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Highlights • The small intestine is an essential constituent of the digestive system and plays a major role in the absorption of nutrients. • Acute mesenteric ischemia remains an emergency case. • Failure to adapt and the inadequate nutritional supply result in Short bowel syndrome. • A minimal indispensable length is required for nutritional autonomy. • Parenteral Nutrition still presents a pertinent problem of complications, charges and impairment in quality of life., Introduction The small bowel is an essential organ for maintaining adequate nutrition. Decrease in length could be associated with malnutrition and may require that the patient receives parenteral nutritional support. We report a case of a 59-year-old man who survived32 years with a short bowel of 35 cm length without any parenteral nutrition. Case presentation A 59-year-old gentleman, with a history of hypercoagulable state, presented for severe abdominal pain and obstipation of one day's duration. Upon presentation, the patient was hemodynamically unstable, with abdominal guarding and tenderness upon physical examination. Laboratory studies showed metabolic acidosis with leukocytosis and electrolyte disturbances, and an abdominal CT scan showed thickening of the sigmoid and multiple air-fluid levels. The patient was operated urgently for suspicion of mesenteric ischemia, however, he was found intraoperatively to have a very short dilated small bowel with jejunotransverse anastomosis. Discussion The necessity for surgical resection of the small bowel can arise for a sum of reasons. However, the removal of a big amount of small bowel may not be adaptive and appropriate digestion will no more be possible. In the aftermath of the resection, patients require parenteral nutrition for a certain period after which they may switch to enteral and oral nutrition, and subsequently intestinal adaptation by thickening and growth of the remaining intestinal villi. Conclusion Patients with a short bowel, particularly those surgically removed, can survive even with a very short remaining bowel length, as a result of intestinal adaptation, nutrition enhancement, and elimination of parenteral nutrition.

Highlights • Combined refeeding and home parenteral nutrition in traumatic intestinal failure. • Peritonitis due to abdominal trauma. • Received Hartman’s procedure and jejunostomy. • Parenteral nutrition at home. • Prevent prolonged length of stay at hospital., Background Intestinal failure is a decrease in intestinal function under the minimum absorption requirements of macronutrients, water, and electrolytes. Hartman's procedure with jejunostomy is used as a surgical procedure to prevent further damage in cases of abdominal trauma. Providing parenteral nutrition at home is needed to prevent nutritional deficiencies and prolonged length of stay. Presentation of case We reported two cases, involving two men aged 25 and 14 years old who had peritonitis due to abdominal trauma and received laparotomy. Both patients had Hartman’s procedures and jejunostomy less than 60 cm from the Treitz ligament. Both patients were diagnosed as bowel failure with an SGA C score. Supervised home parenteral nutrition was done by refeeding jejunostomy at the distal stoma. After supervision of parenteral nutrition, the SGA score increased from C to B. Three months later the patients underwent jejunal reanastomosis. Patients went home one week later without complications. At postoperative follow-up at one month and one year, both patients did not experience any complications. Discussion HPN is now a method used to provide nutritional support for patients with IF. This helps patients to meet their nutritional needs, also preventing psychosocial disorders and reduction of their quality of life. Conclusions Based on these two cases, nurse supervised combined refeeding and home parenteral nutrition showed good results with an increase in nutritional status of SGA C to SGA B. Supervision of home parenteral nutrition can be considered as adjunctive therapy in patients with high intestinal failure before undergoing reanastomosis.

Background: With the introduction of glucagon-like peptide-2 (GLP-2) in the treatment of short bowel syndrome (SBS), there is emerging evidence that GLP-2 may play a role in the restoration of the disturbed homeostatic feedback in the gut-liver axis and may ameliorate SBS-associated liver damage.We have previously presented that daily subcutaneous injections with 1 and 10 mg of glepaglutide improved intestinal function in patients with SBS. As exploratory endpoints, we here assessed the effect of glepaglutide on liver function. Methods: Liver tests, transient elastography (TE) with controlled attenuation parameter (CAP), indocyanine green (ICG) kinetics, soluble CD163 (sCD163), soluble mannose receptor (sMR), and lipopolysaccharide binding protein (LBP) were assessed in 18 patients with SBS in a randomised, cross-over, dose-finding phase 2 trial before and after three weeks of treatment with glepaglutide. This trial is completed and registered at ClinicalTrials.gov: NCT02690025. Findings: Between Feb 2016 and Jan 2017, 22 patients with SBS were screened. Of these, 18 patients were randomised and treated with glepaglutide; 16 patients completed the trial. Treatment with glepaglutide was associated with increase in TE and ICG-elimination. In the 10 mg dose group, glepaglutide increased sCD163 by 0·44 mg/mL (P = 0·0498), and alkaline phosphatase (ALP) decreased in the 1 mg dose group by 33 U/L (P = 0·032). CAP, sMR, LBP, liver transaminases, and INR were not affected. Interpretation: Glepaglutide may improve hepatic excretory function, but at the same time activate resident liver macrophages and increase liver stiffness. The excretory and the stiffness findings may to some extent relate to increased splanchnic blood flow which would not influence the marker of macrophage activation. Thus, glepaglutide exerted diverse effects on liver status that call for attention in future studies. Funding: Zealand Pharma. Keywords: Short bowel syndrome, Transient elastography, Indocyanine green, Soluble CD163, Soluble mannose receptor

Short-bowel syndrome represents the most common cause of intestinal failure and occurs when the remaining intestine cannot support fluid and nutrient needs to sustain adequate physiology and development without the use of supplemental parenteral nutrition. After intestinal loss or damage, the remnant bowel undergoes multifactorial compensatory processes, termed adaptation, which are largely driven by intraluminal nutrient exposure. Previous studies have provided insight into the biological processes and mediators after resection, however, there still remains a gap in the knowledge of more comprehensive mechanisms that drive the adaptive responses in these patients. Recent data support the microbiota as a key mediator of gut homeostasis and a potential driver of metabolism and immunomodulation after intestinal loss. In this review, we summarize the emerging ideas related to host-microbiota interactions in the intestinal adaptation processes.