A pilot study of the use of epidermal growth factor in pediatric short bowel syndrome

Sigalet, David L.; Martin, Gary R.; Butzner, J. Decker; Buret, André G.; Meddings, Jonathan B.

doi:10.1016/j.jpedsurg.2005.01.038

Cited by 64 publications

(33 citation statements)

References 26 publications

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“…These mice have short intestinal villi, reduced cell proliferation, and subsequent development of NEC-573 EGF-R SIGNALING IN FETAL INTESTINE like lesions together with susceptibility to colitis and defective recovery from gut resection (8,29). Clearly, EGF supplementation is beneficial to intestinal development, postnatal maturation, and adaptation (30,31). It increases expression of anti-apoptotic proteins while suppressing pro-apoptotic proteins thus maintaining intestinal integrity (31).…”

Section: Discussionmentioning

confidence: 99%

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Hydrocortisone and Indomethacin Negatively Modulate EGF-R Signaling in Human Fetal Intestine

et al. 2007

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Concomitant use of hydrocortisone and the nonspecific cyclo-oxygenase (COX)-inhibitor indomethacin increases the risk for intestinal perforations in preterm infants. We determined whether this was associated with insufficient epidermal growth factor receptor (EGF-R) signaling. We tested the effect of EGF, hydrocortisone, and indomethacin on its activation, cell proliferation and migration, COX-2 expression, and prostaglandin E 2 (PGE 2 ) production. Human small intestine epithelial cell line FHsInt74 and EGF-Rdeficient mice [EGF-R (-/-)] were used as models. The data revealed that EGF-R signaling had a bimodal positive effect on fetal enterocyte: 1) it increased cell proliferation and migration synergistically with hydrocortisone and 2) up-regulated COX-2 mRNA expression and subsequent PGE 2 production. Correlating with this, COX-2 protein expression was down-regulated in EGF-R (-/-) intestine. Despite a positive effect on cell proliferation with EGF, hydrocortisone blunted the stimulatory effect of EGF on COX-2 expression and PGE 2 production. Addition of indomethacin even further inhibited the EGF-stimulated PGE 2 synthesis. The data suggest that concomitant use of indomethacin and hydrocortisone on preterm infants, who physiologically synthesize only low levels of EGF-R ligands, may lead to intestinal problems related to failure in cytoprotective and regenerative events.

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Section: Discussionmentioning

confidence: 99%

“…Thus, EGF ligands might be useful for preterm infants. Indeed, EGF has been used incidentally in congenital microvillus atrophy (32), prevention of NEC (33), and pediatric short bowel syndrome (30). Association of EGF-R signaling to carcinogenesis has prevented routine EGF substitution.…”

Section: Discussionmentioning

confidence: 99%

Hydrocortisone and Indomethacin Negatively Modulate EGF-R Signaling in Human Fetal Intestine

et al. 2007

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“…Several authors have investigated the synergistic role of EGF in experimental studies along with other factors such as interleukin-11, bombesin and neurotensin, and found that they further enhance the adaptive action of EGF [76][77][78]. Promising results with the use of EGF were reported in a pilot study by Sigalet et al [79] who investigated the effect of enterally administered recombined EGF on nutrient absorption and tolerance feeding in infants with severe PSBS (<25% bowel length for predicting age). EGF was given orally with foods in a daily dose of 100 µg/kg for six weeks The results showed improvement in nutrient absorption, increased tolerance with enteral feeding and possible improvement of infection rate.…”

Section: Epidermal Growth Factor (Egf)mentioning

confidence: 99%

Short-Bowel Syndrome in Children — An Update in Management Strategies

Zavras¹,

Misiakos²,

Velaoras³

et al. 2015

Pediatric Nursing, Psychiatric and Surgical Issues

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“…22-24 Additionally, several other growth modulating factors may also be applicable for clinical study-including KGF, EGF, and HGF-with only EGF having undergone a Phase I trial. 25 One obstacle to the use of many of these factors is the small targeted population, which may have little appeal for many pharmaceutical companies. Another obstacle is the fact that some of these factors (eg, EGF) no longer have an active patent.…”

Section: Considerations For Clinical Application Of Humoral Factorsmentioning

confidence: 99%

Novel Agents in the Treatment of Intestinal Failure: Humoral Factors

Yang

Teitelbaum

2006

Gastroenterology

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Modalities to care for patients who suffer from intestinal failure comprise 2 basic approaches: supportive care and interventions that promote the normal adaptive process of the gastrointestinal tract. During this adaptation, the gastrointestinal tract and other organs release a number of humoral factors, which are critical to promote increased intestinal growth and function. The 3 lectures, summarized below, discuss 3 of the more well-known factors: human growth hormone, epidermal growth factor, and glucagon-like peptide-2. Details regarding these factors will be discussed in the remainder of this section. In addition, a variety of other factors possess similar trophic activity and may have great functional relevance in the adaptive process. This summary will briefly discuss factors involved in the process of short bowel syndrome (SBS) adaptation and where future directions will go in taking these factors toward clinical usage.

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A pilot study of the use of epidermal growth factor in pediatric short bowel syndrome

Cited by 64 publications

References 26 publications

Hydrocortisone and Indomethacin Negatively Modulate EGF-R Signaling in Human Fetal Intestine

Hydrocortisone and Indomethacin Negatively Modulate EGF-R Signaling in Human Fetal Intestine

Short-Bowel Syndrome in Children — An Update in Management Strategies

Novel Agents in the Treatment of Intestinal Failure: Humoral Factors

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