Growth failure occurs through a decrease in insulin-like growth factor 1 which is independent of undernutrition in a rat model of colitis

Ballinger, Anne

doi:10.1136/gut.46.5.695

Cited by 157 publications

(153 citation statements)

References 44 publications

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“…7 The finding that some children with IBD fail to achieve their growth potential, despite nutritional intervention, supports this hypothesis also in the clinical setting. Table 5).…”

Section: Discussionsupporting

confidence: 64%

“…[2][3][4] Although IBDassociated malnutrition is considered the main source of these complications, 5 recent evidence in IBD animal models suggests a direct adverse effect of systemic inflammation on the GH/IGF-1 axis. 6,7 Ballinger et al…”

Section: Discussionmentioning

confidence: 99%

“…6 Indeed, in this same animal model, increased plasma levels of the proinflammatory cytokine interleukin (IL)-6, together with reduced plasma concentrations of insulin-like growth factor (IGF)-1, differentiated colitic rats from pair-fed controls. 7 On the basis of these results, Ballinger et al suggested that inflammation acts mainly at hepatocyte/IGF-1 level to impair linear growth. 7 Tumour necrosis factor (TNF)-a, IL-1b and IL-6 have been shown to decrease hepatic growth hormone (GH)-receptor synthesis, and, in turn, hepatic IGF-1 and IGF-binding protein-3 (IGFBP-3) production.…”

Section: Introductionmentioning

confidence: 99%

“…7 On the basis of these results, Ballinger et al suggested that inflammation acts mainly at hepatocyte/IGF-1 level to impair linear growth. 7 Tumour necrosis factor (TNF)-a, IL-1b and IL-6 have been shown to decrease hepatic growth hormone (GH)-receptor synthesis, and, in turn, hepatic IGF-1 and IGF-binding protein-3 (IGFBP-3) production. [8][9][10] Furthermore, recent results from our group suggest that TNF-a is implicated in the GH resistance associated with chronic liver disease.…”

Section: Introductionmentioning

confidence: 99%

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Infliximab reverses growth hormone resistance associated with inflammatory bowel disease

Gentilucci¹,

Caviglia

Picardi³

et al. 2005

Aliment Pharmacol Ther

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SUMMARYBackground: Increasing evidence shows that inflammation plays a major role in the aetiology of catabolism and wasting observed in inflammatory bowel disease via growth hormone resistance. Aim: To evaluate the effect of infliximab treatment on the growth hormone/insulin-like growth factor-1 axis. Methods: Fourteen adults with active Crohn's disease or ulcerative colitis underwent three infliximab infusions at a dose of 5 mg/kg for induction of remission, plus two maintenance infusions 8 weeks apart. Blood samples were collected for the analysis of serum growth hormone, insulin-like growth factor-1, insulin-like growth factor-binding protein-3 and acid labile subunit. Results: Serum insulin-like growth factor-1 and insulinlike growth factor-binding protein-3 concentrations, which were significantly lower in inflammatory bowel disease patients before treatment compared with con-

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“…7 The finding that some children with IBD fail to achieve their growth potential, despite nutritional intervention, supports this hypothesis also in the clinical setting. Table 5).…”

Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Infliximab reverses growth hormone resistance associated with inflammatory bowel disease

Gentilucci¹,

Caviglia

Picardi³

et al. 2005

Aliment Pharmacol Ther

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“…If this is the case, our experiments indicate that a persistent state of IGF-I resistance may exist following the removal of the insult and this possibility requires further investigation. Our data may also explain the lack of catch-up growth observed in rats administered IGF-I following experimental colitis (Ballinger et al 2000). In children with juvenile idiopathic arthritis, high-dose treatment with GH leads to a rise in systemic levels of IGF-I and has been reported to reduce the worsening growth retardation but does not seem to result in normalisation of height (Simon et al 2003).…”

Section: Discussionsupporting

confidence: 50%

The restricted potential for recovery of growth plate chondrogenesis and longitudinal bone growth following exposure to pro-inflammatory cytokines

MacRae¹,

Farquharson²,

Ahmed³

2006

Journal of Endocrinology

109

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Childhood chronic inflammatory disease can be associated with transient and permanent growth retardation. This study examined the potential for spontaneous growth recovery following pro-inflammatory cytokine exposure. Murine ATDC5 chondrogenic cells and postnatal metatarsals were exposed to interleukin (IL)-1 , IL-6 and tumour necrosis factor-(TNF ), and their growth and proliferative capacity were determined following recovery. TNF and IL-1 reduced chondrocyte proliferation and aggrecan and collagen types II and X expression at minimum concentrations of 10 ng/ml and 0·1 ng/ml respectively. TNF but not IL-1 exposure led to increased caspase-3 activity and altered cellular morphology, consistent with reduced viability. Cytokine exposure particularly inhibited proteoglycan synthesis. This effect was dose and duration dependent. Compared with the control, IL-1 and TNF led to a 71% and 45% reduction in metatarsal growth after 8 days of exposure respectively (P<0·05). An additive effect of IL-1 combined with TNF was observed (110% decrease; P<0·05). Metatarsals exposed to IL-1 or TNF individually for a 2-day period, and allowed to recover spontaneously in the absence of cytokines for a further 6 days, showed normal growth trajectories. In combination, growth was 59% lower (P<0·01) compared with control metatarsals at the end of the recovery period. Exposure to the combination for 4 days followed by a 4-day recovery period resulted in 87% decrement compared with controls (P<0·05). IL-6 did not alter any parameter studied. IL-1 and TNF exert diverse inhibitory effects on ATDC5 chondrocyte dynamics and metatarsal growth. The extent of recovery following cytokine exposure depends on the duration of exposure, and may be incomplete following longer periods of exposure.

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Interventions for growth failure in childhood Crohn's disease

Newby

Sawczenko

Thomas

et al. 2006

Cochrane Database of Systematic Reviews

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In addition to these randomized controlled trials, a body of lower quality evidence does exist relevant to two other important interventions; the use of supplemental enteral nutrition (Morin 1980; Belli 1988; Israel 1995) and the judicious use of surgical interventions in pre-pubertal children with refractory disease (Alperstein 1985; Lipson 1990; McLain 1990). Newer treatments, such as infliximab, are now becoming more widely used and may offer advantages in promoting growth. These effects are as yet unstudied. This review highlights the need for large, multi centre studies of the different treatment options in paediatric Crohn's disease and the importance of standardised measurements of growth, such as height velocity standard deviation scores and height standard deviation scores as outcome measures.

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Growth failure occurs through a decrease in insulin-like growth factor 1 which is independent of undernutrition in a rat model of colitis

Cited by 157 publications

References 44 publications

Infliximab reverses growth hormone resistance associated with inflammatory bowel disease

Infliximab reverses growth hormone resistance associated with inflammatory bowel disease

The restricted potential for recovery of growth plate chondrogenesis and longitudinal bone growth following exposure to pro-inflammatory cytokines

Interventions for growth failure in childhood Crohn's disease

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