Ulcerative colitis

Moderator :Dr.Shamil Nuri (Internist,

Gastroenterologist)

Presenter : Dr.Surafel N(RIII)

 Outline
 Introduction to IBD
 Ulcerative colitis
• Epidemiology
• Ethology
• Pathophysiology
• Clinical feature
• Diagnosis
• Treatment
 Introduction
 IBD is characterized by chronic or relapsing immune
activation and inflammation within the GI tract.
 Crohn disease (CD) and UC are the 2 major forms of
IBD;
 less common, but increasingly recognized, are
• Microscopic colitides,
• Primarily collagenous colitis and
• Lymphocytic colitis .
• CD and UC share many clinical and
epidemiologic characteristics,
• suggesting that underlying causes may be
similar.
• The 2 diseases are most often considered, as
distinct syndromes with divergent treatments
and prognoses .
• CD cannot be distinguished from UC on clinical
grounds “IBD-U”(10%)
 Ulcerative colitis
• UC only affects the colon and rectum.
• UC, inflammation starts in the rectum and extend
proximally
• Is continuous, and is superficial
• Only affecting the epithelial layer of the mucosa.
 Epidemiology and Risk
• Western
• the incidence of both CD and UC were in a range
between 5 and 15 per 100,000.
• In the 21st century, the prevalence
of IBD exceeds 0.3%.
• Africa and Asia,20th century :limited data
• At the turn of the 21st century, the evolution of
IBD had manifest global spread
 CD vs UC
 In developed countries, UC emerged first and
then CD followed
 In the past 20 years, CD has generally
overtaken UC in incidence rates.
 In developing countries in which IBD is
emerging, UC is typically more common than
CD
 In India, for example, there are reports of a
UC/CD ratio of 8 : 1 (previously 10 : 1)
 AGE & SEX
• At any age, although the most common ages of
diagnosis are in adolescence and early adulthood.
 Pediatric IBD (patients <18 years of age) comprises
~20–25% of all IBD patients and about 5% of all
IBD patients are <10 years of age
• Very early onset IBD (VEOIBD) has been defined
as IBD that occurs in children <6 years of age
• Infantile IBD in children <2 years of age.
 Etiology & Pathogenesis
 Currently unknown but appears to be multifactorial
 The current hypothesis is that CD and UC result
from;
• Overly aggressive T-cell mediated immune responses
• To specific components of the intestinal microbiota
• In genetically susceptible individuals, and
• That disease expression is triggered by additional
environmental factor .
ETIOLOGY & PATHOGENESIS
DYSREGULATED Immune Response and
Inflammation
Disease location & Clinical Feature
 Disease location in UC
Based on the extent
 Proctitis :limited to the rectum
 Proctosigmoiditis :limited to the rectum and sigmoid
colon and not involving the descending colon
 Left-sided or distal ulcerative colitis: that extends as
far as the splenic flexure
 Extensive colitis :extending proximal to the splenic
flexure but sparing the cecum
 Pancolitis :extends throughout the colon to the
cecum
 The Montreal Classification of UC disease
location is stratified by
• Proctitis (E1, limited to the rectum),
• Left sided colitis (E2, up to the splenic flexure),
and
• Pancolitis(E3, extending beyond the splenic
flexure)
 Disease Location at initial presentation

• 45%: Rectosigmoid,
• 35%: have disease extending beyond the sigmoid
but not involving the entire
colon, and
• 20% :Pancolitis

• The disease typically is most severe distally and

progressively less severe proximally
• There are racial differences in IBD location and
behavior
• UC: Pancolonic disease is more common than left-
sided colitis or proctitis among African Americans,
Hispanics, and Asian patients with UC.

• Older Asian patients with UC (age >60) tend to have

a more aggressive disease course.
 Involvement
• Continuous and symmetric involvement is the
hallmark of UC ,

• With a sharp transition between diseased and

uninvolved segments of the colon.

• Inflammation starts from the rectum & extend

proximally
There are exceptions to this general rule
 Rectal sparing
 topical medical therapy can result in areas of sparing.
 <5% Adult onset, and 1/3 of pediatric onset UC.
 left-sided UC :75% of patients with have
• Peri-appendiceal inflammation in the colon
• Patchy inflammation in the cecum
 Backwash ileitis, which can be observed in patients
with pancolitis or PSC
 Clinical feature
 Diarrhea: frequent and small in volume as a
result of rectal inflammation.
• Associated symptoms include colicky abdominal
pain, urgency, tenesmus, and incontinence
 Systemic symptoms including;
• Fever, fatigue, weight loss & Anemia symptom
 The onset of symptoms is usually gradual, &
 Progressive over several weeks.
 May be preceded by a self-limited episode of
rectal bleeding that occurred weeks or
months earlier
 The symptom complex & severity of symptoms tends to differ
according to the extent of disease
 Proctitis often have local symptoms
• Tenesmus, urgency, and passage of mucus and blood per rectum,
• Abdominal pain is rare.
• May have constipation accompanied by frequent discharge of
blood and mucus.

 Extensive colitis
• usually have more diarrhea, weight loss, fever, clinically
significant blood loss, and abdominal pain.
 In general, severity of symptoms correlates
with the severity of disease,

 However, active disease may be found at

colonoscopy in patients who are
asymptomatic
 Physical examination
• Is often normal, especially in patients with
mild disease.
• Patients with moderate to severe UC
• May have abdominal tenderness to palpation,
• fever, hypotension, tachycardia, and pallor.
• Rectal examination may reveal evidence of
blood.
• Muscle wasting and peripheral edema .
 Acute complications

 Severe bleeding – 10% of patients.

 Massive hemorrhage - 1-3 % of patients
 Fulminant colitis (extend beyond mucosa)
• More than 10 stools per day,
• Continuous bleeding, abdominal pain,
distension, and
• Acute, severe toxic symptoms including fever
and anorexia.
 …
 Toxic megacolon is characterized by colonic
diameter ≥6 cm or cecal diameter >9 cm and the
presence of systemic toxicity
 Perforation
• Most commonly occurs as a consequence of toxic
megacolon.
• However, first episode of ulcerative colitis due to
lack of scarring from prior attacks of colitis.
• Perforation with peritonitis has 50% mortality in
patients with UC
 Chronic complications
 Long-term complications of ulcerative colitis
include
• Strictures(5–10% )
• Dysplasia, and
• Colorectal cancer (CRC).
 Factors that are associated with an increased
risk of CRC include
• Extent and duration of UC
• Endoscopic and histological severity of
inflammation,
• Positive family history of sporadic colorectal
cancer (2X),
• Postinflammatory pseudopolyps (2X), and
• PSC(4X)
 Extraintestinal manifestations(EIM)
• Although ulcerative colitis primarily involves the
bowel,
• It is associated with manifestations in other
organ systems.
• 10% initial presentation
• 25% lifetime
• With the exception of primary sclerosing
cholangitis and ankylosing spondylitis, EIMs
tend to follow the clinical course of the colitis.
EXTRAINTESTINAL FEATURES & associated
autoimmune diseases
 Potential precipitants of UC may include

 Recent smoking cessation ,

 Nonsteroidal anti-inflammatory drug
(NSAID) use and
 Enteric infections
 C. diff infection
(CDI) (The prevalence of CDI among patients
with newly diagnosed or relapsing IBD ranges
from 5% to 47% )…increased mortality of UC
 Diagnosis
• No single symptom, sign, or diagnostic test
establishes the diagnosis of IBD.
• Rather, the diagnosis is established through
 A complete assessment of the clinical presentation
 With confirmatory evidence from
• Radiologic,
• Endoscopic, and
• Pathologic findings (in most cases)
 LABORATORY FINDINGS
 Unlikely to be completely normal in IBD,
• CBC: Anemia, WBC(N or high)
• Low albumin, Myoglobin(disease severity and
prognosis )
• LFT(ALP)
• Electrolyte abnormalities
• Fecal calprotectin or lactoferrin may be elevated
due to intestinal inflammation
 ESR & CRP
• Non-specific ,can sths be normal
• Correlate with Endoscopic severity of disease
• prognostic significance and
• have a role in predicting the risk of
colectomy and
• response to therapy
 Serologic testing :adjunct to diagnosis
 -ve pASCA (anti–
Saccharomyces cerevisiae antibodies)
 +ve pANCA....
• UC : pANCA in 60%-65%, ASCA in 5%
• CD: pANCA in 20%-25%, ASCA in 41%-76%
• Pooled sensetivity is low to dx UC
• Currently the added value of serologic panels in the diagnosis of IBD is not
clear and is not routinely recommended.

 Genetic testing is not currently routinely recommended for diagnosis, but

• May have future potential in precision medicine
 Stool studies for DDX
 Infectious(C. difficile ,other)
 Testing for STI, ( C. trachomatis, N. gonorrhoeae,
HSV, and Treponema pallidum)
 HIV Testing(CMV)
 Endoscopy & Biopsy
 Ileocolonoscopy
• To determine the endoscopic extent and severity
of colonic disease
• Allows for evaluation of the terminal ileum that
would be suggestive of CD and
• Should be avoided in hospitalized patients with
severe colitis.
 Flexible sigmoidoscopy
• The hallmark of UC is
• Symmetric and continuous inflammation that
begins at the anorectal junction
• Inflammation extends proximally without
interruption for the entire extent of
disease.
 Endoscopic findings in US
 The earliest endoscopic sign of UC
• A decrease or loss of the normal vascular
pattern, with mucosal erythema and edema
• Quiescent disease, the only feature
 As disease progresses,
• the mucosa becomes granular and friable.
 More severe inflammation,
• The mucosa may be covered by yellow-brown
mucopurulent exudates
• Mucosal ulcerations (punctate, annular,or
linear)
• Friable mucosa that bleeds spontaneously
• Narrowing of the lumen (marked edema)
 long-standing UC, Nonneoplastic pseudopolyps
 Long-standing inflammation
• Loss of normal colonic architecture
• Muscular hypertrophy,
• Loss of the normal haustral fold pattern,
• Decreased luminal diameter, and shortening
• The resultant featureless appearance of the colon
• lead-pipe appearance seen on barium enema.
• Strictures ,as a result of focal muscular
hypertrophy (Malignancy must be excluded )
• AGA: Upper Endoscopy not recommended for
pt with normal terminal ileum study and not
upper GI symptoms
 Biopsy
• Multiple biopsy specimens should be taken
from throughout the colon and rectum
• to map the histologic extent of disease and
to confirm the diagnosis.
• Even from endoscopic ally normal appearing
segment.
 Microscopically,

 Findings are confined to the mucosa

 The early stage of UC
• Marked by edema of the lamina propria and
• congestion of capillaries and venules often with
extravasation of red blood cells.
 Then an acute inflammatory cell infiltrate
• Neutrophils, lymphocytes, plasma cells, and
• macrophages, often accompanied by increased
numbers of eosinophils and mast cells.
 Then Cryptitis
• Is associated with discharge of mucus from
goblet cells and
• increased epithelial cell turnover.
• This results in the characteristic histopathology
• Goblet cell mucin depletion, formation of
exudates, and epithelial cell necrosis
 ultimately to crypt abscesses, crypt branching,
shortening , and crypt atrophy.
• None of these features are specific for
ulcerative colitis,
• However;the presence of two or more
histologic features is highly suggestive of
ulcerative colitis
 IMAGING
• Abdominal imaging is not required for the
diagnosis of ulcerative colitis but may be
performed in patients who present with symptoms
of colitis

• Small intestine imaging like MRI and CT not

routinely required in all patients with normal
appearance of the terminal ileum on colonoscopy
(AGA:2019)
• AGA 2019: However, indication for SI study(CT,MRI
or VCE)
• Abdominal symptoms not explained by
endoscopically active disease,
• With suspicion of CD (such as predominantly watery
diarrhea, weight loss, or abdominal pain), or
• Proximal extent of involvement cannot be evaluated
because of severity of inflammation .
• Plain films is indicated in ASUC.
 Plain Films
 Plain films is indicated in all pt ASUC.
 Severe or fulminant ulcerative colitis
 Extent of disease
• Presence or absence of fecal material
• May identify proximal constipation(left-sided)
• Mucosal thickening or
• "thumbprinting" secondary to edema,
 Plain film..
Acute complication
 Fulminant colitis(Colonic dilatation)
 Toxic megacolon
 Perforation
• Free air
 Double contrast barium enema
•
 CT &MRI
• May demonstrate marked thickening of the
bowel wall, but this finding is nonspecific and
• MRI have lower sensitivity than barium
enema for early mucosal disease, but
• Are equivalent in patients with established
and severe disease
 Ultrasound with Doppler
 Help to know the extent of the disease
• Thickened hypoechoic mucosal layer in
patients with active ulcerative colitis.
• More severe cases may be associated with
transmural bowel wall thickening .
• However, these findings are not specific for
UC and
• May be seen in colitis due to other causes
 Assessment of disease extent and severity
 Is important for
• Therapeutic decision making and Prognostication
 Purely clinical, endoscopic, or histologic, and others
that combination
 Commonly used for UC are:
1. The Montreal Classification(Extent)
2. Truelove and Witts ( Mild, Moderate, Sever)
3. Mayo Score , Ulcerative Colitis Endoscopic Index of
Severity
4. American College of Gastroenterology Ulcerative
Colitis Activity Index
 Treatment
Goal Of UC Treatment
 Symptomatic remission
 Endoscopic remission: Mucosal healing
 Deep remission
 Histologic remission ????
 Obtaining and maintaining a steroid-free remission
 Prevention of morbidity including hospitalization and
Surgery
 Prevention of Cancer
 Normalization of patients’ health-related QOL
 Preventing therapy-related adverse events
 Treatment options for UC
 MEDICAL THERAPY
 Aminosalicylates (ASA)
 Glucocorticoids
 Immunomodulators
 Biologic Therapies
 Newer Agents
 Adjunctive Therapies, Antibiotics, Probiotics, and Intestinal
Microbiota,Transplantation
 Nutritional Therapy
 Cytapheresis
 SURGICAL THERAPY
 Aminosalicylates
Sulfasalazine(Parent compound )
Sulfapyridine-free(mesalamine,olsalazine,balsalazide
• MOA: Had anti-inflammatory activity topically
• Preparation :oral ,Rectal(suppository, gel, foam,
enema)
 Oral-Administered Therapies
• have demonstrated efficacy for induction and
maintenance of remission in mildly to moderately
active UC
• Comparable efficacy,
• No RCT severely active disease
 Rectally-Administered Therapies
• 5-ASA enemas, up to splenic flexure ,5-ASA
suppositories, distal 5-8 cm of rectum) & 5-ASA
foam(mid-segmoid)
• They are effective for inducing remission in
patients with mildly to moderately active distal
UC,
• As an adjunctive therapy to oral agents in patients
with more extensive colitis
 Efficacy
• Mesalamine enemas have been shown to be
comparable to oral sulfasalazine in the treatment of
active distal UC, with fewer side effects ,lower cost
• Effect is dose dependent .
• In fact, are more effective than topical
glucocorticoid enemas for distal colitis
• A combination of topical and oral mesalamine also
is more effective than either agent alone
• In patients with left-sided colitis or pancolitis,
suggesting a dose-response effect .
 S/E profile

• Nephrotoxicity
• N&V ,hemolysis, neutropenia, agranulocytosis,
folate deficiency, reversible male infertility,
neuropathy; (Sulfasalazine)
• Paradoxical disease exacerbation, pancreatitis,
hepatitis, pericarditis, pneumonitis, nephritis
• Secretory diarrhea (olsalazine)
• Pregnancy :No evidence of teratogenicity
 Glucocorticoids
Classic:
Methylprednisolone,prednisone,hydrocortisone
 Preparation: IV,oral,Rectal
• their efficacy and rapid induction of clinical
improvement is well established,
 not recommended for long-term use
• Not effective for maintenance
• leads to significant AEs use
no trial to date assessing the efficacy of
mesalamine therapy, as a maintenance after steroid
Budesonide ,multimatrix (MMX)
• High hepatic first-pass metabolism,
• Low systemic steroid exposure, and
• Fewer AEs
• Effective for induction therapy for mild to
moderate UC
• No data for maintenance use
 S/E of glucocorticoid are :
• Sleep and mood disturbance, acne, striae,
hirsutism,
• glucose intolerance, hypertension,
• bone loss, narrow-angle glaucoma,cataracts,
• infection, edema, impaired wound healing,
aseptic necrosis
• proximal myopathy, adrenal suppression,
 Principles of glucocorticoid use
• Use an effective dose
• Do not overdose.
• Do not treat for excessively long periods.
• Anticipate side effects
 Steroid response
 Steroid-responsive disease – Clinical response
to high-dose glucocorticoids (prednisone 40 to
60 mg/day or equivalent) within 30 days for
oral therapy or 7 to 10 days for intravenous
therapy
 STEROID-DEPENDENT ULCERATIVE COLITIS
• if glucocorticoids cannot be tapered to less
than 10 mg/day within three months of
starting steroids without recurrent disease, or
• if relapse occurs within three months of
stopping glucocorticoids
 Steroid-refractory disease –
• Lack of a meaningful clinical response up to doses
of prednisone 40 to 60 mg/day (or equivalent)
within 30 days for oral therapy or 7 to 10 days
for intravenous therapy
• Approach: We have to reevaluate the
patient ,r/o alternative diagnosis( infection, CD)
• Transition to glucocorticoid-sparing agent,
immune modulators or biologics ,or newer agent
 Immunomodulators
 6-Mercaptopurine,Azathioprine
 Cyclosporine/ tacrolimus
• Used as steroid sparing or reducing agent
• S/E: leukopenia, thrombocytopenia, bone
marrow suppression, pancreatitis,
hepatitis, infection; lymphoma
• Pregnancy: Teratogenic in animals, but large series
in renal do not show an increase in birth defects
 Biologic agent
 Anti-TNF antibodies
 infliximab,adalimumab,golimumab,certolizumab pegol
 S/E :
• Infections, Upper respiratory tract
disseminated TB, increased risk of
systemic fungal infection
• Delayed hypersensitivity reactions
• lymphoma
• Contraindicated in heart failure because of
increased mortality
• Pregnancy: Growing amount of evidence supporting safety,
but still relatively limited data in humans.
 Other Newer agent
 Integrin inhibiters
• Vedolizumab
• Natalizumab
 Anti IL-12/IL-23
• Ustekinumab
 JAK Inhibiters
• Tofacitinib
 S1P Inhibitors (sphingosine-1-phosphate receptor)
• Ozanimod
Treatment for UC :Guidelines Summary
 Induction and maintenance therapy

 Selection of induction and maintenance

therapies for UC should be based on disease
extent, severity, and prognosis.
 INDUCTION REMISSION(AGA: 2019)

 Mildly active ulcerative proctitis, rectal 5-ASA (1 g/d )

 Mildly active left-sided UC, rectal 5- ASA enemas at a dose
of at least 1 g/d combined with oral 5-aminosalicylate at a
dose of at least 2 g/d compared with oral
5-aminosalicylate therapy alone for induction of remission
 Mildly active left-sided UC who are intolerant or
nonresponsive to oral and rectal 5-ASA at appropriate doses
• Oral budesonide MMX 9 mg/d is Recommend for induction
of remission
• Topically acting budesonide MMX also
reccommended(BSG:2019)
 ….
• Mildly active extensive colitis, oral 5-ASA at a dose of at
least 2 g/d is recommended.(AGA)
• Oral 5 ASA + 5ASA Enema is rec(BSG:2019)
• UC of any extent who fail to respond to 5-ASA therapy,
oral systemic corticosteroids recommended to induce
remission(AGA)

• Any extent of UC low dose (2–2.4 g/d) of 5-ASA

recommended as compared with a higher dose (4.8 g/d)
(AGA)
 Treatment response to 5ASA
• Symptomatic improvement and a decrease in
bleeding can be seen within a few days.
• However, complete healing usually requires
four to six weeks or longer, and
• It is recommend continued treatment for six
to eight weeks followed by a gradual taper
and discontinuation as tolerated(Uptodate)
 Maintenance of remission for mild
UC(AGA:2019)
• Proctitis, we recommend rectal 5-ASA at a dose of 1 g/d
• Maintenance therapy is not recommended in patients
with a first episode of mild ulcerative proctitis that has
responded promptly to treatment(UPTODATE)
• Left-sided or extensive UC, AGA recommend oral 5-ASA
therapy (at least 2 g/d)).
• AGA recommend against systemic corticosteroids for
maintenance of remission in patients with UC
When do we discontinue maintenance RX?

• Discontinuation of medication in these patients

should only be considered if they have been in
remission for two years and are averse to taking
medication(Uptodate)
• For patients who had been in remission for more
than 2 years however, no statistically significant
difference was observed between relapse rates
[5/28 vs 6/23, or 18% vs 26%, respectively], but
patient numbers were very small. (ECCO)
Induction of remission; Moderate to sever
UC Outpatients(AGA)
• Moderately to severely active ulcerative
colitis :Outpatient
• Moderately active UC ACG recommend oral
budesonide MMX (AGA2019)
• Moderately to severely active UC of any extent,
ACG recommend oral systemic corticosteroids
(AGA2019)

• AGA 2020
AGA 2020-naïve to biologic agent
AGA:2020-biologic agent exposed
 Steroid tapering
• AGA 2019:
• Although the optimal tapering regimen has
not been determined, the dose is usually
reduced over 8–12 weeks
 Up-to-date
• Glucocorticoids should be tapered after the
patient has been stable for two to four weeks.
• Steroids should be tapered over eight weeks by
decreasing the dose by 5 to 10 mg every week
until a daily dose of 20 mg is reached, and
then by 2.5 mg every week .
• More rapid reduction has also been associated
with early relapse and may be associated with
adrenal insufficiency
 Maintenance remission ;moderate to sever UC: AGA

• AGA 2019:
• Previously moderately to severely active UC
now in remission due to corticosteroid
induction, ACG suggest thiopurines for
maintenance of remission compared with no
treatment or corticosteroids
Hospitalized Acute severe UC(ASUC)
treatment
 Antibiotic -uptodate

 We recommend intravenous antibiotics (eg,

ciprofloxacin and metronidazole) in patients
with severe colitis and
• high grade fever,
• leukocytosis with extreme numbers of
immature neutrophils (band form count
greater than 700/microL), and
• peritoneal signs or megacolon
Maintenance treatment of ASUC -AGA
 …
• In Those ASUC who respond for iv steroid it
should be changed to po in 3-5 days then
tapering will continued as mentioned
• The maintenance treatment will be with 6-
mercaptopurine (6-MP)/azathioprine (AZA)..
 Other supportive RX for ASUC
• NSAIDs, opioids, and medications with anticholinergic side
effects should be avoided in ASUC
• All patients with ASUC should be assessed for the presence of
toxic megacolon on a regular basis during the hospital
admission
• In patients with ASUC, we recommend DVT prophylaxis to
prevent venous thromboembolism (VTE) (strong
recommendation, low quality of evidence)
• We suggest against total parenteral nutrition for the purpose
of bowel rest in ASUC
Colorectal cancer prevention in ulcerative
colitis

• Screening and subsequent surveillance

colonoscopy to assess for dysplasia in individuals
with UC of extent greater than the rectum should
start 8 years after diagnosis is
recommended(AGA:2019)
• Patients with UC and PSC should undergo a
screening colonoscopy at the time of diagnosis of
UC and surveillance annually thereafter.
• Chromoendoscopy involves the topical
application of indigo carmine or
methylene blue to enhance mucosal
irregularities and facilitate targeted biopsies
• Chromoendoscopy appears to be superior to
standard white light colonoscopy, but its
superiority over high-definition white light
endoscopy is less clear based on low-quality
data.
• Up-to-date :targeted and random biopsies is
an acceptable alternative, and multiple
biopsies are required to adequately sample
the colon
• AGA
Surgery
 The goals of surgical treatment are
• to remove the entire diseased colon
• preserving continence and
• sexual function and
• elimination of colorectal cancer (CRC) risk
• There are multiple surgical options for UC including
• subtotal colectomy with ileostomy, and a Hartman
pouch or mucus fistula;
• colectomy with ileorectal anastomosis;
• proctocolectomy with Brooke ileostomy;
• proctocolectomy with continent ileostomy;
• Restorative proctocolectomy with IPAA; and
• proctocolectomy with ileal pouchanal transition zone
anastomosis
• Probiotics are living organisms in foods and dietary
supplements
• RCT: Conflicting result
• Helminths :some beneficial effect seen for UC but
need further study
• IMT (larger Canadian study& . A multicenter trial
Australia RCT) shows benefit for UC,NOT CD
• AGA(2019)
 Nutritional therapy-UC
 In UC,
 TPN does not appear to have a role as primary
therapy;
 studies of bowel rest in combination with IV steroids
were no more effective than steroids alone.
 Enteral nutrition is preferred,
• Fewer complications than parenteral nutrition and
• does not deprive the colon of short chain fatty acids
needed for the metabolism and repair of colon
epithelial cells
 Cytapheresis

 Reduction of peripheral blood levels of

leukocytes has been proposed as a therapeutic
option for treating UC
 Reference
• Sleisenger & Fordtran's Gastrointestinal & Liver
Disease 11Edition
• Harrison Principles of Internal Medicine 20th
edition
• Up-To-date 2018
• American Gastroenterology Association guideline
2019/2020
• British Society of Gastroenterology guideline 2019
• European Crohn's and colitis Organization guideline
2017
THANK YOU!!!