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Pyloric stenosis: a postoperative ultrasonic study.

Six infants with hypertrophic pyloric stenosis and 20 control infants were studied ultrasonically on four occasions during the first year of life. At each examination the total diameter and muscle wall thickness of the pylorus were measured. Initially the pylorus was significantly (P less than 0.05) larger in the hypertrophic pyloric stenosis group but returned to normal values by 6 months postoperation. The control group showed a small increase in size of the pylorus over the 12 month period.

Humans↗

Transient neonatal myasthenia gravis and pyloric stenosis.

The case report describes the occurrence of hypertrophic pyloric stenosis in a premature infant with neonatal myasthenia gravis. The infant presented for pyloromyotomy on the nineteenth day of life. Diagnosis of myasthenia gravis was made based on maternal history and clinical findings of poor muscle tone, weak suck, and weak cry. The anesthetic management is discussed with reference to the problems of newborn myasthenia gravis and pyloric stenosis as they relate to anesthetic drugs and techniques.

Anesthesia↗

Risk of infantile hypertrophic pyloric stenosis after maternal postnatal use of macrolides.

A case report has suggested that exposure to erythromycin through breast milk might cause infantile hypertrophic pyloric stenosis. This study therefore examined whether macrolides, transmitted via breast milk, increase the risk of infantile hypertrophic pyloric stenosis in neonates. A population-based cohort study was conducted, based on data from a prescription registry, the Danish Birth Registry and North Jutland County's hospital discharge registry, Denmark, and comprising 1166 pregnant women who had been prescribed macrolides from birth to 90 d postnatally, and 34,690-41,778 pregnant women as controls. The odds ratios for infantile hypertrophic pyloric stenosis varied between 2.3 and 3.0 according to different periods of postnatal exposure, and after stratification for gender they were 10.3 [95% confidence interval (95% CI) 1.2-92.3] for girls and 2.0 (95% CI 0.5-8.4) for boys. The use of macrolides during breast-feeding increases the risk of infantile hypertrophic pyloric stenosis.

Abnormalities, Drug-Induced↗

The role of ultrasonography in the diagnosis of pyloric stenosis: a decision analysis.

BACKGROUND/PURPOSE: The appropriate role for ultrasonography (US) as a replacement for the upper gastrointestinal series (UGI) in vomiting infants remains undefined. The authors have used decision analysis techniques to determine whether the use of ultrasonography as an initial screen in vomiting infants is cost effective when compared with the UGI as the only study. METHODS: Two diagnostic strategies were compared: 1) UGI alone and 2) ultrasonography followed by an UGI series in 50% of cases when ultrasonography scan was negative for pyloric stenosis. The test sensitivity (US, 0.9; UGI, 1.0) and test specificity (US, 1.0; UGI, 1.0) and the incidence of pyloric stenosis among vomiting infants presenting to the community pediatrician (0.30) or after a negative examination by an experienced examiner (0.02 to 0.18) were obtained from a review of the literature. The relative charges for ultrasonography and UGI were obtained from a national survey from which the cost ratio of US to UGI was estimated to range from 0.67 to 1.81 with a median of 1.06. RESULTS: Under these baseline assumptions, UGI only was the preferred strategy. The results of the decision analysis were sensitive to, or dependent on, assumptions made regarding the incidence of pyloric stenosis, the US to UGI cost ratio, the sensitivity of the US, and the proportion of patients that proceed to UGI when the US scan was negative for pyloric stenosis. When at least 50% of patients whose US scan was negative for pyloric stenosis proceeded to a UGI, UGI remained the preferred strategy for all cost ratios examined (0.6 to 1.7). Even when no patients proceeded to UGI, the cost ratio of US to UGI had to be less than 0.7 under the typical incidence (0.30) of pyloric stenosis among vomiting infants presenting to the community pediatrician for US to be cost effective. Finally, only UGI was indicated when an olive was not appreciated by an experienced examiner. CONCLUSION: Under assumptions that fit most clinically relevant circumstances, the UGI as the initial study is the most cost-effective radiological diagnostic test in the evaluation of the vomiting infant.

Contrast Media↗

Birth defects in relation to Bendectin use in pregnancy. II. Pyloric stenosis.

To test the hypothesis that the use of Bendectin in pregnancy increases the risk of pyloric stenosis, we determined rates of antenatal Bendectin exposure among 325 infants with pyloric stenosis and among two control groups comprising infants with other defects; one consisted of 3,153 infants with other conditions, and the other, a subset of that group, consisted of 724 infants with defects that may have had their origins at any time in pregnancy. Comparisons between the cases and the two control series yielded estimated relative risks of 0.9 (95% confidence interval, 0.6 to 1.2) and 1.0 (0.7 to 1.4), respectively. The findings from this large case-control study suggest that Bendectin does not increase the risk of pyloric stenosis.

Abnormalities, Drug-Induced↗

[Hypertrophic pyloric stenosis--an indication for sonography].

The pyloric region of 58 infants who presented with vomiting was examined by real-time ultrasound. Transverse diameter of the pylorus and single wall thickness were measured. In 18 patients sonographic diagnosis of hypertrophic pyloric stenosis (HPS) was made and subsequently confirmed by surgery. The mean (+/- one standard deviation) of the transverse diameter and of the pyloric wall thickness in patients with HPS was 15 (+/- 1) mm. and 5.5 (+/- 0.7) mm., respectively. Forty infants matched for age and sex distribution without gastrointestinal symptoms served as controls. The measurements for the transverse diameter were 9.6 (+/- 1.8) mm. and for the wall thickness 1.9 (+/- 0.5) mm. Diameter values of patients with HPS were significantly (p less than 0.001) higher than those of the control group and those of the remaining 40 patients without HPS. Real-time sonography proved a reliable tool in the diagnosis of HPS.

Age Factors↗

Prognosis of patients with gastric cancer and pyloric stenosis: histological differentiation.

The clinicopathology of gastric cancer with pyloric stenosis was examined with special reference to histological differentiation. One hundred sixteen patients treated in Department of Surgery II, Kyushu University Hospital, were classified into differentiated (DT: n = 47) and undifferentiated types (UT: n = 69). The UT group was significantly younger than the DT group (P < 0.05). There were no differences in the incidence of serosal invasion, liver metastasis, lymph node metastasis, and the clinical stage between the groups. The incidence of peritoneal dissemination of the UT group was 41% (28/69), a value significantly higher than the 23% (11/47) for the DT group (P < 0.05). The 5-year survival rates of the DT and UT groups were 27% and 16%, respectively, with survival time for the UT group being significantly less than that of the DT group (P < 0.05). In patients with pyloric stenosis and an undifferentiated adenocarcinoma with the risk of peritoneal dissemination, intensive adjuvant chemotherapy seems essential to improve the prognosis.

Adenocarcinoma↗

Oesophageal atresia and pyloric stenosis - an association.

The incidence of pyloric stenosis is higher in infants with oesophageal atresia than in the general paediatric population. Techniques in oesophageal atresia repair, such as gastrostomy, may be responsible for this. Pyloric stenoses occurred in two cases of oesophageal atresia repair using gastrostomy and transpyloric feeding tubes.

Esophageal Atresia↗

The inheritance of pyloric stenosis explained by a multifactorial threshold model with sex dimorphism for liability.

The inheritance of pyloric stenosis is explained by a multifactorial threshold model with an underlying assumption that the liability for the disease is distributed in males and females showing a sex dimorphism. From the available data on familial occurrences of pyloric stenosis, it is shown, that an extra maternal effect is not required to explain the familial risk of pyloric stenosis, as opposed to the earlier literature. Explicit expressions for familial risks of a discontinuous trait exhibiting dimorphism of liability are presented, based on a model originally proposed by Rice et al [1981], which do not require the approximation of univariate normality of a conditional bivariate normal distribution.

Factor Analysis, Statistical↗

Pyloric stenosis presenting as severe prolonged jaundice. A case report.

A 17-day-old infant with pyloric stenosis presenting with severe neonatal jaundice is described. The bilirubin level rose to 371 mumol/l and an exchange transfusion was considered. No history of frequent or forceful vomiting was given and the usual symptoms and signs of pyloric stenosis were absent. Radiographic studies revealed features typical of hypertrophic pyloric stenosis. At laparotomy a pyloromyotomy was performed and the jaundice subsided rapidly.

Humans↗

The association of sex ratio anomalies with pyloric stenosis.

Published family data were examined for evidence of aberrant sex ratios in relatives of pyloric stenosis index cases. An excess of males over females was found among unaffected members of sibships in which there occurred more than one case of pyloric stenosis. The male excess among affected members of these sibships did not differ from that among index cases without affected sibs. An unusual frequency of spontaneous abortions in these subships, which might account for the observed excess of males, was not observed. No evidence was found of sex ratio anomalies in other classes of relative of pyloric stenosis index cases, whether or not the index cases had affected sibs.

Abortion, Spontaneous↗

Multinodular adult hypertrophic pyloric stenosis.

A case of multinodular hypertrophic pyloric stenosis is described in a 57-year-old woman. Over a 3-month interval, there was progressive enlargement of several mucosal nodules overlying hypertrophied muscularis, and one nodule obstructed the pyloric opening. Diagnosis was made at operation and symptoms resolved after Billroth I gastrectomy.

Female↗

Pyloric stenosis and direct hyperbilirubinemia with alpha-1-antitrypsin deficiency.

The occurrence of unconjugated hyperbilirubinemia in infants with pyloric stenosis is common. We report an infant who presented with projectile vomiting secondary to pyloric stenosis. In addition, he had conjugated hyperbilirubinemia which proved to be due to alpha-1-antitrypsin deficiency of PiZZ phenotype. This is the first case report of such an association. Infants with pyloric stenosis and conjugated hyperbilirubinemia should be investigated for underlying infectious, metabolic causes or anatomical defects of the biliary tree.

Humans↗

Primary hypertrophic pyloric stenosis in the adult.

Analysis of 100 consecutive patients with pyloric outlet obstruction revealed that 37% of the obstructions were secondary to peptic ulcer disease and 42% were caused by malignant neoplasm. Only a single patient with primary hypertrophic pyloric stenosis was identified, and whether this lesion is a cause or effect of peptic ulcer disease remains unclear. Similarly, the association of this entity with congenital pyloric stenosis is unknown.

Adult↗

Study of the interstitial cells of Cajal in infantile hypertrophic pyloric stenosis.

BACKGROUND & AIMS: The interstitial cells of Cajal form a network in close association with the smooth muscle of the gut. They are regarded as pacemaker cells and might be involved in motility disorders. Their distribution was studied in a common disorder with a dysfunction of the pyloric sphincter called infantile hypertrophic pyloric stenosis. METHODS: Specimens from 27 infants with pyloric stenosis and 12 controls were processed for immunohistochemistry using a specific antiserum raised against c-kit, a tyrosine kinase receptor expressed by interstitial cells. RESULTS: In the normal pylorus, numerous interstitial cells were labeled throughout the tissue. In pyloric stenosis, c-kit immunoreactivity was absent in the major part of the tissue. Interstitial cells were observed only in the inner part of the musculature, near the submucosal edge, and in the antrum, at the proximal end of the biopsy specimens. CONCLUSIONS: The lack of interstitial cells in the pylorus possibly contributes to the motility disturbance of infantile pyloric stenosis.

Female↗

The pathology of infantile hypertrophic pyloric stenosis after healing.

INTRODUCTION: Infantile hypertrophic pyloric stenosis (IHPS) is a common surgical affection of unknown etiology. The muscular hypertrophy is known to resolve within a few months after pyloromyotomy (PM). The pathology of IHPS has been studied extensively at the time of PM, but the fate of the pylorus after healing remains unknown. MATERIALS AND METHODS: We had the rare opportunity to study two pyloric biopsy specimens obtained 4 months and 2 years (respectively) after an uncomplicated PM for IHPS. They were compared with the initial specimen in one case, with 26 other specimens of IHPS, and with five normal controls. Immunohistochemistry using the avidin-biotin complex (ABC) system was performed for S-100 and nerve growth factor receptor, as markers for the enteric nervous system, and for the tyrosine kinase receptor c-kit, as a marker for the interstitial cells of Cajal (pacemaker cells). NADPH-diaphorase histochemistry was performed as a marker for the neuronal enzyme nitric oxide synthase, which produces the inhibitory neurotransmitter nitric oxide. RESULTS: In both cases of IHPS, after healing, the circular musculature was not hypertrophic. For all markers studied, the distribution appeared similar to that in the normal pylorus. In contrast, all specimens obtained at the time of PM displayed a severe reduction of the different markers in the hypertrophic musculature. DISCUSSION: The pathological features observed in the circular layer in IHPS appear to resolve within a few months after PM. This suggests that the involvement of the enteric nervous system in IHPS might be milder than generally assumed. The etiology remains obscure, but our occasional observations may provide new insight into the pathophysiology of IHPS, and are in agreement with the excellent longterm clinical outcome for IHPS.

Biomarkers↗

Lack of intestinal pacemaker (C-KIT-positive) cells in infantile hypertrophic pyloric stenosis.

The pathogenesis of infantile hypertrophic pyloric stenosis (IHPS) is not well understood. Recent studies have shown that the protonocogene c-kit is essential for the development or maintenance of autonomic gut motility, and also show that the c-kit gene protein product (C-KIT) positive cells in the mammalian gut are responsible for intestinal pacemaker activity. This study examines cells in the pyloric muscles of 23 patients (16 with IHPS, 7 controls) for the presence of the C-KIT (C-KIT+), using immunohistochemical techniques with antihuman C-KIT sera. In the controls, many C-KIT immunoreactive (IR+) cells were observed in the muscle layers. The myenteric plexuses were demarcated by a moderate number of C-KIT-IR+ cells. However, in the IHPS patients, C-KIT-IR were either absent or significantly reduced. No C-KIT-IR+ cells were found around the myenteric plexuses. These findings suggest that a lack of c-kit expression (as an indicator of intestinal pacemaker activity) in the hypertrophic pyloric smooth muscles may be an important factor in the pathogenesis of IHPS.

Biological Clocks↗