Kelly A. Miller

Hemangioma of the umbilical cord mimicking an omphalocele

A hemangioma of the umbilical cord was misdiagnosed as an omphalocele both antenatally and immediately after birth. The girl was full term and had no other anomalies. Complete resection, including an intraabdominal component, was performed on the first day of life. This rare anomaly and its possible pitfalls are discussed, and the literature is reviewed.

Intestinal production of IL-6 initiates systemic inflammation in a murine model of intestinal ischemia reperfusion1

Abstract Purpose: Intestinal ischemia/reperfusion (I/R) injury disrupts the gut barrier and activates systemic inflammation and multisystem organ failure (MOF). Our reported murine model of intestinal I/R demonstrated dose-dependent local injury and mortality [Gastroenterology (1998) 114:A-1587]. We hypothesized that the release of proinflammatory cytokines from the gut modulates systemic inflammation. Methods: Balb/c mice underwent 50 minutes of superior mesenteric artery occlusion with reperfusion. All survived long-term (>16 hours). Controls were sham operated. Serum levels of IL-6 and TNF-α were measured at 0, 1, 4, and 16 hours by ELISA. Small bowel and liver mRNA were evaluated for production of IL-6 and TNF-α by semiquantitative RT-PCR, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) standard and a Student t-test for data analysis (p Results: Serum levels of IL-6 were significantly elevated at 4 and 16 hours versus controls ( Fig. 1 , left). The serum level of TNFα was not elevated. There was a significant elevation of IL-6 mRNA at 1 and 4 hours in the jejunum ( Fig. 1 , center) Download : Download high-res image (129KB) Download : Download full-size image FIGURE 1 . and TNFα mRNA at 4 hours. No significant increase in liver IL-6 ( Fig. 1 , right) or TNF-α mRNA was seen. Conclusions: In this model of ischemia reperfusion injury, the intestine is a major source of the proinflammatory cytokine IL-6 but not of TNF-α. The rapid appearance of IL-6 mRNA in the jejunum suggests that the intestine, not the liver, initiates systemic inflammation and MOF by a distinct cytokine pattern.

Endogenous interleukin 10 does not protect against local or systemic injury in a murine model of intestinal ischemia and reperfusion1

Abstract Purpose: Ischemia/reperfusion of the small intestine disrupts gut barrier function and activates systemic inflammation. The anti-inflammatory cytokine interleukin-10 (IL-10) is protective in murine models of acute sepsis, yet its role during gut injury is unknown. We therefore undertook to investigate this question. Methods: Mice genetically deficient in IL-10 (IL-10 −/− ) on a C57BL/10 background, their wild-type littermates, and Balb/c mice underwent 30 to 80 minutes of occlusion of the superior mesenteric artery. Sixteen hours after reperfusion, survival was documented and the small bowel scored for histologic damage. Results: The LD 50 of IL-10 −/− mice was 35 minutes of occlusion, identical to that of the wild-type mice. The small bowel of all animals that died was distended, with localized jejunal hemorrhage. LD 50 Occlusion (min) Histologic Injury Score (n = 3) C57BL/10 (IL-10 +/+ ) 35 30 3.0 ± 1.0 C57BL/10 (IL-10 −/− ) 35 30 2.0 ± 0.0 Balb/c 60 50 4.3 ± 4.0 Balb/c 60 20 0.3 ± 0.6 No significant difference in intestinal damage was observed between surviving IL-10 −/− and IL-10 +/+ mice after 30 minutes of occlusion. Balb/c mice were more resistant to intestinal ischemia, demonstrated by an LD 50 at 60 minutes of occlusion. Furthermore, equivalent mucosal damage in Balb/c mice required 50 minutes of occlusion as compared with that seen in 30 minutes with occluded C57BL/10 mice. Conclusions: Interleukin-10 does not play a significant protective role either locally or systemically in this model of ischemia/reperfusion. The resistance of the Balb/c strain suggests that an alternate mechanism modulates the response to intestinal ischemic/reperfusion injury.