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Inflammatory Bowel Disease
This document discusses inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn's disease. IBD is characterized by chronic inflammation of the gastrointestinal tract. The document covers the etiology, pathophysiology, clinical presentation, complications, and management of both Crohn's disease and ulcerative colitis. Treatment involves the use of aminosalicylates, corticosteroids, immunomodulators, antibiotics, and in some cases surgery. Lifestyle modifications like avoiding certain foods and behaviors are also recommended.
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Inflammatory Bowel Disease
- 1. Inflammatory Bowel Disease Dr. Abhimanyu Parashar Assistant Professor Dept. Of Pharmacy Practice MMCP, Mullana, Ambala
- 2. IBD It isan idiopathic bowel disease which includes ulcerative colitis (UC) & crohn’s disease (CD) UC & CD are chronic, relapsing inflammatory diseases of the gut may be associated with a range of extra intestinal manifestations
- 3. CD or Regionalenteritis It is an idiopathic chronic ulcerative IBD, characterised by transmural, non-caseating granulomatous inflammation affecting most commonly the segment of terminal ileum and/or colon though any part of the GIT may be involved
- 4. Ulcerative Colitis Idiopathicform of acute & chronic ulcero-inflammatory colitis affecting chiefly the mucosa & submucosa of the rectum & descending colon, though it may involve the entire length of large bowel
- 5. Etiopathogenesis 1. Infectiousmechanisms 2. Immunologic mechanisms i) humoral factors ii) cell mediated immunologic factors iii) immunodeficiency 3. Others i) psychological factors ii) genetic factors iii) racial factors iv) diet v) social habits vi) drugs
- 6. Infectious mechanisms Bacterialinfections: mycobacteria dysentery bacilli chlamydia Viral infections: roatvirus EB virus intestinal cytopathic virus Certain protozoal & fungal infections
- 7. Immunologic mechanisms i)Humoral factors a) the specific anti-colon antibodies to E.coli causes the lesion, but no correlation b/n the levels of these antibodies & activity of the IBD b) Increased synthesis of Ig G by the lymphoid cells of diseased bowel, produce antibody mediated damage but IBD was observed in agammaglobulinaemia also
- 8. c) Circulating immunecomplexes produces extra intestinal lesions of IBD but their role in intestinal lesions of IBD is not established d) IgE mediated hypersensitivity reaction leads to excessive histamine release by mast cells in the bowel wall may cause oedema of bowel wall in IBD But administration of antihistamines does not alter the course of the disease
- 9. Cell mediated immunologicfactors a) Decreased number of peripheral T cells. b) presence of T cells sensitized to various bowel antigens may be cytoyoxic to mucosa c) Antibody dependent cellular cytotoxicity (ADCC) may occur by interaction of K cells with humoral antibodies
- 10. immunodeficiency Immunodeficiency ofIgA in crohn’s disease has been suggested more recently as possible immune mechanism for the lesion
- 11. Others Psychological factors: individuals who are sensitive, dependent on others & unable to express themselves suffer from irritable colon Genetic factors: certain HLA have also been found to be associated with IBD
- 12. Racial factors: highincidence of IBD have been identified in Jews & in whites Diet: milk, fibres & diet rich in CH provokes IBD Social habits: smokers are more prone to develop IBD Drugs: women who are on Ocs have increased risk of IBD
- 13. Pathologic changes -CD CD may involve any portion of GIT but affects most commonly 15-25 cms of terminal ileum which may extend into the caecum & sometimes into the ascending colon Transmural inflammatory cell infiltrate: It consists of chronic inflammatory cells (lymphocytes, plasma cells & macrophages) – the classical microscopic feature
- 14. Non-caseating, sarcoid- likegranulomas Present in all layers of affected bowel & in regional lymph nodes Patchy ulceration of mucosa Which may form deep fissures, accompanied by inflammatory infiltrates of lymphocytes & plasma cells Widening of submucosa due to oedema & foci of lymphoid aggregates
- 15. In chronic condition,fibrosis is prominent in all the layers disrupting muscular layer Regardless of the site, bowel wall injury is excessive & intestinal lumen is often narrowed The mesentery first becomes thickened & oedematous & then fibrotic Ulcers tend to be deep & elongated & extend along the longitudinal axis of the bowel, atleast into the submucosa
- 16. The cobblestone appearanceof the bowel wall results from deep mucosal ulceration intermingled with nodular submucosal thickening
- 17. Pathologic changes -UC The characteristic feature is the continuous involvement of rectum & colon without any uninvolved skip areas as seen in CD The appearance of colon may vary depending upon the stage & intensity of the disease because of remissions & exacerbations Mucosa shows linear & superficial ulcers, usually not penetrating the muscular layer
- 18. The intervening intactmucosa may form inflammatory pseudo polyps The muscle layer is thickened due to contraction producing shortening & narrowing of the affected colon with loss of normal haustral folds giving garden-hose appearance Because of remission & exacerbations it is characterised by alternating active disease process & resolving colitis
- 19. Crypt distortion, cryptitis& focal accumulations of neutrophils forming crypt abscesses Marked congestion, dilation & hemorrhages from mucosal capillaries Superficial mucosal ulcerations, usually not penetrating into the muscle coat, except in severe cases & is accompanied by nonspecific inflammatory cell infiltrate of lymphocytes, plasma cells, neutrophils, some eosinophils & mast cells in the lamina propria
- 20. Goblet cells aremarkedly diminished in cases of active disease Areas of mucosal regeneration & mucodeplition of lining cells In long-standing cases, epithilial cytologic atypia ranging from mild to marked dysplasia & some times developing into carcinoma in situ & frank carcinoma
- 21. Types of UC • Proctitis - ulcerative colitis affecting only the rectal mucosa. • Proctosigmoiditis – It involves rectum and the colon • Colitis- It involves other parts of the colon.
- 22. Complications - CD Malabsorption Fistula formation Stricture formation Carcinoma Bleeding Hypochromic anemia Systemic complications like, arthritis, iritis, skin lesions, liver disease, renal stones, gall stones, weight loss, growth failure
- 23. Complications of -UC Toxic megacolon Perianal fistula Carcinoma Stricture formation
- 24. CLINICAL PRESENTATION Clinical presentation Crohn’s disease Ulcerative colitis Malaise, fever Common Un common Abdominal tenderness Common May be present Rectal bleeding Less 100% Illeal Very common Rare Granulomas Common Rare Fistulas Common Rare
- 26. Management Goals: toinduce remission in active disease to maintain remission / prevent relapse
- 27. CD Mild tomoderate disease Active CD: oral/parenteral steroids- most effective & safer than oral aminosalicylates CD of colon: aminosalicylates Crohn’s ileitis- mesalazine should be used as 5 aminosalicylic acid is not released in the small bowel from sulfasalazine or olsalazine
- 28. Dose of aminosalicylatesrequired for CD is more than of UC especially in small bowel disease Prednisolone/prednisone 20-60 mg PO/D for 8-12 weeks Or budesonide CR 9 mg PO/D for 8-12 weeks Aminosalicylates: Sulfasalazine 2-4 g PO/d in DD Mesalazine 3-4.8 g PO/d in DD Olsalazine 2-3 g PO/d in DD
- 29. Metronidazole is aseffective as sulfasalazine for colonic disease Metronidazole 20 mg/kg PO/d in DD Severe disease: Hydrocortisone 100 mg IV Q6H or Hydrocortisone 300-400 mg by CIVIF/d or Methylprednisolone 60-80 mg IV/d in DD or by CIVIF for 5-10 days Oral steroids should be substituted when disease activity has subsided Prednisolone or prednisone 40-60 mg/d PO Gradually reducing to zero over 8-12 weeks
- 30. Chronically active disease: Patients who do not respond to steroids or require continuous steroids to control disease activity AZT 6-MP Surgery should be considered if more than 5-10 mg of prednisolone/d is required AZT 2-2.5 mg/kg PO/d or 6-MP 1-1.5 mg/kg PO/d
- 31. Newer agents: Infliximab-monoclonal antibody directed against the proinflammatory cytokine TNF-alpha Effective in patients with refractory & acutely or chronically active disease Dose: 5 mg/kg IVIF Maintenance therapy: AZT & 6-MP effective as prophylactic agents in patients with frequent relapses & in those who are steroid dependent AZT 2-2.5 mg/kg/PO/d 6-MP 1-1.5 mg/kg/PO/d
- 32. Management - UC Mild disease- topical therapy for proctitis Moderate/severe/more extensive- oral/IV Aminosalicylates: Effective in inducing remission in active colitis/proctitis Response is dose realted Sulfasalazine 6g/d Mesalazine 4g/d Olsalazine 3g/d ADRs of s & o are dose related hence should be started at low doses & titrated to recommended dose
- 33. Immunosupressive agents: AZT& 6-MP, effective for both remission induction & maintenance therapy Takes 3-6 months to achieve benefit Significant ADRs Active proctitis/distal colitis: I-line: Topical steroids alone or with oral aminosalicylates Prednisolone sod.phosphate 20 mg/100ml/d enema rectally at night or twice daily
- 34. Hydrocortisone acetate 10%foam rectally/d at night or twice daily or Prednisolone 5 mg rectally twice daily Along with, Sulfasalazine 2-4 g/PO/d in 3-4 DD Mesalazine 1-1.5 g/PO/d in 3 DD Olsalazine 1-1.5 g/PO/d in 2-3 DD CTE: 5-aminosalicylic acid enemas are superior to topical steroids Combination oral & topical 5 AS therapy is more effective than either therapy alone
- 35. II-line: Addition ofan oral CS to I-line Prednisolone or prednisone 20-60 mg/PO/d for 8-12 weeks Extensive UC: Mild to moderate disease: Prednisolone or prednisone 20-60 mg/PO/d for 8-12 weeks and/or Oral aminosalicylate
- 36. Severe disease: Morethan 6 bloody stools/d Temp more than 37.5 Pulse more than 100 bpm Hb less than 100g/l S.Alb less than 35 g/l Fluid, electrolyte or blood replacement should be considered Early surgical consulatation is essential
- 37. Hydrocortisone 100 mgIV Q6H or by CIVIF or Methylprednisolone 60-100 mg IV/d in DD or by CIVIF For 5-10 days and should be substituted with oral steroids If deteriorating or failure to respond consider colectomy or IV cyclosporin Avoid: Loperamide & other antidiarrhoeals & anticholinergics in severe disease as it may leads to toxic megacolon
- 38. Chronically active disease: AZT, 6-MP, surgery AZT 2-2.5 mg/kg PO/d or 6-MP 1-1.5 mg/kg PO/d ADRs of s&o are dose related hence should be started at low doses & titrated to recommended dose Proctocolectomy, ileal pouch anal anastomosis may be considered for the traetment of chronic refractory disease
- 39. Maintenance therapy: Toreduce the relapse-aminosalicylates or immunosupressive agents Sulfasalazine 2-3 g/Po/d in 3-4 DD Incidence of ADRs increases with increase in dose Mesalazine 1-1.5g/PO/d in 3 DD Olsalazine 1-1.5 g/PO/d in 2-3 DD ADR: watery diarrhoea (10-15%)
- 40. Patients responded totopical AMS preparations may continue to use as maintenance therapy at reduced doses Mesalazine 2-4 g in 60 ml enema rectally 2-3 times a week A prolonged remission may be achieved with, AZT 2-2.5 mg/kg/Po/d or 6-MP 1-1.5 mg/kg/PO/d
- 41. Pouchitis: In patientswho have undergone ileal-pouch anal anastomosis may develop inflammation of ileal pouch Metronidazole 20mg/kg/po/d in DD, probiotic is also useful
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- 44. DRUGS TreDaOStEment oMpAINtTiEoNAnNCsE DOSE SITE OF ACTION Sulfasalazine 3 – 4 gm/day 2 – 4 g/day colon Olsalazine 2 – 3 gm/day 1g/day colon Balsalazide 2 – 6.75 gm/day 2 – 6.75g/day colon Mesalamine (DR) 2.4 – 4.8 gm/day 2.4-4.8g/day Distal ileum and colon Mesalamine (enema) 1 – 4 g/day 0.8 – 4.8 g/day Rectum and terminal colon Mesalamine (SR) 2 – 4 g/day 1.5 – 4 g/day Small bowel and colon Mesalamine suppository 1 – 1.5g/day 0.5 – 1 gm/bedtime Rectum and terminal colon
- 45. corticosteroids DRUGS DOSE Methylprednisolone (IV) 40 – 60mg/day Prednisolone ( IV) 60 – 80 mg/day Hydrocortisone IV 300mg/day Prednisone( oral) 20 – 60mg/day Budesonide( oral) 9 mg/day Hydrocortisone enema 100 – 200 mg/day
- 46. DRUGS ROUTE REMISSIONDOSE MAINTENANCE DOSE Azathioprine Oral 2–3 mg/kg/day 2–3 mg/kg/day 6-Mercaptopurine Oral 1–1.5 mg/kg/day 1–1.5 mg/kg/day Cyclosporine IV 2–4 mg/kg/day Not indicated Oral 4–8 mg/kg/day Not indicated Tacrolimus IV 0.01 mg/kg/day Not indicated Oral 0.1–0.2 mg/kg/day Not indicated Methotrexate IM 25 mg/wk 25 mg/wk Oral 15–25 mg/wk 15–25 mg/wk Infliximab IV 5 mg/kg 5–10 mg/kg
- 47. ANTIMICROBIALS DRUGS REMISSIONDOSE MAINTANANCE DOSE Metronidazole Oral 10–20 mg/kg/day Not indicated Ciprofloxacin Oral 1–1.5 g/day Not indicated
- 48. FOODS TO AVOID • Alcohol (Mixed Drinks, Beer, Wine) • Butter, Mayonnaise, Margarine, Oils • Carbonated Beverages • Coffee, Tea, Chocolate • Corn Husks • Dairy Products (If Lactose Intolerant) • Fatty Foods (Fried Foods) • Foods High In Fiber • Gas-producing Foods (Lentils, Beans, Legumes, Cabbage, Broccoli, Onions) • Nuts And Seeds (Peanut Butter, Other Nut Butters) • Raw Fruits • Raw Vegetables • Red Meat And Pork • Spicy Foods • Whole Grains And Bran