DISEASES OF THE SMALL INTESTINE
Abdullah Alyouzbaki Lecturer of Medicine/Mosul Medical College Gastroenterologist and hepatologist 20/12/2015Disorders causing malabsorption: Coeliac disease
Coeliac disease is an inflammatory disorder of the small bowel occurring in genetically susceptible individuals, which results from intolerance to wheat gluten and similar proteins found in rye, barley and, to a lesser extent, oats.Coeliac disease
The condition occurs worldwide but is more common in northern Europe. The prevalence is approximately 1%, 50% of these people are asymptomatic. ‘silent’ coeliac disease ‘latent’ coeliac disease – genetically susceptible people who may later develop clinical coeliac disease.Coeliac disease: Pathophysiology
Celiac disease: presentationCeliac disease can present at any age. In infancy, it occurs after weaning on to cereals . typically presents with diarrhea, malabsorption and failure to thrive.
Celiac disease: presentation
older children:non-specific features such as delayed growth. Features of malnutrition are found on examination and mild abdominal distension. pubertal delay, leading to short stature in adulthood.Celiac disease: presentation
In adults: usually during the third or fourth decade females > males. The presentation is highly variable: florid malabsorption, while others develop non-specific symptoms, such as tiredness, weight loss, folate deficiency or iron deficiency anaemia. oral ulceration, dyspepsia and bloating. mild under-nutrition and osteoporosis.Celiac disease: Investigations
Duodenal biopsy: Endoscopic small bowel biopsy is the gold standard. The histological features are usually characteristic but other causes of villous atrophy should be considered.A Normal. B Subtotal villous atrophy . There is blunting of villi, crypt hyperplasia and inflammatory infiltration of the lamina propria.
Celiac disease: Investigations
Celiac disease: InvestigationsCeliac disease: Investigations
Antibodies:Anti tissue transglutamase antibodies and Anti-endomysial antibodies of the IgA :They are sensitive (85–95%) and specific (approximately 99%) for the diagnosis, except in very young infants.IgG antibodies, however, must be analysed in patients with coexisting IgA deficiency. they usually become negative with successful treatment.Celiac disease: Investigations
Haematology and biochemistry:A full blood count may show microcytic or macrocytic anaemia from iron or folate deficiency and features of hyposplenism (target cells, spherocytes and Howell– Jolly bodies). Biochemical tests may reveal reduced concentrations of calcium, magnesium, total protein, albumin or vitamin D.Celiac disease: Investigations
Celiac disease : Management
Exclusion of wheat, rye, barley and initially oats, although oats may be re-introduced safely in most patients after 6–12 months.Frequent dietary counselling.Mineral and vitamin supplements.Measurement of tTG or anti-endomysial antibodies.Celiac disease: Complications
Risk of malignancy, particularly of enteropathy-associated T-cell lymphoma, small bowel carcinoma and squamous carcinoma of the esophagus. Ulcerative jejuno-ileitis. Osteoporosis and osteomalacia.Coeliac disease : still diarrhea in spite of gluten free diet??
Non Compliance , Non Compliance ,…..Non compliance.Associations : pancreatic insufficiency , microscopic colitis, inflammatory bowel disease.Complications: ulcerative jejunitis , enteropathy associated T-cell lymphoma, small bowel carcinoma and refractory coeliac disease.Dermatitis herpetiformis
intensely itchy blisters over the elbows, knees, back and buttocks. Immunofluorescence shows granular or linear IgA deposition at the dermoepidermal junction.Dermatitis herpetiformis
Almost all patients have partial villous atrophy on duodenal biopsy, identical to that seen in coeliac disease, even though they usually have no gastrointestinal symptoms. The rash usually responds to a gluten free diet but some patients require additional treatment with dapsone.Small bowel bacterial overgrowth(‘blind loop syndrome’) The normal duodenum and jejunum contain fewer than 10⁴/mL organisms, which are usually derived from saliva.The count of coliform organisms never exceeds 10⁴/mL.In bacterial overgrowth, there may be 108–1010/mL organisms, most of which are normally found only in the colon.
Small bowel bacterial overgrowth(‘blind loop syndrome’)
Small bowel bacterial overgrowth(‘blind loop syndrome’):Clinical features The patient presents with watery diarrhoea and/or steatorrhoea, with anaemia due to B12 deficiency. These arise because of deconjugation of bile acids, which impairs micelle formation, and because of bacterial utilisation of vitamin B12.Small bowel bacterial overgrowth(‘blind loop syndrome’):Investigations Barium follow-through . Jejunal contents for bacteriological examination can also be aspirated at endoscopy (Gold standard) . non-invasively using hydrogen breath tests. Low serum levels of vitamin B12, with normal or elevated folate levels because the bacteria produce folic acid.
Small bowel bacterial overgrowth(‘blind loop syndrome’):Management Treatment of the underlying cause of small bowel bacterial overgrowth Tetracycline (250 mg 4 times daily for 7 days) is then the treatment of choice, Metronidazole (400 mg 3 times daily) or ciprofloxacin (250 mg twice daily) is an alternative. Some patients require up to 4 weeks of treatment and, in a few, continuous rotating courses of antibiotics are necessary. Intramuscular vitamin B12 supplementation.
Whipple’s disease This rare condition is characterised by infiltration of small intestinal mucosa by ‘foamy’ macrophages, which stain positive with periodic acid–Schiff (PAS) reagent. Caused by infection with the Gram positive bacillus Tropheryma whipplei.The disease is a multisystem .
Whipple’s disease
Whipple’s disease Diagnosis: characteristic features on small bowel biopsy, with characterisation of the bacillus by polymerase chain reaction (PCR). Management: often fatal if untreated . Responds well, at least initially, to intravenous ceftriaxone (2 g daily for 2 weeks), followed by oral co-trimoxazole for at least 1 year.Ileal resection
Ileal resection
The most common scenario is in patients with Crohn’s disease.Diarrhea usually responds well to colestyramine, a resin which binds bile salts in the intestinal lumen. Aluminium hydroxide can be used as an alternative.Short bowel syndrome
Digestion and absorption are normally completed within the first 100 cm of jejunum, and enteral feeding is usually still possible if this amount of small intestine remains. The presence of some or all of the colon can markedly improve these losses by increased water reabsorption. The presence of an intact ileocaecal valve ameliorates the clinical picture by slowing small intestinal transit and reducing bacterialovergrowth.Short bowel syndrome:Clinical features
Diarrhoea and steatorrhoea. Dehydration and signs of hypovolaemia are common, weight loss, loss of muscle bulk and malnutrition.Short bowel syndrome:Management
In the immediate post-operative period: total parenteral nutrition (TPN) should be started and PPI therapy given to reduce gastric secretions. Enteral feeding should be cautiously introduced after 1–2 weeks under careful supervision and slowly increased as tolerated.If less than 75 cm of small bowel remains, TPN is also needed.Detailed nutritional assessments at regular intervals Monitoring of fluid and electrolyte balance.Short bowel syndrome:Management
Adequate calorie and protein intake, Fats are a good energy source and should be taken as tolerated. Medium-chain triglyceride are given because they are more easily absorbed.• Replacement of vitamin B12, calcium, vitamin D, magnesium, zinc and folic acid.Loperamide (2–4 mg 4 times daily) or codeine phosphate (30 mg 4–6 times daily) for diarrhoea.Octreotide (50–200 μg 2–3 times daily by subcutaneous injection) reduces gastrointestinal secretions. some require long-term home TPN for survival .Small bowel transplantation.Radiation enteritis and proctocolitis
The risk varies with total dose, dosing schedule and the use of concomitant chemotherapy. Acute injury: nausea, vomiting , abdominal pain and diarrhea . When the rectum and colon are involved, rectal mucus, bleeding and tenesmus occur. rectal changes at sigmoidoscopy resemble ulcerative proctitis or ulcerative colitis. Barium follow-through showing small bowel strictures, ulcers and fistulae.Radiation enteritis and proctocolitis
Chronic Phase :Proctocolitis , Bleeding from telangiectasia, Small bowel strictures, Fistulae: rectovaginal , colovesical , enterocolic ; Adhesions, Malabsorption: bacterial overgrowth, bile salt malabsorption(ileal damage).Radiation enteritis and proctocolitis
Radiation enteritis and proctocolitis:ManagementDiarrhoea : codeine phosphate, diphenoxylate or loperamide. Local corticosteroid enemas can help proctitis. Antibiotics may be required for bacterial overgrowth. Nutritional supplements. Colestyramine (4 g as a single sachet) is useful for bile salt malabsorption. Endoscopic argon plasma coagulation therapy may reduce bleeding from proctitis. Surgery should be avoided, if possible, because the injured intestine is difficult to resect and anastomose, but may be necessary for obstruction, perforation or fistula.
ISCHAEMIC GUT INJURY
Ischaemic gut injury is usually the result of arterial occlusion. Severe hypotension and venous insufficiency are less frequent causes. The presentation is variable, depending on the different vessels involved and the acuteness of the event. Diagnosis is often difficult.Acute small bowel ischaemia
An embolus from the heart or aorta to the superior mesenteric artery is responsible for 40–50% of cases, thrombosis of underlying atheromatous disease for approximately 25%, and non-occlusive ischaemia due to hypotension complicating myocardial infarction, heart failure, arrhythmias or sudden blood loss for approximately 25%. Vasculitis and venous occlusion are rare causes.Acute small bowel ischaemia
The clinical spectrum ranges from transient alteration of bowel function to transmural haemorrhagic necrosis and gangrene. Almost all develop abdominal pain that is more impressive than the physical findings. In the early stages, the only physical signs may be a silent, distended abdomen or diminished bowel sounds, peritonitis only developing later.Acute small bowel ischaemia
Leucocytosis, metabolic acidosis, hyperphosphataemia and hyperamylasaemia are typical. Plain abdominal X-rays show ‘thumb-printing’ due to mucosal oedema.Mesenteric or CT angiography reveals an occluded or narrowed major artery with spasm of arterial arcades, although most patients undergo laparotomy on the basis of a clinical diagnosis without angiography.Acute small bowel ischaemia
Resuscitation, management of cardiac disease and intravenous antibiotic therapy, followed by laparotomy, are key steps. If treatment is instituted early, embolectomy and vascular reconstruction may salvage some small bowel.In these rare cases, a ‘second look’ laparotomy should be undertaken 24 hours later and further necrotic bowel resected. In patients at high surgical risk, thrombolysis may sometimes be effective.Chronic mesenteric ischaemia
This results from atherosclerotic stenosis of the coeliac axis, superior mesenteric artery and inferior mesenteric artery. At least two of the three vessels must be affected for symptoms to develop. The typical presentation is with dull but severe mid- or upper abdominal pain developing about 30 minutes after eating. Weight loss is common because the patient is reluctant to eat, and some experience diarrhoea.Chronic mesenteric ischaemia
Physical examination shows evidence of generalised arterial disease. An abdominal bruit is sometimes audible but is non-specific. The diagnosis is made by mesenteric angiography. Treatment is by vascular reconstruction or percutaneous angioplasty, if the patient’s clinical condition permits. The condition is frequently complicated by intestinal infarction, if left untreated.Chronic mesenteric ischaemia
DISEASES OF THE SMALL INTESTINE Lec2Abdullah Alyouzbaki Lecturer of Medicine/Mosul Medical College Gastroenterologist and hepatologist 22/2/2016
Protein-losing enteropathy
Protein-losing enteropathy
The diagnosis can be confirmed by measurement of faecal clearance of α1-antitrypsin or 51Cr-labelled albumin after intravenous injection. Other investigations should be performed to determine the underlying cause. Treatment is that of the underlying disorder, with nutritional support and measures to control peripheral oedema.Ulceration of the small intestine
Adverse food reactionsAdverse food reactions are common and are subdivided into food intolerance and food allergy, the former being much more common. In food intolerance, there is an adverse reaction to food which is not immune-mediated and results from pharmacological (histamine, tyramine or monosodium glutamate), metabolic (lactase deficiency)or other mechanisms (toxins or chemical contaminants in food).
Lactose intolerance
In most populations, enterocyte lactase activity declines throughout childhood.In cases of genetically determined (primary) lactase deficiency, jejunal morphology is normal. ‘Secondary’ lactase deficiency occurs as a consequence of disorders which damage the jejunal mucosa, such as coeliac disease and viral gastroenteritis. Unhydrolysed lactose enters the colon, where bacterial fermentation produces volatile short-chain fatty acids, hydrogen and carbon dioxide.Lactose intolerance
Clinical features In most people, lactase deficiency is completely asymptomatic. However, some complain of colicky pain , abdominal distension, increased flatus, borborygmi and diarrhoea after ingesting milk or milk products. The lactose hydrogen breath test is a useful non-invasive confirmatory investigation.Lactose intolerance
Dietary exclusion of lactose is recommended, although most sufferers are able to tolerate small amounts of milk without symptoms. Addition of commercial lactase preparations to milk has been effectiveFood allergy
Food allergies are immune-mediated disorders, most commonly due to type I hypersensitivity reactions with production of IgE antibodies, although type IV delayed hypersensitivity reactions are also seen. The most common culprits are peanuts, milk, eggs, soya and shellfish.Clinical manifestations occur immediately on exposure and range from trivial to life-threatening or even fatal anaphylaxis ‘gastrointestinal anaphylaxis’ consists of nausea, vomiting, diarrhoea and sometimes cardiovascular and respiratory collapse. Fatal reactions to trace amounts of peanuts are well documented.Food allergy
The diagnosis of food allergy is difficult . Skin prick tests. Double-blind placebo-controlled food challenges are the gold standard, but are laborious and are not readily available. In many cases, clinical suspicion and trials of elimination diets are used.Food allergy
Treatment of proven food allergy consists of detailed patient education and awareness, strict elimination of the offending antigen. Anaphylaxis should be treated as a medical emergency with resuscitation, airway support and intravenous adrenaline (epinephrine).INFLAMMATORY BOWEL DISEASE IBD
Ulcerative colitis and Crohn’s disease are chronic inflammatory bowel diseases which have a protracted relapsing and remitting course, usually extending over years. The diseases have many similarities and it is sometimes impossible to differentiate between them.INFLAMMATORY BOWEL DISEASE
Both diseases most commonly start in the second and third decades of life, with a second smaller incidence peak in the seventh decade. Life expectancy in patients with IBD is similar to that of the general population.Pathophysiology of IBD
Genetic• Both CD and UC common in Ashkenazi Jews• 10% have first-degree relative/≥1 close relative with IBD• High concordance in identical twins (40–50% CD; 20–25% UC)IBD associated with other inflammatory conditions (esp. ankylosing spondylosis and psoriasis)Pathophysiology of IBD
Environmental• UC more common in non-smokers and ex-smokers• CD more common in smokers (relative risk = 3)• CD associated with low-residue, high-refined-sugar diet• Commensal gut microbiota altered (dysbiosis) in CD and UC• Appendicectomy protects against UC
Ulcerative colitis
Inflammation invariably involves the rectum (proctitis) and spreads proximally in a continuous manner to involve the entire colon in some cases (pancolitis). In long-standing pancolitis, the bowel can become shortened and post-inflammatory ‘pseudopolyps’ develop; these are normal or hypertrophied residual mucosa within areas of atrophy. The inflammatory process is limited to the mucosa and spares the deeper layers of the bowel wall (Fig. 22.50). Both acute and chronic inflammatory cells infiltrate the lamina propria and the crypts (‘cryptitis’). Crypt abscesses are typical.Crohn’s disease The sites most commonly involved are, in order of frequency, the terminal ileum and right side of colon, colon alone, terminal ileum alone, ileum and jejunum. The entire wall of the bowel is edematous and thickened, and there are deep ulcers which often appear as linear fissures; thus the mucosa between them is described as ‘cobblestone’.
Crohn’s disease These may penetrate through the bowel wall to initiate abscesses or fistulae involving the bowel, bladder, uterus, vagina and skin of the perineum. mesenteric lymph nodes are enlarged and the mesentery is thickened.
Crohn’s disease Crohn’s disease has a patchy distribution and the inflammatory process is interrupted by islands of normal mucosa.On histological examination, the bowel wall is thickened with a chronic inflammatory infiltrate throughout all layers.
Histology of Crohn’s disease. A Inflammation is ‘transmural’; there is fissuring ulceration (arrow), with inflammationextending into the submucosa (SM). B At higher power, a characteristic non-caseating granuloma is seen.
Clinical features of IBD: Ulcerative colitis
The cardinal symptoms are rectal bleeding with passage of mucus and bloody diarrhoea. The presentation varies, depending on the site and severity of the disease , as well as the presence of extra-intestinal manifestations. The first attack is usually the most severe and is followed by relapses and remissions. Emotional stress, intercurrent infection, gastroenteritis, antibiotics or NSAID therapy may all provoke a relapse.Clinical features of IBD: Ulcerative colitis
Proctitis causes rectal bleeding and mucus discharge, accompanied by tenesmus. Some patients pass frequent, small volume fluid stools, while others pass pellety stools. Constitutional symptoms do not occur. Left-sided and extensive colitis causes bloody diarrhoea with mucus, often with abdominal cramps. In severe cases, anorexia,malaise, weight loss and abdominal pain occur, and the patient is toxic, with fever, tachycardia and signs of peritoneal inflammation.Clinical features of IBD:Crohn’s disease The major symptoms are abdominal pain, diarrhoea and weight loss. Ileal Crohn’s disease may cause sub acute or even acute intestinal obstruction.The pain is often associated with diarrhoea, which is usually watery and does not contain blood or mucus.Almost all patients lose weight because they avoid food, since eating provokes pain. Weight loss may also be due to malabsorption, and some patients present with features of fat, protein or vitamin deficiencies.
Clinical features of IBD:Crohn’s disease Crohn’s colitis presents in an identical manner to ulcerative colitis, but rectal sparing and the presence of perianal disease are features which favour a diagnosis of Crohn’s disease.
Complications of IBD
Life-threatening colonic inflammation:This can occur in both ulcerative colitis and Crohn’s colitis. In the most extreme cases, the colon dilates (toxic megacolon) and bacterial toxins pass freely across the diseased mucosa into the portal and then systemic circulation. An abdominal X-ray should be taken daily because, when the transverse colon is dilated to more than 6 cm, there is a high risk of colonic perforation.Complications of IBD
Haemorrhage:Haemorrhage due to erosion of a major artery is rare but can occur in both conditions.Fistulae:These are specific to Crohn’s disease. Enteroenteric fistulae can cause diarrhoea and malabsorption due to blind loop syndrome. Enterovesical fistulation causes recurrent urinary infections and pneumaturia. An enterovaginal fistula causes a faeculent vaginal discharge. Fistulation from the bowel may also cause perianal or ischiorectal abscesses, fissures and fistulae.Complications of IBD
Cancer The risk of dysplasia and cancer increases with the duration and extent of uncontrolled colonic inflammation. The risk is particularly high inpatients who have concomitant primary sclerosing cholangitis for unknown reasons. Tumors develop in areas of dysplasia and may be multiple. Patients with long-standing colitis are therefore entered into surveillance programs beginning 10 years after diagnosis. If high-grade dysplasia is found, panproctocolectomy is usually recommended because of the high risk of colon cancer.Extra-intestinal complications
InvestigationsInvestigations are necessary to confirm the diagnosis, define disease distribution and activity, and identify complications. Full blood count may show anaemia resulting from bleeding or malabsorption of iron, folic acid or vitamin B12. Serum albumin concentration falls as a consequence of protein-losing enteropathy, inflammatory disease or poor nutrition. The ESR and CRP are elevated in exacerbations and in response to abscess formation.
Investigations
Faecal calproctectin has a high sensitivity for detecting gastrointestinal inflammation and may be elevated, even when the CRP is normal. It is particularly useful in distinguishing inflammatory bowel disease from irritable bowel syndrome at diagnosis, and for subsequent monitoring of disease activity. Bacteriology: stool microscopy, culture and examination for Clostridium difficile toxin or for ova and cysts, blood cultures and serological tests should be performed.Investigations: Endoscopy
Patients who present with diarrhoea plus raised inflammatory markers or alarm features, such as weight loss, rectal bleeding and anaemia, should undergo ileocolonoscopy.Flexible sigmoidoscopy is occasionally performed to make a diagnosis, especially during acute severe presentations when ileocolonoscopy may confer an unacceptable risk.In ulcerative colitis, there is loss of vascular pattern, granularity, friability and contact bleeding, with or without ulceration. In Crohn’s disease, patchy inflammation, with discrete, deep ulcers, strictures and perianal disease (fissures, fistulae and skin tags), is typically observed, often with rectal sparing.Investigations: Endoscopy
In Crohn’s disease, wireless capsule endoscopy ,enteroscopy may be required.All children and most adults with Crohn’s disease should have upper gastrointestinal endoscopyInvestigations: Radiology
Barium enema is a less sensitive investigation than colonoscopy in patients with colitis and, where colonoscopy is incomplete, a CT colonogram is preferred.Small bowel imaging is essential to complete staging of Crohn’s disease. Traditional contrast imaging by barium follow-through demonstrates affected areas of the bowel as narrowed and ulcerated, often with multiple strictures. This has now largely been replaced by MRI enterography, which is a sensitive way of detecting extra intestinal manifestations and of assessing pelvic and perineal involvement.Investigations: Radiology
A plain abdominal X-ray is essential in the management of patients who present with severe active disease. Dilatation of the colon , mucosal edema (thumb-printing) or evidence of perforation may be found.Management of IBD
Although medical therapy plays an important role, optimal management depends on establishing a multidisciplinary team-based approach involving physicians, surgeons, radiologists, nurse specialists and dietitians. The key aims of medical therapy are to:• treat acute attacks (induce remission)• prevent relapses (maintain remission) •prevent bowel damage• detect dysplasia and prevent carcinoma• select appropriate patients for surgery.DISEASES OF THE SMALL and LARGE INTESTINE Lec3
Abdullah Alyouzbaki Lecturer of Medicine/Mosul Medical College Gastroenterologist and hepatologist 14/3/2016
Ulcerative colitis: Active proctitis
Most patients with ulcerative proctitis respond to a 1 g mesalazine suppository but some will additionally require oral 5-aminosalicylate (5-ASA) therapy. Topical corticosteroids are less effective and are reserved for patients who are intolerant of topical mesalazine. Patients with resistant disease may require treatment with systemic corticosteroids and immunosuppressants.Active left-sided or extensive ulcerative colitis
In mild to moderately active cases, the combination of a oral and a topical 5-ASA preparation.The topical preparation is typically withdrawn after 1 month. The oral 5-ASA is continued long-term to prevent relapse. In patients who do not respond to this approach within 2–4 weeks, oral prednisolone (40 mg daily, tapered by 5 mg/week over an 8-week total course) is indicated. Corticosteroids should never be used for maintenance therapy. At the first signs of corticosteroid resistance or in patients who require high corticosteroid doses to maintain control, immunosuppressive therapy with a thiopurine should be introduced.Severe ulcerative colitis
Patients who fail to respond to maximal oral therapy and those who present with acute severe colitis are best managed in hospital and should be monitored jointly by a physician and surgeon:• clinically: for the presence of abdominal pain,temperature, pulse rate, stool blood and frequency.• by laboratory testing: haemoglobin, white cell count, albumin, electrolytes, ESR and CRP• radiologically: for colonic dilatation on plain abdominal X-rays.Medical management of fulminant ulcerative colitis:
• Admit to hospital for intensive therapy and monitoring• Intravenous fluids and correction of electrolyte imbalance• Transfusion if haemoglobin < 100 g/L (< 10 g/dL)• IV methylprednisolone (60 mg daily) or hydrocortisone (400 mg daily)• Antibiotics until enteric infection excluded• Nutritional support• Subcutaneous low-molecular-weight heparin for prophylaxis of venous thromboembolism• Avoidance of opiates and anti diarrhoeal agents• Consider infliximab (5 mg/kg) or ciclosporin (2 mg/kg) in stable patients not responding to 3–5 days of corticosteroidsMedical management of fulminant ulcerative colitis:
Patients who develop colonic dilatation (> 6 cm), those whose clinical and laboratory measurements deteriorate and those who do not respond after 7–10 days’ maximal medical treatment usually require urgent colectomy.Maintenance of remission
Life-long maintenance therapy is recommended for all patients with left-sided or extensive disease but is not necessary in those with proctitis. Once-daily oral 5-aminosalicylates are the preferred first-line agents. Sulfasalazine can be considered in patients with coexistent arthropathy. Patients who frequently relapse despite aminosalicylate drugs should be treated with thiopurines.Crohn’s disease Crohn’s disease is a progressive condition which may result in stricture or fistula formation if suboptimally treated. It is therefore important to agree long-term treatment goals with the patient; these are to induce remission and then maintain corticosteroid-free remission with a normal quality of life.
Crohn's disease : Induction of remission
Corticosteroids remain the mainstay of treatment for active Crohn’s disease. The drug of first choice in patents with ileal disease is budesonide, since it undergoes 90% first-pass metabolism in the liver and has very little systemic toxicity. If there is no response to budesonide within 2 weeks, the patient should be switched to prednisolone , which has greater potency.Crohn's disease : Induction of remission
As an alternative to corticosteroid therapy, enteral nutrition with either an elemental (constituent amino acids) or polymeric (liquid protein) diet may induce remission.Some patients with severe colonic disease require admission to hospital for intravenous corticosteroids. In severe ileal or panenteric disease, induction therapy with an anti-TNF agent is appropriate, provided that acute perforating complications, such as abscess, have not occurred. Randomised trials have demonstrated that combination therapy with an anti-TNF antibody and a thiopurine is the most effective strategy for inducing and maintaining remission in luminal Crohn’s patients.Crohn's disease :Maintenance therapy
Immunosuppressive treatment with thiopurines (azathioprine and mercaptopurine) forms the core of maintenance therapy, but methotrexate is also effective and can be given once weekly, either orally or by subcutaneous injection. Combination therapy with an immunosuppressant and an anti-TNF antibody is the most effective strategy but costs are high and there is an increased risk of serious adverse effects. Cigarette smokers should be strongly counselled to stop smoking at every possible opportunity. Those that do not manage to stop smoking fare much worse, with increased rates of relapse and surgical intervention.Surgical treatment: Ulcerative colitis
The choice of procedure is either panproctocolectomy with ileostomy, or proctocolectomy with ileal–anal pouch anastomosis.Surgical treatment: Crohn’s disease The indications for surgery are similar to those for ulcerative colitis. Operations are often necessary to deal with fistulae, abscesses and perianal disease, and may also be required to relieve small or large bowel obstruction. In contrast to ulcerative colitis, surgery is not curative and disease recurrence is the rule. Surgery should be as conservative as possible in order to minimize loss of viable intestine and to avoid creation of a short bowel syndrome.