Inflammatory bowel disease (IBD) represents a group of idiopathic, chronic, inflammatory intestinal conditions. Its two main disease categories are: Crohn's disease (CD) and ulcerative colitis (UC), which feature both overlapping and distinct clinical and pathological features. While these diseases have, in the past, been most evident in the developed world, their prevalence in the developing world has been gradually increasing in recent decades. This poses unique issues in diagnosis and management which have been scarcely addressed in the literature or in extant guidelines. Depending on the nature of the complaints, investigations to diagnose either form of IBD or to assess disease activity will vary and will also be influenced by geographic variations in other conditions that might mimic IBD. Similarly, therapy varies depending on the phenotype of the disease being treated and available resources. The World Gastroenterology Organization has, accordingly, developed guidelines for diagnosing and treating IBD using a cascade approach to account for variability in resources in countries around the world.
Pancreatitis occurs in approximately 4% of patients treated with the thiopurines azathioprine or mercaptopurine. Its development is unpredictable and almost always leads to drug withdrawal. We identified patients with inflammatory bowel disease (IBD) who had developed pancreatitis within 3 months of starting these drugs from 168 sites around the world. After detailed case adjudication, we performed a genome-wide association study on 172 cases and 2,035 controls with IBD. We identified strong evidence of association within the class II HLA region, with the most significant association identified at rs2647087 (odds ratio 2.59, 95% confidence interval 2.07-3.26, P = 2 × 10(-16)). We replicated these findings in an independent set of 78 cases and 472 controls with IBD matched for drug exposure. Fine mapping of the HLA region identified association with the HLA-DQA1*02:01-HLA-DRB1*07:01 haplotype. Patients heterozygous at rs2647087 have a 9% risk of developing pancreatitis after administration of a thiopurine, whereas homozygotes have a 17% risk.
Summary
Background Distinguishing Crohn’s disease from intestinal tuberculosis in endemic areas is challenging as both conditions have overlapping clinical, radiological, endoscopic and histological characteristics. Furthermore, high rates of latent tuberculosis confer a considerable risk of reactivation once therapy for established Crohn’s disease is started.
Aim To review current strategies in differentiating these two conditions, and in managing Crohn’s disease, in populations with high rates of tuberculosis.
Methods Literature review and clinical experience.
Results While various clinical, radiological, endoscopic and histological parameters may aid in differentiating Crohn’s disease from intestinal tuberculosis, these remain imperfect and as treatment options differ misdiagnosis has grave consequences. We propose a diagnostic algorithm, based on currently available evidence and experience, to aid in this dilemma. We also discuss approaches to the management of Crohn’s disease, including agents targeting tumour necrosis factor‐α, in patients at risk of developing tuberculosis.
Conclusions A diagnosis of Crohn’s disease in individuals at risk for tuberculosis should only be made after careful interpretation of clinical signs, abdominal imaging and systematic endoscopic and histological assessment. Newer techniques for the diagnosis of latent tuberculosis still need to be validated in this environment, and guidelines on the treatment of latent tuberculosis in this setting require clarification.
Background:The histological differential diagnosis of Crohn’s disease and intestinal tuberculosis can be very challenging, as both are chronic granulomatous disorders with overlapping histological features.Aim:To evaluate selected clinical and histological parameters in colonic biopsy specimens for their ability to discriminate between Crohn’s disease and intestinal tuberculosis.Methods:25 patients with Crohn’s disease and 18 patients with intestinal tuberculosis were selected for this study on the basis of established clinical, radiological and histological criteria. Clinical data and selected histological parameters in colonoscopic biopsy specimens were assessed retrospectively. A total of 103 and 41 biopsy sites were evaluated in patients with Crohn’s disease and intestinal tuberculosis, respectively.Results:Clinical parameters helpful in differentiating intestinal tuberculosis from Crohn’s disease included chest radiographic features of tuberculosis (56%v0%), perianal fistulae (0%v40%) and extraintestinal manifestations of Crohn’s disease (0%v40%). Histopathological features that seemed to reliably differentiate between intestinal tuberculosis and Crohn’s disease included confluent granulomas, ⩾10 granulomas per biopsy site and caseous necrosis (in biopsy samples of 50%, 33% and 22% of patients with intestinal tuberculosis, respectively,v0% of patients with Crohn’s disease). Features that were observed more often in patients with intestinal tuberculosis than in those with Crohn’s disease included granulomas exceeding 0.05 mm2(67%v8%), ulcers lined by conglomerate epithelioid histiocytes (61%v8%) and disproportionate submucosal inflammation (67%v10%).Conclusion:Clinical features and selected histological parameters in colonoscopic biopsy specimens can help in differentiating between Crohn’s disease and intestinal tuberculosis.
Patients with IBD who receive thiopurines are at increased risk of non-melanoma skin cancer. The risk is highest in Caucasian patients, and is negligible in other groups.
This study demonstrates a protective association of childhood helminth infection against the development of IBD and supports the "hygiene hypothesis" that improved living conditions may increase the incidence of IBD. Our epidemiologic conclusions provide support that helminths may have immunomodulatory effects which provides protection against the development of IBD later in life.
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