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A 15-month-old girl with celiac disease presented with microcephaly and developmental delay. Head growth resumed during a gluten-free diet. Subsequent gluten ingestion resulted in no head growth, areflexia, and increased celiac antibodies. All resolved with gluten elimination. Poor head growth may precede other clinical manifestations of celiac disease.

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BACKGROUND AND OBJECTIVES: The purpose of the present study was to evaluate the results of diagnostic laparoscopy in children with chronic recurrent abdominal pain. PATIENTS AND METHODS: Thirteen children with chronic recurrent abdominal pain were subjected to diagnostic laparoscopy. Ages varied from 10 to 17 years. There were six males and seven females. Abdominal pain was present from 3 weeks to 12 months (mean, 2 months). Extensive laboratory and imaging studies did not contribute to the diagnosis. In all patients, the pain was disabling and severe enough to warrant repeated visits to the pediatrician, emergency room visits, or hospital admissions, as well as absence from school. RESULTS: All children recovered uneventfully. Laparoscopic findings that identified the cause of abdominal pain were obtained in 12 of 13 patients. Laparoscopic appendectomy was done in all patients. There were no operative complications. One child presented three months later with incomplete small bowel obstruction, which resolved with conservative management. There were no other postoperative complications. Follow-up varied from six months to three years. Abdominal pain resolved in ten patients. One patient presented eight months later with biliary dyskinesia. She improved following laparoscopic cholecystectomy and later on sphincterotomy, but her pain has not yet completely resolved. One patient presented six months later with abdominal pain secondary to intestinal adhesions. Her pain completely resolved after laparoscopic lysis of adhesions. A third patient who developed lower abdominal pain six months after laparoscopy improved with conservative management and antibiotics for pelvic inflammatory disease. CONCLUSIONS: Diagnostic laparoscopy is a valuable procedure in the management of children with chronic recurrent abdominal pain. In the present study, laparoscopic examination revealed the cause of abdominal pain in most patients, and this pain resolved in most cases. Based on our experience, we recommend diagnostic laparoscopy early in the course of debilitating chronic recurrent abdominal pain in children. Appendectomy should be done when no other significant cause of abdominal pain has been identified, even if the appendix looks normal.

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BACKGROUND: Nonspecific esophageal motility disorders (NEMDs) have been identified in up to 50% of adults with noncardiac chest pain or dysphagia. This study sought to determine the incidence of NEMDs in children with upper gastrointestinal tract symptoms and to evaluate the clinical course of pediatric patients with these manometric abnormalities. METHODS: The study involved 154 children aged 4 to 18 years (mean age, 11.6+/-2.6 years [SE]) who had upper gastrointestinal, swallowing-related symptoms. The children were evaluated by 24-hour intraesophageal pH monitoring, esophageal manometry, and esophagogastroduodenoscopy. RESULTS: Gastroesophageal reflux (GER) was diagnosed by pH study in 109 (71%) of 154 patients, and examination of biopsy specimens demonstrated esophagitis in 70 children with GER. Results of esophageal manometry were abnormal in 30 (67%) of 45 children without GER. A variety of motility disorders were diagnosed in 17 of the patients without GER, whereas NEMDs were diagnosed in the remaining 13 children (mean age, 10.6+/-2.7 years; 10 boys, 3 girls). Patients with GER showed normal esophageal wave propagation; however, mean lower esophageal sphincter pressure was significantly lower in patients with GER than in children with NEMDs. The children with NEMDs exhibited a diverse array of symptoms, including esophageal food impaction in 4 of the 13 patients. During a 36.2+/-4.3-month follow-up period, no correlation was found between therapeutic intervention and clinical course in the 13 patients with NEMDs. Symptomatic improvement occurred in 6 of 13 patients, including 3 children for whom no pharmacologic therapy was prescribed. CONCLUSIONS: These data indicate that NEMDs represent a 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 NEMDs should be considered in children who have this finding.

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Two distinct quinoprotein amine oxidases were found in Aspergillus niger mycelia grown on n-butylamine medium and purified using chromatographic techniques. The respective enzymes were termed AO-I, which had already been isolated, and AO-II, a new enzyme found in this study. HPLC indicated that their molecular masses are 150 kDa and 80 kDa, respectively. On SDS/PAGE, the enzymes gave a similar but distinct mobility, which corresponds to 75 kDa for the subunit dimeric AO-I and 80 kDa for monomeric AO-II. The absorption spectra of both enzymes were different from each other; the absorption maxima in the visible region were at 490 nm for AO-I and 420 nm for AO-II. The enzymes showed positive quinone staining, comparable substrate specificity, and sensitivity to inhibitors typical for copper/topa quinone-containing amine oxidases, but they had different copper contents and also differed in their N-terminal sequences. Their peptide maps showed almost identical patterns, with the exception of two additional bands for AO-II. Among the peptides obtained from digestion of AO-II, peptides with sequences corresponding to the N-terminal part of AO-I were detected. Polyclonal antibodies raised against AO-I and AO-II recognized both enzymes, but with different specificities. Using precipitation with AO-I, the antibody prepared against AO-II was purified and was shown to be specific only for AO-II. The cDNA of AO-I was cloned and sequenced. A highly conserved tetrapeptide sequence, Asn-Tyr-Glu-Tyr, was identified in which the first tyrosine residue (Tyr404) that could be converted to topa quinone was present in the 670-residue deduced amino acid sequence. Northern blot analysis indicated that AO-I was highly expressed in A. niger grown on n-butylamine as a single nitrogen source. Genomic Southern blot analysis confirmed that both enzymes are likely to be encoded by the same gene.

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OBJECTIVE: To determine the importance of acid reflux-induced dysmotility in the genesis of noncardiac chest pain in children. METHOD: We performed esophageal manometries during intraesophageal perfusion with 0.9% NaCl or 0.1 N HCl in 19 children (age, 14.5 +/- 0.5 yr) with gastroesophageal reflux, biopsy-proven esophagitis, and complaints of at least one episode of chest pain per day. RESULTS: Baseline esophageal motilities were normal in all patients. Eight of 19 children (42%) complained of chest pain during intraesophageal acid perfusion. In three of these eight patients, complaints of chest pain during acid perfusion were temporally associated with "conversion" of previously normal motility patterns to manometric tracings, indicating esophageal dysmotility. Compared with findings during saline perfusion, esophageal acid exposure in these three children resulted in significant increases in both the duration (13.6 +/- 4.0 vs 3.2 +/- 0.2 s, p < 0.05) and amplitude (105.2 +/- 7.8 vs 61.2 +/- 2.1 mm Hg, p < 0.05) of esophageal contractions during wet swallows. Symptoms of chest pain resolved in all patients after therapy with H2-receptor antagonists. CONCLUSIONS: These data represent the first demonstration of acid-induced esophageal dysmotility in children with chest pain and suggest that reflux-induced motor abnormalities contribute to the onset and/or exacerbation of chest pain in pediatric patients with gastroesophageal reflux and esophagitis.

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Esophageal motility was studied in 31 patients with mild to moderate esophagitis and in 48 patients without esophagitis to determine the effect of esophageal inflammation on lower esophageal sphincter pressure, and the amplitude, duration, and velocity of esophageal contractions. There were no significant differences in any of these parameters associated with esophageal inflammation. We conclude that mild to moderate esophagitis does not cause serious esophageal dysfunction in children.

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The relationship between gastric Helicobacter pylori colonization and esophagitis was determined in 457 children undergoing endoscopic evaluation of abdominal pain and/or vomiting. In all patients, biopsies of the esophagus were examined histologically, and two antral biopsies were analyzed for the presence of H. pylori, using standard microbiological and histochemical techniques. The incidence of biopsy-proven esophagitis was similar in H. pylori-positive (15/56 patients) and -negative (94/401; p = NS) groups. Clinical improvement, after 2 months of antisecretory therapy with H2-receptor antagonists, was independent of H. pylori status (11/15 vs. 68/94 responders; p = NS). All 26 H. pylori-negative nonresponders became asymptomatic with a second course of H2-blockers. The 4/15 H. pylori-positive patients (all of whom had associated gastritis/duodenitis) who failed antisecretory therapy responded clinically to treatment with amoxicillin plus bismuth subsalicylate. These data indicate that primary treatment of biopsy-confirmed esophagitis in children should include anti-secretory agents, regardless of H. pylori status. A small percentage of H. pylori-positive patients with esophagitis and concomitant gastroduodenal inflammation may require additional antibacterial therapy, suggesting that presence of the organism should be assessed in all pediatric patients undergoing upper endoscopic evaluation.

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The charts of 54 children diagnosed with antral H. 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 (> or = 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 by H. pylori is highly predictive of mucosal pathology in children. Initial therapy should be directed toward achieving bacterial eradication, as opposed to gastric acid suppression.

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A 14-year-old patient who was eventually found to have Gardner syndrome initially presented at the age of 3 years with a desmoid tumor involving the scalp. A careful review of the family history revealed a high incidence of colonic cancer, which prompted endoscopic evaluation of the patient. The discovery of adenomatous polyps in the colon confirmed the diagnosis of Gardner syndrome. In patients with hard or soft tissue tumors, the possibility of Gardner syndrome should be kept in mind, and a thorough family history taken. Early diagnosis may prevent malignant transformation of colonic polyps.

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Over a one-year period, 95 children and adolescents presenting with epigastric pain and/or vomiting, and without associated risk factors for development of peptide disease, underwent endoscopic antral biopsies for pathologic diagnosis and to detect presence of Campylobacter ss. pylori (C. pylori). Additional biopsies of the esophagus, stomach, and duodenum were obtained for histologic evaluation. C. pylori was identified in 16 patients (16.8%), all of whom had evidence of acute and/or chronic gastritis. Significant discriminating factors between C. pylori-positive and -negative subjects included age at presentation (positive vs negative = 14.6 vs 9.9 years, P less than 0.01), biopsy-confirmed gastritis (100% vs 30.4%, P less than 0.001), and diagnosis of duodenitis alone (0% vs 46.8%, P less than 0.001). Risk for bacterial colonization was significantly higher in the presence of endoscopic gastritis (P less than 0.001). Among C. pylori-positive patients, none responded to standard antiulcer therapy (H2-receptor antagonists, antacids). Symptomatic and histologic remission was achieved utilizing combined therapy with bismuth subsalicylate and antibiotics. Seven of 79 C. pylori-negative patients with biopsy-proven gastritis who responded poorly to antisecretory therapy had the organism identified in follow-up antral biopsies; these patients improved clinically following treatment for C. pylori. These data suggest that C. pylori is a significant factor in the etiology of upper gastrointestinal tract inflammatory disease in pediatrics, and presence of the organism should be evaluated, particularly in children with evidence of acute and/or chronic gastritis.

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The incidence and temporal patterns of gastroesophageal reflux (GER) in infants presenting with an apparent life-threatening event (ALTE) was compared with GER characteristics of infants evaluated for persistent emesis, utilizing continuous 24 h intraesophageal pH monitoring. These data indicate that the incidence of significant GER was similar in both groups, despite the absence of a clinical vomiting history in 46% of ALTE patients. Furthermore, infants with ALTE demonstrate a significantly higher incidence of sleep reflux when compared with control infants presenting with vomiting alone (27 vs. 0%, p less than 0.001). Awake GER beyond the first two postprandial hours was not observed in either study group. Monitoring results, therefore, indicate that significant GER is common in infants with ALTE; and these infants manifest an apparently unique pattern of GER distinct from that observed in age-matched controls with GER alone. Possible relationships between GER in ALTE patients and the development/onset of apneic episodes are discussed.

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We evaluated five children with severe psychomotor retardation who developed frequent vomiting and poor weight gain after surgical placement of a feeding gastrostomy tube. Prolonged pH probe testing before surgery did not reveal notable gastroesophageal reflux (GER). Treatment with 12-hour gastrostomy tube feeding resulted in a marked reduction in vomiting; after one year of continuous feeding, all patients had achieved significant weight gain (mean, 44.0%). Esophageal manometrics and 24-hour pH probe testing before and at the end of the 12-month continuous-feeding period demonstrated low pressures of the lower esophageal sphincter and significant GER in the five children studied. These results indicate that children may develop symptomatic GER after gastrostomy tube placement. In such patients continuous gastrostomy tube feeding may result in a cessation of vomiting and achievement of significant weight gain. Definitive antireflux surgery can then be performed with the patient in an improved nutritional state.

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A new 24-h ambulatory esophageal pH monitoring system (AMBI 24) was evaluated in 72 pediatric patients with suspected gastroesophageal reflux (GER). Forty-seven of these patients were monitored at home and the other 25 in our hospital. This system was employed without complication in infants and a full range of pediatric patients, as well as in older children with severe psychomotor delay. The data obtained were consistent with those reported utilizing standard monitoring equipment, and the results served as the basis for subsequent medical management. The results of this study, therefore, suggest that this method of esophageal pH monitoring is a safe and effective means of evaluating GER while allowing for patient mobility.

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