Objective To study the presentation and treatment in two infants who presented with refractory Sandifer syndrome (SS).Study Design We retrospectively reviewed the cases of two infants who presented to our outpatient clinic with SS who were refractory to conventional treatment.Results We report two patients with refractory SS who responded to treatment with hypoallergenic formula.Conclusion It is important to consider a diagnosis of milk protein allergy responsive to hypoallergenic formula in patients with SS who are refractory to conventional antireflux treatment.

Liver abscesses in CGD are generally refractory to antibiotics and drainage procedures. Hepatic resection after failing medical therapy has been the accepted treatment. Recent literature has demonstrated a beneficial effect of corticosteroids in CGD. We report successful management of multiple, difficult to drain liver abscesses in a 10 year old child with CGD, using corticosteroids. There are no formal guidelines for steroid use in CGD liver abscesses in children. There was no clinical or radiological recurrence of the abscesses after discontinuation of steroids.

Idiopathic isolated benign non-traumatic biliary strictures are a rare cause of obstructive jaundice in children. The treatment has been surgical with resection of the stricture and biliary-enteric anastomosis. We report a case of an idiopathic isolated benign non-traumatic inflammatory biliary stricture successfully treated with endoscopic dilatation in a 26-month-old male with persistent obstructive liver disease after surgical resection of an adjacent lymph node.

INTRODUCTION Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently used for fever control and are generally considered to be safe. Prolonged use and higher doses of NSAIDs are associated with gastrointestinal complications (1); even chronic "minidose" use of aspirin (<100 mg/d) is associated with gastrointestinal bleeding (2). These complications from NSAID use are a significant cause of mortality in adults (3). Herein we describe 4 children who were hospitalized for gastrointestinal bleeding and hematemesis after receiving only 1 or 2 doses of ibuprofen. Four patients, ages 16 to 36 months, developed hematemesis within 24 hours after receiving 1 or 2 age- and weight-appropriate doses of ibuprofen for fever control. In each patient esophagogastroduodenoscopy demonstrated an antral gastric ulcer. Although chronic use of NSAIDs has been associated with gastric ulcers, gastric ulcers have not been described in children receiving short-term NSAID therapy. METHODS AND RESULTS During a 1-year period, 4 children were admitted to our institution for hematemesis after receiving only 1 or 2 weight-appropriate doses of ibuprofen for fever. A retrospective chart review was performed. The mean age was 23.5 ± 9.0 months. All of the patients had fever higher than 101.5°F. Two of the 4 children had a cough and 2 had rhinitis. Three of the 4 children received a single dose of ibuprofen and the fourth received 2 doses. All 4 children developed hematemesis at home within 24 hours of starting ibuprofen. None of the patients were receiving other medications and none had a history of gastrointestinal problems. Hemoglobin values ranged from 6.4 to 10.9 g/dL. All other laboratory results, including coagulation studies, were normal (Table 1).TABLE 1: Patient demographics, symptoms, and laboratory dataAll of the patients had esophagogastroduodenoscopy performed during their first hospital day. In each patient an isolated gastric antral ulcer was visualized (Fig. 1). Multiple gastric biopsy specimens were obtained from each patient and stained using hematoxylin and eosin and Gomori methenamine silver stain. This showed evidence of mild gastritis, which included mucin depletion and foveolar hyperplasia consistent with drug-induced reactive gastritis. There was no histological or culture evidence of Helicobacter pylori infection in any patient. Biopsies from the esophagus and duodenum had normal findings. All of the patients were treated with lansoprazole, a proton pump inhibitor (PPI; Prevacid; TAP Pharmaceuticals, Lake Forest, IL) for at least 2 months and there was no further reduction in hemoglobin values, indicating resolution of their gastrointestinal bleeding.FIG. 1: Gastric antral ulceration in 1 subject (arrow).DISCUSSION Chronic use of NSAIDs has been associated with gastroduodenal injury, including gastritis, gastric and duodenal ulcers, and gastrointestinal bleeding (1). Gastric or duodenal ulcers are detected during endoscopy in as many as 15% to 30% of adult chronic NSAID users (4). In pediatric patients with juvenile rheumatoid arthritis receiving chronic NSAID therapy, >75% of patients with abdominal pain had gastritis, antral erosions, or ulcers (5). Two studies reporting the safety of acetaminophen and ibuprofen in children have shown that there were no statistical differences in gastrointestinal complications (6,7). However, in both studies, hospitalizations for gastrointestinal bleeding occurred only in those receiving ibuprofen (6,7). Factors associated with NSAID-associated gastrointestinal complications include existing ulcers, high dose or multiple use of NSAIDs, comorbid illnesses such as rheumatoid arthritis, concomitant corticosteroid or anticoagulant use, coinfection with Helicobacter pylori, and prolonged continuous use. The greatest risk of developing gastrointestinal complications is during the first 30 days after the start of treatment (8). The proposed mechanism of NSAID-induced gastrointestinal injury is referred to as the "dual injury hypothesis" because of the direct and indirect toxic effects on the gastrointestinal mucosa. NSAIDs have direct toxic effects on the gastrointestinal mucosa and indirect effects through active hepatic metabolites and decreases in protective mucosal prostaglandins (9). Hepatic metabolites are excreted into the bile and subsequently into the duodenum, where they cause mucosal damage to the stomach during duodenogastric reflux and mucosal damage to the small intestine by antegrade passage through the gastrointestinal tract (9). Patients who develop gastrointestinal bleeding caused by NSAID-associated ulcers should discontinue their use of NSAIDs. PPIs are the medication of choice to promote the healing of ulcers. PPIs promote more rapid healing of gastric ulcers than the use of histamine 2–receptor antagonists (10). The PPI lansoprazole received US Food and Drug Administration approval for the treatment of NSAID-associated ulcers. Our report is unique in that our patients received only 1 or 2 self-administered weight- and age-appropriate doses of ibuprofen before developing gastrointestinal bleeding. This is in contrast to previous studies in which subjects were randomized to receive acetaminophen or ibuprofen (6,7). Three of the 4 families reported giving the medication before daytime naps or at bedtime. It is possible that this led to delayed gastric emptying of the NSAID and direct mucosal damage. We did not determine the relationship between NSAID administration and food ingestion in this group of patients. Endoscopic studies in adults have shown that a single 650-mg dose of aspirin is frequently associated with gastric mucosal injury. Gastric petechiae (mucosal and submucosal hemorrhage) become evident within 1 hour after aspirin ingestion and small gastric erosions appear within several hours (11). In young children these lesions may progress more frequently to ulcers and gastrointestinal bleeding. Although it would have been desirable to perform follow-up endoscopic examinations in our patients, this was not practical because of their young age and the rapid resolution of their symptoms. Although the number of patients in our report is small, these findings suggest initially treating fever with acetaminophen instead of NSAIDs. This is based on our reported experience, as well as that of others who reported hospitalizations because of gastrointestinal bleeding in patients receiving ibuprofen only (6,7). Because of the relative young age of our described patients, patients younger than 36 months may be at an increased risk for the development of gastrointestinal bleeding after the use of NSAIDs.

Purpose: Patients with hiatal hernias are usually asymptomatic or have only vague, intermittent symptoms such as epigastric pain, nausea and reflux symptoms. In this report, we describe two children with a hiatal hernia who initially presented with severe, iron deficiency anemia. Results: The first patient was a 20 month old boy, born prematurely at 26 weeks. At 18 months, he had 2 episodes of hematemesis. He had a hemoglobin of 5.8, a hematocrit of 19.8, WBC of 12,200, and platelets of 570,000. Serum iron was 36 and TIBC 452, with a transferrin saturation of 8%. Stool for occult blood was intermittently positive. He was transfused with packed red blood cells. An upper gastrointestinal series showed a large hiatal hernia that was later confirmed by upper endoscopy. The endoscopy and biopsies showed evidence of reflux esophagitis. A pH study showed significant reflux. The patient underwent hiatal hernia repair and Nissen fundoplication at 24 months. Since the surgery his hemoglobin and hematocrit have remained normal for 14 months. The second patient was a 6 year old boy referred to Pediatric Hematology and Oncology with a hemoglobin of 6.0 and a hematocrit of 18.9. He had platelets of 357,000and a WBC of 11,100. Serum iron was 12, total iron binding capacity was 487, with a transferrin saturation of 2%. He had a 2 day history of abdominal pain and vomiting. An upper GI series showed a hiatal hernia and upper endoscopy showed severe erosions of the gastric fundus. He had an exploratory laparotomy and hiatal hernia repair, suture repair of the esophageal hiatus and lesser curvature anterior gastropexy. Since the surgery his hemoglobin and hematocrit have remained normal for 7 months. Conclusions: Severe iron deficiency anemia may be associated with hiatal hernia. In our first patient, the anemia may have resulted from the reflux esophagitis secondary to the hiatal hernia. In our second patient the anemia was due to gastric erosions that may have resulted from prolapse of the gastric fundus into the esophagus. Hiatal hernia should be considered in patients with severe iron deficiency anemia.

Chronic pancreatitis is rare in children. A number of potential etiologies have been identified, including gene mutations of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR), the cationic trypsinogen gene (PRSS1) and pancreatic secretory trypsin inhibitor (SPINK1). It is not clear whether individuals with the combination of CFTR and SPINK1 are at increased risk for chronic pancreatitis. We present a case of a 12 year old male who had mutations in both the CTFR and SPINK1 and early onset of severe chronic pancreatitis. Case report: The patient was a 12 year old male who had been previously healthy, although he had intermittent vague abdominal pain for several years. He had no history of chronic respiratory disease. The family history was unknown. At 12 years of age he was hospitalized 3 times for pancreatitis. Abdominal ultrasound and magnetic resonance cholangiopancreatography showed a dilated pancreatic duct with atrophy and calcifications of the gland. Endoscopic retrograde cholangiopancreatography showed chronic pancreatitis with moderate side branch ectasia, and a diffusely dilated (6mm), irregular pancreatic duct with numerous filling defects. Sphincterotomy was performed and a white, soft, stone-like material was removed from the duct with a partially inflated balloon. A temporary pancreatic duct stent was placed acutely and the patient was started on therapy with pancreatic enzymes. After this, the patient remained free of abdominal pain. An evaluation determined that the patient had 2 CFTR gene mutations, (Delta F508, the most common mutation, and D1152H, a rarely described mutation) and an additional SPINK1 mutation. This patient developed severe chronic pancreatitis at an early age and was found to have 2 CFTR mutations and a SPINK1 mutation. The CFTR mutations predispose to abnormalities in pancreatic duct secretion, whereas the SPINK1 mutation causes damage at the level of the acini. The combined effects of these defects may explain why this patient developed chronic pancreatitis at an early age.

Purpose: Biliary dyskinesia, a motility disorder of the gallbladder, causes poor emptying and pain. Quantitative cholecystokinin cholescintigraphy (QCC) identifies patients with abnormal gallbladder emptying. Ten patients (8 female, 2 male, mean age 13.8 y) with chronic right upper quadrant pain were evaluated for biliary dyskinesia using QCC. Abdominal complaints were present for a mean of 13.6 months. Epigastric pain, nausea and vomiting, food intolerance and diarrhea and/or constipation were also reported. Methods: Abdominal ultrasound, upper GI series and abdominal CT scan were done. Abnormal gallbladder ejection fractions after cholecystokinin were defined as less than 35% excretion. Results: Nine patients had normal endoscopies with one showing histological evidence of esophagitis. All patients had normal liver function. None of the patients had Helicobacter pylori. The average gallbladder ejection fraction in this group of patients was 16.97%. All 10 patients had a laparoscopic cholecystectomy and histology showed mild chronic cholycystitis in 8 of 10 patients; two had normal gallbladders. Gallstones were found surgically in 2 patients that had normal imaging studies. The mean follow up period following surgery was 23.8 months. The four patients with significant right upper quadrant pain before surgery had complete resolution of their abdominal symptoms following cholecystectomy with no other significant gastrointestinal complaints. The six patients who had continuing abdominal complaints following surgery reported right upper quadrant pain in addition to a combination of epigastric pain, vomiting and or constipation/diarrhea before surgery. Conclusions: (1) Cholecystectomy may not relieve all abdominal complaints in documented cases of biliary dyskinesia. (2) Cases of biliary dyskinesia with abdominal complaints confined to the right upper quadrant are more likely to respond to cholecystectomy. (3) Cases of biliary dyskinesia with multifocal abdominal complaints are less likely to respond completely to cholecystectomy. (4) Biliary dyskinesia may be part of a more global motility disturbance.

Objectives To determine the clinical presentation, radiographic, endoscopic and manometric findings, and clinical outcome of esophageal food impaction (EFI) in pediatric patients. Methods We retrospectively reviewed the clinical course of 12 pediatric patients with EFI over a 10-year period. Results All 12 patients described initially presented to our emergency department for care. Four patients (25%) required previous endoscopic intervention for disimpaction of EFI. Eleven required endoscopic removal of their EFI, and 1 patient’s food impaction resolved spontaneously. The mean duration of food impaction was 20 hours prior to endoscopic intervention. Endoscopy demonstrated an esophageal stricture in 1 patient with a history of trisomy 21 and tracheoesophageal fistula repair. While there was no visual evidence of esophagitis in any patient, 5 of 7 had histologic evidence of esophagitis. Upper gastrointestinal series demonstrated the esophagus to be anatomically normal in 10 of 12 patients (83%); 1 patient had an esophageal stricture and another an esophageal web. Four of 8 patients studied had nonspecific esophageal motility abnormalities. Conclusions EFI in children is not generally associated with underlying esophageal anatomic abnormalities. Esophagitis and nonspecific esophageal motility disorder abnormalities may be etiologic factors. Endoscopic removal of the EFI was safe and effective and is recommended as there is little likelihood of spontaneous resolution of EFI in children.

Lactose intolerance (LI), a consequence of decreased or absent intestinalβ-galactosidase activity is common in the pediatric population. Treatment generally includes dietary lactose restriction, use of exogenous lactase or a combination of the two. To evaluate the effectiveness of these therapies we interviewed 100 patients (58 male, 42 female, aged 4-19 y, mean=11.0 y) 6-36 months after diagnosed as being LI by a positive hydrogen breath test, using a standardized questionnaire. The interview included questions about initial symptoms, present diet, use of exogenous lactase and present symptoms. Participants also graded their symptom severity. Of the 100 subjects interviewed, 60% were on a lactose-free diet, 67% used lactase tablets, and 42% used both. Data analysis showed a significant (p<0.01) reduction in the frequency of abdominal pain, diarrhea, gassiness, bloating and abdominal distention, whether they were on a lactose-restricted diet or taking lactase tablets. Diet restriction alone resulted in a significant decrease in the reported symptoms of abdominal pain by 50%, diarrhea by 83%, bloating by 66%, gassiness by 60%, and abdominal distension by 66%. Lactase tablets alone resulted in a significant decrease in abdominal pain by 47%, diarrhea by 60%, bloating by 41%, gassiness by 44% and abdominal distension by 66%. However, children who were both lactose-restricted and used lactase tablets had an even greater decrease of symptom occurrence (p<0.001) when compared to either alone. The results describing severity of symptoms were similar, showing a significant (p<0.01) reduction of abdominal pain, diarrhea and gassiness employing either therapy alone. Combining therapies resulted in a more significant (p<0.001) reduction of symptom severity than either alone. Use of single or combined therapies however, had no effect on the occurrence or severity of bloating and abdominal distention. Conclusions: A large percentage of pediatric patients continue to utilize treatment for their lactose intolerance up to 3 years following diagnosis. Treatment of lactose intolerance by either dietary restriction or use of exogenous lactase causes a significant reduction of symptoms and symptom severity, and the efficacy of these modalities increases significantly when these two modalities are combined.

Gallbladder dyskinesia is defined as abnormal contractility of the gallbladder. This motility disorder of the biliary tree has not been extensively studied in the pediatric population. In this report we describe four patients presenting with chronic right upper quadrant abdominal pain who were evaluated with gallbladder emptying scans. Their mean age was 14.2±1.7 (range 11 to 18) years. All four patients were female. Abdominal complaints were prevalent for a mean of 6.3 ± 3.8 weeks. The following symptoms were also reported; nausea and vomiting in 3, epigastric pain in 2 and nocturnal pain in 2 patients. There was no clear correlation between the onset of the abdominal pain and the meals. No patients had pain radiating to the back or subscapular area. All patients had normal liver function tests initially. Evaluations included a normal abdominal ultrasound, upper G.I. series, and abdominal CT scan in all patients. Three patients had a normal upper endoscopy, with one patient demonstrating biopsy confirmed esophagitis. None of the patients were positive for Helicobacter pylori by serology, Clo-test or histology. Delayed gallbladder emptying was demonstrated utilizing cholescintigraphy with Tc99m Choletec. The mean ejection fraction measured in these patients was 12.9 ± 6.7%. Abnormal gallbladder ejection fractions after cholecystokinin were defined as less than 35% excretion. All 4 patients underwent laparoscopic cholecystectomy. Histology demonstrated mild chronic cholecystitis in all 4 patients. The mean follow-up was 13.0 ± 2.9 weeks (range 8 to 20 weeks). Three of the 4 patients have remained asymptomatic. One of the patients had a subsequent sphincterotomy because of persistent pain and elevated biliary pressure.In conclusion, delayed gallbladder emptying identified gallbladder dyskinesia in 4 of 4 children with chronic right upper quadrant pain. Symptoms resolved in 3 of 4 patients after cholecystectomy, while one patient required an endoscopic sphincterotomy. A gallbladder emptying study should be performed in children with right upper quadrant pain and negative routine evaluation.

Nonspecific esophageal motility disorders (NEMD) comprise up to 50% of manometric diagnoses in adults with non-cardiac chest pain or dysphagia. This study sought to determine the incidence of NEMD in children with upper gastrointestinal tract symptoms, and to evaluate the clinical course of pediatric patients with these abnormalities. Study design: We studied 154 children, 4 to 18 years of age (mean ± sem: 11.6 ± 2.6 years), utilizing 24 hour intraesophageal pH monitoring, esophageal manometry and esophagogastroduodenoscopy. Results: Gastroesophageal reflux (GER) was demonstrated by pH studies in 109 of 154 patients (71%). In subjects with GER, manometric studies demonstrated reduced lower esophageal sphincter pressures and normal esophageal wave propagation; and, in biopsies showed esophagitis in 70 patients. Biopsy-confirmed Helicobacter pylori gastritis was found in 11 of 154 patients (7%). Esophageal manometries were abnormal in 30 of 45 subjects without GER (67%), and these included 13 children with NEMD (mean age: 10.6 ± 2.7 years; M:F = 10:3). Children with NEMD manifested a diverse group of symptoms, including 4 of 13 patients who presented with esophageal food impaction. Over a 36.2 ± 4.3 month follow-up period, no correlation was found between therapeutic intervention and the clinical course in the 13 patients with NEMD. Symptomatic improvement occurred in 6 of 13 patients, including in 3 children for whom no pharmacologic therapy was offered. Conclusions: These data indicate that NEMD represents the most common group of esophageal manometric abnormalities in children with upper gastrointestinal tract symptoms and without GER. Food impaction appears to be a relatively frequent complication, and NEMD should be considered in children presenting with this finding.

Three pediatric age siblings with hereditary pancreatitis required therapeutic intervention for intractable pain resulting in malnutrition. One had recurrent pseudocysts. The first patient, a 6-year-old girl was status post biliary sphincterotomy and pancreaticojejunostomy. Endoscopic retrograde cholangiopancreatography (ERCP) demonstrated narrowing proximally and distally within the remaining pancreatic duct. A stent was placed across the pancreatic duct. This relieved her abdominal pain. Serial stents were placed at variable intervals and then removed. The patient experienced prolonged symptom-free intervals, but required additional periods of serial stent placement for 2 recurrences of abdominal pain. Her brother developed pancreatic pseudocysts at 2 years of age. ERCP showed pancreas divisum and multiple pseudocysts. He was treated with external drainage and sphincterotomy. The pseudocysts resolved and he did well. At 5 years of age, he had recurrence of pseudocysts. ERCP with cannulation of the minor papilla demonstrated a large pseudocyst communicating with an irregular pancreatic duct. A stent was placed across the minor papilla and past the origin of the pseudocyst. The pseudocyst resolved within 1 week. The stent was replaced twice and then removed. The patient has been free of abdominal pain with no recurrence of pseudocysts for more than one year. The last patient had ERCP performed at 6 years of age for reoccurence of abdominal pain that demonstrated a dilated pancreatic duct, which bifurcated and ended abruptly in the body of the pancreas. At 9 years of age, she developed intractable abdominal pain. Repeat ERCP showed total occlusion of the dilated pancreatic duct in the head of the pancreas. Biliary sphincterotomy did not relieve her symptoms. She subsequently underwent a 90% subtotal pancreatectomy. The body and tail of the pancreas were shrunken, nodular, and calcified. The patient has remained well in 6 months of follow-up. Conclusions: Ductal anomalies may play a role in symptomatology and possibly progression of disease in hereditary pancreatitis in children. Endoscopically-placed stents are effective therapy for hereditary pancreatitis. Persistent relief of symptoms may be due to dilating strictures within the pancreatic duct. Pancreas divisum may contribute to disease when present in patients with hereditary pancreatitis.

Polypoid lesions of the gallbladder in children are rare. We report a case of a gallbladder polyp in a 14-year-old boy who presented with recurrent right upper quadrant abdominal pain. Ultrasound examination of the abdomen revealed a polypoid lesion of the gallbladder. His symptoms resolved after laparoscopic cholecystectomy. Histological examination of the gallbladder demonstrated a benign adenomatous polyp. Although the experience with polypoid lesions of the gallbladder in children is limited, we currently recommend cholecystectomy because these lesions are associated with acalculous cholecystitis, and because their long-term effects are unknown.

Purpose This report describes a female infant with stage 4 multifocal ganglioneuroblastoma with gastric involvement. Patient The patient had a right cervical tumor, a left posterior mediustinal tumor, bilateral adrenal tumors, and bony and bone marrow metastases. The tumor cells were diploid and lacked N-myc gene amplification. The gastric involvement, which did not produce clinical symptoms, was only detected by meticulous exploration during laparotomy. Results Our patient achieved only a partial response to alternating cycles of cyclophosphamide, vincristine, and adriamycin; and etoposide and cisplatin. She currently has stable, unresectable disease with elevated catecholamines. Conclusions Multifocal ganglioneuroblastomas may arise from either neuroblastic rests or aberrant deposits of neuroblasts. The latter mechanism may have accounted for our patient's gastric tumor. Patients with multifocal ganglioneuroblastomas warrant meticulous radiographic and surgical evaluation to completely document the full extent of disease, and to ensure appropriate staging and therapy.

once a day. Fourteen of the 18 patients had been tried on a hydrolyzed casein formula for at least 1 week without improvement. Parental counseling, as previously described by Taubman,4 had been tried for each patient without a decrease in crying time. Esophagogastroduodenoscopy (EGD) was performed in each patient using a flexible Olympus XP10 endoscope (Olympus Corp., Lake Success, New York) after intravenous sedation with meperidine (1 mg/kg) or after receiving chloral hydrate 50-75 mg/kg 1 hour prior to the procedure. Esophagitis was diagnosed endoscopically by the presence of friability, erythema, ulceration, or granularity. Biopsies were taken under di-

Journal of Pediatric Gastroenterology and NutritionVolume 19, Issue 3 p. 360-360 Inflammatory Bowel Disease: PDF Only 123 NONSPECIFIC ESOPHAGEAL MOTILITY DISORDERS (NEMD) IN CHILDREN J Rosario, J Rosario Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this authorM S Medow, M S Medow Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this authorH E Bostwick, H E Bostwick Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this authorM S Halata, M S Halata Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this authorS Berezin, S Berezin Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this authorS M Schwarz, S M Schwarz Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this author J Rosario, J Rosario Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this authorM S Medow, M S Medow Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this authorH E Bostwick, H E Bostwick Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this authorM S Halata, M S Halata Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this authorS Berezin, S Berezin Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this authorS M Schwarz, S M Schwarz Dept of Peds, New York Medical College, Valhalla, NYSearch for more papers by this author First published: 01 October 1994 https://doi.org/10.1002/j.1536-4801.1994.tb11426.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume19, Issue3October 1994Pages 360-360 RelatedInformation

Journal of Pediatric Gastroenterology and NutritionVolume 19, Issue 3 p. 359-359 Inflammatory Bowel Disease: PDF Only 121 ESOPHAGEAL DYSMOTILITY ELICITED BY ACID IN CHILDREN WITH ESOPHAGITIS M S Medow, M S Medow Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this authorM S Glassman, M S Glassman Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this authorM S Halata, M S Halata Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this authorL J Newman, L J Newman Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this authorH E Bostwick, H E Bostwick Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this authorS Berezin, S Berezin Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this author M S Medow, M S Medow Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this authorM S Glassman, M S Glassman Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this authorM S Halata, M S Halata Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this authorL J Newman, L J Newman Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this authorH E Bostwick, H E Bostwick Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this authorS Berezin, S Berezin Dept. of Pediatrics, New York Medical College, Valhalla, N.Y.Search for more papers by this author First published: 01 October 1994 https://doi.org/10.1002/j.1536-4801.1994.tb11424.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume19, Issue3October 1994Pages 359-359 RelatedInformation

The charts of 54 children diagnosed with antralH. pylori were reviewed, to establish the incidence of gastroduodenal inflammation and compare therapeutic efficacies of antisecretory vs. antibacterial therapy. Histology demonstrated normal mucosa in three cases (6%) and gastric/duodenal inflammation (≥ Whitehead grade 3) in 51 biopsies (94%). 23/43 children (53%) initially responded to H2-blockers; however, by 10 mo, 13 had relapsed clinically. All of these patients subsequently responded to amoxicillin plus bismuth subsalicylate. Of the 20 children who failed to enter remission after an initial course of H2-blockers, all became symptom-free after treatment with amoxicillin/bismuth. Compared to antisecretory agents, antibacterial treatment induced clinical remission in 11/11 patients (p<0.001), who remained symptom-free for 10±0.2 mo. Clinical remissions were maintained in significantly more patients following amoxicillin/bismuth vs. H2-blockers (44/54 vs. 10/43 courses,p<0.001); and, the cumulative probability of remaining asymptomatic was significantly greater in the antibiotic group (p<0.001). These data suggest that gastric colonization byH. pylori is highly predictive of mucosal pathology in children. Initial therapy should be directed toward achieving bacterial eradication, as opposed to gastric acid suppression.

A 12-year-old girl is described who developed rectal bleeding 5 months after being diagnosed as having a Coombs-positive hemolytic anemia. Colonoscopy showed that the rectal bleeding was due to ulcerative proctitis. This is the first case report of Coombs-positive hemolytic anemia preceding the onset of ulcerative proctitis in a child.