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Eytan Wine

Publications and source records attributed to Eytan Wine.

7 recordsLinked to original sources
PubMed2006

Biliary atresia with choledochal cyst: implications for classification.

BACKGROUND & AIMS: To illustrate the limitations of the embryonic and perinatal classification system of biliary atresia (BA), we present a child with an antenatal diagnosis of choledochal cyst (CC) associated with BA and review the published literature. METHODS: Medline and Pubmed were searched for "BA and CC," "cystic biliary atresia," "BA and cysts," and "biliary cystic malformations." RESULTS: A 7-week-old with an antenatal diagnosis of CC was found to have BA associated with CC. The literature search identified 88 cases of BA with CC. Sixty-seven cases had type 1 BA (atresia of the common bile duct), 2 had type 2 BA (atresia of the common hepatic duct), and 19 had type 3 BA (atresia of the porta hepatis). Of the 27 cases of antenatal diagnosis of BA with CC only 1 had associated congenital anomalies. Outcome analysis showed poor outcomes were significantly more common (P = .009) and occurred earlier (P = .0249) in patients with type 3 BA. Children with type 3 BA were 5.4 times more likely to develop poor outcomes compared with type 1 (hazard ratio, 5.4; 95% confidence interval, 1.03-27.8). CONCLUSIONS: BA associated with CC forms a distinct subtype of BA, characterized by a preponderance of type 1 BA, a relatively good clinical outcome after surgery, and an absence of associated congenital anomalies. Antenatal diagnosis of many affected infants supports their inclusion within the embryonic BA group and suggests that a broader interpretation of the embryonic phenotype and further classification of BA based on genetic susceptibility may be required.

Biliary Atresia↗
PubMed2006

Polymorphisms in the TNF-alpha promoter and variability in the granulomatous response in patients with Crohn's disease.

Granulomas may be found in 30-70% of patients with Crohn's disease (CD). The etiology of granuloma formation in CD is presently unknown. Elevated levels of TNF-alpha are found within granuloma tissue, and are required to maintain granuloma formation in animal models. TNF-alpha production has been shown to influenced by TNF-alpha promoter polymorphisms. We hypothesized that heterogeneity for granulomas in CD might be influenced by the TNF-alpha promoter genotype. Patients with confirmed CD that had undergone full colonoscopy with multiple biopsies and/or surgical resection, served as the study group. One hundred healthy individuals served as a control population for genotyping. Patients and controls underwent genotyping for four TNF-alpha polymorphisms: 238G/A, 308 G/A,857 C/T, and 863 C/A. Inclusion and exclusion criteria were met in 155 patients (1-68 y). Polymorphisms in the TNF promoter were found in 16.6% (238G/A), 14.5% (308 G/A), 36.6% (857 C/T) and 30.7% (863G/A). No significant association was found for any of the individual polymorphisms with presence or absence of granulomas. In conclusion, we did not find an association between individual polymorphisms in the TNF-alpha promoter and presence of granulomas in CD. The reason for heterogeneity in granuloma formation in patients with CD remains elusive.

Adult↗
PubMed2005

Pediatric gastrointestinal diseases: are drugs the answer?

Owing to the lack of large randomized controlled studies, which would produce level 1 evidence, to guide management of gastrointestinal disorders in children, data are often extrapolated from adult studies to aid in treatment strategies. However, there are unique aspects to the management of children and adolescents with these chronic diseases, including issues of growth, side effects, long-term outcomes and psychosocial factors that might not be considered in adult trials. There is a major need for increased research in this population. In the future, a better understanding of the pathophysiologic mechanisms of these diseases should guide the development of rational novel therapies with better safety profiles for children with gastrointestinal disorders.

Adrenal Cortex Hormones↗
PubMed2005

TNF promoter polymorphisms and modulation of growth retardation and disease severity in pediatric Crohn's disease.

OBJECTIVES: Delayed growth is common in pediatric Crohn's disease (CD). Multiple factors have been shown to affect growth in this situation, the most prominent being the presence and severity of inflammation and inadequate nutritional intake. Inflammation, anorexia, and weight loss are all manifestations of circulating TNF-alpha, which is elevated in CD. The ability to secrete TNF-alpha may be affected by polymorphisms in the TNF-alpha promoter. The aim of our study was to determine whether growth retardation and disease severity in pediatric onset CD are affected by TNF promoter genotype. METHODS: Genotyping for TNF-alpha and NOD2/CARD15 single nucleotide polymorphisms was performed in 87 patients with detailed growth records. Parameters including disease location and disease severity were recorded, and the effect of these polymorphisms on Z-scores for height and weight at disease onset and during follow-up were analyzed. RESULTS: Lower age of onset was linked to more height retardation, while the presence of colonic disease and the absence of ileal disease were more likely to predict the absence of growth retardation. The presence of two polymorphisms thought to decrease circulating TNF-alpha was associated with higher mean Z-scores for height and a trend toward less growth retardation. Two other polymorphisms were modestly associated with disease severity. CONCLUSION: Polymorphisms in the TNF-alpha promoter may independently modulate growth and disease severity in pediatric onset CD. The effect of these polymorphisms does not appear to be mediated via weight loss, and is relatively modest.

Adenine↗
PubMed2004

Pediatric Crohn's disease and growth retardation: the role of genotype, phenotype, and disease severity.

BACKGROUND: Delayed growth is a well-established feature of pediatric Crohn's disease. Several factors have been shown to affect growth, including disease location, severity, and treatment. The recently discovered NOD2 gene has been correlated to ileal location of Crohn's disease and subsequently could affect growth through the resulting phenotype or as an independent risk factor. The aim of our study was to determine if growth retardation is affected by genotype independently of disease location or severity. METHODS: Genotyping for 3 NOD2 single-nucleotide polymorphisms was performed in 93 patients with detailed growth records. Parameters including disease location, disease severity, and NOD 2 genotype and their effect on z scores for height and weight at disease onset and during follow-up were analyzed. RESULTS: NOD2 mutations were correlated with ileal location but not with disease severity or growth retardation. Ileal involvement was significantly associated with height retardation at disease onset and the lowest z score during follow-up. Use of steroids affected weight but not height. Regression models for growth variables revealed that the strongest association with impaired growth is with disease severity (weight- and height-failure odds ratios: 6.17 and 4.52, respectively). CONCLUSIONS: Severity of disease is correlated with growth failure for both height and weight. Location of disease is a weaker predictor of disordered growth and is correlated with growth retardation but not growth failure. The NOD2 genotype was not correlated with growth retardation or growth failure.

Child↗