**2.3 Treatment**

A curative treatment for inflammatory bowel disease is yet to be identified. Strategies for the management of IBD involve treatment of flares and maintenance of remission. Although a wide range of therapies including enteral nutrition (Zachos et al., 2007), antibiotics (Lal and Steinhart, 2006) and complementary medicines (Langmead and Rampton, 2006) are used in IBD, the mainstay of treatment has been with anti-inflammatory and immunomodulatory drugs. Corticosteroids, 5-aminosalicylates (5ASA), azathioprine (AZA), mercaptopurine (6MP), methotrexate (MTX) and cyclosporin A (CSA) have been the most commonly used drugs. In an attempt to reduce steroid exposure and maintain remission, immunomodulatory therapy is being used earlier, for prolonged periods and in combination. The concern is of an increased risk of side effects with this approach. Estimates suggest that up to 30% of patients may not respond to this treatment and may require more aggressive strategies. The increased understanding of the pathogenesis of IBD, has led to investigation in to a number of therapies targeted towards the abnormal cytokine expression seen in patients with IBD. Of these, only the monoclonal antibodies against tumour necrosis factor are currently in clinical use but other targets have been identified and are undergoing laboratory and clinical study. Infliximab (IXB) and adalimumab (ADA) are the two antitumour necrosis factor (anti-TNF) drugs available in the United Kingdom and a number of

Evaluating Lymphoma Risk in Inflammatory Bowel Disease 315

Classification of Tumours of Haemopoietic and Lymphoid Tissues, updated in 2008 (see Table 1), is now widely accepted (Swerdlow et al., 2008) and categorises lymphoid

Mature T lymphocytes - cytotoxic or killer T cells, helper T cells or T regulatory cells

**Non-Hodgkin's Lymphoma** 

Precursor B-cell lymphoblastic lymphoma Precursor T-cell lymphoblastic lymphoma

Lymphoplasmacytic lymphoma T-cell prolymphocytic leukaemia Splenic marginal zone lymphoma T-cell large granular lymphocytic leukaemia Hairy cell leukaemia Aggressive NK-cell leukaemia Plasma cell neoplasms Adult T-cell lymphoma/leukaemia

Nodal marginal zone B-cell lymphoma Enteropathy-type T-cell lymphoma Follicular lymphoma (grades 1, 2, 3a and 3b) Hepatosplenic T-cell lymphoma

Mantle cell lymphoma Mycosis fungoides Diffuse large B-cell lymphoma Peripheral T-cell lymphoma unspecified

Mediastinal (thymic) large B-cell lymphoma Angioimmunoblastic T-cell lymphoma Intravascular large B-cell lymphoma Anaplastic large cell lymphoma

Diffuse follicle centre lymphoma Subcutaneous panniculitis-like T-cell

lymphoma Extranodal NK-/T-cell lymphoma, nasal type

**Precursor B-cell lymphomas Precursor T-cell and NK-cell lymphomas** 

Blastic NK-cell lymphoma

**Mature T-cell and NK-cell lymphomas** 

lymphoma

neoplasms in to those derived from:

 B cell progenitors - bone marrow derived T cell progenitors - thymus derived

**Mature B-cell lymphomas** 

Small lymphocytic lymphoma

Extranodal marginal zone B-cell MALT

Primary effusion lymphoma Burkitt lymphoma

**B-cell proliferations of uncertain malignant potential** 

Lymphomatoid granulomatosis Post-transplant lymphoproliferative disorder

Mature B lymphocytes - B cells or plasma cells

studies have proven their efficacy (Hanauer et al., 2006, Hanauer et al., 2002, Jarnerot et al., 2005). A third, pegylated anti-TNF drug, certolizumab has also been studied and appears to have equivalent clinical efficacy (Sandborn et al., 2007a). Despite medical therapy, up to 50- 70% of patients with CD will undergo surgery within 5 years of diagnosis and UC patients have a 20-30% lifetime risk of colectomy (Cosnes et al., 2005).
