on the physiology and pathophysiology of gastrin, the authors concentrate on situations of hypergastrinemia, which they divide into a hyperhydrochloric and a hypohydrochloric variety. Among the former, which they subdivide into preoperative and postoperative, the authors discuss problems of differential diagnosis versus peptic ulcers in patients so afflicted. To that end they propose diagnostic policies comprising among other instrumental and laboratory tests the study of gastric secretion, blood gastrin levels in basal conditions and after stimulation by a protein meal, BBS, secretin, and calcium. From analysis of the results of such tests they were able to find a precise nosographic placement for postoperative hypergastrinemia, and from there they arrived at surgical programs aiming to correct postoperative peptic ulcers on the basis of their etiology and pathogenesis.

Topics: Gastrectomy; Gastrins; Humans; Hyperparathyroidism; Peptic Ulcer; Postoperative Complications; Pyloric Stenosis; Stomach Diseases; Vagotomy; Zollinger-Ellison Syndrome

Topics: Anemia, Pernicious; Calcium; Dietary Proteins; Duodenal Ulcer; Gastric Juice; Gastrins; Gastritis; Glucagon; Humans; Hyperplasia; Intestine, Small; Kidney Failure, Chronic; Pyloric Antrum; Pyloric Stenosis; Secretin; Stomach Neoplasms; Stomach Ulcer; Vagotomy; Zollinger-Ellison Syndrome

Topics: Animals; Bile Acids and Salts; Child; Child, Preschool; Cholera Toxin; Diarrhea; Diarrhea, Infantile; Gastrins; Gastroesophageal Reflux; Gastrointestinal Diseases; Gastrointestinal Hormones; Gastrointestinal Motility; Humans; Infant; Infant, Newborn; Intestinal Absorption; Intestine, Small; Intestines; Metals; Proteins; Pyloric Stenosis; Syndrome

Topics: Diarrhea; Drainage; Dumping Syndrome; Duodenal Ulcer; Female; Gallbladder; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Gastrointestinal Motility; Humans; Intestine, Small; Male; Pancreas; Peptic Ulcer Perforation; Postoperative Complications; Pyloric Antrum; Pyloric Stenosis; Pylorus; Recurrence; Stomach; Stomach Ulcer; Vagotomy

Parietal cell vagotomy has been in clinical use for 7 years in elective treatment of nonobstructive duodenal ulcer, and for even a shorter period for complicated cases and for gastric ulcer The evolution of the surgical technique has not yet come to an end and the ability to perform the procedure is still improving. It can therefore be questioned, if this operation is yet ripe for a realistic clinical trial, and the great variation in recurrence rate reported in pilot series as well as in prospective randomized clinical trials points to the possibility that we will have to wait several years before the anticipated mean recurrence rate is known. At present it can be stated that even if gastric emptying is not quite undisturbed, the addition of a drainage procedure in nonobstructive cases is unnecessary. The same may be true in some patients with pyloric obstruction. Furthermore, the mortality rate is very low and the incidence of moderate-to-severe dumping and diarrhea is virtually nil.

Topics: Animals; Clinical Trials as Topic; Denmark; Diarrhea; Drainage; Dumping Syndrome; Duodenal Ulcer; Gastric Juice; Gastrins; Gastrointestinal Motility; Humans; Peptic Ulcer; Pilot Projects; Postoperative Complications; Pyloric Stenosis; Recurrence; Stomach; Stomach Ulcer; Vagotomy

An account is given of the process by which the Primary Hyperacidity pathogenesis of Pyloric Stenosis of Infancy (PS) evolved. The initial discovery that fasting gastrins were high at birth and continued to rise within the first 4 days was the starting point. Since acidity was also rising at the same time it was proposed that the usual negative feed-back between gastrin and stomach acidity was not mature in the first few weeks of life. The gastrin model for producing PS in puppy dogs was a further incentive to believe that relatively high gastrins, and secondary high acidity would thereby repeatedly cause sphincter contraction and lead to hypertrophy. When gastrin was found to be normal in PS babies we considered and accepted, the less complicated hypothesis that a Primary Inherited Hyperacidity itself was the driving force. Such a theory explained nearly all the clinical features. When we further considered the expected consequences of an initially ineffective negative feed -back and its later maturation, the known peak acidity in neonatal development was explained. This phenomenon also provided an explanation for the remaining previously unexplained time sensitive features of the condition.

Topics: Animals; Disease Models, Animal; Dogs; Fasting; Gastrins; Humans; Hypertrophy; Infant; Pyloric Stenosis

The cause of pyloric stenosis of infancy (PS) is at present unknown. A theory of causation is proposed which is consistent with all the known clinical features of this condition. It is based on the knowledge that PS babies are hypersecretors of acid which pre-dates the development of PS and is an inherited constitutional feature. This acidity will become temporarily and dangerously high due to an insensitivity of the negative feed-back between gastrin and gastric acidy within the first few weeks of life. Normal babies who have inherited normal acidity will also experience peak acid secretions at that time but will be much less acid than babies destined to develop PS. Acid entering the duodenum causes contraction of the pyloric sphincter. Hyperacidity will naturally lead to repeated pyloric sphincter contractions and sphincter hypertrophy. Inappropriate repeated feeding of the vomiting PS baby by a first-time overanxious mother to her ever hungry baby, by provoking feed related sphincter contraction is considered to play a significant part in pathogenesis. Should the baby with PS survive beyond the age of around 6weeks, the matured negative feed-back between gastrin and acid will ensure that dangerous hyperacidity is kept in check. This coupled with the natural pyloric canal widening with age, will lead then to an long lasting cure. This theory explains satisfactorily all the known and hitherto unexplained features of this condition.

Topics: Child; Female; Gastric Acid; Gastrins; Humans; Hypertrophy; Infant; Pyloric Stenosis; Pylorus

Topics: Age Factors; Female; Gastric Acid; Gastrins; Humans; Infant; Infant, Newborn; Male; Pyloric Stenosis

Despite multiple and often contradictory research, no firm conclusions regarding the role of hypergastrinaemia in infantile hypertrophic pyloric stenosis (IHPS) have been established. Evaluation of somatostatin, the main physiological antagonist of gastrin, has not been assessed in previous studies. Long-term evaluation following pyloromyotomy suggests persistent abnormalities in gastrin and somatostatin in IHPS. The objective of this case-controlled study was to compare fasting serum gastrin and somatostatin levels in IHPS. Serum sample were collected from 39 children with IHPS at the time of pyloromyotomy and 20 age-matched controls with no evidence of gastrointestinal disease. Standard radioimmunoassay techniques were used to detect circulating levels of the hormones. A two-tailed t-test was used for statistical analysis. The levels of the two hormones (mean +/- SEM) revealed that there was no evidence of hypergastrinaemia in IHPS compared with controls (75.6 +/- 16.1 and 68.1 +/- 7.8 ng l(-1), respectively), but that the level of somatostatin was significantly elevated (38.9 +/- 6.4 and 30.5 +/- 5.8 ng l(-1), p = 0.016). An inverse trend in the gastrin/somatostatin levels could not be identified in IHPS.. Somatostatin but not gastrin is raised in IHPS. Somatostatin is known to inhibit the actions of inhibitory neurotransmitters in the pylorus and may explain the development of pylorospasm, which is believed to be important in the development of pyloric tumours. These results do not agree with a previous long-term follow-up study, but reflect the hormonal imbalance at the time of pyloric hypertrophy.

Topics: Biomarkers; Case-Control Studies; Fasting; Gastrins; Humans; Hypertrophy; Infant; Pyloric Stenosis; Somatostatin

Because somatostatin (SS) inhibits basal and stimulated gastric acid secretion and gastrin release, it is conceivable that decreased gastric SS concentration may be one of the factors responsible for hypergastrinemia found in patients formerly operated on for hypertrophic pyloric stenosis (HPS). To investigate this issue, the SS-like immunoreactivity (SLI) concentration was estimated in antral and fundic mucosal samples from control and HPS children. In addition, SS binding to cytosol from gastric mucosa (fundus and antrum), fasting serum gastrin levels, and serum gastrin response to a standard breakfast were studied. The mean fundic and antral SLI concentrations were significantly lower in HPS children than in controls. The depletion of fundic and antral SLI content was associated with an increase in the number of gastric SS binding sites. The fasting serum gastrin levels and serum gastrin responses to the standard breakfast (after 60 minutes) of HPS children were significantly higher than those of controls. Since, together with the increase of SS binding to gastric mucosa, there is an increase in the gastrin serum levels, despite the inhibitor effect of SS on gastrin release, the binding capacity cannot be the main factor determining the response to SS in children with HPS. The present results suggest that both SS and gastrin have a role in the pathogenesis of HPS.

Topics: Adolescent; Binding Sites; Child; Child, Preschool; Female; Follow-Up Studies; Gastric Fundus; Gastric Mucosa; Gastrins; Histocytochemistry; Humans; Hypertrophy; Male; Pyloric Antrum; Pyloric Stenosis; Radioimmunoassay; Somatostatin; Stomach

Pyloric stenosis produces gastric hypersecretion and is thought to stimulate the growth of the gastric mucosa in the rat, the dog, and man. However, the mechanisms behind the hypersecretion and the trophic effect of pyloric stenosis are little known. The purpose of the present study was to examine whether the postulated trophic effects described include growth of the histamine-producing enterochromaffin-like (ECL) cells and whether circulating gastrin can be held responsible.. Pyloric stenosis was produced in rats by tying a ligature around the pylorus, thereby narrowing the passage through the sphincter. The animals were left for 4 to 12 weeks.. The operation dilated the stomach, increased the serum gastrin concentration approximately twofold, and increased the oxyntic mucosal weight, volume, and surface area but not the mucosal thickness and total DNA content. The interglandular space was increased, and the DNA concentration was reduced. The density of the ECL cells (that is, the number of ECL cells per visual field) was reduced at 4 weeks and back to control values at 8 and 12 weeks. The calculated total volume of the ECL cell population was unchanged at first but showed a less than twofold increase 12 weeks after the operation. The volume density of the ECL cells (that is, the proportion of the mucosa made up of ECL cells) was reduced at 4 and 8 weeks and was back to normal at 12 weeks. The ECL cells are rich in histidine decarboxylase (HDC); whenever the cells are stimulated, the enzyme activity increases. The HDC activity in the oxyntic mucosa was reduced at first and returned to control values 12 weeks later.. Pyloric stenosis per se does not affect the total number of oxyntic mucosal cells, but causes the ECL cell population to grow somewhat, probably because of the moderate hypergastrinemia. Interestingly, however, there was no increase in the HDC activity, suggesting that the ECL cells are not much activated by the operation.

Topics: Animals; Cell Count; Disease Models, Animal; Enterochromaffin Cells; Gastrins; Gastritis, Hypertrophic; Male; Parietal Cells, Gastric; Pyloric Stenosis; Rats; Rats, Sprague-Dawley

Since somatostatin inhibits basal and stimulated gastric acid secretion and gastrin release, it is conceivable that decreased gastric somatostatin concentration may be one of the factors responsible for gastric hypersecretion found in patients who have undergone long-term pylorotomy for hypertrophic pyloric stenosis. To investigate this proposal the somatostatin-like immunoreactivity concentration was determined in antral and fundic mucosa samples from control and long-term pyloromyotomized children. In addition, somatostatin binding to cytosol from gastric (fundus and antrum) mucosa and fasting serum gastrin levels and serum gastrin response to a standard breakfast were also studied. The mean fundic and antral somatostatin-like immunoreactivity concentrations were significantly lower in long-term pyloromyotomized children than in control children. The depletion of fundic and antral somatostatin-like immunoreactivity content was associated with an increase in the number of gastric somatostatin binding sites. The fasting serum gastrin levels and serum gastrin response to a standard breakfast (after 60 min) in long-term pyloromyotomized children was significantly higher than those in control children. Since, together with the increase of somatostatin binding to gastric mucosa, there is an increase in the gastrin serum levels, despite the inhibitory effect of somatostatin on gastrin release, the binding capacity cannot be the main factor determining the response to somatostatin in long-term pyloromyotomized children. The present results suggest that both somatostatin and gastrin have some pathophysiologic importance in long-term pyloromyotomized children.

Topics: Adolescent; Binding Sites; Child; Child, Preschool; Female; Gastric Mucosa; Gastrins; Humans; Male; Pyloric Stenosis; Radioimmunoassay; Somatostatin

The effects of 4-week indomethacin administration (1mg/kg/day, orally) on gastrin cell (G-cell), somatostatin cell (D-cell) and prostaglandin E2 (PGE2) of gastric mucosa were examined in pyloric stenosis rats. As a result, pyloric stenosis rats showed hypergastrinemia, G-cell hyperplasia and D-cell hyperplasia with normal PGE2 concentration of gastric mucosa compared with sham operated rats. However, indomethacin administration completely abolished these endocrinic changes of pyloric stenosis by reducing PGE2 concentration of gastric mucosa in both fundic and pyloric regions. These results underline the importance of gastric mucosal PGE2 concentration on the proliferation of G-cells and D-cells in pyloric stenosis.

Topics: Administration, Oral; Animals; Disease Models, Animal; Gastric Mucosa; Gastrins; Indomethacin; Male; Pyloric Stenosis; Rats; Rats, Wistar; Somatostatin

To determine the effect of persistent narrowing of the gastric outlet on peptic ulcer disease, changes in gastric hormones induced by pyloric stenosis were studied in an experimental model in the rat. Pyloric stenosis was created by constricting the pylorus to a 4-mm channel. Changes in serum gastrin and plasma somatostatin concentrations, in the length of the lesser curvature, in the size of the fundic and pyloric regions, and in the G-cell and D-cell counts were determined after 4 and 8 weeks (PS4W and PS8W) and compared with those of control groups. The size of the stomach, the serum gastrin concentration, and the corrected G-cell count (indexed to stomach size) were greater in PS8W than in PS4W rats, and both were greater than in respective controls (p < 0.005). Serum somatostatin concentrations were not different, but the total D-cell count and the corrected D-cell count were higher in PS4W and PS8W rats than in controls. Moreover, the total D-cell count and the corrected D-cell count were greater in PS8W than in PS4W (p < 0.05, p < 0.005).

Topics: Animals; Cell Count; Gastric Mucosa; Gastrins; Male; Pyloric Stenosis; Rats; Rats, Wistar; Somatostatin; Stomach

We investigated the effect of 4-weeks famotidine administration (15 mg/kg/day) on gastrin cell (G-cell), somatostatin cell (D-cell) and prostaglandin E2 (PGE2) of gastric mucosa in pyloric stenosis rats. As a result, the increase of G-cell number and serum gastrin level in pyloric stenosis rats were potentiated by famotidine administration. However, the increase of D-cell number in pyloric stenosis was remarkably abolished by famotidine administration, and G/D cell ratio was increased accordingly. Moreover, famotidine administration decreased PGE2 concentration in fundic mucosa of the stomach without altering PGE2 concentration in pyloric mucosa. Our results suggested that famotidine administration in pyloric stenosis had a possibility to worsen the balance of endocrine cell kinetics in stomach, and PGE2 in fundic mucosa would play a roll on the proliferation of D-cell in pyloric stenosis.

Topics: Animals; Cell Count; Dinoprostone; Famotidine; Gastric Acid; Gastric Mucosa; Gastrins; Hydrogen-Ion Concentration; Male; Pyloric Stenosis; Rats; Rats, Wistar; Somatostatin

Topics: Child, Preschool; Follow-Up Studies; Gastrins; Humans; Hypertrophy; Infant; Infant, Newborn; Postoperative Period; Pyloric Stenosis; Time Factors

Since little is known about the pathophysiology of pyloric stenosis, we created a partial gastric outlet obstruction in 13 Wistar rats by placing a nonabsorbable ligature of defined size around the pylorus. Sham operations were performed in 10 rats. The animals from both groups were killed after four months. G-cell count and gastrin content were determined in 10 parallel strips, which were cut by razor blades mounted on a handle. Gastric size and weight as well as thickness of mucosal and muscular layers and serum gastrin concentration were also determined. Body weight of the animals with pyloric stenosis was lower and gastric weight higher than that of the controls. Furthermore, we found an enlarged G-cell area and G-cell hyperplasia, an increased surface area and thickness of the mucosal and muscular layers of the stomach, and in the majority of rats, elevated serum gastrin levels. Total G-cell count was 583,720 +/- 90,561 in the rats with pyloric stenosis and 385,775 +/- 15,820 (mean +/- SEM) in the control rats (P less than 0.04). We conclude that partial gastric outlet obstruction in rats leads to G-cell hyperplasia and that this experiment may serve as a model for pyloric stenosis in man.

Topics: Animals; Body Weight; Cell Count; Chromaffin System; Enterochromaffin Cells; Gastric Mucosa; Gastrins; Hyperplasia; Hypertrophy; Male; Organ Size; Pyloric Stenosis; Rats; Rats, Inbred Strains; Stomach

The gastrointestinal tract harbors several populations of peptide containing nerve fibers. Among the gut neuropeptides are vasoactive intestinal peptide (VIP), substance P, enkephalin, and gastrin releasing peptide (GRP). We have examined specimens from five patients with pyloric stenosis and from five controls immunocytochemically with respect to the density of nerve fibers containing VIP, substance P, enkephalin, or GRP. In the control specimens VIP and enkephalin fibers were fairly numerous, whereas substance P and GRP fibers were few. In the pyloric stenosis patients the density of VIP fibers and enkephalin fibers was reduced in the smooth muscle. In the myenteric ganglia there was no such reduction. Substance P and GRP fibers were rare as in controls. The results indicate a reduction of VIP and enkephalin fibers in smooth muscle in pyloric stenosis patients and may be interpreted to support the view that an impaired neuronal function is involved in the pathophysiology of pyloric stenosis.

Topics: Enkephalins; Female; Fluorescent Antibody Technique; Gastrin-Releasing Peptide; Gastrins; Humans; Hypertrophy; Infant; Infant, Newborn; Male; Muscle, Smooth; Nerve Fibers; Peptides; Pyloric Stenosis; Substance P; Vasoactive Intestinal Peptide

Serum gastrin levels in 16 patients with congenital hypertrophic pyloric stenosis (CHPS) were measured and oesophageal manometric studies were performed in 14 of these 16 patients before and after pyloromyotomy. Hypergastrinaemia was found in the patients with CHPS, and the 7th postoperative serum gastrin level was much higher than the preoperative pressure. However, there was no significant correlation between the LES pressure change and the serum gastrin change. These results indicate that competence of LES after pyloromyotomy in patients with CHPS is maintained not only by endogenous gastrin rise but also by other factors.

Topics: Esophagogastric Junction; Female; Gastrins; Humans; Hypertrophy; Infant; Male; Manometry; Postoperative Complications; Pyloric Stenosis

Topics: Gastrins; Gastrointestinal Hormones; Glucagon-Like Peptides; Humans; Hypertrophy; Infant; Infant, Newborn; Neurotensin; Pyloric Stenosis; Radioimmunoassay; Somatostatin

Topics: Adult; Animals; Gastrins; Humans; Hypertrophy; Infant; Infant, Newborn; Pyloric Stenosis

Topics: Adult; Female; Fetal Blood; Gastrins; Humans; Hypertrophy; Infant, Newborn; Maternal-Fetal Exchange; Pregnancy; Pregnancy Complications, Neoplastic; Pyloric Stenosis; Zollinger-Ellison Syndrome

Topics: Gastrins; Humans; Hypertrophy; Infant; Pyloric Stenosis; Radioimmunoassay

Genitourinary anomalies were looked for in patients with congenital hypertrophic pyloric stenosis. In a prospective series of 64 patients investigated by intravenous pyelography, 13 were abnormal (20.6%). In a retrospective series of 232 patients, 6 had anomalies of the upper urinary tract (2.7%). In this latter series the incidence of inguinal hernia (3.4%), undescended testes (3.0%), and hypospadias (0.9%) was determined. In another 10 patients urinary tract anomalies (5), urinary infection (2), and a significant family history (3) were found associated with congenital pyloric stenosis. As the incidence of these anomalies is greater than expected, which suggests an interrelationship, a hypothesis has been proposed linking genetic factors and the metabolism of gastrin with the etiology of congenital hypertrophic pyloric stenosis.

Topics: Female; Gastrins; Hernia, Inguinal; Humans; Hypertrophy; Kidney Neoplasms; Male; Prospective Studies; Pyloric Stenosis; Retrospective Studies; Urogenital Abnormalities; Wilms Tumor

Topics: Female; Gastrins; Gastroenteritis; Gastroesophageal Reflux; Gastrointestinal Diseases; Humans; Hypertrophy; Infant; Infant, Newborn; Male; Pyloric Stenosis; Secretin

Topics: Adult; Duodenal Ulcer; Female; Gastrins; Humans; Insulin; Male; Middle Aged; Pyloric Stenosis; Stimulation, Chemical; Stomach Ulcer

Blood serum immunoreactive gastrin level (IRG) was measured in infants with hypertrophic pyloric stenosis before and after corrective surgery and in a control group children of corresponding age. No significant difference in IRG level was found between the stenotic infants and the control group. In the stenotic infants IRG values were higher at the seventh day after than before the operation and significantly higher in those infants in whom gain of body weight was noted during that time as compared with the infants without gain of weight. These observations remain in agreement with the view that the main role of gastrin in infants is trophic action on the mucosa of the upper gastrointestinal tract.

Topics: Body Weight; Gastrins; Humans; Hypertrophy; Infant; Pyloric Stenosis; Radioimmunoassay

Topics: Female; Gastrins; Humans; Hypertrophy; Infant; Infant, Newborn; Male; Peptones; Pyloric Stenosis; Stomach

Topics: Dumping Syndrome; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Postgastrectomy Syndromes; Pyloric Stenosis; Stomach Neoplasms

In conscious fullgrown minipigs simple SPV alone, SPV and pyloric stenosis and SPV and pyloroplasty were performed. After a liquid test meal the motoric and secretory function of the stomach were examined simultaneously by a modified method of intestinal perfusion and aspiration. After simple SPV initially a marked decrease of gastric volume and normal emptying into the duodenum were found. With additional pyloric stenosis no significant change was found. The pyloroplasty lead to an increase of gastric volume and delayed emptying. The acid secretion after feeding reduced by SPV was not changed significantly neither by pyloroplasty nor by pyloric stenosis. The baseline values of serum gastrin were elevated after SPV as well as after SPV in combination with pyloric stenosis or pyloroplasty. After food stimulation there was a delayed increase of gastrin after SPV which differed from that after SPV with pyloric stenosis or pyloroplasty only during the first hour. These results show that after SPV no further improvement of the motoric and secretory function can be achieved by an additional pyloroplasty. Furthermore these findings permit the conclusion that even after SPV with additional artificial pyloric stenosis no delayed gastric emptying occurs and that there is no negative effect postoperatively on the acid secretion and gastrin production.

Topics: Animals; Digestion; Gastric Juice; Gastrins; Gastrointestinal Motility; Hydrogen-Ion Concentration; Male; Pyloric Stenosis; Pylorus; Stomach; Swine; Vagotomy

This case describes an extraordinarily elevated total bilirubin level that reverted to normal 9 1/2 wk after Fredet-Ramstedt pyloromyotomy. Although the etiology of jaundice occurring in patients with IHPS remains uncertain, theories implicating inhibition of the glucuronyl transferase system have been proposed. Infants with IHPS have a documented hypergastrinemia. An hypothesis is offered, illustrated by this case, to explain the inhibition of the glucuronyl transferase system with resultant hyperbilirubinemia by the hypergastrinemia of idiopathic hypertrophic pyloric stenosis.

Topics: Exchange Transfusion, Whole Blood; Gastrins; Glucuronosyltransferase; Humans; Hypertrophy; Infant, Newborn; Jaundice, Neonatal; Male; Methods; Pyloric Stenosis

The aim of this study was to look for a difference in fasting serum gastrin levels or in serum gastrin response to oral feeding between infants with hypertrophic pyloric stenosis and normal controls. Fasting serum gastrin levels were measured by radioimmunoassay in 10 patients with pyloric stenosis, before pyloromyotomy and 7 and 15 days after it, and in 11 controls. In addition, the serum gastrin responses to a casein hydrolysate meal were studied in both groups (in the patients, 7 days after operation). The fasting serum gastrin levels in the patients did not differ from those in the controls before operation, but they did so after it. The serum gastrin response to feeding in patients after pyloromyotomy was no greater than in controls.

Topics: Caseins; Female; Gastrins; Humans; Hypertrophy; Infant; Infant, Newborn; Male; Postoperative Period; Protein Hydrolysates; Pyloric Stenosis

Topics: Gastrins; Humans; Infant, Newborn; Pyloric Stenosis

A study was designed and carried out to determine if the canine model of hypertrophic pyloric stenosis is applicable to other species and to demonstrate the transplacental passage of gastrin. Results of the study show that (1) pentagastrin does not induce hypertrophic pyloric stenosis in the rabbit; (2) human gastrin does not cross the canine placenta, and (3) gastrin has no documented and little inferred role in the etiology of CHPS.

Topics: Animals; Dogs; Female; Gastrins; Hypertrophy; Pentagastrin; Placenta; Pregnancy; Pyloric Stenosis; Rabbits

In order to evaluate the potential role of gastrin in the etiology of pyloric stenosis, serum gastrin levels were measured in cord blood of affected infants, matched controls, and mothers of both. No differences were identified when values from infants with pyloric stenosis were compared with those from control infants. Mean cord serum gastrin levels of the infants were significantly greater than the mean maternal gastrin levels. The data effectively dismiss the possibility that elevated serum gastrin concentration in mother or infant at the time of delivery can be implicated as a cause of pyloric stenosis.

Topics: Fetal Blood; Gastrins; Humans; Hypertrophy; Infant, Newborn; Pyloric Stenosis

Topics: Age Factors; Duodenal Ulcer; Female; Gastrins; Humans; Hypertrophy; Infant; Male; Pyloric Stenosis; Radioimmunoassay

The serum immunoreactive gastrin (IRG) level in infants with confirmed idiopathic hypertrophic pyloric stenosis (IHPS) has been determined and compared to that found in vomiting infants without IHPS, in normal infants, and in normal adults. The mean serum IRG level of normal infants (103 +/- 9 pg/ml (mean +/- SEM) exceeded that of normal adults (28 +/- 5 pg/ml). The preoperative mean serum IRG level in IHPS infants (256 +/- 26 pg/ml) was significantly higher than that of both normal infants and vomiting infants without IHPS (93 +/- 9 pg/ml). Twenty-five per cent (5/20) of the IHPS infants had serum IRG levels within the upper range of normal infants. Fasting serum IRG levels in IHPS infants were not altered immediately by pyloromyotomy. The results from this study suggest a relationship between gastrin and idiopathic hypertrophic pyloric stenosis.

Topics: Adolescent; Adult; Antigens; Female; Gastrins; Humans; Hypertrophy; Infant; Infant, Newborn; Male; Pyloric Stenosis; Vomiting

Recently attempts have been made to demonstrate the possible role of hypergastrinemia in the production of congenital hypertrophic pyloric stenosis in infants. Eleven infants with congenital hypertrophic pyloric stenosis, ranging in age from three to 11 weeks, were evaluated for fasting and postprandial serum gastrin levels. Two to ten weeks following successful pyloromyotomy, a similar evaluation was undertaken to demonstrate the possible role of elevated serum gastrin levels in the etiology of congenital hypertrophic pyloric stenosis. The average fasting and postprandial serum gastrin levels in infants with congenital hypertrophic pyloric stenosis did not differ significantly from levels noted in control infants. Similarly, no statistically significant difference was noted between the pre- and postoperative levels of serum gastrin in the affected infants. Several experimental studies have been reported within the past few years describing the production of hypertrophic pyloric stenosis in the offspring of dogs injected with pentagastrin during pregnancy. The results of our study minimize the direct importance of serum gastrin in the production of congenital hypertrophic pyloric stenosis. The role of the hormone secretin in the etiology of this condition is hypothesized.

Topics: Female; Gastrins; Humans; Hypertrophy; Infant; Infant, Newborn; Male; Pyloric Stenosis; Secretin

Topics: Adult; Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Humans; Meat; Pyloric Stenosis; Secretory Rate; Time Factors

Pentagastrin and acetyl choline were shown to contract isolated strips of the circular pyloric muscle from baboons. These findings are compatible with the hypothesis that gastrin may have a part to play in the development or maintenance of congenital hypertrophiic pyloric stenosis of infancy.

Topics: Acetylcholine; Animals; Gastrins; Haplorhini; Hypertrophy; Papio; Pentagastrin; Pyloric Stenosis; Pylorus

Present knowledge about gastrointestinal peptide hormones is discussed from three points of view: (a) diagnostic significance of these hormones; (b) states characterized by over-production or deficiency of peptide hormones; (c) clinical application and perspectives of gastrointestinal hormones. The data in the literature are subjected to a critical analysis; in addition, the author's own experiments are discussed.

Topics: Anemia, Pernicious; Celiac Disease; Cholecystokinin; Duodenal Ulcer; Duodenum; Esophageal Diseases; Gastrins; Gastrointestinal Hormones; Humans; Peristalsis; Pyloric Stenosis; Secretin; Spasm; Zollinger-Ellison Syndrome

Topics: Animals; Gastrins; Humans; Hypertrophy; Infant; Pentagastrin; Pyloric Stenosis; Rabbits

Basal and meat extract stimulated plasma gastrin (PG) levels and basal and stimulated gastric acid secretion were evaluated pre and postoperatively in duodenal ulcer patients who underwent parietal cell vagotomy without antral drainage (normal duodena) (PC, n=32) or selective vagotomy with drainage (pyloric stenosis) (SV +P, n=11). Before operation, both groups had comparable basal PG values of 52+/-13 pg/ml (PCVP) AND 51+/-18 PG/ML (SV+P), while the peak gastrin level to meat extract stimulation was 173+/-40 pg/ml for the total group of patients. After both operations basal PG levels increased (107+/-18 pg/ml (PCV) and 152+/-45 pg/ml (SV+P) and the gastrin response to meat extract stimulation was augmented after PCV, while the response after SV+P was the same as before operation. Patients with PCV often demonstrated an acid response following meat extract stimulation (3.6+/-0.9 mEq HC1/hr), and pentapeptide stimulation (18.8+/-2.0 mEq/hr) while patients with SV/P showed a minimal response (1.3+/-1.2 mEq HC1/hr meat extract), and 10.7+/-1.8 mEq/hr pentapeptide stimulation. The comparatively intact acid response in the PCV patients may augur a high ultimate recurrence rate.

Topics: Adult; Aged; Drainage; Duodenal Ulcer; Female; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Insulin; Male; Middle Aged; Pyloric Stenosis; Secretory Rate; Stomach; Vagotomy

Fasting plasma gastrin levels were measured in babies with pyloric stenosis and in normal babies of similar age. There was no difference in gastrin levels either before or after operation between the babies with pyloric stenosis and normal babies. Similarly, neither the fasting blood glucose nor the fasting gastric pH of the babies with pyloric stenosis differed significantly from the values obtained in normal babies. Our findings do not support the hypothesis that gastrin in the fasting baby has an aetiological role in the development of hypertrophic pyloric stenosis of infancy. An alternative hypothesis is suggested.

Topics: Animals; Blood Glucose; Dogs; Fasting; Female; Gastric Lavage; Gastrins; Gastroenterostomy; Humans; Hydrogen-Ion Concentration; Infant; Infant, Newborn; Male; Pentagastrin; Pyloric Antrum; Pyloric Stenosis

Observations on the plasma gastrin response to feeding protein in patients with the dumping syndrome, patients with pyloric stenosis, and patients asymptomatic after gastric surgery suggested that the duodenum might be important in the mechanism of gastrin release. This duodenal role was confirmed by the finding that when the stimulus was placed directly in the duodenum peak gastrin levels occurred earlier than when the stimulus was placed directly in the stomach.

Topics: Dietary Proteins; Dumping Syndrome; Duodenal Ulcer; Duodenum; Gastrins; Humans; Pyloric Stenosis; Secretory Rate; Time Factors; Vagotomy

Topics: Adult; Calcium; Diagnosis, Differential; Duodenal Ulcer; Female; Gastrectomy; Gastric Acidity Determination; Gastrins; Gastritis; Humans; Infusions, Parenteral; Male; Middle Aged; Peptic Ulcer; Pyloric Stenosis; Radioimmunoassay; Vagotomy; Zollinger-Ellison Syndrome

Topics: Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastrins; Humans; Pepsin A; Peptic Ulcer; Pyloric Stenosis; Radioimmunoassay; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Dumping Syndrome; Duodenal Ulcer; Duodenum; Gastrins; Humans; Pyloric Stenosis; Vagotomy

Topics: Drainage; Duodenal Ulcer; Gastric Mucosa; Gastrins; Humans; Insulin; Meat; Pyloric Stenosis; Vagotomy

Topics: Abdominal Muscles; Animals; Cell Division; Diet; Gastric Dilatation; Gastric Juice; Gastric Mucosa; Gastrins; Male; Organ Size; Pyloric Stenosis; Rats

Topics: Animals; Animals, Newborn; Dogs; Duodenal Ulcer; Female; Gastrins; Injections, Subcutaneous; Pregnancy; Pregnancy, Animal; Pyloric Stenosis

Topics: Blood Protein Electrophoresis; Gastric Juice; Gastrins; Gastroenterostomy; Humans; Postoperative Complications; Pyloric Stenosis; Radioimmunoassay; Serum Albumin; Serum Globulins; Zollinger-Ellison Syndrome

Topics: Animals; Atmospheric Pressure; Cats; Female; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hypercapnia; Hypoxia; Male; Peptic Ulcer; Peptic Ulcer Hemorrhage; Pulmonary Heart Disease; Pyloric Stenosis

Topics: Duodenal Ulcer; Gastrectomy; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Humans; Pyloric Stenosis; Pylorus; Stomach Ulcer; Vagotomy

Topics: Duodenal Ulcer; Gastrins; Hemorrhage; Humans; Peptic Ulcer; Pyloric Stenosis; Stomach Ulcer; Vagotomy

Topics: Duodenal Ulcer; Gastrectomy; Gastrins; Humans; Pyloric Stenosis; Stomach Ulcer; Vagotomy