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At least 145 records · Page 8Linked to original sources
PubMed2003

Hypertrophic pyloric stenosis in infants: US evaluation of vascularity of the pyloric canal.

PURPOSE: To determine if there is increased flow to the pylorus in infants with hypertrophic pyloric stenosis (HPS) and, if so, whether the flow is localized to the muscle layer, mucosal layer, or both. MATERIALS AND METHODS: Seventy-five infants examined for clinical suspicion of HPS were prospectively recruited for the study. Color scale was standardized at 4.2-4.4 cm/sec. Color Doppler flow at ultrasonography (US) was graded as follows: Grade 1 meant no signal; grade 2, two to five flow signals; and grade 3, extensive or continuous flow. Flow to the muscle or mucosal layer was documented and confirmed with spectral analysis. Infants without HPS served as control patients. Descriptive analyses were conducted to assess the demographic data and US results. Significance was assessed with chi2 or t tests. P <.05 was considered to indicate a significant difference. RESULTS: HPS was present in 41 infants with a mean age of 5 weeks +/- 2.0 (SD). Their mean flow grade was 2.80 +/- 0.4 in muscle and 2.88 +/- 0.4 in mucosa. HPS was not present in 34 infants with a mean age of 5.9 weeks +/- 4.5. Their mean flow grade was 1.26 +/- 0.5 in muscle and 1.15 +/- 0.5 in mucosa (P <.001). There was no significant difference in flow grades when the dimensions of the pyloric muscle and mucosa were compared. There was no significant difference in age between the HPS and control patient groups. CONCLUSION: Increased flow accompanies and may conceivably represent an integral component of the changes that occur with infantile HPS.

Blood Flow Velocity↗
PubMed1993

[Effect of indomethacin on endocrine kinetics of the stomach in experimental pyloric stenosis model].

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.

Administration, Oral↗
PubMed2002

A quantitative study of the neural changes underlying pyloric stenosis in dogs.

This study aimed to quantify the neural changes in congenital pyloric stenosis in dogs and to study the comparative anatomy between this condition in dogs and that in infantile hypertrophic pyloric stenosis. Eight specimens from the pylorus of dogs with pyloric stenosis and six control specimens were examined using conventional histology and immunohistochemistry for a range of neural antigens. The changes in the proportion of nerves immunoreactive for each antigen were quantified and analysed statistically. The morphology of the nerves in the diseased dogs was similar to that in controls. Only vasoactive intestinal peptide was reduced in expression in dogs (median proportion in control dogs 0.57, in diseased dogs 0.17; P = 0.065). This study demonstrates both morphological similarities and significant differences between closely related conditions in dogs, humans and other species.

Animals↗
PubMed2002

Sonographic diagnosis of hypertrophic pyloric stenosis: preliminary experience.

The value of ultrasound diagnosis for suspicion of infantile hypertrophic pyloric stenosis (HPS) was assessed in three consecutive years using ultrasound measurement of pyloric muscle thickness (PMT), pyloric diameter (PD) and pyloric length (PL) in Tikur Anbessa Hospital which is a tertiary referral and teaching hospital. Among all patients 39 patients (36 males and 3 females) had Infantile Hypertrophic Pyloric Stenosis confirmed by surgery, with male to female ratio of 12:1. Ultrasound correctly diagnosed all of the cases. Sixty- six patients were negative by Ultrasound, Barium meal studies and clinical follow up. The mean Pyloric Muscle Thickness (4.46 Vs 1.81), Pyloric Length (19.1 Vs 11.55) and Pyloric Diameter (14.05 Vs 8.4) between patients with and with out pyloric stenosis were significantly different (p < 0.05). A PMT of 3 mm and above was observed in all cases of HPS, and was never observed in the absence of HPS (100% sensitivity and specificity). A pyloric muscle thickness of 3 mm and above is recommended as a diagnostic cutoff and upper gastrointestinal series (UGIS) can be reserved for those who might fall in the grey zone (i.e. PMT of 2-3 mm).

Chi-Square Distribution↗
PubMed1983

Ultrasound diagnosis of hypertrophic pyloric stenosis: real-time application and the demonstration of a new sonographic sign.

The diagnosis of hypertrophic pyloric stenosis (HPS), a common problem of infancy, is usually based on medical history. When the diagnosis is in question a barium upper gastrointestinal series has been the diagnostic imaging procedure of choice. In this study real-time ultrasound was used in 27 infants in whom pyloric stenosis was suspected. The published criteria for the ultrasound diagnosis of pyloric stenosis were used to evaluate the results. Fourteen examinations were true-positive, 12 were true-negative, and one was false-negative. The authors termed the hypertrophied muscle, which was demonstrated in longitudinal section, the "ultrasonic cervix sign" of hypertrophic pyloric stenosis. It was concluded that real-time ultrasound is a simple and accurate method for the diagnosis of HPS and should be the initial imaging procedure.

Evaluation Studies as Topic↗
PubMed1990

Pyloric stenosis with esophageal involvement in Behçet's syndrome.

A 43-yr-old man with a diagnosis of Behçet's syndrome since 1977 developed esophageal aphthous ulcerations, duodenal ulcer, and pyloric stenosis. The pyloric stenosis was due to edematous hypertrophy of the pyloric ring. The evidence strongly suggested that these findings were complications of Behçet's syndrome.

Adult↗
PubMed1975

Infantile hypertrophic pyloric stenosis in Belfast, 1957-1969.

Infants with hypertrophic pyloric stenosis born in Belfast during the 13 years 1957-1969 have been reviewed. Their distribution shows a bias towards higher social classes, breast feeding, and primogeniture. Obstetric factors and parental ages seem to be of no importance. More affected infants were born during winter months than would be expected. The overall incidence of infantile pyloric stenosis in this community has fallen during the period under review. Clinically, the patients started vomiting at a mean age of 22 days and it is recommended that the condition should not be called 'congenital'. The size of the tumour is mainly determined by the size of the patient, rather than by his age or duration of symptoms. Attention is drawn to the occurrence of haematemesis in 17-5% and melaena in 2-9% of infants. Jaundice occurred in 1-8% of patients in this series, and is attributed to the adverse effect of starvation on hepatic glucuronyl transferase activity. Other conditions noted in these patients included inguinal hernia, partial thoracic stomach, and phenylketonuria. Subsequent growth and development were in the anticipated range.

Age Factors↗
PubMed1979

Esterolytic activity of blood serum in infants with hypertrophic pyloric stenosis.

Esterolytic activity of blood serum was determined in infants with hypertrophic pyloric stenosis and in healthy control children. The substrates hydrolyzed mainly by arylesterase (EC. 3.1.1.2), i.e. p-nitrophenyl esters of acetic, propionic and butyric acid were used. It was found that in infants with hypertrophic pyloric stenosis the rate of p-nitrophenyl propionate hydrolysis was significantly higher than that of the acetate or butyrate. In control group children all three substrates were hydrolysed at similar rates, and these were significantly lower than in infants with hypertrophic pyloric stenosis.

Carboxylic Ester Hydrolases↗
PubMed2006

Endoscopic therapy of benign pyloric stenosis and gastric outlet obstruction.

PURPOSE OF REVIEW: To examine the short and long-term success rates of balloon dilation of pyloric stenosis. RECENT FINDINGS: Several large studies have demonstrated high rates of success for the relief of symptoms from pyloric stenosis using through-the-scope balloons. These dilating balloons readily increase the diameter of the stenotic pylorus on average from 6 to 16 mm. Patients who require more than two dilations are at high risk of endoscopic failure and the need for surgical intervention. Rapid re-stenosis rates are observed in patients with malignant pyloric obstruction. Since many patients with benign pyloric stenosis have underlying ulcer disease, helicobacter infection is a relatively common finding. Eradication of this infection at the time of balloon dilation will ensure higher long-term success rates. SUMMARY: In summary, benign pyloric stenosis can be readily treated with endoscopic balloon dilation and should be the first-line therapy.

Adult↗
PubMed1992

[Effect of famotidine on gastrin cell, somatostatin cell, and prostaglandin E2 concentration of stomach in experimental pyloric stenosis model].

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.

Animals↗
PubMed1986

Pyloric stenosis: an unusual complication of Behçet's disease.

A 20-yr-old Japanese man with longstanding Behçet's disease had pyloric stenosis and multiple duodenal ulcers. The pyloric stenosis was due to edematous hypertrophy of the pyloric ring and was unrelated to duodenal ulceration. The evidence suggests that the pyloric stenosis and multiple duodenal ulceration were a manifestation of Behçet's syndrome and not merely incidental peptic ulcer disease.

Adult↗
PubMed1999

The development of hypertrophic pyloric stenosis in a patient with prostaglandin-induced foveolar hyperplasia.

BACKGROUND: Hypertrophic pyloric stenosis (HPS) has been described in association with several obstructive antropyloric lesions including idiopathic foveolar hyperplasia (gastric mucosal hypertrophy), feeding tubes, eosinophilic gastroenteritis, and hypertrophic antral polyps. Non obstructive antral webs have also been described with HPS. PATIENT AND METHODS: We present a case of gastric-outlet obstruction in association with HPS, namely, prostaglandin-induced foveolar hyperplasia. This entity has been previously described, but rarely in association with HPS. We report a female infant requiring prostaglandin therapy for pulmonary atresia who developed dose-related prostaglandin-induced foveolar hyperplasia and symptoms of progressive non-bilious vomiting. RESULTS: Initially, ultrasonography demonstrated evidence of antral mucosal hypertrophy as the cause for gastric-outlet obstruction. The patient subsequently developed progressive thickening of the antropyloric muscle, resulting in sonographic appearances of hypertrophic pyloric stenosis. Pyloromyotomy was eventually required for treatment of HPS. CONCLUSION: A common denominator of most of the above-described entities is thickening and/or hypertrophy of the antral mucosa. We suggest that the antropyloric musculature may hypertrophy in an effort to overcome the gastric-outlet obstruction caused by the adjacent thickened antral mucosa. In other words, these entities may represent examples of "secondary" hypertrophic pyloric stenosis.

Female↗
PubMed1994

Diagnosis of hypertrophic pyloric stenosis: value of sonography when used in conjunction with clinical findings and laboratory data.

OBJECTIVE: This study aimed to determine the value of sonography in the diagnosis of hypertrophic pyloric stenosis in patients with no palpable olive-shaped mass. MATERIALS AND METHODS: One hundred and five children with projectile vomiting but no palpable mass had sonography because of possible hypertrophic pyloric stenosis. The patients' history, signs and symptoms, and results of laboratory tests were incorporated into the statistical analysis. Using medical history, signs and symptoms, and laboratory results in one case and history, signs and symptoms, laboratory results, and pyloric measurements based on sonographic findings in another case, we composed the best predicting logistic regression models. RESULTS: The ability to predict hypertrophic pyloric stenosis is greatly increased by adding information obtained from sonography. At 91% specificity of the final model, only 5% of the patients with no evidence of the abnormality actually had hypertrophic pyloric stenosis. The positive predictive value is thus 94%, and the negative predictive value is 95%. CONCLUSION: The results justify the use of sonography as the diagnostic procedure of choice for infants suspected of having hypertrophic pyloric stenosis.

Female↗
PubMed2001

In vivo visualization of pyloric mucosal hypertrophy in infants with hypertrophic pyloric stenosis: is there an etiologic role?

OBJECTIVE: Infantile hypertrophic pyloric stenosis (IHPS) is a common condition which presents in infants at 2-12 weeks of postnatal life, and whose cause remains obscure. Multiple associated abnormalities have been recognized within the external hypertrophied pyloric muscle layer, but the internal component of the pyloric mucosa has received scant attention in the literature to date. Our purpose in this study was to show that pyloric mucosal redundancy is a constant finding in infants with IHPS, to discuss its possible cause, and to explore the hypothesis of a relationship between pyloric mucosal redundancy and the development of IHPS. MATERIALS AND METHODS: We identified 102 consecutive infants with surgically confirmed IHPS and determined the thickness of the pyloric mucosa compared with the thickness of the surrounding hypertrophied muscle. Fifty-one infants who did not have pyloric stenosis served as controls. RESULTS: Mean mucosal thickness in patients with IHPS approximated mean muscle thickness, with a ratio of 0.89. In infants with IHPS, the pyloric mucosa constitutes approximately one third of the cross-sectional diameter of the pyloric mass and fills and obstructs the pyloric canal. CONCLUSION: Mucosal redundancy is a constant associated finding in IHPS. Although the origin of the redundancy and a cause-and-effect relationship are difficult to establish, our findings support the hypothesis that hypergastrinemia may be implicated in the pathogenesis of IHPS, and suggest that mucosal thickening could be implicated as one of the initiating factors in its development.

Female↗
PubMed1975

"Burned-out" pyloric stenosis: an elusive gastric outlet obstruction.

Four cases of infantile pyloric stenosis are presented to illustrate the difficulties found in diagnosing pyloric stenosis. Clinical, histological, surgical, and roentgenologic examination must be combined to determine the optimum treatment. All patients exhibited failure to thrive and gain weight normally, but few showed palpable tumors upon abdominal examination. The results of upper gastrointestinal examination are often more confusing than helpful, but previously performed Gl studies have been rewarding. The main problem is to rule out pylorospasm, and a trial of treatment with antispasmodics is essential. The presence or absence of a residual muscle mass at surgery would call for pylorotomy or pyroplasty, respectively.

Female↗
PubMed2004

The impact of a clinical guideline on imaging children with hypertrophic pyloric stenosis.

PURPOSE: The purpose of the study was to evaluate the impact of a clinical pathway on the volume of imaging studies performed in children with suspected clinical diagnosis of hypertrophic pyloric stenosis. The pathway suggested referral to surgeons for clinical evaluation for palpation of the olive prior to ordering imaging studies. Only those children in whom the olive could not be palpated would be referred for imaging, and it was anticipated that imaging volume would be reduced following guideline implementation. MATERIALS AND METHODS: The database of the Health Policy and Clinical Effectiveness Department was used to evaluate all patients who had surgery for hypertrophic pyloric stenosis. The presence of a palpable olive and the type of imaging were evaluated both prior to and after the implementation of the clinical guideline. RESULTS: Prior to the guideline, 85 infants had surgery for pyloric stenosis, with 83 of the 85 (97%) having imaging. After the implementation of the guideline, 90 infants had surgery for pyloric stenosis with 84 of 90 patients imaged (92%). A chi-square analysis demonstrated no significant difference in the percentage of children imaged in the two groups (P = 0.104). Approximately one in five children referred for vomiting were diagnosed with hypertrophic pyloric stenosis. CONCLUSION: No significant change in imaging volume occurred following initiation of a guideline which recommended clinical evaluation for palpation of the olive prior to ordering imaging studies. Multiple factors probably contributed to the lack of demonstrated changes.

Critical Pathways↗
PubMed1986

[Sonographic diagnosis of hypertrophic pyloric stenosis].

50 infants admitted during the years 1981 to 1985 for suspected hypertrophic pyloric stenosis were examined sonographically. A pyloric cockade of 14 mm or more in diameter is diagnostic. A diameter up to 10 mm can be considered normal, whereas values between 11 and 13 mm represent borderline cases, which need consideration of the clinical symptoms and repeated controls. Because of its accuracy sonography can replace X-ray examinations in most of the cases with suspected hypertrophic pyloric stenosis.

Diagnosis, Differential↗