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At least 559 records · Page 31Linked to original sources
PubMed1989

Gastric emptying in adults treated for infantile hypertrophic pyloric stenosis.

The gastric emptying rate was scintigraphically determined in 6 women and 26 men who had undergone medical or surgical treatment for infantile hypertrophic pyloric stenosis a median of 29 years previously. Dyspeptic complaints were reported by four of the seven medically treated and nine of the 25 surgically treated group. No intergroup difference was demonstrated in the gastric emptying rate of liquid or solid food, and neither group differed significantly from the normal values. The gastric emptying rate, measured as in this study, thus was uninfluenced by treatment.

Adult↗
PubMed1987

Pyloric stenosis in Western Australia, 1971-84.

Analyses of hospital records and census data for 1971-84 showed no significant increase in incidence of infantile hypertrophic pyloric stenosis in Western Australia. No link was found between breast feeding and incidence of disease. Low birth weight, short gestation pregnancies, and paternal family history of the disease were significant features.

Australia↗
PubMed1995

Evolving asymmetric hypertrophic pyloric stenosis associated with histologic evidence of eosinophilic gastroenteritis.

The most frequently occurring and important cause of gastric outlet obstruction in the neonate and young infant is infantile hypertrophic pyloric stenosis (IHPS). A reported association of IHPS and eosinophilic gastroenteritis [1] raises interesting questions about the possible etiologic relationship between the two entities. It is plausible that the observed sonographic pyloric muscular wall thickness in IHPS may in part be dependent on the degree and duration of an allergic gastroenteropathy. A recent report suggests that endoscopy may be a more reliable diagnostic method than sonography in the patient with evolving IHPS [2]. Our recent experience with a patient with evolving IHPS supports the findings described in these prior reports.

Eosinophilia↗
PubMed2006

Helicobacter pylori and infantile hypertrophic pyloric stenosis: is there a possible relationship?

BACKGROUND: Recently, it has been suggested that Helicobacter pylori might be a cause of some cases of infantile hypertrophic pyloric stenosis (IHPS) in infancy on the basis of its epidemiologic and clinical features. We performed this study to evaluate the possible relationship between IHPS and H. pylori. DESIGN: In consecutive infants with IHPS, we performed upper gastrointestinal endoscopy with biopsy before pyloromyotomy. The endoscopic appearance of the pylorus was noted to validate endoscopic features of IHPS. RESULTS: Sixteen infants, 15 male, 14 white, mean age 42 days, range 21 to 104 days, were studied. The index case had chronic active gastritis on biopsy with organisms suspicious for H. pylori. Four others had chronic active gastritis, six more had focal or mild chronic gastritis, five were normal, and none had H. pylori on histology or immune histochemical staining in selected cases. All patients had negative rapid urease test. Most common endoscopic findings of IHPS were thickened prominent asymmetric pyloric folds and pin-hole pylorus that could not be intubated by the pediatric endoscope. CONCLUSION: H. pylori was not specifically identified in our patients with IHPS. The presence of H. pylori-like organisms in the gastric mucosa in our index case and finding of chronic active gastritis in several others may indicate the possibility of an acquired infectious etiology for IHPS.

Biopsy↗
PubMed1998

Active collagen synthesis in infantile hypertrophic pyloric stenosis.

M-57 antibody, which is capable of distinguishing newly-synthesized type I procollagen from fully-processed, mature collagen, was used to examine the expression of collagen synthesis in hypertrophic pyloric muscle from patients with infantile hypertrophic pyloric stenosis (IHPS). Seven specimens from IHPS patients were removed at the time of operation; age-matched normal pyloric tissue of 5 post-mortem cases was obtained as controls. Immunohistochemistry was performed using antibody of the amino-terminal end of the procollagen type I propeptide (M-57). Newly-synthesized procollagen (M-57) was strongly detected in both the connective tissue septa between circular muscle bundles, and among the circular-muscle fibers in patients with IHPS. No M-57 staining was observed among the circular-muscle fibers in controls. Our findings show that the hypertrophic circular muscle in IHPS is actively synthesizing collagen, and this may be responsible for the characteristic "firm" nature of the pyloric tumor.

Antibodies, Monoclonal↗
PubMed1990

Balloon catheter dilatation for hypertrophic pyloric stenosis.

Balloon dilating catheters (BDC) have provided a non-operative means of managing obstructive lesions within the gastrointestinal tract. Its potential utility in infants with hypertrophic pyloric stenosis (HPS) was studied. Six patients with HPS underwent balloon catheter dilatation of the pylorus under the direct observation of the surgeon. The pylorus was exposed using a standard right upper quadrant incision. The BDC was passed transorally into the stomach and manipulated into the pyloric canal by the surgeon. The balloon was inflated with saline to a maximum pressure of 50 psi for 2 minutes. Four patients were dilated with a 10-mm diameter balloon catheter, and in two patients, a 15-mm balloon was used. Success was defined as the complete and longitudinal disruption of the seromuscular ring without violation of mucosal integrity. Using this criterion, none had successful pyloric dilatation. No disruption occurred in three patients, partial disruption in two. These patients subsequently underwent a Ramstedt pyloromyotomy. Complete disruption was observed in one; however, a breach of the mucosa was evident. This was repaired without incident. All seromuscular breaks occurred at the point of vascular entry along the lesser curve, presumably the weakest point of the ring. Pyloric dilatation using BDC does not reliably disrupt the muscular ring. This preliminary report recognizes that major refinements must occur before this method will supplant the time-honored surgical pyloromyotomy for HPS.

Catheterization↗
PubMed1988

Trends in infantile hypertrophic pyloric stenosis in Olmsted County, Minnesota, 1950-1984.

In the 35-year period, 1950-1984, 154 Olmsted County, Minnesota, infants were diagnosed with definite infantile hypertrophic pyloric stenosis (IHPS). Patients were identified using outpatient and inpatient records of all providers of care to the circumscribed population, and ascertainment was complete insofar as diagnosed cases are concerned. The overall incidence of IHPS was 2.6 per 1000 person-years (95% confidence interval: 2.2-3.0), with a male:female ratio of 4.1:1. A dramatic rise in incidence was seen among male infants over the study period, but not for females, so that by 1980-1984 the rates for the two sexes were 6.2 and 0.9 per 1000 person-years, respectively. Improvements in diagnostic capabilities and case identification may have occurred but seem unlikely to entirely account for these changes. Aetiologic hypotheses should reflect the different trends for male and female infants.

Cohort Studies↗
PubMed1990

Clinical, haematological and biochemical findings and the results of treatment in cattle with acute functional pyloric stenosis.

The clinical features and changes in blood and rumen fluid, and the results of therapy are described in 10 cows suffering from acute functional pyloric stenosis. The general condition of the cows was moderately to severely disturbed. The abdomen of most of them was distended on one or both sides and the rumen was excessively full. Defecation was reduced or absent. In most of them there was moderate or severe abomasal reflux-syndrome. Exploratory laparotomy or slaughter revealed a grossly distended abomasum which was filled with ingesta but not displaced. The omasum, reticulum and rumen of most of the cows were dilated secondarily and filled with ingesta. Six of the cows were treated by the administration of a solution of sodium chloride, glucose and potassium chloride intravenously, and metoclopramide intramuscularly. Five cows recovered within a short time, general condition, appetite and defecation were again normal and the abomasal and ruminal function returned within three days.

Acute Disease↗
PubMed1977

Dominantly-inherited polycystic kidneys in infants: association with hypertrophic pyloric stenosis.

Newborn male fraternal twins presented at 10 days of age will bilateral flank masses; intravenous urograms showed polycystic kidney disease. Both babies also had hypertrophic pyloric stenosis (HPS). Their father has radiographic and sonographi findings of previously unsuspected polycystic kidneys and has a history of HPS in infancy. The association of dominantly-inherited polycystic kidneys (DPK) and HPS in this family is probably due to chance. However the authors speculate that the autosomal gene for DPK may occur at one of several loci that carry the genetic liability for HPS, A DISORDER TRANSMITTED BY POLYGENIC INHERITANCE.

Diseases in Twins↗
PubMed1988

Prenatal gastric dilatation and infantile hypertrophic pyloric stenosis.

Fetal sonography showed persistent gastric dilatation with no other abnormalities. Following uneventful pregnancy and delivery, the patient presented with typical clinical and radiologic features of infantile hypertrophic pyloric stenosis. Literature review indicates that this association was never reported.

Adult↗
PubMedDate not supplied

Palliation of pyloric stenosis caused by gastric cancer using an endoscopically placed covered ultraflex stent: covered stent inside an occluded uncovered stent.

A 71-year-old man developed pyloric stenosis caused by gastric cancer. Vomiting and nausea resolved after the insertion of an uncovered Ultraflex stent (length 10 cm, inner diameter 18-23 mm) through a 7-cm-long stenosis, and the patient was able to eat a soft diet. After 6 weeks, stent occlusion occurred due to tumor ingrowth and accumulation of food residue. Endoscopic observation showed a very narrow residual lumen. A covered Ultraflex stent (length 10 cm, inner diameter 18-23 mm) was inserted through the first stent and expanded to its maximum diameter over the next 2 days. The patient's vomiting and nausea improved rapidly. He died 6 months after the second stenting procedure, from metastatic tumor spread, having remained free of nausea and vomiting. In this case, a covered metallic stent prevented tumor ingrowth and maintained gastrointestinal patency.

Aged↗
PubMed2004

A histological study of the hph-1 mouse mutant: an animal model of phenylketonuria and infantile hypertrophic pyloric stenosis.

AIM: To quantify the chronological sequence of changes in the morphology and immunoreactivity for neurotransmitters in the pylorus of an animal model of infantile hypertrophic pyloric stenosis and phenylketonuria. METHOD: Thirty specimens of pylorus from hph-1 mice and age/sex matched controls (age range: 10-180 days) were examined using conventional histology and immunohistochemistry for a variety of antigens: protein gene product 9.5, a pan neuronal marker; vasoactive intestinal polypeptide; nitric oxide synthase two antigens coalesced to the same inhibitory neurons in humans; substance P, a potent excitatory neurotransmitter; and calcitonin gene related peptide, a neurotransmitter implicated in the somatic afferent innervation of the stomach. The changes in the morphology of the muscle layers were quantified and statistically analysed for each age group (10, 20, 40, 90 and 180 days). RESULTS: Between 10 and 90 days of age, all muscle layers of the hph-1 mice were hypertrophied, for example, 10 days, hph-1 longitudinal muscle mean diameter = 3.4, control = 1.8; hph-1 circular muscle width = 11.5, control = 4.7. The hph-1 mice were significantly smaller during this period (40 days, hph-1 weight = 10 g, control = 25 g). There was no change in the pattern of expression of the antigens examined within the hph-1 mice compared with the controls. CONCLUSION: Hph-1 mice develop a transient smooth muscle hypertrophy of the pylorus attended by gastric distension and failure to gain weight. These changes resolve as the pyloric muscle hypertrophy resolves.

Age Factors↗