Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) includes two classic entities, Crohn\u2019s disease (CD) and ulcerative colitis (UC), and a third undetermined form (IBD-U). Ulcerative colitis is an idiopathic IBD affecting primarily the mucosal layer of the colon. UC is more frequent between ages 15 and 35. The disease extent is variable; inflammation can be restricted either to the distal rectum or to the entire colon. According to Scandinavian, North American, and UK studies, UC incidence in children ranges from 2.1 to 4.2 cases/year/100,000 population. Most common symptoms include rectal bleeding, abdominal pain, and diarrhea. Pediatric UC activity evaluation is evaluated with a sixth variable which is the pediatric UC activity index (PUCAI). Diagnosis is based on laboratory assessment and endoscopic and histologic evaluation. Treatment options depend on the extent and severity of disease. Medical treatment should be proposed first. Surgery should be reserved to patients with severe and/or refractory disease or with serious pharmacological side effects. Crohn\u2019s disease is a chronic, relapsing, inflammatory disorder which could develop in any part of the gastrointestinal tract. The incidence of CD in children is increasing worldwide, ranging from 2.5 to 11.4 per 100,000, with an estimated prevalence of 58/100,000 which is rising in both developed and developing countries. In genetically predisposed children, an interaction between luminal contents and the mucosa leads to a dysregulated inflammation, which is the most recognized mechanism of pediatric CD. Classical symptoms and signs are abdominal pain, diarrhea, weight loss, fever, and failure to thrive. Diagnosis is based on serologic tests, fecal markers, and endoscopic findings. Conventional therapy is based on the shift from drugs with a better safety profile but lower efficacy (mesalazine, sulfasalazine, antibiotics) to those with improved efficacy but a greater risk of side effects (steroids, immunomodulators, biologicals, surgery)

Diaphragm Repair with a Novel Cross-Linked Collagen Biomaterial in a Growing Rabbit Model

Neonates with congenital diaphragmatic hernia and large defects often require patch closure. Acellular collagen matrices (ACM) have been suggested as an alternative to synthetic durable patches as they are remodeled by the host or could also be used for tissue engineering purposes.2.0x1.0 cm diaphragmatic defects were created in 6-weeks old New-Zealand white rabbits. We compared reconstruction with a purpose-designed cross-linked ACM (Matricel) to 4-layer non-cross-linked small intestinal submucosa (SIS) and a 1-layer synthetic Dual Mesh (Gore-Tex). Unoperated animals or animals undergoing primary closure (4/0 polyglecaprone) served as age-matched controls. 60 (n = 25) resp. 90 (n = 17) days later, animals underwent chest x-ray and obduction for gross examination of explants, scoring of adhesion and inflammatory response. Also, uniaxial tensiometry was done, comparing explants to contralateral native diaphragmatic tissue.Overall weight nearly doubled from 1,554±242 g at surgery to 2,837±265 g at obduction (+84%). X-rays did show rare elevation of the left diaphragm (SIS = 1, Gore-Tex = 1, unoperated control = 1), but no herniation of abdominal organs. 56% of SIS and 10% of Matricel patches degraded with visceral bulging in four (SIS = 3, Matricel = 1). Adhesion scores were limited: 0.5 (Matricel) to 1 (SIS, Gore-Tex) to the left lung (p = 0.008) and 2.5 (Gore-Tex), 3 (SIS) and 4 (Matricel) to the liver (p<0.0001). Tensiometry revealed a reduced bursting strength but normal compliance for SIS. Compliance was reduced in Matricel and Gore-Tex (p<0.01). Inflammatory response was characterized by a more polymorphonuclear cell (SIS) resp. macrophage (Matricel) type of infiltrate (p<0.05). Fibrosis was similar for all groups, except there was less mature collagen deposited to Gore-Tex implants (p<0.05).Matricel induced a macrophage-dominated inflammatory response, more adhesions, had appropriate strength but a lesser compliance compared to native tissue. The herein investigated ACM is not a viable option for CDH repair