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Published on: September 12, 2019
Serum concentrations of tumour necrosis factor alpha in childhood chronic inflammatory bowel disease
S H Murch1, V A Lamkin, M O Savage
1Department of Paediatric Gastroenterology, St Bartholomew's Hospital, West Smithfield, London.
Insights
Tumour necrosis factor alpha (TNF alpha) rises during relapses of ulcerative colitis and colonic Crohn's disease in children. This inflammation marker may contribute to growth failure in pediatric inflammatory bowel disease.
Area of Science:
- Pediatric Gastroenterology
- Immunology
- Biochemistry
Background:
- Chronic inflammatory bowel disease (IBD) in children can lead to growth impairment.
- The role of specific inflammatory markers in IBD-related growth failure is not fully understood.
Purpose of the Study:
- To investigate the association between serum tumour necrosis factor alpha (TNF alpha) levels and disease activity in children with IBD.
- To explore the potential contribution of TNF alpha to growth failure in pediatric IBD.
Main Methods:
- Serum TNF alpha concentrations were measured using enzyme-linked immunosorbent assay (ELISA).
- Measurements were taken in healthy children and in children with IBD during remission and relapse.
- Disease indices and height velocity were also assessed.
Main Results:
- Elevated serum TNF alpha was observed in children with relapsing ulcerative colitis and colonic Crohn's disease.
- Children with relapsing small bowel Crohn's disease did not show increased TNF alpha levels.
- Growth velocity was significantly depressed in children with relapsing large bowel IBD compared to those in remission.
Conclusions:
- Serum TNF alpha elevation is associated with relapse in colonic forms of pediatric IBD.
- TNF alpha may play a role in growth failure in pediatric IBD through cachexia and potential inhibition of growth hormone release.
Abstract:
Serum tumour necrosis factor alpha (TNF alpha) concentrations were measured by enzyme linked immunoadsorbent assay in 31 normal children and during 65 episodes of clinical remission and 54 episodes of relapse in 92 children with chronic inflammatory bowel disease. An appreciable rise in TNF alpha was found only in children in relapse of ulcerative colitis and colonic Crohn's disease. The group of children with small bowel Crohn's disease in relapse did not show increases of TNF alpha above control concentrations, despite an equivalent rise in disease indices. Height velocity was depressed in children with relapse of large bowel Crohn's disease and ulcerative colitis compared with the equivalent condition in remission. The impairment of growth velocity was significantly greater in relapse of large bowel Crohn's disease and ulcerative colitis than in small bowel Crohn's disease alone, although for the subgroups in stage 1 puberty (prepubertal) the differences were not significant. Inadequate growth in chronic inflammatory bowel disease is currently ascribed to inadequate nutrition and TNF alpha may contribute to this through its cachexia inducing effects. It may, in addition, diminish pituitary growth hormone release. These results suggest that production of TNF alpha may be associated with growth failure in relapse of colonic inflammatory bowel disease.
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