INFLAMMATORY BOWEL DISEASE (IBD)

DR. FANDY A. G. GOSAL, MPPM, SP.PD-KGEH

DEFINISI

Inflammatory Bowel Disease (IBD) adalah penyakit radang kronis pada saluran pencernaan dan
dibagi menjadi Chron’s disease dan ulcerative colitis. IBD terjadi pada individu yang rentan
secara genetik setelah respon imun yang berlebihan terhadap rangsangan normal seperti
makanan dan flora usus.
 Ulcerative colitis (UC) melibatkan peradangan difus pada mukosa kolon. Paling sering UC
mempengaruhi rektum (proktitis), tetapi dapat meluas ke sigmoid (proctosigmoiditis), di luar
sigmoid (kolitis ulseratif distal), atau mencakup seluruh usus besar hingga sekum (pankolitis).
 Chron’s disease (CD) menyebabkan ulserasi transmural pada bagian manapun dari saluran
pencernaan, yang paling sering mempengaruhi ileum terminal dan usus besar.
PATOFISIOLOGI

 Under physiologic conditions, homeostasis normally exists between the commensal

microbiota, epithelial cells that line the interior of the intestines (intestinal epithelial cells/
IEC), and immune cells within the tissues.
 Hypothesis: each of the three major host compartments are affected by specific environment
(smoking, antibiotics, enteropathogens) and genetic factors, that, in a susceptible host,
cumulatively and interactively disrupt homeostasis during the course of one's life, and in so
doing, culminate in a chronic state of dysregulated inflammation.
 IBD is currently considered an inappropriate immune response to the endogenous commensal
microbiota within the intestines, with or without some component of autoimmunity.
MANIFESTASI KLINIS ULCERATIVE COLITIS

 Diarrhea
 Rectal bleeding
 Tenesmus (a sensation of incomplete evacuation)
 Passage of mucus
 Crampy abdominal pain
 Can present acutely, but symptoms usually have been present for weeks to months
MANIFESTASI KLINIS CHRON’S DISEASE

 Vary considerably depending on the region of gastrointestinal involvement.

 Manifestations vary based on the underlying etiology of inflammation, fistula
formation, or stricture formation
 Right lower quadrant pain, weight loss, and non-bloody diarrhea are suggestive of
Crohn disease flare-up
 Fistula formation may result in fecaluria, pneumaturia, and rectovaginal fistulas.
DIAGNOSIS

 Requires a combination of clinical findings, inflammatory laboratory markers,

imaging findings, and endoscopic biopsies
 Hematologic findings include microcytic anemia, leukocytosis, and thrombocytosis,
inflammatory markers such as the erythrocyte sedimentation rate (ESR), and high-
sensitivity C-reactive protein (hsCRP) are commonly elevated
 Fecal calprotectin levels can be used as a marker for intestinal inflammation. Levels
of perinuclear antineutrophilic cytoplasmic and anti-saccharomyces cerevisiae
antibodies may be elevated in Crohn disease. 
DIAGNOSIS

 Abdominal x-ray can assess for the presence of free air, bowel obstruction, or toxic megacolon.
 Barium studies are done to characterize the bowel disease; a lead pipe appearance indicates
ulcerative colitis; sparing of the rectum is indicative of Crohn disease and thumb printing is
indicative of mucosal inflammation. Further, the barium studies may reveal skip lesions and
stricture formation in the ileum, which are indicative of Crohn disease.
 Ultrasound (US), computed tomography (CT), and magnetic resonance imaging (MRI) have all
been used in the diagnosis of IBD or to assess for complications.
 Endoscopy evaluation with either esophagogastroduodenoscopy, colonoscopy, or both is
essential to obtaining biopsies to confirm a diagnosis of IBD.
TREATMENT

 Stepwise approach
 First step in pharmacologic therapy: aminosalicylates (sulfasalazine, balsalazide,
delzicol, asacol HD, apriso, pentasa, salofalk granu-stix)
 If the patient does not respond to an appropriate dose of aminosalicylates, the second
step is the addition of corticosteroids, which tend to result in a significant decrease in
inflammation. Once the response is seen, the dose can be tapered > Prednisone,
hydrocortisone, methylprednisone.
TREATMENT

 The immune-modifying agents (e.g Anti-TNF agents) are the step three drugs. These
are used when the patient does not respond to corticosteroids, steroids are required for
prolonged periods, or the steroids cannot be tapered down without recurrence of
symptoms.
 Lately, a step-down approach is being favored more for patients with high-risk or
severe disease. This includes the early introduction of higher step medications such as
anti-TNF agents with rapid de-escalation when the response is seen.
PROGNOSIS

 The prognosis for both UC and CD depends on the extent of the disease and treatment
response.
 Patients with IBD tend to have much higher mortality compared to the general
population. Causes of death include primary disease, infections, and respiratory
illness
 The cumulative risk of colorectal cancer is estimated to be as high as 30% for those
with the disease of 30 years or more. The extraintestinal manifestation of primary
sclerosing cholangitis leads to liver failure
COMPLICATIONS

Intestinal Extra Intestinal

 Osteoporosis
 Hemorrhage
 Deep vein thrombosis
 Strictures  Anemia
 Colon perforation  Gallstones

 Anal fistulas  Primary sclerosing cholangitis

 Aphthous ulcers
 Pelvic or perirectal abscesses
 Arthritis
 Toxic megacolon
 Iritis
 Cholangiocarcinoma, colon cancer  Pyoderma gangrenosum
TERIMA KASIH