A Masking Effect: A Case of Initial Presentation of Ulcerative Colitis After Discontinuing Growth Hormone Therapy.

Background: The inflammation and repair of the intestinal mucosa in inflammatory bowel disease (IBD) involve a complex interplay between innate, adaptive immune responses, and hormones. This may explain the relapsing clinical course of the disease. Methods: We present the first reported case of a patient presenting their initial flare of ulcerative colitis immediately after discontinuing growth hormone (GH) therapy, suggesting treatment with GH or growth factors may prevent the development of IBD. Results: This is a case of a 13-year-old female with a history of GH deficiency, presenting with an 8-week history of abdominal pain, blood-stained diarrhea, and fecal calprotectin greater than 8000 mcg/g, 2 weeks after discontinuing GH therapy. The patient subsequently underwent an esophagoduodenoscopy and colonoscopy with biopsies showing histological features consistent with ulcerative colitis. Conclusions: The finding of withdrawing GH or growth factors therapy potentially unmasking IBD in this patient raises a question of whether growth factors can inhibit the development of IBD and suggests beneficial effects of treatment with GH or growth factors as adjuvant therapy for IBD.

13C-breath tests for sucrose digestion in congenital sucrase isomaltase-deficient and sacrosidase-supplemented patients.

BACKGROUND: Congenital sucrase-isomaltase deficiency (CSID) is characterized by absence or deficiency of the mucosal sucrase-isomaltase enzyme. Specific diagnosis requires upper gastrointestinal biopsy with evidence of low to absent sucrase enzyme activity and normal histology. The hydrogen breath test (BT) is useful, but is not specific for confirmation of CSID. We investigated a more specific 13C-sucrose labeled BT. OBJECTIVES: Determine whether CSID can be detected with the 13C-sucrose BT without duodenal biopsy sucrase assay, and if the 13C-sucrose BT can document restoration of sucrose digestion by CSID patients after oral supplementation with sacrosidase (Sucraid). METHODS: Ten CSID patients were diagnosed by low biopsy sucrase activity. Ten controls were children who underwent endoscopy and biopsy because of dyspepsia or chronic diarrhea with normal mucosal enzymes activity and histology. Uniformly labeled 13C-glucose and 13C-sucrose loads were orally administered. 13CO2 breath enrichments were assayed using an infrared spectrophotometer. In CSID patients, the 13C-sucrose load was repeated adding Sucraid. Sucrose digestion and oxidation were calculated as a mean percent coefficient of glucose oxidation averaged between 30 and 90 minutes. RESULTS: Classification of patients by 13C-sucrose BT percent coefficient of glucose oxidation agreed with biopsy sucrase activity. The breath test also documented the return to normal of sucrose digestion and oxidation after supplementation of CSID patients with Sucraid. CONCLUSIONS: 13C-sucrose BT is an accurate and specific noninvasive confirmatory test for CSID and for enzyme replacement management.

Epidermal growth factor reduces ischemia-reperfusion injury in rat small intestine.

OBJECTIVE: To measure the effect of pre-ischemic administration of intraluminal epidermal growth factor on the changes in intestinal permeability induced by 30 mins of superior mesenteric artery occlusion, followed by 2 hrs of reperfusion. DESIGN: Prospective, randomized, placebo-controlled experimental study. SETTING: University basic science research laboratory. SUBJECTS: Healthy, young, adult, male Sprague-Dawley rats. INTERVENTIONS: A 10-cm segment of small intestine was isolated and studied in situ in rats that were anesthetized with fentanyl and mechanically ventilated. Intestinal ischemia-reperfusion injury was induced by temporary occlusion of the superior mesenteric artery for 30 mins, followed by 2 hrs of reperfusion. Three groups were studied: time controls with a sham operation, saline-treated ischemia-reperfusion, and epidermal growth factor-treated ischemia-reperfusion. Epidermal growth factor, 100 ng/min, was infused intraluminally, beginning 30 mins before and continued until 40 mins after ischemia. MEASUREMENTS AND MAIN RESULTS: Intestinal permeability was measured for each 10-min time period by using chromium-labeled EDTA. Histopathologic injury was assessed by light microscopy. After superior mesenteric artery occlusion, intestinal permeability increased approximately ten-fold and was sustained for 2 hrs of reperfusion in saline-treated rats. Pretreatment with epidermal growth factor significantly reduced the permeability changes during reperfusion by >60% compared with saline-treated animals (p <.05). Histopathologic sections revealed apparently more extensive loss of epithelial cells and mucosal disruption in saline-treated intestine compared with epidermal growth factor-treated intestine. CONCLUSION: Pre-ischemic administration of intraluminal epidermal growth factor significantly protects against intestinal ischemia-reperfusion injury.

Lipopolysaccharide-induced gastrointestinal injury in rats: role of surface hydrophobicity and bile salts.

Sepsis of gastrointestinal origin can lead to life-threatening complications in vital organs due to bacterial overgrowth and/or translocation from the lumen into the blood. In a rat model of endotoxemia, changes in surface hydrophobicity (associated with barrier integrity) of the gastrointestinal mucosa were examined. Rats were treated with Escherichia coli lipopolysaccharide (LPS), and gastric and ileal tissue were collected for determination of surface hydrophobicity by contact angle analysis. A role for bile salts in hydrophobicity changes was tested by quantifying bile salts in the lumen of both the stomach and ileum after LPS and by the administration of LPS to bile duct-ligated rats. A single intraperitoneal dose of LPS induced a dose- and time-dependent reduction in hydrophobicity of both the stomach and ileum, with the stomach showing greater sensitivity at an earlier time than the ileum. LPS also induced gastric bleeding, reflux of bile acid into the gastric lumen, and decreased levels of bile salt in the ileum. The LPS-induced reductions in surface hydrophobicity of the stomach were prevented by prior bile duct ligation. We conclude that LPS disrupts gastrointestinal barrier integrity, in part by mechanisms involving bile constituents and an attenuation in the mucosa's hydrophobic characteristics.