RT Book, Section
A1 Kasper, Dennis L.
A1 Fauci, Anthony S.
A1 Hauser, Stephen L.
A1 Longo, Dan L.
A1 Jameson, J. Larry
A1 Loscalzo, Joseph
SR Print(0)
ID 1128786885
T1 Inflammatory Bowel Diseases
T2 Harrison's Manual of Medicine, 19e
YR 2016
FD 2016
PB McGraw-Hill Education
PP New York, NY
SN 9780071828529
LK accessmedicine.mhmedical.com/content.aspx?aid=1128786885
RD 2024/04/16
AB Inflammatory  bowel  diseases  (IBDs)  are  chronic  inflammatory  disorders  of  unknown  etiology  involving  the  gastrointestinal  (GI)  tract.  Peak  occurrence  is  between  ages  15  and  30  and  between  ages  60  and  80,  but  onset  may  occur  at  any  age.  Epidemiologic  features  are  shown  in  Table  148-1.  Pathogenesis  of  IBD  involves  activation  of  immune  cells  by  unknown  inciting  agent  (?  microorganism,  dietary  component,  bacterial  or  self-antigen)  leading  to  release  of  cytokines  and  inflammatory  mediators.  Genetic  component  suggested  by  increased  risk  in  first-degree  relatives  of  pts  with  IBD  and  concurrence  of  type  of  IBD,  location  of  Crohn’s  disease  (CD),  and  clinical  course.  Reported  associations  include  HLA-DR2  in  Japanese  pts  with  ulcerative  colitis  (UC)  and  a  CD-related  gene  called  CARD15  on  chromosome  16p.  CARD15  mutations  may  account  for  10%  of  CD  risk.  Other  potential  pathogenic  factors  include  serum  antineutrophil  cytoplasmic  antibodies  (ANCA)  in  70%  of  pts  with  UC  (also  in  5–10%  of  CD  pts)  and  antibodies  to  Saccharomyces  cerevisiae  (ASCA)  in  60–70%  of  CD  pts  (also  in  10–15%  of  UC  pts  and  5%  of  normal  controls).  Granulomatous  angiitis  (vasculitis)  may  occur  in  CD.  Acute  flares  may  be  precipitated  by  infections,  nonsteroidal  anti-inflammatory  drugs  (NSAIDs),  and  stress.  Onset  of  UC  often  follows  cessation  of  smoking.