Inflammatory bowel disease (IBD) encompasses chronic inflammatory disorders of the gastrointestinal tract, primarily including ulcerative colitis (UC) and Crohn's disease (CD), with varying prevalence and incidence rates in different populations. The etiology remains unclear but is believed to involve genetic, environmental, and immunologic factors, leading to characteristic symptoms such as diarrhea, abdominal pain, and weight loss, along with extraintestinal manifestations. Treatment is multifaceted, including pharmacologic options like aminosalicylates and corticosteroids, nutritional support, and potential surgical interventions.

1. Inflammatory Bowel Disease (IBD)

2. Overview
• IBD Definition: generic term for a group of chronic,
idiopathic, relapsing inflammatory disorders of the
gastrointestinal tract.
• Two forms of idiopathic IBD are:
– Ulcerative colitis (UC)
• Mucosal inflammatory condition that is limited to the rectum and colon
– Crohn’s disease (CD)
• Transmural inflammatory condition that can affect any part of the GI tract,
from the mouth to the anus

3. Epidemiology
• Rates of IBD are highest in North America, Northern Europe,
and Great Britain
• Ulcerative colitis (UC)
– Incidence: 6 – 15.5 cases per 100,000 per year in the U.S.
– Prevalence: 7.6-246 per 100,000 persons per year in the U.S.
• Crohn’s disease (CD)
– Incidence: 6-15cases per 100,000 per year in the U.S.
– Prevalence: 3.6-214 per 100,000 persons per year in the U.S.

4. Epidemiology
• The peak incidence occurs in the second or third decade of life with
a second peak occurring between the ages of 60 and 70
• IBD affects both sexes somewhat equally overall
– 20% to 30% more woman are affected with CD
– Slightly more men (60%) are affected with UC
• Caucasians are affected more than non-whites for both UC and CD

5. Etiology
• The exact etiology of IBD is unknown.
• Dysregulation of the inflammatory response within the GI tract in response to
environmental or microbiologic factors is thought to be the prevailing
mechanism
• It is postulated that the cause of IBD is a combination of:
– Infectious factors: viruses, protozoans, and mycobacteria may promote alteration of the
intestinal barrier and/or propagate an inflammatory response
– Genetic factors: First-degree relatives with IBD…a 20-fold increase risk
– Immunologic mechanisms: an abnormal regulation of the normal immune response or an
autoimmune reaction to self-antigens
– Environmental causes
• Psychological factors
• Lifestyle, Dietary, and drug-related causes

6. Ulcerative Colitis (UC) Pathophysiology
• The inflammatory response in UC is propagated by atypical type 2
helper T cells that produce proinflammatory cytokines such as
interleukin (IL)-1, IL-6, and tumor necrosis factor- (TNF-)
• UC is confined to the rectum and colon
• Lesions affect the mucosal and submucosal layers
• In UC, the mucosal appearance includes edema, mucopus,
erosions, and the lesions are continuous in nature
– Lesions are sometimes referred to as having a “lead pipe” appearance
• Fistulas, strictures, perforations are rare

7. Crohn’s Disease (CD) Pathophysiology
• CD is characterized by a transmural inflammatory process
• Cytokines thought to play major roles in CD are derived from T-helper type 1 cells and
include interferon-, transforming growth factor-, TNF-, and IL-1, IL-6, IL-8, IL-12, and
IL-23.
• TNF-, IL-12, and IL-23 are major contributors to the inflammatory process and
development of fibrosis in CD.
• Lesions can occur anywhere in the GI tract but the terminal ileum is the most common site
• In CD, the mucosal appearance often includes ulcers, strictures, fistulas and the lesions
are discontinuous and segmented
– Lesions are sometimes said to give a “cobblestone” appearance
• Fistulas and strictures are common
• Nutritional deficiencies are common

8. Extraintestinal Manifestations of IBD
• Both UC and CD are associated with the development of symptoms and
organ involvement outside of the GI tract and these are referred to as
extra intestinal manifestations
• Several of these have immunologic components associated with them
• Extra intestinal manifestations include hepatobiliary complications; joint
complications; ocular complications; dermatologic complications;
hematologic, coagulation, and metabolic abnormalities

9. Clinical Presentation of IBD
• Presenting symptoms common to both UC and CD include:
– Diarrhea
– Abdominal cramping
– Fever
– Rectal bleeding
– Weight loss
• Most people with IBD have periods of exacerbations and
remissions

10. UC Clinical Presentation
• There is a wide range of presentation in UC
• There is no standard disease severity scoring system
– The arbitrary distinctions of mild, moderate, severe, and fulminant
disease activity are generally accepted and used in treatment
guidelines
– These classifications are determined by clinical signs and symptoms

11. UC Clinical Presentation
• Mild
– Less than 4 stools per day, with or without blood, with no systemic
disturbance and a normal erythrocyte sedimentation rate (ESR)
• Moderate
– Four or more stools per day but with minimal systemic disturbance
• Severe
– More than 6 stools per day with blood and systemic disturbance
• Fulminant
– More than 10 stools per day with continuous bleeding that may require
transfusion, abdominal tenderness, colonic dilation, and additional marked
systemic disturbance/toxicity

12. UC Clinical Presentation
• Systemic disturbance includes:
– Fever (temperature > 99.5 degrees Fahrenheit)
– Tachycardia (HR > 90-100 bpm)
– Anemia (hemoglobin < 75% of normal)
– ESR > 30 mm/h
– Abdominal tenderness
– Bowel wall edema

13. UC Clinical Presentation
• In addition to determining disease severity,
determining disease extent or which parts of the
colon are involved is important
– Distal disease (AKA left-sided disease) – inflammation
limited to areas distal to the splenic flexure
– Extensive colitis – inflammation extending proximal to
the splenic flexture
– Proctitis – inflammation confined to the rectum
– Proctosigmoiditis – inflammation involving the rectum
and sigmoid colon
– Pancolitis – inflammation occurring in the majority of the
colon

14. CD Clinical Presentation
• Presentation of CD is highly variable
• Treatment guidelines use the presence of signs and symptoms
as their marker for disease activity and severity
• The primary classifications used are:
– Mild to Moderate disease
– Moderate to Severe disease
– Severe to Fulminant disease

15. CD Clinical Presentation
• Mild to Moderate Disease
– Ambulatory patients who are able to tolerate food and beverage intake
– Absence of fever, dehydration, systemic toxicity, abdominal
tenderness, mass, obstruction
– No weight loss or a non-significant weight loss
• Less than 10% of body weight

16. CD Clinical Presentation
• Moderate to Severe Disease
– Those who fail to respond to treatment for mild/moderate disease
OR
– Those with more prominent symptoms such as fever, abdominal
pain/tenderness, intermittent nausea/vomiting, dehydration, significant
weight loss, significant anemia

17. CD Clinical Presentation
• Severe to Fulminant Disease
– Those with persistent symptoms despite the use of corticosteroid or
biologic treatment
OR
– Those with high fever, persistent vomiting, rebound tenderness,
evidence of intestinal obstruction or abscess

18. Selected Complications
• Toxic Megacolon
– IBD patients are at increased risk of developing toxic megacolon, which
is a segmental or total colonic distension of greater than 6cm with acute
colitis and signs of systemic toxicity
• Colon Cancer
– IBD patients are at higher risk of colorectal carcinoma (CRC)
– Risk factors for CRC include: young age at IBD onset (<50 years old),
severe inflammation, positive family history of CRC
– Screening colonoscopy should be performed at 8 years after onset of
IBD symptoms with subsequent screenings every 1 to 2 year if negative

19. IBD Diagnosis
• The diagnosis of IBD is made on clinical suspicion confirmed by a thorough
medical evaluation using:
– Sigmoidoscopy or colonoscopy
– Biopsy
– Stool examinations
– Barium radiographic contrast studies
– Laboratory testing: ESR, CRP, faecal calprotectin, CBC ( Leukocytosis, Hgb)
• The presence of extraintestinal manifestations may also aid in establishing a
diagnosis

20. Treatment of IBD
Goals of Therapy
• IBD is a chronic lifelong illness characterized by exacerbations
and periods of remission.
• Goals of therapy include:
– Provide relief of symptoms (induce remission)
– Improve quality of life
– Maintain adequate nutritional status
– Relieve intestinal inflammation
– Decrease frequency of recurrence
– Resolve complications

21. Nonpharmacologic Therapy: Nutritional Support
• Proper nutritional support is an important aspect
– Individual patients can try avoiding specific foods that may exacerbate their symptoms
• Nutritional needs of patients with IBD may be adequately addressed with
enteral supplementation in acute or chronic situations
• Parenteral nutrition has a more limited role in IBD and is reserved for
patients with severe malnutrition or those who fail enteral therapy

22. Nonpharmacologic Therapy: Nutritional Support
• Probiotic therapy involves the reestablishment of normal bacterial flora
within the gut by oral administration of live bacteria such as
nonpathogenic Escherichia coli, bifodbaceria, lactobacilli, Streptococcus
thermophilus, Saccharomyces boulardii
• Probiotics have demonstrated some effectiveness in inducing and
maintaining remission in some trials for patients with UC
• Evidence of probiotic use in the induction and maintenance of CD is less
compelling and has led to recommendations not supporting widespread
use

23. Nonpharmacologic Therapy: Surgery
• Even with many medications available to treat IBD, many
patients will require surgery
• Surgical procedures may involve resection of segments of
intestine that are affected, correction of complications
– (e.g., fistulas, strictures, obstructions, perforations, etc.), or drainage of
abscesses

24. Pharmacologic Treatment of IBD
• Aminosalicylates
• Corticosteroids
• Immunomodulators
• Tumor necrosis factor (TNF)-inhibitors and other biologics
• Miscellaneous agents (antimicrobials)

25. Pharmacotherapy for IBD
• Treatment selection is dependent on the
– Type (UC or CD)
– Severity (mild, moderate, severe, fulminant)
– Site of disease (proctitis, distal disease, extensive disease, small
intestine involvement, etc.)
– Need for acute treatment or maintenance therapy

26. UC Pharmacotherapy
• Proctitis – inflammation confined to the rectum
– Topical therapy used most often
• Distal disease (AKA left-sided disease) – inflammation limited to areas
distal to the splenic flexure
– May use either systemic or topical therapy or a combination
• Extensive colitis – inflammation extending proximal to the splenic
flexure
– Must use systemic therapy. May add topical therapy to systemic therapy if
needed/appropriate
• Pancolitis – inflammation occurring in the majority of the colon
– Must use systemic therapy. May add topical therapy to systemic therapy if
needed/appropriate

28. Mild/Moderate DISTAL UC
• Treatment of ACTIVE Disease
1. First-line therapy: topical (enema/suppository) amino salicylates
2. If inadequate or no response to #1, use an oral amino salicylate or
topical corticosteroid
• May combine oral and topical amino salicylates

29. Mild/Moderate DISTAL UC
• Remission/Maintenance Therapy:
– Mesalamine suppository or enema used 3 times per week
OR
– Oral aminosalicylate tapered to a maintenance dose
• Topical or oral corticosteroids have no role in maintenance
therapy

30. Mild/Moderate EXTENSIVE UC
• Treatment of ACTIVE Disease
1. First-line therapy: Oral aminosalicylate
2. If #1 doesn’t work, use budesonide 9mg/day for up to 8 weeks
• Remission/Maintenance Therapy
1. Preferred: Oral aminosalicylate
2. If used budesonide for induction, then budesonide 6mg/day for up to 3
months plus oral aminosalicylate at maintenance dose

31. Moderate/Severe UC
• Treatment of ACTIVE disease
1. First-line therapy: Oral aminosalicylate PLUS prednisone 40-
60mg/day
2. If inadequate or no response to #1, ADD azathioprine,
mercaptorpurine, infliximab, adalimumab, or golimumab
• Remission/Maintenance Therapy
1. Taper prednisone, then after 1 to 2 months reduce oral
aminosalicylate dose to maintenance dose
2. Continue azathioprine, mercaptopurine, infliximab, adalimumab, or
golimumab if previously added

32. Severe/Fulminant UC
• Treatment of ACTIVE disease
1. 7 to 10 day course of intravenous corticosteroids (hydrocortisone)
2. Patients refractory to IV corticosteroids (no response in 5 to 7 days)
are candidates for IV cyclosporine

33. Severe/Fulminant UC
• Remission/Maintenance Therapy
1. If remission achieved with IV hydrocortisone: Change IV
hydrocortisone to oral prednisone and ADD azathioprine,
mercaptopurine, adalimumab, or golimumab. Attempt to withdraw
prednisone after 1 – 2 months. Can also consider adding oral
aminosalicylate into the mix.
2. If corticosteroid refractory disease and needed cyclosporine to achieve
remission: Change IV cyclosporine to oral cyclosporine and ADD
either azathioprine or mercaptopurine.
– May consider TNF-inhibitor at maintenance dose in the future, but if using oral
cyclosporine, must use azathioprine or mercaptopurine with it

34. Refractory UC
• Oral tacrolimus (has been used in combination with oral
aminosalicylates, AZA, or 6-MP)
• Vedolizumab
• Surgery

35. CD Pharmacotherapy

36. CD Pharmacotherapy
Mild/Moderate CD
• Treatment of ACTIVE disease
– First-line therapy: Oral aminosalicylate
– Alternative therapies:
• Budesonide 9mg daily up to 8 weeks
• Metronidazole 10 – 20mg/kg/day for up to 10 weeks
• Ciprofloxacin 500mg bid for 6 to 10 weeks
• Rifaximin 800mg bid for 12 weeks
• Ciprofloxacin 500mg bid + metronidazole 250mg tid for 10 weeks

37. Mild/Moderate CD
• Specific choice of agent(s) for active disease can be informed
by location of disease
– Ileocolonic or colonic
• Sulfasalazine OR oral mesalamine OR metronidazole +/- ciprofloxacin
– Perianal
• Sulfasalazine or oral mesalamine and/or metronidazole
– Small bowel
• Oral mesalamine or metronidazole
• Budesonide 9mg/day for terminal ileal or ascending colonic disease

38. Moderate/Severe CD
• Treatment of ACTIVE disease
1. First-line: Aminosalicylate OR metronidazole +/- ciprofloxacin
PLUS prednisone at a dose of 40-60mg/day until resolution of
symptoms or resumption of weight gain (7-28 days)
2. If steroid refractory and/or fistulizing disease
• Add infliximab, adalimumab, or certolizumab +/- azathioprine,
mercaptopurine, or methotrexate
• If no response to TNF-inhibitor and/or immunomodulator, change to
natalizumab or vedolizumab

39. Severe/Fulminant CD
• Treatment of ACTIVE disease
1. May need surgical intervention (mass, obstruction, abscess, etc.)
2. Administer IV hydrocortisone 100mg every 6 to 8 hours
3. If no response to hydrocortisone in 5 to 7 days, then IV cyclosporine
4mg/kg/day OR infliximab is not attempted before

40. Remission/Maintenance Therapy for Crohn’s Disease
• No role for long-term corticosteroid use
• First Line: Azathioprine or 6-mercaptopurine plus or minus oral
aminosalicylate
– If intolerant to AZA or 6-MP, then try methotrexate
• Second Line: TNF-inhibitor plus or minus azathioprine or 6-
mercaptopurine or methotrexate (if intolerant of AZA or 6-MP)
• Alternative: Vedolizumab

41. Refractory CD
• Oral tacrolimus (has been used in combination with oral
aminosalicylates, AZA, or 6-MP)
• Natalizumab
• Surgery

42. Aminosalicylates
• MOA
– Not completely understood but postulated to diminish inflammation by
inhibiting cyclooxygenase and lipoxygenase, thereby decreasing
prostaglandins, leukotrienes resulting in decreased inflammation
• Agents
– Sulfasalazine
– Mesalamine
• Suppository
• Enema
• Oral formulations
– Olsalazine
– Balsalazide

43. Aminosalicylates
• Sulfasalazine
– Prototype aminosalicylate
– The drug is cleaved by colonic bacteria to an active portion
Mesalamin (5-aminosalicylate or 5-ASA) and an inactive carrier
molecule (sulfapyridine)
– AVOID in patients with a SULFA allergy
• Mesalamine
– Available in various formulations including a rectal suppository,
enema, and various oral formulations that release the drug at different
points in the GI tract

44. Aminosalicylates
• Olsalazine
– A dimer of two 5-ASA molecules linked by an azo bond
– Mesalamine is released in the colon after colonic bacteria cleave the
azo bond
– High incidence of diarrhea as an adverse effect (up to 25% of patients)
• Balsalazide
– A mesalamine prodrug that couples mesalamine with an inert carrier
molecule and is enzymatically cleaved in the colon to release
mesalamine

45. Aminosalicylates
• Different amino salicylate products have different sites of action
and hence location of the disease in the GI tract is factored into the
selection of an agent
– Suppositories have local activity in the rectum and are useful in
proctitis
– Enemas have local activity in the rectum and distal colon and are useful to
treat left-sided disease
– Different oral formulations release drug at different points in the small
intestine and colon

46. Corticosteroids
• MOA
– Corticosteroids are used to suppress acute inflammation in the treatment
of IBD, and may be given parenterally, orally, or rectally.
– They modulate the immune system and inhibit production of cytokines and
mediators.
• Agents
– Prednisone
– Prednisolone
– Methylprednisolone
– Hydrocortisone
– Budesonide

47. Corticosteroids
• Corticosteroids work very quickly to suppress inflammation
and reduce flare-ups
• Corticosteroids should NOT be used for maintenance therapy
• Budesonide has a high ratio of local anti-inflammatory to
systemic effect due to an extensive first pass metabolism
– Administered orally in a controlled-release formulation designed to
release in the terminal ileum or the colon depending on the product
– This results in a decrease in systemic effects and systemic adverse
effects

48. Patient Counseling
For Mesalamine and Hydrocortisone Enema Administration
• An enema is a procedure introducing liquid into the rectum and
colon through the anus
• Enemas are most commonly used as laxatives to relieve
constipation or to deliver medication to the rectum and colon
for inflammatory bowel disease

49. How to Use an Enema
• Shake to mix (particularly mesalamine and hydrocortisone
enemas because they are suspensions)
• Remove the cap/cover from the applicator tip
– Hold the bottle at the neck so you don’t accidently squeeze out any
medication

50. How to Use an Enema (Administration)
• Get into appropriate position (either of the following positions)
– Lie on the floor on left side with right knee bent
• This is the most comfortable position and hence the one most patients prefer
– Lie on floor on stomach and then bring both knees to chest
• For enemas used for IBD, specifically mesalamine and
hydrocortisone enemas, it is recommended to
– Remain in the position the enema was administered in for at least 30
minutes to allow the thorough distribution of the medication
– Retain the enema all night (preferably 8 hours), if possible
• Hence, these enemas are typically administered at bedtime

51. Immunomodulators
• MOA
– Immunosuppressive actions through a variety of mechanisms
• Agents
– Azathioprine
– Mercaptopurine
– Methotrexate
– Cyclosporin

52. Azathioprine (AZA) and Mercaptopurine (6-MP)
• Are effectively used in long-term treatment of both UC and CD
• Generally reserved for patients who fail 5-ASA therapy or are refractory to
or dependent on corticosteroids
• May be used in conjunction with 5-ASAs, corticosteroids, and TNF-
inhibitors
• Are indicated for IBD maintenance therapy due to a long onset of
action
– Onset of action can range from a few weeks to up to 12 months before
benefits are seen

53. Methotrexate (MTX)
• Useful for the treatment and maintenance of CD; data
supporting use in UC is lacking
Cyclosporine
• Used in severe flares of IBD not responding to IV
corticosteroids
• Poses a risk of nephrotoxicity and neurotoxicity

54. Tumor Necrosis Factor (TNF) Inhibitors
• MOA
– Inhibits endogenous TNFα. Elevated levels of TNFα have been found in involved tissues of
various disease states including CD and UC. Biological activities of TNFα include the induction
of proinflammatory cytokines, enhancement of leukocyte migration, activation of neutrophils and
eosinophils, and the induction of acute phase reactants and disease degrading enzymes.
• Indicated for both CD and UC
– Moderate to severe active disease
– Maintenance therapy in moderate to severe disease
– Fistulizing disease
• Agents
– Infliximab
– Adalimumab
– Certolizumab
– Golimumab

55. Other Biologics: Natalizumab
• MOA
– A humanized monoclonal antibody that targets integrin molecules
expressed on the cell surface of leukocytes. Integrins bind to vascular
receptors in the gut, allowing leukocytes to migrate across the vacular
endothelium. Natalizumab blocks this process and inhibits the
inflammatory cascade.
• Indication: Induction and maintenance treatment of CD
refractory to conventional therapies and TNF inhibitors.

56. Other Biologics: Vedolizumab
• MOA
– reduces chronically inflamed gastrointestinal parenchymal tissue associated
with ulcerative colitis and Crohn disease by binding specifically to the
alpha-4-beta-7-integrin receptor and blocking its interaction with mucosal
addressing cell adhesion molecule-1. This inhibits the movement of memory
T-lymphocytes across the endothelium into inflamed gastrointestinal tissue
• Indications: Induction and maintenance in adults with moderate to
severe active UC and CD who have had an inadequate response with,
lost response to, or were intolerant to a TNF inhibitor or
immunomodulator; or had an inadequate response with, were
intolerant to, or demonstrated dependence on corticosteroids.

57. Drug Brand Name Initial Dose (g) Usual Range
Sulfasalazine Azulfidine
Azulfidine EN
500 mg-1 g
500 mg-1 g
4-6 g/day
4-6 g/day
Mesalamine suppository Rowasa 1 g 1 g daily to three times weekly
Mesalamine enema Canasa 4 g 4 g daily to three times weekly
Mesalamine (oral) Asacol HD
Apriso
Lialda
Pentasa
Delzicol
1.6 g/day
1.5 g/day
1.2-2.4 g/day
2 g/day
1.2 g/day
2.8-4.8 g/day
1.5 g/day once daily
1.2-4.8 g/day once daily
2-4 g/day
2.4-4.8 g/day
Olsalazine Dipentum 1.5 g/day 1.5-3 g/day
Balsalazide Colazal 2.25 g/day 2.25-6.75 g/day
Azathioprine Imuran, Azasan 50-100 mg 1-2.5 mg/kg/day
Cyclosporine Gengraf
Neoral, Sandimmune
2-4 mg/kg/day IV
2-8 mg/kg/day oral
2-4 mg/kg/day IV
Agents for the Treatment of Inflammatory Bowel Disease

58. Agents for the Treatment of Inflammatory Bowel Disease
Mercaptopurin
e
Purinethol 50-100 mg 1-2.5 mg/kg/day
Methotrexate No branded IM
injection
15-25 mg IM weekly 15-25 mg IM weekly
Adalimumab Humira 160 mg SC day 1 80 mg SC 2 (day 15), and then 40
mg every 2 weeks
Certolizumab Cimzia 400 mg SC 400 mg SC weeks 2 and 4, and
then 400 mg SC monthly
Infliximab Remicade 5 mg/kg IV 5 mg/kg weeks 2 and 6, 5-10
mg/kg every 8 weeks
Natalizumab Tysabri 300 mg IV 300 mg IV every 4 weeks
Budesonide Enterocort EC, Uceris 9 mg 6-9 mg daily
Vedolizumab Entyvio 300 mg IV 300 mg IV weeks 2 and 6 and
then every 8 weeks

59. Drug(s) Adverse Drug Reaction Monitoring Parameters Comments
Sulfasalazine Nausea, vomiting, headache
Rash, anemia, pneumonitis
Hepatotoxicity, nephritis
Thrombocytopenia, lymphoma
Folate, complete blood
count, Liver function
tests, Scr, BUN
Increase the dose
slowly, over 1-2 weeks
Mesalamine Nausea, vomiting, headache GI disturbances
Corticosteroids Hyperglycemia, dyslipidemia
Osteoporosis, hypertension,
acne
Edema, infection, myopathy,
psychosis
Blood pressure, fasting
lipid panel, Glucose,
vitamin D, bone density
Avoid long-term use if
possible or consider
budesonide
Azathioprine/
mercaptopurin
e
Bone marrow suppression,
pancreatitis
Complete blood count
Liver dysfunction, rash,
arthralgia
Scr, BUN, liver function
tests,
genotype/phenotype
Drug Monitoring Guidelines

60. Drug Monitoring Guidelines
Methotrexate Bone marrow suppression,
pancreatitis
Complete blood count, Scr,
BUN
Check baseline pregnancy test
Pneumonitis, pulmonary fibrosis,
hepatitis
Liver function tests Chest x-ray
Infliximab Infusion-related reactions
(infliximab), infection
Blood pressure/heart rate
(infliximab)
Need negative PPD and viral
serologies
Adalimumab Heart failure, optic neuritis,
demyelination, injection site
reaction, signs of infection
Neurologic exam, mental
status
Certolizumab Lymphoma Trough concentrations
(infliximab)
Natalizumab
Vedolizumab
Infusion-related reactions Brain MRI, mental status,
progressive multifocal
leukoencephalopathy
Vedolizumab not associated
with PML

61. THANK YOU