As early as 1975, the triad of GI mucosal injury, presence of bacteria in the gut, and introduction of a metabolic substrate (eg, feedings) was proposed as the etiology of bowel necrosis [3] (Fig 2).

[24] Adequate bowel length was preserved in infants with massive intestinal necrosis, allowing for their survival. There was no major morbidity in study infants, and only 30% required a second ...

No significant difference in the risk for MACE was observed between patients with IBD receiving JAK vs TNF inhibitors.