A study of mucosal gut immunity in infants who develop Hirschsprung's-associated enterocolitis

Turnock, R. R.; Spitz, Lewis; Ströbel, Stephan

doi:10.1016/0022-3468(92)90375-h

Cited by 19 publications

(7 citation statements)

References 9 publications

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“…They examined the rectal suction biopsies of 20 patients with HD of which 8 developed HAEC. They [47] found no evidence of a significant deficiency or difference in population in the IgA, IgM and IgG plasma cells in the lamina propria in patients with HD, HAEC or the normal controls. Overall, there is evidence that the IgA function and formation is normal within the cells but that there is a deficiency in the transfer of the immunoglobulin into the lumen to assist the mucin in its role in the front line of immunological response, however, this hypothesis has not been proven conclusively.…”

Section: Intestinal Wall Defencementioning

confidence: 91%

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New insights into the pathogenesis of Hirschsprung’s associated enterocolitis

Murphy

Puri

2005

Ped Surgery Int

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The management of Hirschsprung's disease (HD) has made dramatic strides over the last 20 years. Research into the embryological development and migration of ganglion cell has enabled a greater understanding of the pathogenesis of the disease. Coupled with new techniques in surgery, such as laparoscopy-assisted pull-through and the transanal pull-through, this knowledge has led to improved outcomes for children with HD. However, although our appreciation of Hirschsprung's associated enterocolitis and its aetiology has increased, there are continued references in the literature to a multitude of theories of pathogenesis. The purpose of this review is to delineate the theories and demonstrate the evidence supporting or otherwise contradicting each other.

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Section: Intestinal Wall Defencementioning

confidence: 91%

“…Turnock et al [47] attempted to answer the question of whether or not there is a pre-morbid deficiency of the intestinal immune response in patients whom develop HAEC. They examined the rectal suction biopsies of 20 patients with HD of which 8 developed HAEC.…”

Section: Intestinal Wall Defencementioning

confidence: 99%

New insights into the pathogenesis of Hirschsprung’s associated enterocolitis

Murphy

Puri

2005

Ped Surgery Int

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“…Even in the absence of mortality, postoperative EC is consequently a major cause of morbidity that justifies further investigation to clarify its pathophysiology and effective prevention. Research have addressed patients' characteristics, mechanical factors, type of technique, mucin production, gut immunity, mucosal genes, bacterial and viral agents, neuroendocrine cells, and retention of a residual aganglionic segment or transitional zone but have not demonstrated an unequivocal pathogenesis [17,20,[24][25][26][27][28][29][30][31]; a coexisting proximal dysplastic colon has been correlated with unsatisfactory outcome after HD surgery, suggesting a pathogenic relationship or an additive effect of both malformations [5,6].…”

Section: Discussionmentioning

confidence: 97%

An approach to minimize postoperative enterocolitis in Hirschsprung's disease

Estevão‐Costa

Fragoso

Campos

et al. 2006

Journal of Pediatric Surgery

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“…No differences in lymphocyte numbers have been demonstrated in the distal bowel of HSCR or HAEC patients vs. normal neonates[18]. However, there are increased lymphocytes in the ganglionated bowel of HSCR patients that develop diversion colitis (HAEC equivalent) 33 .…”

Section: Historical Investigations Into Haec Pathophysiologymentioning

confidence: 99%

Hirschsprung's associated enterocolitis

Gosain

Brinkman²

2015

Current Opinion in Pediatrics

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Purpose of Review Hirschsprung’s Disease (HSCR) is characterized by an absence of ganglion cells in the distal hindgut, extending from the rectum to a variable distance proximally, and results from a failure of cranial-caudal neural crest cell migration. Hirschsprung’s-Associated Enterocolitis (HAEC) is a condition with classic manifestations that include abdominal distention, fever and foul-smelling stools, and is a significant and life-threatening complication of HSCR. The purpose of this review is to critically evaluate recent findings regarding the pathophysiology of HAEC. Recent Findings Several recent studies have investigated the etiology of HAEC in humans and mouse models. These studies suggest that alterations in the intestinal barrier, including goblet cell number and function and Paneth cell function, impaired gastrointestinal mucosal immunity, including B-lymphocyte trafficking or function and secretory IgA production, and dysbiosis of the intestinal microbiota may contribute to the development of HAEC. Summary Recent studies add to the body of literature suggesting that the intestinal defects observed in HSCR are not restricted to the aganglionic segment but extend to the mucosal immune system within and beyond the gastrointestinal tract. Future studies further dissecting mechanisms of HAEC and validating these findings in human patients will allow for development of directed therapeutic interventions.

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A study of mucosal gut immunity in infants who develop Hirschsprung's-associated enterocolitis

Cited by 19 publications

References 9 publications

New insights into the pathogenesis of Hirschsprung’s associated enterocolitis

New insights into the pathogenesis of Hirschsprung’s associated enterocolitis

An approach to minimize postoperative enterocolitis in Hirschsprung's disease

Hirschsprung's associated enterocolitis

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