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At least 271 records · Page 15Linked to original sources
PubMed2004

Clinical relevance of advances in genetics and pharmacogenetics of IBD.

Crohn's disease and ulcerative colitis result from an inappropriate response of the mucosal immune system to the normal enteric flora in a genetically susceptible individual. During the past decade, exciting progress has been made in our understanding of the contribution of genetics to inflammatory bowel disease susceptibility and phenotype. This article reviews recent advances in the genetics of inflammatory bowel disease and explores how they might impact on clinical practice. Current knowledge of the genetic basis for disease susceptibility, phenotype, and response to therapy is explored and the factors currently limiting the translation of this knowledge to clinical practice is discussed.

Carrier Proteins↗
PubMed2004

Current concepts and controversies in surgery for IBD.

Surgery improves the quality of life in patients with Crohn's disease (CD) and cures patients with chronic ulcerative colitis (CUC). There are several surgical controversies primarily involving techniques and long-term outcomes. Some debates are long standing; whether to perform a double-stapled ileal pouch-anal anastomosis (IPAA) or a mucosectomy and hand-sewn anastomosis, and whether to divert or not to divert in patients with CUC undergoing an IPAA. Other issues are more recent, such as the effects of age, pregnancy, pouch salvage, and laparoscopic IPAA. In patients with Crohn's disease the anastomosis technique, the management of perianal disease, and the role of laparoscopic surgery are topics of debate. This review shows the current concepts and controversies in the surgical management of patients with CUC or CD.

Adult↗
PubMed2004

Colonic leptin: source of a novel proinflammatory cytokine involved in IBD.

Leptin, a peptide encoded by the obese (ob) gene, is primarily secreted by adipocytes and is a critical hormone that controls body weight due to its central effects. Recently, additional roles for leptin in the gastrointestinal tract have been suggested because gastric lining cells also produce and release leptin in response to meal-related stimuli. While gastric epithelia might thus directly contribute to circulating leptin following a meal, here we show that inflamed colonic epithelial cells express and release leptin apically into the intestinal lumen. In addition, we demonstrate leptin expression and secretion in vitro in epithelial cells. In response to luminal leptin, model intestinal epithelia critically activate the NF-kappaB, a key signaling system to pro-inflammatory stimuli. The inflammatory effect of luminal leptin was characterized in vivo in mice administered intrarectal leptin. Leptin induced epithelial wall damage and neutrophil infiltration that represent characteristic histological findings in acute intestinal inflammation. These observations provide evidence for an intraluminal biological signaling of leptin and a new pathophysiological role for intraluminal leptin during states of intestinal inflammation such as inflammatory bowel disease.

Animals↗