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MICROSCOPIC COLITIS
By
Omar Mohammed Saleh
Assistant Lecturer of Tropical
Medicine and Gastroenterology-
HUCOM-2015.
OBJECTIVES:
 Definition
 Epidemiology
 Etiology
 Pathophysiology
 Diagnosis
 Treatment
 Complications and Prognosis
DIARRHEA:
 Diarrhea is defined in adults by abnormal stool
weight (>200 g/day), consistency (loose or liquid),
and/or frequency (>3 times/day). A 4-week
symptom duration is generally considered as a
cutoff point to distinguish acute (<4 weeks) from
chronic (>4 weeks) diarrhea.
DEFINITION:
 Microscopic colitis is a clinical syndrome of
unknown etiology, characterized by chronic watery
diarrhea in the absence of macroscopic changes in
the large bowel. Ianiro G, et al. Microscopic colitis. WJG. 2012.
Types :
1. Lymphocytic colitis
2. Collagenous colitis
3. Incomplete MC
4. MC not otherwise specified
5. Paucicellular LC
6. MC with giant cells
7. Pseudomembranous CC
8. MC with granulomatous inflammation
9. Cryptal LC
EPIDEMIOLOGY:
Is it a missed disease ?
OR
Under diagnosed illness !!
RISK FACTORS:
 Female gender
 Older age
 Concomitant autoimmune diseases
 Solid organ transplantation
ETIOLOGY:
 Multifactorial
 Idiopathic
 Autoimmune phenomena; 30-50 % of MC have
autoimmune diseases
 Drugs
 Familial
 Possible enteric infections or toxins
 Smoking
REVIEW OF THE LITERATURE, MODIFIED FROM
BEAUGERIE AND PRADI
Drug- induced microscopic colitis
Low likelihoodIntermediate likelihoodHighly likelihood
Cimetidine
Gold salts
piasciedine
Carbamazepine
Celecoxib
Duloxetine
Fluvastatin
Flutamide‘
Oxetorone
Madopar
Paroxetine
Simvastatin
stalevo
Acarbose
Aspirin and NSAIDs
Clozapine
Entocapone
Flavonoid
Lansoprazole
Omeprazole/esomeprazo
le
Ranitidine
Sertraline
ticlopidine
PATHOPHYSIOLOGY:
PATHOGENESIS:
 Still not clearly understood !
 Genetic; family cluster, diseases with strong genetic
component
 Infectious element , chronic inflammation
 Bile salts; increased malabsorption, response to
bile acid binding agents
 Abnormal immune response to luminal
antigens…….> cytotoxic tissue damage
 In CC, dysfunction of subepithelial myofibroblast 
excessive Collagen deposition  mechanical
diffusion barrier
PATHOGENESIS:
DIAGNOSIS:
Clinical presentation:
 Chronic watery diarrhea
 Abdominal pain
 Weight loss
 Fecal incontinence
Unremarkable findings
Physical
examination
Laboratory
tests
Colonoscopy
examination
 Histopathological examination of the taken biopsy is
the golden tool for making diagnosis
Lymphocytic colitisCollagenous colitis
1-Intraepithelial lymphocytosis
(≥20IEL per 100 surface
epithelial cells
2-Inflammation in the lamina
propria consisting of mainly
lymphocytes and plasma cells
3-Epithelial damage, such as
flattening and detachment
4-Subepithelial collagen layer
not present or less than
<10um
1-Thickening of a
subepithelial collagen layer of
more than 10um
2-Inflammation in the lamina
propria consisting of mainly
lymphocytes and plasma cells
3-Epithelial damage, such as
flattening and detachment
4-Intraepithelial lymphocytosis
(IEL) could be present, but is
not necessary for the
diagnosis of CC
AWARENESS:
Colonoscopy
Biopsy from
normal
mucosa
Histopahology
criteria of MC
TREATMENT:
 Aim of treatment :
to induce clinical remission and improve the patient’s
quality of life.
Treatment algorithm:
Confirm diagnosis/ rule out other disorders
Withdrawal of medications causing MC
Dietary changes; avoid caffeine, lactose
Trial of loperamide (mild cases)
Corticosteroids: budesonide, prednisolone
Probiotics
Immunosuppressive drugs
Surgery !
BUDESONIDE:
 Potent glucocorticoid with a high local anti-inflammatory
effect.
 A PH and time dependent formulation, enables its
release to the colon.
 Downregulation of cytokines with an important role in the
inflammation pathways, including nuclear factor-KappaB,
TNF-α, and the interleukins 1 and 6.
 15 times higher binding affinity to the glucocorticoid
receptor than prednisolone.
 High first-pass effect (over 90%) which is carried out by
hepatic cytochrome P450 (CYP3A4 and CYP3A5)
enzymes  minimal systemic absorption.
COMPLICATIONS AND PROGNOSIS:
 Dehydration and electrolyte imbalance
 Progression to IBD
 Colonic perforation
 Malignant transformation; very rare with CC
 Very rare toxic megacolon
 Prognosis:
 Many cases are self limited
 Other symptomatic cases show relapsing-remission
course
 Impaired HRQoL
 Extra-intestinal disorders (immune-mediated);
Arthritis, spondylitis, thyroiditis, pyoderma gangrenosum.
CONCLUSION:
 MC is not uncommon disease.
 Pathophysiology ???
 Lab tests are non specific
 Biopsy is essential from normal colonoscopic mucosa in
cases of CNBD
 Budesonide is the only evidence based treatment
available
 Consider MC in celiac disease not responding to gluten
free diet.
 Long term outcome is good
 Further studies are needed !
Microscopic colitis
Microscopic colitis

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Microscopic colitis

  • 1. MICROSCOPIC COLITIS By Omar Mohammed Saleh Assistant Lecturer of Tropical Medicine and Gastroenterology- HUCOM-2015.
  • 2. OBJECTIVES:  Definition  Epidemiology  Etiology  Pathophysiology  Diagnosis  Treatment  Complications and Prognosis
  • 3. DIARRHEA:  Diarrhea is defined in adults by abnormal stool weight (>200 g/day), consistency (loose or liquid), and/or frequency (>3 times/day). A 4-week symptom duration is generally considered as a cutoff point to distinguish acute (<4 weeks) from chronic (>4 weeks) diarrhea.
  • 4. DEFINITION:  Microscopic colitis is a clinical syndrome of unknown etiology, characterized by chronic watery diarrhea in the absence of macroscopic changes in the large bowel. Ianiro G, et al. Microscopic colitis. WJG. 2012. Types : 1. Lymphocytic colitis 2. Collagenous colitis 3. Incomplete MC 4. MC not otherwise specified 5. Paucicellular LC 6. MC with giant cells 7. Pseudomembranous CC 8. MC with granulomatous inflammation 9. Cryptal LC
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  • 7. EPIDEMIOLOGY: Is it a missed disease ? OR Under diagnosed illness !!
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  • 11. RISK FACTORS:  Female gender  Older age  Concomitant autoimmune diseases  Solid organ transplantation
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  • 13. ETIOLOGY:  Multifactorial  Idiopathic  Autoimmune phenomena; 30-50 % of MC have autoimmune diseases  Drugs  Familial  Possible enteric infections or toxins  Smoking
  • 14. REVIEW OF THE LITERATURE, MODIFIED FROM BEAUGERIE AND PRADI Drug- induced microscopic colitis Low likelihoodIntermediate likelihoodHighly likelihood Cimetidine Gold salts piasciedine Carbamazepine Celecoxib Duloxetine Fluvastatin Flutamide‘ Oxetorone Madopar Paroxetine Simvastatin stalevo Acarbose Aspirin and NSAIDs Clozapine Entocapone Flavonoid Lansoprazole Omeprazole/esomeprazo le Ranitidine Sertraline ticlopidine
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  • 17. PATHOGENESIS:  Still not clearly understood !  Genetic; family cluster, diseases with strong genetic component  Infectious element , chronic inflammation  Bile salts; increased malabsorption, response to bile acid binding agents  Abnormal immune response to luminal antigens…….> cytotoxic tissue damage  In CC, dysfunction of subepithelial myofibroblast  excessive Collagen deposition  mechanical diffusion barrier
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  • 20. DIAGNOSIS: Clinical presentation:  Chronic watery diarrhea  Abdominal pain  Weight loss  Fecal incontinence
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  • 23.  Histopathological examination of the taken biopsy is the golden tool for making diagnosis
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  • 25. Lymphocytic colitisCollagenous colitis 1-Intraepithelial lymphocytosis (≥20IEL per 100 surface epithelial cells 2-Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells 3-Epithelial damage, such as flattening and detachment 4-Subepithelial collagen layer not present or less than <10um 1-Thickening of a subepithelial collagen layer of more than 10um 2-Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells 3-Epithelial damage, such as flattening and detachment 4-Intraepithelial lymphocytosis (IEL) could be present, but is not necessary for the diagnosis of CC
  • 27. TREATMENT:  Aim of treatment : to induce clinical remission and improve the patient’s quality of life. Treatment algorithm: Confirm diagnosis/ rule out other disorders Withdrawal of medications causing MC Dietary changes; avoid caffeine, lactose Trial of loperamide (mild cases) Corticosteroids: budesonide, prednisolone Probiotics Immunosuppressive drugs Surgery !
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  • 29. BUDESONIDE:  Potent glucocorticoid with a high local anti-inflammatory effect.  A PH and time dependent formulation, enables its release to the colon.  Downregulation of cytokines with an important role in the inflammation pathways, including nuclear factor-KappaB, TNF-α, and the interleukins 1 and 6.  15 times higher binding affinity to the glucocorticoid receptor than prednisolone.  High first-pass effect (over 90%) which is carried out by hepatic cytochrome P450 (CYP3A4 and CYP3A5) enzymes  minimal systemic absorption.
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  • 31. COMPLICATIONS AND PROGNOSIS:  Dehydration and electrolyte imbalance  Progression to IBD  Colonic perforation  Malignant transformation; very rare with CC  Very rare toxic megacolon  Prognosis:  Many cases are self limited  Other symptomatic cases show relapsing-remission course  Impaired HRQoL
  • 32.  Extra-intestinal disorders (immune-mediated); Arthritis, spondylitis, thyroiditis, pyoderma gangrenosum.
  • 33. CONCLUSION:  MC is not uncommon disease.  Pathophysiology ???  Lab tests are non specific  Biopsy is essential from normal colonoscopic mucosa in cases of CNBD  Budesonide is the only evidence based treatment available  Consider MC in celiac disease not responding to gluten free diet.  Long term outcome is good  Further studies are needed !