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PubMed2001

Absence of Epstein-Barr virus in smooth muscle cells of idiopathic hypertrophic pyloric stenosis.

CONTEXT: The etiology of idiopathic hypertrophic pyloric stenosis (IHPS) is unknown. Epstein-Barr virus (EBV) infects smooth muscle cells and is associated with leiomyomas and leiomyosarcomas of immunocompromised persons, including persons with the acquired immunodeficiency syndrome. OBJECTIVE: To determine whether EBV is causally associated with IHPS. DESIGN: Biopsy samples of the pylorus were obtained from 10 infants with projectile vomiting and pyloric hypertrophy on ultrasound, with confirmation of hypertrophy at the time of pyloromyotomy. The presence of EBV infection was tested by in situ hybridization for EBV-encoded RNA 1 (EBER1) in smooth muscle cells of IHPS. SETTING: Biopsy specimens were obtained from children treated for IHPS at a tertiary referral hospital and were tested in a clinical molecular diagnostics laboratory. RESULTS: All of the 10 smooth muscle biopsies were negative for EBER1. Cellular U6 RNA was detected in all smooth muscle samples, confirming that the RNA in the specimens was intact and capable of detection by in situ hybridization. CONCLUSIONS: The absence of EBER1 in 10 cases of clinically diagnosed and histopathologically confirmed cases of IHPS effectively excludes EBV infection of smooth muscle cells as a causal factor in the pathogenesis of IHPS.

Biopsy↗
PubMed2006

The continuing enigma of pyloric stenosis of infancy: a review.

Striking features of the descriptive epidemiology of pyloric stenosis of infancy have been identified but until recently have not suggested any useful etiologic lead. The disease first received serious attention approximately 100 years ago and has since occurred throughout the Western world at a rate between 2 and 5 per thousand live births; it appears to be uncommon elsewhere. Its age distribution is essentially limited to the period between the third and eighth weeks after birth. It is 4 to 5 times more common in boys than girls. It is less common in blacks than whites in the United States and less common among Asians than whites in the United States and elsewhere. Its incidence is highest in first-born infants. Evidence on a role for maternal age is not consistent. The disease re-occurs in families with sufficient frequency to incite the interest of geneticists, although no genetic model yet proposed offers a better basis for counseling than do the empiric observations on which it is based. Monozygous twins are concordant for the disease not much more frequently than are dizygous twins, and indeed not a great deal more often than nontwin siblings, which should prompt a search for environmental explanations of the disease's familial nature. Sharp declines in the incidence of the disease in Denmark and Sweden during the 1990s led to the hypothesis that infants sleeping in the prone position-a practice discouraged with some success by Scandinavian campaigns to reduce the frequency of sudden infant death syndrome (SIDS)-may also be at increased risk of pyloric stenosis. If supported, this hypothesis may offer the first-ever possibility of reducing the frequency of this disease, as well as SIDS. If the hypothesis is not supported, the recent declines in the disease in Denmark and Sweden add another facet to its enigmatic nature.

Birth Order↗
PubMed1992

Sonographic diagnosis of infantile hypertrophic pyloric stenosis.

Twenty-five consecutive sonographic examinations performed at Flinders Medical Centre for possible infantile hypertrophic pyloric stenosis (IHPS) were analyzed retrospectively. The results and a pyloric muscle index calculated by a formula using length, diameter, muscle thickness, and body weight were compared with the clinical outcome (surgery or conservative management). In the children without IHPS, the calculated pyloric muscle index was less than 0.2, whereas in infants with proven pyloric stenosis, the index was greater than 0.2 (P < 0.001). This result suggested that the published index upper limit of > 0.4 to 0.46 was not valid in our institution. Pyloric length to muscle thickness ratio was also found to predict IHPS. A simplified index, including only length and muscle thickness, is proposed, whereby length (mm) plus 3.64 times thickness (mm), when greater than 25, implies IHPS.

Humans↗
PubMed2001

Erythromycin-induced pyloric stenosis in infants.

(1) Several cases of pyloric stenosis have occurred in infants treated with erythromycin during the first weeks of life. (2) A disturbing report of a cluster of cases is enough to avoid erythromycin use in neonates.

Anti-Bacterial Agents↗
PubMedDate not supplied

Pyloric stenosis and eosinophilic gastroenteritis in infants.

Eosinophilic gastroenteritis is known to cause gastric outlet obstruction in adults, but has been reported only rarely in infants presenting with pyloric stenosis, a common form of gastric outlet obstruction in children. We describe two infants who presented with classic clinical and radiographic evidence of pyloric stenosis and who were found to have histologic evidence of eosinophilic gastroenteritis on gastric antral biopsies. Their presentation is compared with the clinical and laboratory findings of 47 other infants with pyloric stenosis.

Dietary Proteins↗
PubMed2004

[Pyloric stenosis management in France in 1999: a postal survey].

OBJECTIVE: The aim of this postal survey was to know how were treated infants with hypertrophic pyloric stenosis in France in 1999. METHODS: A questionnaire was sent to all French members of the Association Des Anesthésistes Réanimateurs Pédiatriques d'Expression Française (Adarpef). RESULTS: Half the cases of pyloric stenosis treated in France in 1999 were related by the survey. Preoperative management was short lasting (24 h) while the advised guidelines regarding biologic criteria for operation were poorly followed. Nevertheless, crush induction was only performed in 80%. CONCLUSION: The management of infants with pyloric stenosis must be improved, at least to obtain the generalization of crush induction.

Analgesics, Opioid↗
PubMed1980

Atypical muscle hypertrophy in pyloric stenosis.

Four types of atypical hypertrophy in pyloric stenosis in 17 infants are described. In all instances, the antropyloric deformity differs from that in the classic case, and usually delays early diagnosis. However, it is important that these forms of muscle hypertrophy be appreciated, for just as in the classic case, pyloromyotomy is curative. The radiologist is in the best position to make the diagnosis providing he is aware of the four atypical configurations we have encountered: (1) persistent lesser curve mass or identation; (2) funnel-shaped antrum; (3) spiculated antrum; and (4) pyloric niche/diamond sign.

Humans↗
PubMed1987

Abnormalities of peptide-containing nerve fibers in infantile hypertrophic pyloric stenosis.

The distributions of nerve cells and fibers with immunoreactivity for the peptides enkephalin, gastrin-releasing peptide, neuropeptide Y, somatostatin, substance P, and vasoactive intestinal peptide were examined in specimens of myenteric plexus and external muscle from the pylorus of 20 infants with hypertrophic pyloric stenosis. These were compared with peptide distributions in pyloric samples from unaffected infants and adults. In the normal pylorus the circular muscle was richly supplied with fibers reactive for enkephalin, neuropeptide Y, substance P, and vasoactive intestinal peptide. In pyloric stenosis, these immunoreactive fiber bundles were either missing or less than 5% of normal. In contrast, there were reactive cell bodies and nerve fibers in the myenteric plexuses of both normal and affected specimens. In the samples from cases of stenosis, swollen nerve fibers that appeared to be in the process of degeneration were frequently encountered. It is concluded that infantile hypertrophic pyloric stenosis is associated with a loss of peptide immunoreactivity in nerve fibers in the circular muscle, although the same peptides are still revealed in fibers and in nerve cell bodies in the myenteric plexus.

Enkephalin, Leucine↗
PubMed1991

Modified Ramstedt's pyloromyotomy for the treatment of infantile hypertrophic pyloric stenosis.

Thirty-seven infants with hypertrophic pyloric stenosis had a modified Ramstedt pyloromyotomy performed. The incidence of postoperative vomiting was low (16%), with no infant suffering sustained vomiting requiring re-exploration for incomplete pyloromyotomy. The modified Ramstedt's pyloromyotomy is a simple procedure and may confer an advantage in the postoperative course of the recovering infant.

Female↗
PubMed2000

Is Helicobacter pylori a cause of infantile hypertrophic pyloric stenosis?

My hypothesis is that infantile hypertrophic pyloric stenosis (IHPS) is caused in some cases by Helicobacter pylori (HP) a bacterium commonly found in the human stomach. IHPS is an idiopathic condition of infancy. It occurs at about 5 weeks of age in 3 per 1000 newborns. Children with IHPS have structurally normal pylori at birth and do not resemble children with congenital anomalies. Some nonspecific evidence (temporal distribution, seasonality, familial clustering, leukocytic infiltrates, and increased risk with bottle feeding) are compatible with an infectious etiology. Some other epidemiologic features of IHPS, such as its strong male predominance, its racial and social class variation, and a possible drop in its incidence, are also features of HP infection. Clinical features of IHPS, such as vomiting, hematemesis, and esophagitis, are also consistent with HP. Finally, children with IHPS appear to be more likely to develop chronic conditions, such as peptic ulcers, now known to be caused by HP.

Female↗
PubMed2006

Conservative treatment of infantile hypertrophic pyloric stenosis with intravenous atropine sulfate does not replace pyloromyotomy.

Pyloromyotomy as described by Weber and Ramstedt has been the standard therapy for infantile hypertrophic pyloric stenosis since the 1960's and conservative therapy has been abandoned. The objective of this study was to test the effectiveness of systemic atropine applied intravenously for 7 days as a conservative therapeutic strategy and as an alternative to primary operation. Forty-two consecutive term infants with infantile hypertrophic pyloric stenosis were enrolled in the study over a period of 5 years. After confirmation of the diagnosis they all received intravenous atropine at a dose of 0.04 mg/(kg day) and increased by 0.01 mg/(kg day) up to 0.12 mg/(kg day), given as 6-8 single doses per/day. Nine pairs of parents requested that their child should be operated before completing the 7 days of medical therapy. Surgery was necessary in 8 of the remaining 33 infants (24,.2%) who did not improve after 7 days of conservative treatment. Successful treatment with i.v. atropine sulfate was achieved only in 25/33 term infants at an average maximal dose of 0.11 mg/(kg day), without any major side effects. Intravenous atropine sulfate has been considered as a potential alternative therapeutic strategy in the treatment of infantile hypertrophic pyloric stenosis. Clinical improvement however was often not seen before the 6th or 7th day of intravenous treatment. A success rate for the conservative approach of only 75% at day 7 in our study does not favour atropine therapy, in view of success rates above 95% with surgical repair.

Atropine↗
PubMedDate not supplied

[Population prevalence of congenital hypertrophic pyloric stenosis in the Donetsk region of Ukraine].

The population prevalence of congenital hypertrophic pyloric stenosis in Donetsk region in the course of 11 years (1989-1999) has been descriptively studied. Its frequency is 0.73:1000 or 1:1370 newborn infants annual with range of 0.54 to 1.01:1000. It is somewhat lower than that of more wide spread congenital diseases: labial cleft and hemochromatoses. Pyloric stenosis is detected in 42 of 43 populations of Donetsk region. There is a population nonuniformity of the case rate: from 0.19 to 1.9:1000 newborn infants, that the authors are inclined to explain by dissimilarity of a gene pool in the populations due to random migration of the population.

Female↗
PubMed1978

Increased serum immunoreactive gastrin levels in idiopathic hypertrophic pyloric stenosis.

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.

Adolescent↗
PubMed1995

Long-term outcome of endoscopic dilation of nonmalignant pyloric stenosis.

Although the immediate success of endoscopic balloon dilation of nonmalignant and noncongenital pyloric stenosis is known, little information is available on the long-term results of such therapy. Of 19 patients who underwent this treatment at our institution for gastric outlet obstruction, 3 (16%) experienced sustained relief and 16 (84%) had a recurrence of symptoms during a median follow-up period of 45 months. Twelve of the patients who had a recurrence of gastric outlet obstructive symptoms required further therapy. Our results suggest that if followed for a prolonged period of time, patients who have undergone endoscopic balloon dilation of nonmalignant pyloric stenosis have a high recurrence rate of symptomatic gastric outlet obstruction.

Adult↗
PubMed1996

Atypical pyloric stenosis in an infant with familial hyperlipidemia.

A 1-month-old infant presented with a typical pattern of pyloric stenosis but US revealed an intense hyperechogenicity of the thickened pyloric muscle. Cholecystitis and pancreatitis were also present in this child. Familial hyperchylomicronemia was detected. Surgery confirmed the fatty infiltration of the pyloric muscular layer, which was necrotic and inflammatory. Medical management with restriction of fat in the diet led to a complete recovery. This is an exceptional case of pyloric stenosis where the particular echographic appearance of the pyloric muscle led to successful to medical treatment.

Humans↗