ABSTRACT
Pediatric Crohn disease is characterized by clinical and endoscopic relapses. The inflammatory process is considered to be progressive and may lead to strictures, fistulas, and penetrating disease that may require surgery. In addition, medically refractory disease may be treated by surgical resection of inflamed bowel in an effort to reverse growth failure. The need for surgery in childhood suggests severe disease and these patients have an increased risk for recurrent disease and potentially more surgery. Data show that up to 55% of patients had clinical recurrence in the first 2 years after initial surgery. The current clinical report on postoperative recurrence in pediatric Crohn disease reviews the risk factors for early surgery and postoperative recurrence, operative risk factors for recurrence, and prevention and monitoring strategies for postoperative recurrence. We also propose an algorithm for postoperative management in pediatric Crohn disease.
Subject(s)
Aftercare/methods , Crohn Disease/surgery , Postoperative Care/methods , Secondary Prevention/methods , Child , Crohn Disease/diagnosis , Crohn Disease/etiology , Crohn Disease/prevention & control , Digestive System Surgical Procedures/methods , Humans , Recurrence , Risk Factors , Severity of Illness Index , Treatment OutcomeSubject(s)
Abdominal Abscess/diagnosis , Abdominal Abscess/drug therapy , Crohn Disease/diagnosis , Crohn Disease/drug therapy , Fistula/diagnosis , Fistula/drug therapy , Abdominal Abscess/etiology , Abdominal Abscess/pathology , Child , Crohn Disease/complications , Crohn Disease/pathology , Fistula/etiology , Fistula/pathology , Humans , Research ReportABSTRACT
It is estimated that of the >1 million individuals in the United States with inflammatory bowel disease (IBD), approximately 100,000 are children. IBD that begins in childhood affects the individual at a critical period of growth and development. Children with Crohn's disease and ulcerative colitis may experience complications such as growth failure, school absence, and depression. In addition, because children with IBD have fewer environmental confounders such as smoking, children may be an excellent population to study microbial and immune interactions. Despite these opportunities, the discipline of pediatric IBD investigation is still in its infancy. In September of 2005, a group of investigators with expertise in pediatric IBD met in Boston (Massachusetts) to review the current status of childhood IBD research and to develop research priorities that warranted funding from the Crohn's and Colitis Foundation of America. The group included pediatricians, internists, basic scientists, clinical investigators, and members of the administrative staff and board of the Crohn's and Colitis Foundation of America. The research needs in respective areas were outlined by the heads of 10 focus groups, each with expertise in their respective fields (genetics, psychosocial issues, epidemiology, microbiology, immunology, quality improvement, pharmacogenomics, nutrition, growth and skeletal health, and clinical trials). Before the conference, heads of the research focus groups developed their proposals with experts in the field. At the end of the conference, members of the focus groups and members of the steering committee rated the proposed areas of study in terms of feasibility and importance. It was recommended that the Crohn's and Colitis Foundation of America focus its initial efforts in pediatric IBD in 5 areas: the effects of inflammation on growth and skeletal development, the genetics of early-onset IBD, the development of quality improvement interventions to standardize and improve clinical care of children with IBD, the immunology of childhood IBD, and the diagnosis and treatment of psychosocial sequelae of childhood IBD. At the conclusion of the meeting, investigators discussed the formation of a multicenter collaborative network to advance clinical and basic research in the field.
Subject(s)
Inflammatory Bowel Diseases , Child , Humans , Inflammatory Bowel Diseases/diagnosis , Inflammatory Bowel Diseases/physiopathology , Inflammatory Bowel Diseases/psychology , Inflammatory Bowel Diseases/therapy , Pediatrics/methods , Pediatrics/standards , ResearchABSTRACT
Prostaglandin E(2) (PGE(2)) and other cAMP elevating agents inhibited neonatal but not adult T cell dependent Ig production. PGE(2) did not inhibit IL-2-dependent anti-CD3 stimulated neonatal T cell proliferation or T cell-dependent neonatal B cell proliferation. The results could not be explained by differences in the effect of PGE(2) on cAMP production by neonatal and adult B and T cells or by a unique sensitivity of CD5+ B cells to inhibition by PGE(2). The enhanced sensitivity of neonatal T cell dependent Ig production to inhibition by PGE(2) may play a role in the increased susceptibility of neonatal B and T cells to tolerance induction.
