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Four patients with inflammatory bowel disease and severe cystic acne were treated with isotretinoin. Two patients had a successful course of treatment without any gastrointestinal side-effects. One patient had two episodes of profuse rectal bleeding that were probably related to pre-existing haemorrhoids. The fourth patient had a flare-up of his Crohn's disease after starting isotretinoin.
The cause of inflammatory bowel disease (IBD) remains unknown. In this report, an attempt is made to produce a suitable animal model for studying the pathobiology of IBD, especially its pathogenesis. Sprague-Dawley rats were divided into four groups of six (A, B, C, D). The experimental design involved prior parenteral sensitization of groups A and B by a 1.5 percent solution of lambda degraded carrageenan followed by oral administration of the same solution for 30 days to groups A and C. The animals were then sacrificed, and the small intestine was evaluated for injury. Oral carrageenan caused significant intestinal injury as evidenced by ulceration, abnormal villous pattern, degree and extent of inflammation [p = 0.0001 for groups (A + C) versus (B + D)]. Prior sensitization aggravated the effects of oral carrageenan. Overall, the inflammation produced was reminiscent of human IBD in that there was pin-point ulceration, focality of lesions and lymphoid hyperplasia with microgranulomas. It was concluded that this carrageenan model may prove to be particularly useful for studying the pathobiology of human IBD.
Stools from 109 patients with inflammatory bowel disease (13.4%) contained Clostridium difficile or its toxin, an incidence similar to the stools of 99 control patients with diarrhoea (11.9%), but significantly higher than the stools of 77 control patients with a normal bowel habit (1.4%). Sixty-six per cent of the diarrhoea controls, but only 11% of the inflammatory bowel disease patients, reported recent antibiotic use: however, 67% of inflammatory bowel disease patients were taking sulphasalazine. The presence of Cl difficile in the stool was not related to the clinical assessment of inflammatory bowel disease relapse, but it was related to hospital admission. During the one year study, 31 of the 109 patients (28%) with inflammatory bowel disease had one or more stool samples that were positive for Cl difficile.
Therapeutic outcome in inflammatory bowel disease has traditionally been related to disease activity. Recent data suggest that individual differences in drug disposition and metabolism, some of which are genetically determined, may play a significant role in the outcome of therapy for inflammatory diseases. Polymorphisms in the thiopurine methyl transferase gene (TPMT) are known to influence the outcome of therapy with azathioprine although pharmacogenetic analysis of outcome has not entered routine clinical use. The outcome of therapy with drugs such as steroids may be influenced by a wide range of genetic factors including polymorphisms in the multi-drug resistance 1 gene (MDR1), polymorphisms in glucocorticoid receptor genes and potentially other as yet undefined polymorphisms regulating the inflammatory process. Multiple polymorphisms have been identified in MDR1 but their direct contribution to changes in expression and function have not as yet been defined. Lastly, as novel biological agents such as infliximab become established in clinical practice, it is clear that their therapeutic efficacy will likely be modified by polymorphisms downstream of their target molecules. New diagnostic and therapeutic algorithms are needed to directly determine the functional importance of the influence of host genetic factors on choice and dosage scheduling of therapy.
The etiology of inflammatory bowel disease (IBD) is currently unknown. Although there is convincing evidence supporting a critical role for micro-organisms in the pathogenesis of IBD, the specific organisms involved remain undetermined. Mucus-associated bacteria have recently been considered as likely candidates for involvement in IBD; indeed several mucus-associated bacteria species have been shown to induce IBD-like conditions in animal models, and some of these bacteria have been detected in human intestinal tissues. Further studies are required to investigate the possible role of mucus-associated bacteria in human IBD.
BACKGROUND: As platelet factors are important in the inflammatory response, we examined the course of platelet factor 4 and beta-thromboglobulin in relation to disease activity in inflammatory bowel disease and in giant cell arteritis. PATIENTS AND METHODS: In a prospective study, the platelet count, platelet factor 4 and beta-thromboglobulin were measured in 20 patients with Crohn's disease, 18 with ulcerative colitis and 19 with giant cell arteritis, during active and inactive disease, as well as in 51 controls without inflammation. RESULTS: Platelet counts were significantly higher in active vs. inactive Crohn's disease, ulcerative colitis and giant cell arteritis. Levels of platelet factor 4 and beta-thromboglobulin were significantly higher in active inflammatory bowel disease and giant cell arteritis, as well as in inactive inflammatory bowel disease and giant cell arteritis, than in the non-inflammatory controls. A positive correlation was found between the Crohn's disease activity index and the platelet count, platelet factor 4 and beta-thromboglobulin. Also, a positive correlation was found between the ulcerative colitis activity index and beta-thromboglobulin. However, even after 12 months of follow-up, in Crohn's disease and ulcerative colitis the mean levels of platelet factor 4 and beta-thromboglobulin were significantly higher than the levels of the controls. CONCLUSION: Platelet factors were correlated with inflammatory bowel disease activity. Levels of platelet factor 4 and beta-thromboglobulin, however, were markedly raised for a long time in clinically inactive inflammatory bowel disease, which might point to a pre-thrombotic state of disease.
Animal models of inflammatory bowel disease (IBD) have been useful in the identification of those immune responses uniquely involved in IBD pathogenesis and in defining the important roles of environmental influences, such as normal luminal bacterial flora and the genetic composition of the host, in modifying IBD-associated inflammation. Recent studies have focused particular attention on CD4+ T cells which produce excessive quantities either of Th1 cytokines (IFN-gamma and TNF) directed by IL-12 or of a Th2 cytokine (IL-4), relative to the production of suppressive cytokines such as IL-10 and transforming growth factor beta. Such insights will be extremely beneficial in the development of novel approaches to the control of IBD-type inflammation, such as the use of anticytokine therapies and gene therapy, and finally, in the identification of the genetic abnormalities and the antigens driving the inflammation that underlies the human disease.
Inflammatory bowel diseases are characterized by the accumulation of granulocytes and monocytes/macrophages at the site of inflammation. Activation of these cells leads to the release of degradative enzymes, e.g., proteinases and glycosidases, and the production of reactive oxygen metabolites. This has been shown both in animal models of experimental intestinal injury, and in human inflammatory bowel disease. Scavenging of oxygen radicals protected tissue from damage in experimental inflammation models. Human studies with specific oxygen radical scavengers are rare, preliminary results appear promising. The fact that the aminosalicylates used in the treatment of inflammatory bowel disease are potent antioxidants underscores the important role of reactive oxygen metabolites in this setting.
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In patients with inflammatory bowel diseases (IBD) the immune system leads to the polarization of intestinal immune cells towards a T helper one (Th1) pro-inflammatory response. The immunologic factors intervene in intestinal homeostasis and initiate the development of intestinal mucosal inflammation. Cytokines, which are important regulators of inflammation and repair as wells as leukocyte trafficking have become apparent as key immune molecules in the pathogenesis of IBD. In this review, recent advances in our understanding of the cytokine involvement in inflammation and repair in patients with ulcerative colitis (UC) and Crohn's disease (CD) are discussed. Knowledge of objective evidence of inflammatory activity may allow targeted treatment at an earlier stage to avoid the relapse, as well as assessment of new therapeutic strategies for maintenance of remission.
Inflammatory bowel disease (IBD) is a chronic condition that often presents in adolescence. The characteristic manifestations, exacerbations, and treatment of the disease affect the adolescent's physical, physiological, and psychological development. Body image, self-esteem, and dependence/independence issues may lead to noncompliance, further complicating the disease process and its management. This article will review IBD and present treatment options and interventions in the care of the adolescent with IBD.
The cause of the inflammatory bowel diseases Crohn's disease and ulcerative colitis is unknown, but epidemiological evidence suggests that it is multifactorial with a strong genetic component. Several genetic loci probably contribute to disease susceptibility, accounting for the complex pattern of inheritance and heterogeneous clinical manifestations. The combination of candidate gene studies and, more recently, genome-wide searches has resulted in the identification of a number of putative susceptibility loci. With large-scale, fine-mapping studies under way, and accelerating progress in the physical mapping of the human genome, rapid progress is now being made towards the identification of the genes responsible for inflammatory bowel disease.
Inflammatory bowel disease presents in various forms. Its increasing incidence indicates that modern lifestyle triggers disease in genetically susceptible individuals. We present a model for inflammatory bowel disease pathophysiology and review the new biological therapies available. These biological agents have been developed to antagonise the processes of pathogenic inflammation, such as the reduction in T-lymphocyte apoptosis, increase in T-lymphocyte proliferation and increase in T-lymphocyte trafficking into the intestinal mucosa. Inhibitors of various inflammatory cytokines, including some antagonists to tumour necrosis factor, are effective therapies for inflammatory bowel disease. However, this class is associated with the risk of rare, but serious, side-effects, such as opportunistic infections and demyelinating diseases. The administration of anti-inflammatory cytokines, including interleukin-10 and interleukin-11, may theoretically be effective in reducing inflammation, although the clinical development of some of these therapies has been terminated. The selective inhibition of the adhesion molecules involved in T-lymphocyte trafficking can be effective in reducing gut inflammation. Of the selective adhesion molecule inhibitors under investigation, natalizumab has demonstrated efficacy in inflammatory bowel disease. The future of biological therapy for inflammatory bowel disease shows promise.
The idiopathic inflammatory bowel diseases (IBD), comprised of Crohn's disease (CD) and ulcerative colitis (UC), are related, complex genetic disorders. With the completion of the human genomic sequence, identification of genetic variants contributing to IBD susceptibility can now more systematically be identified. Significant genetic linkages have been observed on chromosomes 16, 12, 14, 19, 6, and 1, of which the linkage to CD on chromosome 16 is the most well-established. For many of the other regions, evidence for linkage has been observed for both CD and UC. Candidate gene association studies have largely focused on genes involved in inflammatory pathways, such as cytokines and cytokine receptors. With greater understanding of genetic differences underlying both disease susceptibility and response to medical therapy, the individualization of medical approaches based on this knowledge may soon be possible in patients with IBD.
Diagnosis of chronic inflammatory bowel disease (IBD) in children requires noninvasive, atraumatic diagnostic tools that depict localization and acuity of inflammation and yield only a low radiation dose. This retrospective analysis evaluates the diagnostic potential of FDG-PET. Twenty-six consecutive FDG-PET scans of 23 patients (age: 2-16, years, 14 M, 9 F) with suspected IBD were analyzed in this retrospective study. Results were compared to endoscopic, histologic, and abdominal ultrasound (US) finding. In these examinations, presence of inflammation was evaluated in each patient in 8 bowel segments (score 1-4). Standardized uptake values (SUVs) for FDG-PET were measured for all segments. Sensitivity, specificity, and accuracy were calculated using histology as the standard of reference on a segment-based analysis (pathologic if inflammation score > or = 3 or SUV(max)/SUV(liver)>1.2). With histology as the standard of reference, FDG-PET showed a sensitivity/specificity/accuracy of 98%/68%/8%/3 as compared to endoscopy (90%/75%/82%) and US (56%/92%/75%). For the small bowel, FDG-PET was even more reliable (100%/86%/90%). Because of its high sensitivity and accuracy,FDG-PET is an excellent, noninvasive diagnostic tool for IBD. Depicting inflammation in the whole bowel, while being not traumatic, it is attractive for use especially in children. FDG-PET is especially reliable for the small bowel and can inform application of topical therapy.
In patients with inflammatory bowel disease (IBD), radiologic examinations are important for diagnosis and treatment. With conventional X-ray examinations, mucosal abnormalities, ulcers and fistulas can be visualised, but no information on the extramural extension of the disease can be obtained. Newer radiologic modalities (ultrasound, CT and MRI) offer new diagnostic possibilities. With ultrasound IBD can be diagnosed with good confidence and it can differentiate between Crohn's disease and ulcerative colitis. CT and MRI are indicated not so much to diagnose the disease but rather to determine the severity and spread of disease activity (transmural and extramural inflammation) and to detect complications such as fistulas and abscesses.
Inflammatory bowel disease (IBD) is a disease that affects women of childbearing age. Active disease at conception increases the risk for adverse outcomes and thus postponement of pregnancy until the disease is in remission is the best advice that physicians can give their IBD patients. The majority of medications used to treat IBD are safe in pregnancy and breastfeeding; active, untreated, or undertreated disease is more deleterious than active therapy.
The term "inflammatory bowel disease" includes ulcerative colitis, Leśniowski-Crohn's disease and indeterminate colitis. The history of these diseases in Poland began with Antoni Leśniowski, who in 1904 described an inflammatory tumour of the small intestine with a fistula to ascending colon. The first contemporary clinical descriptions of the main forms of inflammatory bowel disease emerged after 1960, and were made by Warsaw groups and a surgical group from Poznań. The major contributions of Polish investigators to the development of knowledge about ulcerative colitis and Leśniowski-Crohn's disease were made in the fields of immunology and genetics and in studies on kallikrein-kinin and haemostasis systems. The investigators of pathogenetic mechanisms in these diseases come from departments of gastroenterology in Warsaw, Lublin, Gdańsk and Sosnowiec.