Glucocorticoids Improve Enteral Feeding Tolerance in Pediatric Short Bowel Syndrome With Chronic Intestinal Inflammation : Journal of Pediatric Gastroenterology and Nutrition

Secondary Logo

Journal Logo

Original Articles: Gastroenterology

Glucocorticoids Improve Enteral Feeding Tolerance in Pediatric Short Bowel Syndrome With Chronic Intestinal Inflammation

Wang, Fangfang; Gerhardt, Brandi K.; Iwansky, Sarah N.; Hobson, Brandy; Logan, Samantha; Mercer, David F.; Quiros-Tejeira, Ruben E.

Author Information
Journal of Pediatric Gastroenterology and Nutrition 73(1):p 17-22, July 2021. | DOI: 10.1097/MPG.0000000000003058
  • Free



A group of short bowel syndrome (SBS) patients developed chronic intestinal inflammation while struggling weaning off parenteral nutrition (PN). They did not respond to standard management of SBS and food allergy. We treated them with glucocorticoids and described the outcome.


Our study is a retrospective descriptive study. We reviewed records from the intestinal rehabilitation program from 2006 to 2017. We identified 15 patients whose lab values, pathology results, and clinic notes were reviewed.


We had more patients (n = 10) with diagnosis of gastroschisis, and more female patients (n = 9). Seven patients weaned off PN with median treatment duration of 5 months, 5 of which remained on budesonide for significant period of time (median: 7.5 months). One of these 7 patients relapsed, as the patient resumed glucocorticoids because of recurrence of chronic intestinal inflammation. Six of 15 children had significant eosinophils in their initial biopsy, 5 of these children weaned off PN whereas 1 child's gastrointestinal (GI) bleeding stopped. Four patients were not able to decrease PN calorie. Two of these patients’ GI bleeding stopped, the other 2 had normalized histology.


For SBS children with histologically confirmed chronic intestinal inflammation, glucocorticoids may help promote enteral feeding tolerance. Glucocorticoids regimen should be chosen individually. Patients are more likely to respond if initial histology has significant eosinophilic infiltration. Patients may need to remain on glucocorticoids for over 6 months.

See “Glucocorticoid Therapy in Short Bowel Syndrome: A New Fork in the Road?” by Cohran on page 1.

What Is Known/What Is New

What Is Known

  • Chronic inflammation is related to short bowel syndrome and prolonged parenteral nutrition support.
  • Food allergies or small intestine bacterial overgrowth may be a factor in a subset of these patients.
  • Glucocorticoids are used in various inflammatory diseases including inflammatory bowel disease or other chronic intestinal inflammatory processes.

What Is New

  • There is a subset of children with short bowel syndrome who has chronic intestinal inflammation who may benefit from anti-inflammatory therapy.
  • Glucocorticoids may help to promote enteral feeding tolerance in this subset of children with short bowel syndrome and chronic intestinal inflammation.
  • A better response to glucocorticoids was seen when mucosal eosinophilic infiltration was present.

Short bowel syndrome (SBS) is a rare yet costly disease with incidence of 3 per million people, and prevalence around 10,000 to 15,000 (1). Parenteral nutrition (PN) significantly affects SBS patients’ economy and quality of life (2). With the advancement in PN and intestinal rehabilitation programs (IRP), 50% to 70% of SBS patients can wean off PN if managed by IRP experts (3). For pediatric SBS patients, however, maximizing enteral feeding tolerance, minimizing the need of PN while optimizing growth, and development have always been significant challenges.

Chronic inflammation is related to SBS and PN. Aprahamian et al (4) suggested that SBS, independent of PN, is a proinflammatory state. Serum proinflammatory cytokines are significantly higher in SBS patients who were receiving PN, regardless of duration of PN (5). Another study (6) showed that inflammatory bowel disease (IBD)-like symptoms and pathologic changes have been found in pediatric SBS patients, and that there exists an etiology connection between SBS and chronic intestinal inflammation.

Glucocorticoids are used in various inflammatory diseases. As chronic inflammation and systemic immune dysregulation are related to SBS, we believed that glucocorticoids may improve enteral feeding tolerance in SBS patients with bowel inflammation. Treatment strategies and outcomes of glucocorticoids use in SBS were, however, not well established. At the University of Nebraska Medical Center, we had a group of patients from our IRP who were resistant to multiple treatment modalities for SBS. They had histologically proven, chronic intestinal inflammation. We used glucocorticoids as the last resort. In this study, we will describe these patients’ presenting features and treatment outcomes.


Our study was approved by the Institutional Review Board at University of Nebraska Medical Center (IRB # 099-18-EP). We used Current Procedural Terminology codes Z78.9 (on PN) and K91.2 (SBS) or K63.9 (Intestinal Failure) to identify pediatric (ages <18 years) IRP patients who had SBS and were on PN between years 2006 and 2017. We included patients who were on glucocorticoids for biopsy-proven chronic intestinal inflammation and excluded those who took glucocorticoids for posttransplant immunosuppression or severe food allergy. This allowed us to minimize the deviation of purpose of using glucocorticoids and maintained the homogeneity of our patient cohort. The chronic intestinal inflammation was detected by endoscopy and intestinal biopsy. Noted that the chronic intestinal inflammation, we described is different from findings in IBD, none of our included patients had diagnosis of IBD, nor did they have typical endoscopic or histological findings of IBD. All patients received standard treatment for potential complications from SBS and PN before starting glucocorticoids, such as amino-acid-based elemental formula, dietary modifications addressing potential food allergies, treating small intestine bacterial overgrowth, screening for celiac disease whenever appropriate, and so forth. We also ensured that there is no dilated loops in their small bowel series, which may require surgical intervention. Patients had no significant improvement of enteral feeding tolerance before we initiated glucocorticoids. Fifteen patients were included based on the above inclusion criteria.

Patients were monitored by multidisciplinary IRP team including pediatric gastroenterologists, surgeons, nutritionist, nurses, psychologist, and so forth. We saw patients every month at the beginning, and then every 2 to 3 months when they were clinically stable. We kept close contact with our patients and adjusted follow-ups whenever they had new symptoms or following lab results.

For our glucocorticoid therapy, whether to start with prednisolone or budesonide was based on our clinical judgement and parents’ preference. For children who had higher PN calorie requirement, we usually started with oral prednisolone 1 mg · kg−1 · day−1 for 2 to 4 weeks, then gradually tapered and switched to 3 to 9 mg/day budesonide. Budesonide dosing was based on current literature (7,8) on its use in pediatric IBD. As budesonide comes in 3 mg/tablet. We used 3 mg/day for weight <15 kg, 6 mg/day for weight between 15 and 25 kg, and 9 mg/day for weight >25 kg. We also added sulfasalazine 50 to 60 · kg−1 · day−1 divided into 3 doses to the anti-inflammatory therapy in those children with distal intestinal inflammation and/or colitis. For children who had lower PN calorie requirement and milder clinical course, or whose parents refused to use standard glucocorticoids, we treated them with budesonide and sulfasalazine. We gradually decreased and stopped budesonide when patients were clinically stable and showed steady growth and development pattern. We monitored linear growth, metabolic bone disease on a regular basis for these patients. We evaluated all patients’ bone age annually and bone density, when they were older than 5 years old, at least yearly. We checked each patient's calcium, phosphorus, and alkaline phosphatase levels biweekly or weekly, and vitamin D every 3 months. When they were weaned off PN, we still followed up and checked above labs every 3 months. We also monitored their folate level at least 2 times a year, and supplemented accordingly.

Our study was a retrospective descriptive study. Patients’ lab values, pathology results, and clinic notes were reviewed. The variables of interest included sex, race, primary diagnosis, intestinal anatomy, age of starting glucocorticoid therapy, type of glucocorticoids, initial intestinal histology before starting glucocorticoid therapy, duration of glucocorticoid therapy, duration of maintenance therapy if weaned off PN, follow-up intestinal histology, whether they weaned off PN, change of the calorie count over the course of treatment, z scores, and their growth charts.


Six boys and 9 girls were identified over the study period (Table 1) The majority (9/15) of children were Caucasian. Most (10/15) patients had gastroschisis in their primary diagnosis. The small bowel length ranged from 20 to 108 cm with a median of 46 cm. Most patients had more than ½ colon remaining. Among our 15 patients, 8 patients had negative celiac screening. The other 7 patients were not tested, because of no exposure to gluten before diagnosis of chronic intestinal inflammation. Either because of age (< or = 13 months—just elemental formula fed—n = 5) or because of limited intake to elemental formula as only source of enteral nutrition (n = 2). The median age of starting glucocorticoids was 3.3 years. The median duration of PN before glucocorticoid treatment was 3.3 years, as all patients started receiving PN 1 to 2 weeks after birth. The duration of glucocorticoid therapy before the study ended ranged from 1 to 64 months with a median of 18 months. No patient required escalation of treatment, such as biologic therapy.

TABLE 1 - Demographic and basic treatment information of study subjects
ID Sex Race Primary diagnosis Intestinal anatomy Age of starting glucocorticoid therapy, years Type of glucocorticoids Initial intestinal histology before starting glucocorticoid therapy Duration of glucocorticoid therapy before study ended, months Duration of glucocorticoid therapy before off PN, months Duration of maintenance therapy, months Follow-up intestinal histology Weaning off PN, Yes/No
1 M American Indian or Alaskan Native Gastroschisis 80 cm small bowel + ½ colon 10 Budesonide SIBO and chronic small bowel inflammation 12 N/A N/A No follow-up studies No
2 F White Gastroschisis and small bowel volvulus 70 cm small bowel + transverse and descending colon 5 Prednisolone and budesonide Chronic small bowel inflammation 58 N/A N/A Normal histology after 53 months therapy No
3 M White Gastroschisis 56 cm small bowel + ½ colon 3 Prednisolone and budesonide Chronic small bowel inflammation 64 N/A N/A Mild nonspecific inflammation after 59 months therapy No
4 M Hispanic or Latino Necrotizing enterocolitis 20 cm small bowel + whole colon 3 Prednisolone and budesonide Increased eosinophils and chronic inflammation in small bowel and eosinophilic colitis 54 N/A N/A Continued increased eosinophils in distal small bowel and colonic anastomosis, 3 episodes of acute small bowel inflammation No
5 F African American Midgut volvulus 40 cm small bowel + whole colon 4 Prednisone and budesonide Mild intraepithelial lymphocytes, chronic small bowel inflammation 44 36 8 Normal histology after 32 months therapy Yes
6 F White Gastroschisis and intestinal atresia 45 cm small bowel + ½ colon 4 Budesonide Increased eosinophils and chronic inflammation in small bowel 20 5 15 No follow-up studies Yes
7 F White Intestinal atresia and gastroschisis 65 cm small bowel + transverse and descending colon 3 Budesonide Villous blunting and chronic inflammation in small bowel and colon. Gastritis with focal eosinophils 39 6 33 Normal histology 3 months after off PN Yes
8 M White Gastroschisis 32 cm small bowel + transverse and descending colon 1 Prednisolone and budesonide Chronic small bowel inflammation 30 N/A N/A Normal histology after 24 months therapy No
9 F White Gastroschisis and intestinal atresia 108 cm small bowel + whole colon 4 Prednisolone and budesonide Chronic small bowel inflammation 10 3 7 No follow-up studies Yes
10 F White Diaphragmatic hernia 33 cm small bowel + 2/3 colon 4 Budesonide Chronic small bowel inflammation, villous blunting, and nonspecific colitis 4 N/A N/A Normal histology after 4 months therapy No
11 M White Gastroschisis Mid ileal resection, unknown total length of small bowel + whole colon 0.8 Budesonide Increased eosinophils and chronic inflammation in distal small bowel and eosinophilic colitis 9 2 7 No follow-up studies Yes
12 M African American Necrotizing enterocolitis 24 cm small bowel + 42 cm colon 0.7 Prednisolone and budesonide Eosinophilic colitis 5 5 0 No follow-up studies Yes
13 F Hispanic or Latino Intestinal atresia and gastroschisis 47 cm small bowel + whole colon 0.7 Prednisolone and budesonide Chronic small bowel inflammation and eosinophilic colitis 18 3 N/A Not on glucocorticoids continuously, had recurrent chronic small bowel inflammation, intraepithelial lymphocytes while off glucocorticoids Yes§
14 F White Gastroschisis, intestinal atresia and volvulus 51 cm small bowel + ½ colon 3 Budesonide Small bowel villous blunting, patchy chronic inflammation in small bowel and colon 1 N/A N/A No follow-up studies No
15 F African American Necrotizing enterocolitis 85 cm small bowel + 17 cm colon 1 Prednisolone and budesonide Mural hemorrhage, focal erosion, congestion and chronic inflammation in small bowel 7 N/A N/A Not on glucocorticoids continuously, recurrent chronic small bowel inflammation, nonspecific villous blunting while off glucocorticoids No
PN = parenteral nutrition.
SIBO = small intestine bacterial overgrowth. It was diagnosed by small bowel aspirate.
Prednisone or prednisolone was followed by budesonide.
Eosinophilic colitis—increased eosinophils and chronic inflammatory changes.
§Patient relapsed 3 months after off PN and glucocorticoids.

Seven of the 15 patients were able to wean off PN at some point. Most (11/15) patients had significant reduction of PN calorie count after starting glucocorticoid therapy (Table 2). For the 7 children who weaned off PN, the median duration of glucocorticoid treatment was 5 months. Most (5/7) patients remained on budesonide for significant period of time (median: 7.5 months). Patient 7 was initiated on glucocorticoids while receiving low calories through PN. Patient had PN-related complications leading to a possible transplant—central access issues and superior vena cava syndrome. We tried glucocorticoids as there was evidence of chronic intestinal inflammation. The success was that the patient reestablished a good weight gain pattern and patient was off intravenous fluid after 5 months.

TABLE 2 - Changes of parenteral nutrition calories (kcal · kg−1 · day−1) over the course of glucocorticoid treatment
Patient ID Weaning off PN, Y/N 0 Month 3 Months 6 Months 9 Months 1 Year 15 Months 16 Months 2 Years 3 Years 4 Years 5 Years
1 N 24 10 15 10 15 N/A N/A N/A N/A N/A N/A
2 N 58 40 40 33 30 42 42 27 20 20 N/A
3 N 40 60 52 52 44 70 70 55 30 45 44
4 N 65 68 62 50 63 61 61 54 57 N/A N/A
5 Y 54 28 28 25 38 30 30 30 0 N/A N/A
6 Y 23 27 0 0 0 0 0 0 0 N/A N/A
7 Y 10 10 0 0 0 0 0 0 0 N/A N/A
8 N 60 54 58 75 66 50 52 56 N/A N/A N/A
9 Y 23 0 0 0 0 0 0 0 0 N/A N/A
10 N 60 66 N/A N/A N/A N/A N/A N/A N/A N/A N/A
11 Y 75 0 0 0 0 0 0 0 0 N/A N/A
12 Y 80 57 25 0 0 0 0 0 0 N/A N/A
13 Y 55 0 0 25 38 43 48 32 N/A N/A N/A
14 N 79 38 N/A N/A N/A N/A N/A N/A N/A N/A N/A
15 N 77 63 66 41 29 18 71 N/A N/A N/A N/A
PN = parenteral nutrition; Y/N = Yes/No.
GI bleeding stopped after glucocorticoid treatment.
Patient had complication from parenteral nutrition (PN) and was receiving minimal calories through PN. Glucocorticoid therapy was initiated because of struggling with weight gain and biopsy proven chronic intestinal inflammation.
N/A is not applicable as the study ended.

In our 15-patient cohort, 6 patients (patient 4, 6, 7, 11, 12, and 13) had significant eosinophils in their initial pathology finding. Five of these 6 patients were able to wean off PN at some point of the glucocorticoid treatment. The other one had significant symptom improvement (patient 4 GI bleeding stopped).

Two patients, patients 13 and 15, had relapse after stopping glucocorticoids. Patient 13 was on glucocorticoids for 3 months initially and was off PN for 3 months. Due to struggle of weight gain and GI symptoms, however, the child was put back on PN. Then, 5 months later, glucocorticoids were resumed as pathology showed chronic inflammation again. Patient responded well by showing 37% decrease of PN calorie count after 15 months. Patient 15 initially responded well to glucocorticoids, frequent vomiting and high G tube output resolved, PN calorie count reduced from 77 to 66 kcal · kg−1 · day−1. Due to parents’ refusal, glucocorticoids were stopped after 7 months of treatment. The calorie count continued to decrease to only 18 kcal · kg−1 · day−1 even after another 7 months without glucocorticoid treatment. Just 1 month before the study ended, however, the child had severe enteral feeding intolerance. His calorie count increased to 71 kcal/kg, and histology showed acute on chronic small bowel inflammation. As a result, the patient had to be restarted on prednisolone.

Four patients (patients 3, 4, 8, and 10) had difficulty cutting down PN requirement. Among them, patient 3 and 4's repeated histological findings were consistent with intestinal inflammation but their GI bleeding stopped. Patients 8 and 10 had symptom improvement and normalized histology after 24 and 4 months therapy, respectively.

Of the 15 patients, 4 had significant drop in linear growth, defined as drop on z score of more than 0.5, while tracking on weight gain pattern suggestive of side effect from glucocorticoid therapy. The glucocorticoid dose was decreased on those patients. Overall, children's linear growth were not significantly impacted by glucocorticoid therapy (Fig. 1). In addition, there was a good tracking pattern on weight gain in these patients while weaning PN in those who we were able to stop PN or decrease parenteral calories (Table 2). None of the 15 patients developed significant metabolic bone disease.

Average weight and height z-scores before and after glucocorticoid treatment. In the univariate analysis, there is no significant difference for average z-scores of weight and height before and after glucocorticoid treatment. The P values are 0.25 and 0.54 for weight and height, respectively.


Local and systemic inflammation have shown correlation to SBS and PN. Irritation from excessive short-chain fatty acid, low luminal pH, and gut microbiota dysbiosis might contribute to the surface epithelial erosion, which leads to chronic inflammation (9–11). Our 15 children had typical features of chronic bowel inflammation, such as significant lymphocytes, eosinophils, villous blunting, and mucosal congestion. These findings were likely related to SBS. We believed chronic bowel inflammation contributed to their difficulty achieving intestinal adaptation.

We used glucocorticoids for treating various intestinal inflammatory diseases. The effect of glucocorticoids stem from their ability to modulate the immune response and inhibit trafficking of inflammatory cells to the intestine (12). Freeman et al (13) reported pediatric SBS patients who developed IBD after intestinal surgeries benefited from anti-tumor necrosis factor (TNF) and glucocorticoids. We believed that glucocorticoids could potentially reduce chronic intestinal inflammation in SBS patients, increase functional small bowel surface area, and thus promote enteral feeding tolerance.

Of our 15 identified patients, although our other findings were close to the basic demographic information from the Pediatric Intestinal Failure Consortium Report (14) in 2012, we had more girls (60% vs 42.6%) and more children with diagnosis of gastroschisis (67% vs 44%) in the cohort. Common side effects from glucocorticoids include immunosuppression, diabetes, impaired linear growth, and osteoporosis. For pediatric patients, the biggest concern is the negative effect on growth and development. Our 15 patients failed multiple modalities of standard SBS treatment including addressing possible food allergies and were being considered for intestinal transplantation. The subsequent immunosuppression would also include glucocorticoids. Of our 15 patients, 4 had significant drop of their growth chart after starting glucocorticoids. As weight gain pattern was sustained in all these children, the impairment on linear growth was most likely in relation to glucocorticoid therapy. We decreased the dose of glucocorticoids as much as possible. Three of these patients were on budesonide and 1 was on low-dose glucocorticoids because of GI bleeding that recurred when switched to budesonide.

Budesonide with locational specificity and first-pass metabolism has been developed to reduce systemic availability. Recent systemic review (15) suggested that standard glucocorticoids may be more effective in inducing remission in active IBD compared with placebo and budesonide. We considered budesonide for children who had milder clinical course and parents’ preference. These patients (patients 1, 6, and 7) all responded well. Regarding, which type of glucocorticoid regimen to start, we believe the joint decision-making should be based on patients’ clinical features and preference. Close follow-up and adjustment are needed throughout the treatment course.

The duration of glucocorticoid therapy remains unknown. The treatment duration before patients weaned off PN ranged from 2 to 36 months with the median of 5 months. The duration of maintenance glucocorticoids after weaned off ranged from 0 to 33 months with the median of 7.5 months. Studies (16) suggested that for maintenance of remission, budesonide can be used for up to 3 months for Crohn disease and up to 12 months for microscopic colitis. We determined the treatment duration mainly based on clinical judgement and gradually stopped glucocorticoids when patients were clinically stable with normal growth pattern and development. Two of the 15 patients had recurrent enteral feeding intolerance after stoping glucocorticoids. Patients may need to remain on glucocorticoids for a period of time even if they weaned off PN or had significant reduction of PN calories as they may experience regression on enteral tolerance. Due to our relatively small sample size, the exact duration of treatment could not be determined. Future study with large patient cohort should help to address this.

Patient with significant eosinophils in intestinal biopsy may respond well to glucocorticoids. Six of the 15 patients’ initial biopsy showed significant eosinophils, which was likely part of chronic intestinal inflammation. Five of these 6 children weaned off PN at some point after initiated glucocorticoids. The other child's GI bleeding stopped. We were once suspecting the eosinophils in those 6 children might be caused by an allergic reaction to certain food or formula. They did not respond to elemental diet and protein restriction, however. There are very wide differential diagnoses of tissue eosinophilia in gastrointestinal tract. It is known that colonic eosinophilia can be found in IBD. Studies (17,18) suggested children who had colonic eosinophilia with signs of systemic inflammation raised the suspicion of IBD. Our 6 patients responded well to glucocorticoids, which suggested significant eosinophil infiltration might be a good indicator of chronic inflammation related to SBS. These children might benefit from anti-inflammatory treatment.

Management of complex SBS patients remains a challenge. Four children (patients 3, 4, 8, and 10) struggled cutting down PN calorie requirement. Three of them had histological improvement. It suggested that glucocorticoids did help to reduce inflammation from SBS. Patients 4, 8, and 10 had shorter residual small bowel length compared with most other children's in the cohort. The lesser surface area of absorption might contribute to their overall complexity. Case report (19), however, described infant who had as little as 10 cm small bowel thrived without PN. It has also been reported that 27 patients with ultra SBS had successful intestinal rehabilitation (20). In our cohort, patient 12 weaned off PN with 24 cm small bowel. Therefore, the enteral feeding intolerance is likely multifactorial. For some children, elimination of intestinal inflammation was not enough to improve enteral feeding tolerance.

In conclusion, glucocorticoid therapy may help to promote enteral feeding tolerance for SBS children with histologically confirmed, chronic intestinal inflammation. Choice of glucocorticoids should be individualized in children with SBS-related chronic intestinal inflammation. Patients are more likely to respond if their initial histology has chronic intestinal inflammation with significant eosinophilic infiltrate. Patients may need to remain on maintenance glucocorticoids for a period of time as they might relapse with intestinal inflammation leading to GI bleeding in some instances.


1. Carroll RE, Benedetti E, Schowalter JP, et al. Management and complications of short bowel syndrome: an updated review. Curr Gastroenterol Rep 2016; 18:40.
2. Winkler MF, Smith CE. Clinical, social, and economic impacts of home parenteral nutrition dependence in short bowel syndrome. JPEN J Parenter Enteral Nutr 2014; 38: (1 Suppl): 32S–37S.
3. Buchman AL, Scolapio J, Fryer J. AGA technical review on short bowel syndrome and intestinal transplantation. Gastroenterology 2003; 124:1111–1134.
4. Aprahamian CJ, Chen M, Yang Y, et al. Two-hit rat model of short bowel syndrome and sepsis: independent of total parenteral nutrition, short bowel syndrome is proinflammatory and injurious to the liver. J Pediatr Surg 2007; 42:992–997.
5. Bizari L, da Silva Santos AF, Foss NT, et al. Parenteral nutrition in short bowel syndrome patients, regardless of its duration, increases serum proinflammatory cytokines. Nutr Res 2016; 36:751–755.
6. Baxter KJ, Srinivasan JK, Ziegler TR, et al. Pediatric short bowel syndrome and subsequent development of inflammatory bowel disease: an illustrative case and literature review. Pediatr Surg Int 2017; 33:731–736.
7. Escher JC. European Collaborative Research Group on Budesonide in Paediatric IBD. Budesonide versus prednisolone for the treatment of active Crohn's disease in children: a randomized, double-blind, controlled, multicentre trial. Eur J Gastroenterol Hepatol 2004; 16:47–54.
8. Levine A, Kori M, Dinari G. Israeli Pediatric Budesonide Study Group. Comparison of two dosing methods for induction of response and remission with oral budesonide in active pediatric Crohn's disease: a randomized placebo-controlled trial. Inflamm Bowel Dis 2009; 15:1055–1061.
9. Taylor SF, Sondheimer JM, Sokol RJ, et al. Noninfectious colitis associated with short gut syndrome in infants. J Pediatr 1991; 119 (1 Pt 1):24–28.
10. Argenzio RA, Meuten DJ. Short-chain fatty acids in- duce reversible injury of porcine colon. Dig Dis Sci 1991; 36:1459–1468.
11. Piper HG, Fan D, Coughlin LA, et al. Severe gut microbiota dysbiosis is associated with poor growth in patients with short bowel syndrome. J Parenter Enteral Nutr 2017; 41:1202–1212.
12. Hayashi R, Wada H, Ito K, et al. Effects of glucocorticoids on gene transcrip- tion. Eur J Pharmacol 2004; 500:51–62.
13. Freeman JJ, Rabah R, Hirschl RB, et al. Anti-TNF-α treatment for post-anastomotic ulcers and inflammatory bowel disease with Crohn's-like pathologic changes following intestinal surgery in pediatric patients. Pediatr Surg Int 2015; 31:77–82.
14. Squires RH, Duggan C, Teitelbaum DH, et al. podiatric Intestinal Failure Consortium. Natural history of paediatrics intestinal failure: initial report from the paediatrics Intestinal Failure Consortium. J Pedate 2012; 161:723.e2–728.e2.
15. Ford AC, Bernstein CN, Khan KJ, et al. Glucocorticosteroid therapy in inflammatory bowel disease: systematic review and meta-analysis. J Pediatr 1991; 119 (1 Pt 1):24–28.
16. American Gastroenterological Association. AGA Institute Guideline on the Management of Microscopic Colitis: Clinical Decision Support Tool. Gastroenterology 2016; 150:276.
17. Mark J, Fernando SD, Masterson JC, et al. Clinical implications of pediatric colonic eosinophilia. J Pediatr Gastroenterol Nutr 2018; 66:760–766.
18. Conner JR, Kirsch R. The pathology and causes of tissue eosinophilia in the gastrointestinal tract. Histopathology 2017; 71:177–199.
19. Kurkchubasche AG, Rowe MI, Smith SD. Adaptation in short- bowel syndrome: reassessing old limits. J Pediatr Surg 1993; 28:1069–1071.
20. Infantino BJ, Mercer DF, Hobson BD, et al. Successful rehabilitation in pediatric ultrashort small bowel syndrome. J Pediatr 2013; 163:1361–1366.

chronic intestinal inflammation; eosinophils; intestinal adaptation; parenteral nutrition; short bowel syndrome

Copyright © 2021 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition