60. Crohn’s disease and ulcerative colitis. Precancerous states of the gastrointestinal tract

Page created on September 16, 2021. Last updated on October 22, 2021 at 09:27

Crohn disease

Introduction

For introduction, epidemiology, etiology, and pathology, see the corresponding pathology 2 topic.

Clinical features

The cardinal symptoms of CD are crampy abdominal pain (usually right lower quadrant), chronic intermittent diarrhoea, fatigue, and weight loss. Diarrhoea may and may not be bloody. Patients may also present with complications such as aphthous stomatitis, perianal fistula, or abscess.

Crohn disease is associated with certain extraintestinal manifestations, although it’s rare that a patient presents with these. These include arthritis, uveitis, ankylosing spondylitis, erythema nodosum, and pyoderma gangrenosum.

Diagnosis and evaluation

Diagnosis of CD is histological, requiring biopsy. The workup of CD involves MR enterography (to visualise the small bowels) and colonoscopy. Biopsies should be taken from any lesions visible, as well as the terminal ileum. If there are oesophageal or gastric symptoms, upper endoscopy should be performed as well. Laboratory tests should check for anaemia and vitamin deficiencies.

Non-infectious intestinal inflammation correlates directly with the amount of calprotectin in the faeces. Measurement of this marker is useful both for excluding the diagnosis (if negative) and for follow-up.

Treatment

Early treatment is necessary to achieve remission and to maintain it, and to prevent complications. Unfortunately, many patients with CD require surgery due to complications in their lifetime.

Many drugs are used in the treatment of CD, including 5-ASA, corticosteroids, immunosuppressants (azathioprine, 6-MP), and biological therapies, like anti-TNF, anti-integrin, and so on. Choice of treatment depends on the severity. 5-ASA is only effective in colonic Crohn disease. Steroids are often used for induction of remission, rather than for maintenance.

For surgical treatment, see the corresponding surgery – traumatology topic.

Ulcerative colitis

Introduction

For introduction, epidemiology, etiology, and pathology, see the corresponding pathology 2 topic.

Clinical features

The cardinal symptoms of UC are bloody diarrhoea with or without mucus, abdominal pain, faecal urgency, and tenesmus.

Like CD, UC may cause extraintestinal manifestations.

Diagnosis and evaluation

Colonoscopy with biopsy is essential. The diagnosis of UC is made in the patient with chronic diarrhoea, colitis on biopsy, and when other causes of diarrhoea have been ruled out. Stool should be tested for bacterial causes of diarrhoea.

Treatment

Early treatment is necessary to achieve remission and to maintain it, and to prevent complications. Unfortunately, many patients with UC require surgery due to complications in their lifetime.

Many drugs are used in the treatment of UC, including 5-ASA, corticosteroids, immunosuppressants (azathioprine, 6-MP), and biological therapies, like anti-TNF. Choice of treatment depends on the severity. 5-ASA is very effective for UC. Steroids are often used for induction of remission, rather than for maintenance.

UC carries an elevated risk for CRC. Patients should undergo regular (every 1 – 3 years) colonoscopy to assess for dysplasia and malignancy.

For surgical treatment, see the corresponding surgery – traumatology topic.

Precancerous states of the GI tract

Barrett oesophagus

For introduction, see the corresponding pathology 2 topic.

Barrett oesophagus is asymptomatic and is often discovered when a patient is being evaluated endoscopically for GERD. The diagnosis is based on biopsy and histology.

All patients with Barrett oesophagus should be on PPI.

Barrett oesophagus with high-grade dysplasia is treated with mucosectomy (endoscopic resection) or endoscopic ablation, same as T1A oesophageal cancer. No dysplasia or low-grade dysplasia may be managed either with regular surveillance or endoscopic removal.

Oral leucoplakia and erythroplakia

For introduction, see the corresponding pathology 2 topic.

These precancerous lesions should be surgically removed, or alternatively, regularly surveyed. Avoiding risk factors is important to prevent recurrence or progression.

Familial adenomatous polyposis

For introduction, see the corresponding pathology 2 topic.

As FAP is autosomal dominant, there is often a family history of the disease, but not always. Genetic testing is necessary for the diagnosis, which shows the characteristic germline mutation in APC.

Because FAP is associated with a 100% risk of progression to CRC by the age of 45, surgery is required in all cases. Surgery is performed at age 16 – 20, or at the time of diagnosis if later than this.

The preferred surgical procedure is the same as for UC, is restorative proctocolectomy with ileum pouch and anal anastomosis.

Atrophic gastritis

For introduction, see the corresponding pathology 2 topic. See also topic 57 of internal medicine.

Atrophic gastritis is commonly asymptomatic. Autoimmune metaplastic atrophic gastritis (AMAG) may cause pernicious anaemia. Environmental metaplastic atrophic gastritis (EMAG, H. pylori associated) may cause peptic ulcers.

Treatment involves eradication of H. pylori for EMAG, B12 supplements for AMAG, and possibly regular endoscopic surveillance (although this is controversial).


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56. Peptic ulcer disease. Helicobacter pylori infection

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