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One in four loop ileostomies performed to defunction an elective anterior resection is not reversed, and in the presence of significant comorbidity one in three is not reversed. Only 12% is reversed within 12 weeks.

Acidic fibroblast growth factor (FGF-1) and basic fibroblast growth factor (FGF-2) are ubiquitous cytokines found in many tissues. They have effects on multiple cell types derived from mesoderm and neuroectoderm, including endothelial cells. In this review the structure and function of the fibroblast growth factor family and its receptors are described. The evidence implicating both FGF-1 and FGF-2 in the control of blood vessel formation is presented and their involvement in normal and pathological angiogenesis during adult life is then described in more detail.

Conversion after laparoscopic cholecystectomy is less common as consultant caseload increases. This suggests that operation should be undertaken only by surgeons with an adequate caseload. There is a wide variation in conversion rates among hospitals. This has important implications for training as well as for the organization and accreditation of cholecystectomy services on a national basis.

Conclusion-Treatment with anti-CINC antibody aVorded significant protection against pancreatitis associated lung injury. These results suggest that CINC plays an important role in the systemic inflammatory response in AP. (Gut 2000;47:838-844)

Impaired lung function in severe acute pancreatitis is the primary cause of morbidity and mortality in this condition. Preprotachykinin-A (PPT-A) gene products substance P and neurokinin (NK)-A have been shown to play important roles in neurogenic inflammation. Substance P acts primarily (but not exclusively) via the NK1 receptor. NKA acts primarily via the NK2 receptor. Earlier work has shown that knockout mice deficient in NK1 receptors are protected against acute pancreatitis and associated lung injury. NK1 receptors, however, bind other peptides in addition to substance P, not all of which are derived from the PPT-A gene. To examine the role of PPT-A gene products in acute pancreatitis, the effect of PPT-A gene deletion on the severity of acute pancreatitis and the associated lung injury was investigated. Deletion of PPT-A almost completely protected against acute pancreatitis-associated lung injury, with a partial protection against local pancreatic damage. These results show that PPT-A gene products are critical proinflammatory mediators in acute pancreatitis and the associated lung injury.