Abstract Background and Aim Data on factors influencing time to remission in pediatric Crohn's disease (CD) are very limited in the literature. The aim of this retrospective cohort study was to describe the trends of time to clinical remission over the past decade and to identify factors associated with time to clinical remission in children with luminal CD. Methods Patients under 18 years old diagnosed between 2009 and 2019 were included. All data were collected from the patients' medical records. Survival analyses and linear regression models were used to assess the impact of clinical, laboratory, endoscopic, histological, and therapeutic factors on time to clinical remission. Results A total of 654 patients were included in the study. There was no change in the time to clinical remission over the decade. Female sex in adolescents (adjusted bêta regression coefficient [aβ] = 31.8 days, P = 0.02), upper digestive tract involvement (aβ = 46.4 days, P = 0.04) perianal disease (aβ = 32.2 days, P = 0.04), presence of active inflammation on biopsies at diagnosis (aβ = 46.7 days, P = 0.01) and oral 5‐aminosalicylates (5‐ASA) exposure (aβ = 56.6 days, P = 0.002) were associated with longer time to clinical remission. Antibiotic exposure (aβ = −29.3 days, P = 0.04), increased eosinophils (aβ = −29.6 days, P = 0.008) and combination of exclusive enteral nutrition with tumor‐necrosis‐factor‐alpha (TNF‐alpha) inhibitors as induction therapy (aβ = −36.8 days, P = 0.04) were associated with shorter time to clinical remission. Conclusion In children with newly diagnosed Crohn's disease, time to clinical remission did not shorten during the decade. It was associated with baseline clinical and histological data and treatment strategies. Combination of enteral nutrition and TNF‐alpha inhibitors was associated with faster clinical remission.

North American Indian Childhood Cirrhosis (NAIC) has only been described in the Cree-Ojibway First Nations of Northern Quebec. NAIC presents with transient neonatal jaundice and progresses to biliary cirrhosis often requiring liver transplantation (LT) in childhood. Only 30 patients have been described to date and risk factors associated with an earlier progression to LT have not yet been identified. Moreover, NAIC patients seem to experience more fractures than other cholestatic patients, but this has not been confirmed. With this study, we aimed to identify predictors at 6 months from presentation that might suggest progression to end-stage liver disease as well as evaluate bone health in affected patients. The records of all NAIC patients diagnosed between 2000–2020 were reviewed. Subjects were split into 2 groups based on whether they had undergone LT or not (No_LT) before age 18. Recorded complications included: hepatic encephalopathy (HE), variceal bleeding (VB), ascites, spontaneous bacterial peritonitis (SBP), bacteremia, and pulmonary shunts. Laboratory data (alanine aminotransferase, ALT; total bilirubin, TB) were collected at presentation and follow-up. Bone mineral density (BMD) of the lumbar spine (Z-scores) and number of fractures were compared between groups. NAIC patients were then compared to cohorts with other chronic cholestatic diseases such as biliary atresia (BA, n=24) and Alagille syndrome (AS, n=11). A total of 14 patients (M=9, F=5) were diagnosed with NAIC. Average age at presentation was 2.1 months (IQR 1–16.9 months), with 3 patients older than 18 months. Overall, 6 patients were transplanted (avg 8.6±1.7 years), one was listed for LT but died waiting, and 7 remained in a state of compensated cirrhosis. All complications were only observed in the LT group except for VB which also occurred in 2 patients of the No_LT group. Between presentation and 6 months, ALT and TB levels increased more in the LT vs No_LT group (p=ns). There was a greater variation of ALT/TB levels in the LT group (p=0.0047) even once the 3 patients with late referral were excluded (p=0.0381). No patient in the No_LT group had fractures, while 3 did in the LT group. BMD was lower in the LT group vs No_LT group (-2.2±1.2 vs. -1.1±1.3, p=ns). NAIC patients had lower BMD (-1.7±1.3) than those with AS (0.7±0.9, p=0.003) or BA (-0.9±1.4, p=ns) and had a higher prevalence of fractures (21.4% vs. 12.5% for BA and 18.2% for AS patients). In patients with NAIC, variation of ALT/TB levels at 6 months from presentation may be used as an early predictor of unfavorable outcome and progression towards end-stage liver disease. Patients who evolved to LT had more complications, higher prevalence of fractures and lower BMD values. Compared to children with BA or AS, NAIC patients had poorer bone health. None

Abstract Background The European Society of Pediatric Gastroenterology Hepatology and Nutrition suggests that the diagnosis of Celiac disease (CD) can be confirmed solely on the basis of clinical symptoms and bloodwork including a level of transglutaminase IgA-antibodies (TGA) ≥ 10 times the upper limit of normal (10XN). In Canada and the United States, this recommendation has not been endorsed. We recently demonstrated that TGA ≥ 10XN performed at our institution (INOVA Diagnostics’ Quanta Lite) was a reliable predictive test of villous atrophy in patients with suspicion of CD. Aims The aim of the present study was to investigate the rate of supplemental endoscopic or histological findings in a cohort of children with TGA ≥ 10XN and the association of these findings with clinical symptoms. Methods Consecutive children with suspected CD who had an endoscopy between 2011 and 2018 were included in this analysis. Data was extracted from our CD database. The macroscopic and histological findings were reported. We compared these diagnoses to the clinical symptoms. Results From 2011 to 2018, 405 new cases of CD were identified in our pediatric center. In total, 238 (58.7%) patients had baseline TGA levels ≥ 10XN (67.2% females, median (IQR) age 8.4 (4.8–12.2)). The median interval between the first visit to the gastroenterology unit and the endoscopy was 43.0 (21.0–78.0) days. In total, 58% of the endoscopies had macroscopic findings in the bulb (37.8 %) or the duodenum (41.5%) including a mosaic pattern, mucosal fissuring, or erythema. Seven cases (2.8%) of esophagitis were identified during endoscopy; histological analysis confirmed eosinophilic esophagitis in 3 cases (1.2%) and peptic esophagitis in 4 cases. Non-specific gastritis was present in 58 patients (24.4%) and 2 cases of Helicobacter pylori infection were identified. The biopsies showed subtotal/total villous atrophy of duodenum in 171 (71.8%) or partial villous atrophy in 51 patients (29.8 %). Ten patients (4,3%) had villous atrophy in the duodenal bulb alone, with normal biopsies of the second part of the duodenum. Abdominal pain did not correlate with gastritis or duodenitis. However, children with diarrhea had a greater prevalence of visible endoscopic inflammation in the duodenum than those without diarrhea: 53.5% vs 38.9% respectively; P= 0,037. Conclusions Apart from the classical features associated with CD, the supplementary diagnostic yield of endoscopy was low. There were only a few cases of additional diseases identified by the endoscopic procedure in a large cohort of children and adolescents with suspicion of CD. Therefore, these results support the no-biopsy approach in the settings of TGA ≥ 10XN using a reliable diagnostic kit. Funding Agencies None

Rubinstein-Taybi syndrome is a rare disorder associated with mutations in the CREB-binding protein gene (1). It is characterized by broad thumbs and toes, characteristic facies, postnatal failure to thrive, and delayed development (2). These children often have chronic gastrointestinal problems, including gastroesophageal reflux, feeding difficulties, and chronic constipation (2–4). They are not reported to have an increased incidence of atopic disease. Herein is the first report, to the authors’ knowledge, of eosinophilic gastrointestinal disease presenting as dysphagia in this population.

A common feature of cystic fibrosis (CF) is the functional derangement of the exocrine pancreas, which affects output of pancreatic lipase. This condition results in severe dietary malabsorption due to the poor hydrolysis of triacylglycerol (TG) in the lumen of the small intestine. Despite the benefits of pancreatic enzyme supplements, patients with CF present with persistent intestinal fat malabsorption. The aim of the present investigation was to determine whether defects in the intracellular phase of lipid transport occur in this pathophysiology in addition to the known disturbed digestive processes. Our hypothesis was tested by incubating intestinal biopsies from six CF and six healthy subjects with radiolabeled lipid and protein precursors. Lipid esterification and secretion were markedly decreased by 22-31% and 38-42%, respectively, in CF samples, as noted by the low incorporation of [(14)C]palmitic acid into TGs, phospholipids, and cholesteryl esters in patients' duodenal explants and culture media compared with controls (100%). Accordingly, the output of TG-rich lipoproteins was substantially reduced (P < 0.05), and a similar trend was observed for high-density lipoproteins. Because intestinal lipoprotein assembly/secretion shows an absolute requirement for apolipoprotein (apo) B-48, radioactive labeling experiments were performed; these experiments demonstrated a significantly (P < 0.05) diminished synthesis of apoB-48 (40%) and apoA-I (30%). Given the critical role of microsomal triglyceride transfer protein in the formation of apoB-containing lipoproteins, its activity was determined and not found to be altered in CF intestinal tissue. Together, these results suggest that CF malabsorption may also be caused by defects in mucosal mechanisms leading to abnormal lipoprotein delivery into the blood circulation.

Transport mechanisms, whereby alimentary lipids are digested and packaged into small emulsion particles that enter intestinal cells to be translocated to the plasma in the form of chylomicrons, are impaired in cystic fibrosis. The purpose of this paper is to focus on defects that are related to intraluminal and intracellular events in this life-limiting genetic disorder. Specific evidence is presented to highlight the relationship between fat malabsorption and essential fatty acid deficiency commonly found in patients with cystic fibrosis that are often related to the genotype. Given the interdependency of pulmonary disease, pancreatic insufficiency and nutritional status, greater attention should be paid to the optimal correction of fat malabsorption and essential fatty acid deficiency in order to improve the quality of life and extend the life span of patients with cystic fibrosis.

BACKGROUND:Juvenile polyposis and hereditary haemorrhagic telangiectasia are autosomal dominant disorders with distinct and non-overlapping clinical features. The former, an inherited gastrointestinal malignancy predisposition, is caused by mutations in MADH4 (encoding SMAD4) or BMPR1A, and the latter is a vascular malformation disorder caused by mutations in ENG (endoglin) or ACVRL1 (ALK1). All four genes encode proteins involved in the transforming-growth-factor-beta signalling pathway. Although there are reports of patients and families with phenotypes of both disorders combined, the genetic aetiology of this association is unknown.METHODS:Blood samples were collected from seven unrelated families segregating both phenotypes. DNA from the proband of each family was sequenced for the ACVRL1, ENG, and MADH4 genes. Mutations were examined for familial cosegregation with phenotype and presence or absence in population controls. Findings No patient had mutations in the ENG or ACVRL1 genes; all had MADH4 mutations. Three cases of de-novo MADH4 mutations were found. In one, the mutation was passed on to a similarly affected child. Each mutation cosegregated with the syndromic phenotype in other affected family members.INTERPRETATION:Mutations in MADH4 can cause a syndrome consisting of both juvenile polyposis and hereditary haemorrhagic telangiectasia phenotypes. Since patients with these disorders are generally ascertained through distinct medical specialties, genetic testing is recommended for patients presenting with either phenotype to identify those at risk of this syndrome. Patients with juvenile polyposis who have an MADH4 mutation should be screened for the vascular lesions associated with hereditary haemorrhagic telangiectasia, especially occult arteriovenous malformations in visceral organs that may otherwise present suddenly with serious medical consequences.

Studies of the pharmacokinetics of omeprazole in children with gastroesophageal reflux disease (GERD) remain scarce despite the vast number of reports on its efficacy. The objectives of this study were to assess the pharmacokinetics of omeprazole in healthy adults and in children with GERD. Omeprazole (Losec®, delayed-release capsules) was administered orally to 18 healthy adults (mean age 36.8 years) and 12 children with GERD (mean age 6.1 years). Blood samples were collected over 5 hours, and plasma concentrations were assessed using liquid chromatography. Population pharmacokinetic parameters were calculated using NONMEM®. A 1-compartment model with zero-order absorption and a lag time was used. The population approach was well suited to the limited number of samples available, and residual variability was low. Oral clearance (CL/F) and apparent volume of distribution (Vss/F) in healthy adults (Mean ± SD: 0.62 ± 0.27 L/h/kg and 0.76 ± 0.26 L/kg, respectively) were not significantly different than those in children with GERD (0.51 ± 0.34 L/h/kg and 0.66 ± 0.25 L/kg, respectively). Healthy adults displayed a statistically significantly longer delay in drug absorption (Lag time: 0.62 ± 0.15 hours) as compared with that observed in children with GERD (0.12 ± 0.03 hours, P < 0.05). On the basis of these findings, omeprazole dosings on a milligram-per-kilogram basis are recommended with no further adjustments for the treatment of GERD in children.

ABSTRACTAim:To review the authors’ experience with eosinophilic esophagitis.Methods:Between 1993 and 2001, the authors identified 12 patients with eosinophilic esophagitis defined on histologic criteria (≥20 eosinophils per high‐power field in the distal esophageal epithelium). The authors reviewed medical records for details of clinical presentation; laboratory data; radiologic, endoscopic, and histologic findings; and the results of continuous esophageal pH probe monitoring.Results:Seventy‐five percent of the patients were male. The median age at presentation was 10.8 years (range, 1–17 years). Commonly reported symptoms were dysphagia with solid food (66%), epigastric pain (42%), food impaction (50%), and vomiting (8%). Food allergy was reported in 50% and asthma in 33%. Peripheral eosinophilia (>700/mm3) was found in 42%. Upper gastrointestinal series performed in eight patients, showed esophageal luminal narrowing in three. Computed tomography, performed in two patients, revealed thickening of the esophageal wall. Esophageal pH probe monitoring, performed in nine patients, revealed no abnormal acid reflux. All of the monitored patients had episodic alkalinization of the esophagus. Upper endoscopic analysis revealed white specks on the esophageal mucosa in 42%, esophageal narrowing in 33%, esophageal rings in 25%, and esophageal furrowing in 8%. The mean eosinophils per high‐power field was 65 (range, 20–200). Histologic characteristics included juxtaluminar (33%) and peripapillary clusters of eosinophils (33%), increased papillary height (50%), and basal cell hyperplasia (34%).Conclusion:Solid food dysphagia was the most common feature of eosinophilic esophagitis in our patients. Alkalinization of the esophagus was found in all nine pH probe recordings of eosinophilic esophagitis patients and may represent a previously unreported characteristic of the condition.

Clinical Pharmacology & Therapeutics (2003) 73, P48–P48; doi:

BACKGROUND & AIMSAlthough antibiotics are frequently used to treat Crohn's disease, this practice is not supported by strong evidence from randomized trials.METHODSWe conducted a double-blind multicenter study of patients with active Crohn's disease of the ileum, right colon, or both. Patients were randomized to receive oral ciprofloxacin and metronidazole, both 500 mg twice daily, or placebo for 8 weeks. All patients received oral budesonide 9 mg once daily. The primary efficacy measure was the proportion of patients in remission at week 8.RESULTSOf the 134 patients who were randomized, 130 were evaluated for efficacy; 66 received placebo, and 64 received antibiotics. At week 8, 21 patients (33%) assigned to antibiotics were in remission as compared with 25 patients (38%) in the placebo group (P = 0.55; absolute difference, -5%; 95% confidence interval, -21% to 11%). An interaction (P = 0.025) between treatment allocation and disease location on treatment response was identified. Among patients with disease of the colon, 9 of 17 (53%) were in remission after treatment with antibiotics, compared with 4 of 16 (25%) of those who received placebo (P = 0.10). Discontinuation of therapy because of adverse events occurred in 13 of 66 (20%) patients treated with antibiotics, compared with 0 of 68 in the group who received placebo (P < 0.001).CONCLUSIONSIn patients with active Crohn's disease of the ileum, the addition of ciprofloxacin and metronidazole to budesonide is an ineffective intervention, but this antibiotic combination may improve outcome when there is involvement of the colon.

North American Indian childhood cirrhosis (CIRH1A, or NAIC), a severe autosomal recessive intrahepatic cholestasis described in Ojibway-Cree children from northwestern Quebec, is one of several familial cholestases with unknown molecular etiology. It typically presents with transient neonatal jaundice, in a child who is otherwise healthy, and progresses to biliary cirrhosis and portal hypertension. Clinical and physiological investigations have not revealed the underlying cause of the disease. Currently, liver transplantation is the only effective therapy for patients with advanced disease. We previously identified the NAIC locus by homozygosity mapping to chromosome 16q22. Here we report that an exon 15 mutation in gene FLJ14728 (alias Cirhin) causes NAIC: c. 1741C-->T in GenBank cDNA sequence NM_032830, found in all NAIC chromosomes, changes the conserved arginine 565 codon to a tryptophan, altering the predicted secondary structure of the protein. Cirhin is preferentially expressed in embryonic liver, is predicted to localize to mitochondria, and contains WD repeats, which are structural motifs frequently associated with molecular scaffolds.

North American Indian childhood cirrhosis (NAIC, or CIRH1A) is an isolated nonsyndromic form of familial cholestasis reported in Ojibway-Cree children and young adults in northwestern Quebec. The pattern of transmission is consistent with an autosomal recessive mode of inheritance. To map the NAIC locus, we performed a genomewide scan on three DNA pools of samples from 13 patients, 16 unaffected siblings, and 22 parents from five families. Analysis of 333 highly polymorphic markers revealed 3 markers with apparent excess allele sharing among affected individuals. Additional mapping identified a chromosome 16q segment shared by all affected individuals. When the program FASTLINK/LINKAGE was used and a completely penetrant autosomal recessive mode of inheritance was assumed, a maximum LOD score of 4.44 was observed for a recombination fraction of 0, with marker D16S3067. A five-marker haplotype (D16S3067, D16S752, D16S2624, D16S3025, and D16S3106) spanning 4.9 cM was shared by all patients. These results provide significant evidence of linkage for a candidate gene on chromosome 16q22.

BACKGROUND:North American Indian childhood cirrhosis (NAIC) is a distinct, rapidly evolving form of familial cholestasis found in aboriginal children from northwestern Quebec. This is a retrospective review of the 30 patients treated in Quebec since the discovery of NAIC in 1970.METHODS:The clinical records and histologic samples from 30 patients were reviewed. Extensive metabolic, biochemical, viral, genetic, and radiologic studies were performed in most patients.RESULTS:Genetic analysis suggests autosomal recessive inheritance and a carrier frequency of 10% in this population. Gene mapping studies showed that the NAIC gene is located on chromosome 16q22. Typically, patients have neonatal cholestatic jaundice (70%) or hepatosplenomegaly (20%) with resolution of clinical jaundice by age 1 year but persistent direct hyperbilirubinemia. Portal hypertension was documented in 29 patients (91%). Variceal bleeding (15 patients, 50%) occurred as early as age 10 months. Surgical portosystemic shunting was performed in 13 of these 15 patients (87%); 4 (31%) rebled after 1 to 5 years. Fourteen patients died (47%). In 10 (71%), liver disease was the cause. Four children died of liver failure before liver transplantation became available. In transplanted livers, no recurrence of NAIC was observed after 1 to 10 years. Recognized infectious, metabolic, toxic, autoimmune, and obstructive causes of cirrhosis have been eliminated. The histologic features of NAIC show early bile duct proliferation and rapid development of portal fibrosis and biliary cirrhosis, suggesting a cholangiopathic phenomenon.CONCLUSION:Together with gene mapping studies showing that the NAIC gene is different from those of other familial cholestases, these observations suggest that NAIC is a distinct entity that could be classified as "progressive familial cholangiopathy."

The ideal therapy for Helicobacter pylori would cure the infection without resulting in the development of antibiotic resistance. Current therapies have variable cure rates; the reasons for treatment failure include bacterial resistance and poor compliance. Some antibiotics, such as furazolidone, may be affordable agents to treat this infection worldwide. New proton pump inhibitors, such as rabeprazole, can potentiate antibiotics. Nutriceuticals and probiotics demonstrate interesting in vitro activity against H pylori. Children rarely have symptoms to this infection and, therefore, are a suitable group in which to assess different nonaggressive therapies.

91 Fulminant hepatic decompensation is described in biliary atresia patients with advanced biliary cirrhosis. A decreased hepatic microvascularisation was proposed to explain this complication. Case report: A 17 month old female infant with biliary atresia who underwent a Kasai operation at 7 weeks of age, was transferred from Morocco with severe malnutrition, ascites, unexplained fever and recurrent gastrointestinal bleeding. Investigations showed: hemoglobin 64 g/l, albumin 23 g/l, total bilirubin 249 µmol/l, conjugated bilirubin 151 µmol/l, ALT: 151 U/l and AST: 204 U/l. She had received a somatostatin perfusion at 4 µg/kg/hour for the last two weeks which was changed to octreotide 5 µg/kg/hour. An upper endoscopy revealed grade III and IV varices and sclerotherapy was performed. Examination of her ascites revealed a sterile transudate fluid. She was listed for liver transplantation and treated with albumin, diuretics, enteral and parenteral feedings and antibiotic coverage for persistent unexplained fever. Ten days later, she deteriorated with irritability and feeding difficulties. Physical examination was unchanged but transaminases were abruptly elevated: AST 9430 U/l; ALT 3215 U/l. The coagulation profile revealed an INR of 2 and bilirubin as 710 µmol/l total, 421 conjugated. Octreotide perfusion was stopped and transaminases improved to AST 1880 U/l and ALT 1391 U/l gradually over 3 days. Variceal bleed recurred the following day so octreotide was restarted at 3.5 µg/kg/h. The bleeding stopped but transaminases increased again: AST 5330 µl and ALT 2119 U/l. A liver transplantation was performed the following day, with severe hemorrhagic complications. The patient died 24 hour post-transplant during a second reoperation for ongoing intraabdominal bleeding. Conclusion: Octreotide infusion decreases portal blood flow and therefore might have contributed to severe decompensation in our patient. Prolonged octreotide infusion should be carefully monitored and perhaps avoided in patients with biliary atresia and advanced decompensated cirrhosis.

Journal of Pediatric Gastroenterology and NutritionVolume 27, Issue 4 p. 469-469 Annual Meeting of the North American Society for Pediatric Gastroenterology and Nutrition; Orlando, October 22–24, 1998 CLINICAL EXPERIENCE WITH CHRONIC HEPATITIS C VIRUS INFECTION IN CHILDREN D. Levesque, D. Levesque Division of Gastroenterology, Ste Justine Hospital, University of MontrealSearch for more papers by this authorS. Martin, S. Martin Division of Gastroenterology, Ste Justine Hospital, University of MontrealSearch for more papers by this authorE. Drouin, E. Drouin Division of Gastroenterology, Ste Justine Hospital, University of MontrealSearch for more papers by this authorF. Alvarez, F. Alvarez Division of Gastroenterology, Ste Justine Hospital, University of MontrealSearch for more papers by this author D. Levesque, D. Levesque Division of Gastroenterology, Ste Justine Hospital, University of MontrealSearch for more papers by this authorS. Martin, S. Martin Division of Gastroenterology, Ste Justine Hospital, University of MontrealSearch for more papers by this authorE. Drouin, E. Drouin Division of Gastroenterology, Ste Justine Hospital, University of MontrealSearch for more papers by this authorF. Alvarez, F. Alvarez Division of Gastroenterology, Ste Justine Hospital, University of MontrealSearch for more papers by this author First published: 01 October 1998 https://doi.org/10.1002/j.1536-4801.1998.tb01357.xRead the full textAbout 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. Volume27, Issue4October 1998Pages 469-469 RelatedInformation

Journal of Pediatric Gastroenterology and NutritionVolume 25, Issue 2 p. 210-213 Case Report Gastrointestinal Cytomegalovirus Infection Complicating Crohn's Disease in an Adolescent Without AIDS E. Drouin, E. Drouin Division of Gastroenterology-Nutrition, Department of Pediatrics, Quebec, CanadaSearch for more papers by this authorE. Seidman, E. Seidman Division of Gastroenterology-Nutrition, Department of Pediatrics, Quebec, CanadaSearch for more papers by this authorP. Russo, P. Russo Department of Pathology, Ste-Justine Hospital, University of Montreal, Montreal, Quebec, CanadaSearch for more papers by this authorC. Deslandres, Corresponding Author C. Deslandres n/[email protected] Division of Gastroenterology-Nutrition, Department of Pediatrics, Quebec, CanadaAddress correspondence and reprint requests to Dr. C. Deslandres, Division of Gastroenterology-Nutrition, Hôpital Ste-Justine, 3175 Côte Ste-Catherine, Montreal, Quebec, H3T 1C5 Canada.Search for more papers by this author E. Drouin, E. Drouin Division of Gastroenterology-Nutrition, Department of Pediatrics, Quebec, CanadaSearch for more papers by this authorE. Seidman, E. Seidman Division of Gastroenterology-Nutrition, Department of Pediatrics, Quebec, CanadaSearch for more papers by this authorP. Russo, P. Russo Department of Pathology, Ste-Justine Hospital, University of Montreal, Montreal, Quebec, CanadaSearch for more papers by this authorC. Deslandres, Corresponding Author C. Deslandres n/[email protected] Division of Gastroenterology-Nutrition, Department of Pediatrics, Quebec, CanadaAddress correspondence and reprint requests to Dr. C. Deslandres, Division of Gastroenterology-Nutrition, Hôpital Ste-Justine, 3175 Côte Ste-Catherine, Montreal, Quebec, H3T 1C5 Canada.Search for more papers by this author First published: 01 August 1997 https://doi.org/10.1002/j.1536-4801.1997.tb00678.x Dr. E. Drouin's current address is Montreal Children's Hospital, McGill University, Montreal, Quebec, Canada. 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