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PubMed2004

Emerging biologic therapies in inflammatory bowel disease.

Ulcerative colitis and Crohn's disease, the idiopathic inflammatory bowel diseases (IBD), are thought to represent genetically determined, dysregulated immune responses to otherwise innocuous luminal antigens. Although progress in research has advanced our understanding of the immunopathogenesis and begun to elucidate genetic contributions toward susceptibility, limitations of current medical approaches continue to drive the search for better therapeutic agents. Most recently, the introduction of infliximab has heralded a new era of evolving biologically targeted treatments for IBD. Infliximab is currently the only biologic agent approved for the treatment of inflammatory and fistulizing Crohn's disease, but ongoing research continues to generate new biologic agents targeted at specific pathogenic mechanisms involved in the inflammatory process. Undoubtedly, with the success of infliximab, the role of biologic therapy will continue to expand in the future treatment of IBD.

Antibodies, Monoclonal↗
PubMed2006

Advances and perspectives in the genetics of inflammatory bowel diseases.

Several clinical and biological phenotypes define complex diseases such as inflammatory bowel disease (IBD). There is a critical role of the caspase recruitment domain protein 15/nucleotide-binding oligomerization protein 2-dependent (CARD15-NOD2) sensing of bacterial cell wall components in health and disease. The current etiologic model for IBD emphasizes an interaction between susceptibility and modifier genes along with environmental factors. Together, these lead to disease progression. However, further work should clarify the pathophysiological mechanisms leading to IBD and how innate immune signaling confers susceptibility to intestinal inflammation. This is a prerequisite for rational clinical management of IBD. Genetic, functional, serologic testing and development of therapeutics in IBD are discussed.

Crohn Disease↗
PubMed2003

[Inflammatory Bowel diseases in the elderly].

Although often regarded as a disease of young adults, Inflammatory Bowel Disease occurs with greater frequency in the elderly than is generally anticipated. Due to the comorbidity in the elderly, the precise diagnosis of Inflammatory Bowel Disease is overlooked. There is a tendency for both Crohn's disease and ulcerative colitis to involve the distal colon in older patients. As a consequence, the disease is often milder and less complicated than in younger patients. The first wave of the disease in an older age group is characterized by a higher complication rate. The treatment modalities are the same as in the younger age groups. The disease is often overlooked and misdiagnosed. However, since it is a treatable condition, the clinician has to be more suspicious about it in the cases of prolonged diarrhea or other gastrointestinal symptoms in the elderly.

Adult↗
PubMed1997

Factors influencing the relapse of patients with inflammatory bowel disease.

The management of relapse of inflammatory bowel disease (IBD) remains a clinical challenge and a relatively neglected area of current research. Many factors contribute to relapse, and the proper identification of the cause of each case may influence optimal management. Often, relapse is related to the failure of maintenance therapy. Mesalamine sensitivity is difficult to recognize and should be considered when increased doses are associated with the worsening of symptoms. An increase in eosinophil activity could explain seasonal relapses of IBD as a result of exposure to allergens, but other eosinophil activation pathways also will influence the course of IBD. Infection, either enteric or systemic, may trigger a relapse by activating the gastrointestinal mucosal immune system. Nonsteroidal anti-inflammatory drug use is a well-recognized cause of exacerbation of disease. Smoking status is emerging as a complex factor in IBD, and a change in smoking status may influence the course of IBD.

Acute Disease↗
PubMed2003

High prevalence of fatigue in quiescent inflammatory bowel disease is not related to adrenocortical insufficiency.

OBJECTIVES: Inflammatory bowel disease (IBD) patients, with active as well as quiescent disease, frequently complain of fatigue. This often has consequences for patients' work and daily lives. The primary aim of this study was to assess the prevalence and severity of fatigue in IBD patients in remission. Furthermore, we studied the correlation between fatigue and disease activity, quality of life, and biochemical and hematological test results, and the role of (secondary) hypocortisolism. METHODS: Eighty subjects with proven IBD were included. Disease activity was assessed using the Clinical Activity Index for Ulcerative Colitis and the Crohn's Disease Activity Index. Quality of life was measured by the Inflammatory Bowel Disease Questionnaire, and fatigue was assessed using the Multidimensional Fatigue Inventory (MFI). Routine biochemical and hematological tests were performed, and basal cortisol was determined. To evaluate adrenocortical reserve in subjects with a cortisol level of <0.4 micromol/L, a low dose adrenocorticotrophin hormone test was performed. Healthy age- and sex-matched subjects (n = 67) served as controls. RESULTS: More than 40% of the IBD patients in remission suffered from fatigue. Mean MFI scores of the IBD patients were comparable to mean MFI scores reported in cancer patients. The Inflammatory Bowel Disease Questionnaire showed a negative correlation with the MFI (r = -0.735; p < 0.001). No correlation was found between fatigue and basal cortisol levels or other laboratory parameters. CONCLUSION: Fatigue is an important feature in IBD in remission, adversely affecting the quality of life. It does not, however, affect all patients, nor does it seem to be the result of hypocortisolism.

Adrenal Insufficiency↗
PubMed1988

Aberrant expression of monoclonal antibody-defined colonic mucosal antigens in inflammatory bowel disease.

Human proximal colon from patients with inflammatory bowel disease and from controls was studied by two techniques to detect tumor-associated antigen expression. A panel of four murine monoclonal antibodies that recognize tumor-associated antigens was used to test purified colonic mucins for epitope expression by radioimmunoassay and to test formalin-fixed, deparaffinized sections of colon by the immunoperoxidase technique. The panel included monoclonal antibodies 19-9, B72.3, DU-PAN-2, and CSLEX1. Colonic mucins were purified from uninvolved surgical specimens by gel filtration with Sepharose 4B and cesium chloride-guanidine hydrochloride density gradient ultracentrifugation. Purified mucins from uninvolved colonic mucosal specimens from 4 of 7 patients with ulcerative colitis expressed one or more of these epitopes by radioimmunoassay, whereas mucins from 6 disease controls did not. Reactivity patterns were heterogeneous. Immunoperoxidase testing demonstrated staining with two or more antibodies in 14 of 18 involved inflammatory bowel disease segments, whereas control sections rarely stained with these antibodies, with the exception of 19-9. Sections of uninvolved mucosa from 4 of 9 patients with ulcerative colitis stained with two or more antibodies. Staining patterns were heterogeneous. The results demonstrate that colonic expression of tumor-associated epitopes occurs frequently in involved segments from both patients with ulcerative colitis and with Crohn's disease, whereas only patients with ulcerative colitis frequently expressed these epitopes in uninvolved segments.

Antibodies, Monoclonal↗
PubMed2006

Review article: interactions between genotype and response to therapy in inflammatory bowel diseases.

BACKGROUND: More than half of the patients with inflammatory bowel diseases are candidates for immunosuppressive therapy. However, even the most effective drugs used in inflammatory bowel disease are only successful in about two-thirds of patients. Adverse events limit their use in a further substantial proportion of patients. Recent research has focussed on the possibility of predicting a drugs' efficacy and/or toxicity by identifying polymorphic variants in the genes encoding enzymes involved in metabolic pathways. AIM: To highlight recent advances and limitations in the field of pharmacogenetics in inflammatory bowel disease. RESULTS: Recent pharmacogenetic studies have mainly focussed on immunosuppressive agents including corticosteroids, azathioprine, methotrexate and infliximab. Several polymorphic genes encoding enzymes involved in the metabolism of these drugs have been identified including the inosine triphosphate pyrophosphatase in thiopurine therapy, the methylene tetrahydrofolate reductase in methotrexate therapy and polymorphisms in apoptosis genes in infliximab therapy. However, at the present time, genotyping for the variants of the thiopurine methyltransferase gene, an enzyme important for the metabolism of the thiopurine drugs, is the only useful test in clinical practice. CONCLUSIONS: Although the field of pharmacogenetics in inflammatory bowel disease is promising most new targets have so far failed to translate into clinical practice. Future pharmaceutical trials should include pharmacogenetic research to test appropriate candidate genes in a prospective manner.

Anti-Inflammatory Agents↗
PubMed1993

Cluster of inflammatory bowel disease in three close college friends?

Although the etiology of inflammatory bowel disease remains unknown, current evidence favors the interplay of genetic predisposition with environmental factors. Clustering of inflammatory bowel disease in spouses had been described, and supports a role for an environmental agent. We describe three unrelated, unmarried men all attorneys who enjoyed a close, sustained friendship in college, and who within a decade of their contact developed inflammatory bowel disease. We describe the nature of their college contact, the course of their inflammatory bowel disease, and relate our cluster to the scanty literature on clustering in inflammatory bowel disease. Physicians should report similar observations to illuminate the roles of genetics and environment in the development of these illnesses.

Adult↗
PubMed1997

[Tc-99m labeled leukocyte scintigraphy and CT for the evaluation of patients with inflammatory bowel disease].

Seventeen cases (11 patients) of inflammatory bowel disease (IBD) were studied to define the intensity and extent of disease by 99mTc-HMPAO-labeled leukocytes scintigraphy (TLLS), and 10 cases underwent CT examination to evaluate the bowel wall, lymph-nodes, and mesenteric surroundings. Serial TLLS were obtained up to 4 hours and CT was carried out within one week before or after TLLS. The sensitivities of early (1 hour) and delayed (4 hours) TLLS were 91% and 100%, respectively. The respective specificities were 100% and 33%. However, it appeared that mild IBD may yield false negative results in early TLLS while non-specific bowel activity and migration of white cells may cause false positive results in delayed imaging. By setting the diagnostic criteria for labeled leukocyte accumulation on visualization of the small bowel regardless of uptake or activity of the large bowel similar to or greater than lumbar bone marrow, the sensitivity and specificity of delayed TLLS changed to 91% and 83%, respectively. On CT examination, mesenteric lymph-node swelling, periintestinal blurring and dilatation of mesenteric vasa recta were observed in all five patients with active Crohn's disease, while wall thickening and enhancement were seen in four of them. None of the other three cases of inflammatory disease showed positive findings of dilatation of the mesenteric vasa recta, and they revealed relatively low uptake of labeled leukocytes in TLLS. A "scintigram score" was calculated by comparing uptake of tracer in five bowel segments with lumbar bone marrow activity, and a "CT score" was calculated by adding abnormalities of the intestine and mesenteric surroundings. The scintigram score correlated closely with CT score and clinical disease activity. Combined use of CT and TLLS for the evaluation of patients with IBD was an excellent means to obtain the findings of intensity and extent of disease of the bowel wall and mesenteric surroundings and provided useful information in determining the patient management.

Adolescent↗
PubMed2004

Lower prevalence of Helicobacter pylori infection in patients with inflammatory bowel disease but not with chronic obstructive pulmonary disease - antibiotic use in the history does not play a significant role.

BACKGROUND: Patients with inflammatory bowel disease have lower prevalence of Helicobacter pylori infection, but the exact reason for this is not yet clear. AIM: To examine whether the antibiotics frequently used in inflammatory bowel disease are responsible for the lower prevalence of H. pylori infection. Patients with chronic obstructive pulmonary disease on prolonged previous antibiotic therapy were used for comparison. METHODS: Presence/absence of H. pylori infection was detected by a (13)C-urea breath test in 133 patients with inflammatory bowel disease (82 ulcerative colitis, and 51 Crohn's disease) and compared with that of 135 patients with chronic obstructive pulmonary disease and with two age-matched control groups (200 patients each). Primary disease location, duration of disease and detailed analysis of previous and current medication (dose and duration of antibiotics, steroids, 5-aminosalicylic acid) were analysed in each cases. RESULTS: Seventeen of the 133 patients with inflammatory bowel disease [12.2% (10/82) of ulcerative colitis and 13.7% (7/51) of Crohn's disease] and 90/135 patients with chronic obstructive pulmonary disease (66.7%) were positive for H. pylori. A total of 78/200 (39%) for the inflammatory-bowel-disease-group-matched controls and 110/210 (55%) for the chronic-obstructive-pulmonary-disease-matched controls were positive for H. pylori. The history of any antibiotic or steroid therapy had no influence on H. pylori status of patients with inflammatory bowel disease. CONCLUSION: The prevalence of H. pylori compared to the age-matched controls is significantly lower in patients with inflammatory bowel disease but not in those with chronic obstructive pulmonary disease. Antibiotic use is not responsible for the lower prevalence of H. pylori infection in patients with inflammatory bowel disease.

Adolescent↗
PubMed1978

Total parenteral nutrition in inflammatory bowel disease.

Nutritional depletion is a common feature of inflammatory bowel disease. The advent of total parenteral nutrition (TPN) has allowed nutritional repletion or maintenance while total bowel rest is achieved. The experience with total parenteral nutrition in inflammatory bowel disease is varied; our recommendations for use of total parenteral nutrition in specific situations are presented with a description of the techniques for administration in patients with inflammatory bowel disease.

Child↗
PubMed1998

Therapeutic implications of interleukin-10 in inflammatory bowel disease.

Enhanced production of proinflammatory cytokines has been described in inflammatory bowel disease. The effect of interleukin (IL)-10, a cytokine with antiinflammatory activity, or anti-IL-10, on cytokine production by cultured colonic mucosa or blood mononuclear cells from patients with active inflammatory bowel disease was evaluated. Addition of IL-10 to the culture medium of colonic tissues or blood mononuclear cells resulted in inhibition of both IL-1 beta and tumor necrosis factor-alpha production and augmentation of IL-1 receptor antagonist production. Conversely, neutralization of endogenous IL-10 was found to augment both tumor necrosis factor-alpha and IL-1 beta production and inhibit IL-1 receptor antagonist production. In addition, the production of IL-10 by mononuclear cells was suppressed by prednisolone. In conclusion, IL-10 and related molecules may be useful in the treatment of inflammatory bowel disease.

Anti-Inflammatory Agents↗
PubMed2005

HLA-DRB1 alleles may influence disease phenotype in patients with inflammatory bowel disease: a critical reappraisal with review of the literature.

PURPOSE: The HLA region has been implicated in determining the disease susceptibility or the clinical phenotype of inflammatory bowel disease. The aim of this study was to assess the relation between HLA-DRB1 alleles with the clinical features of Crohn's disease and ulcerative colitis and the presence of anti-neutrophil cytoplasmic and anti-Saccharomyces cerevisiae antibodies. METHODS: Blood samples were obtained from 102 Crohn's disease patients, 114 ulcerative colitis patients, and 264 unrelated healthy controls. Anti-neutrophil cytoplasmics were detected by a standard immunofluorescence method, and anti-Saccharomyces cerevisiaes were examined by an enzyme-linked immunosorbent assay immunoglobulin G/immunoglobulin A commercial assay. HLA-DRB1 typing of 26 alleles was performed by polymerase chain reaction sequence-specific primes. Patients were phenotyped according to gender, disease location, extent, and behavior, surgical resection, need of steroid, and anti-neutrophil cytoplasmic/anti-Saccharomyces cerevisiae status. RESULTS: As a whole, after applying Bonferroni's correction for multiple comparisons, no significant association of HLA-DRB1 alleles with Crohn's disease or ulcerative colitis was found. After stratifying HLA-DRB1 alleles by clinical phenotypes of patients with ulcerative colitis, an excess of DRB1*1309*1320*1325*1329 allele (DR13) was found in conjunction with pancolitis (P < 0.0001), surgical resection (P < 0.0003), and extraintestinal manifestations (P < 0.0001). In Crohn's disease patients, an excess of DRB1*0304*0305*0307*0309 allele (DR3) was found in those with colonic disease (P < 0.0001) and patients with extraintestinal manifestations (P = 0.0003). This statistical association, however, emerged in only 3 of 114 patients with ulcerative colitis and in 3 of 102 patients with Crohn's disease. We found no association with the presence of anti-Saccharomyces cerevisiae or anti-neutrophil cytoplasmic. CONCLUSIONS: Some clinical features of Crohn's disease and ulcerative colitis may be influenced by specific HLA-DR alleles; in particular, in ulcerative colitis some alleles appear to segregate with more aggressive disease, whereas in Crohn's disease different alleles cosegregate in patients with colonic disease and extraintestinal manifestations.

Adolescent↗
PubMed2002

Acute surgical emergencies in inflammatory bowel disease.

BACKGROUND: Acute surgical emergencies in patients with inflammatory bowel disease may carry a substantial morbidity, but fortunately today, a low mortality. The aim of this review is to delineate the treatment of acute surgical emergencies that occur in patients with ulcerative colitis and Crohn's disease. METHODS: Suitable English language reports were identified using PubMed search. RESULTS: Inflammatory bowel disease can present in numerous ways as an acute surgical emergency. These include toxic colitis, hemorrhage, perforation, intra-abdominal masses or abscesses with sepsis, and intestinal obstruction. Toxic colitis and perforation are best managed with intestinal resection and fecal diversion. Hemorrhage in ulcerative colitis initially requires colectomy with rectal preservation and ileostomy. In Crohn's disease hemorrhage is often focal and localization and segmental resection are performed. Intra-abdominal abscesses should initially be attempted by computed tomography-guided percutaneous drainage followed subsequently by definitive resection. Perianal disease requires abscess drainage with minimal tissue trauma. Intestinal obstruction should be initially managed nonoperatively, with surgery reserved for complete obstruction or intractability. CONCLUSIONS: Acute surgical emergencies in patients with inflammatory bowel disease are rare and can have a high morbidity. With a multidisciplinary approach, morbidity can be reduced and patients can have a rapid return and improved quality of life.

Abdominal Abscess↗
PubMed2005

Recent advances in the genetics of inflammatory bowel disease.

PURPOSE OF REVIEW: This review addresses recent advances in the mapping and characterization of susceptibility genes for inflammatory bowel disease. The article discusses current information on the relation between CARD15 variants and Crohn disease and the discoveries of SLC22A4/SLC22A5 and DLG5 gene variants that also confer risk for inflammatory bowel disease. RECENT FINDINGS: Much of the recent emphasis in inflammatory bowel disease genetics research has been directed at evaluation of candidate disease susceptibility genes within inflammatory bowel disease linkage intervals. Such studies have elucidated associations of numerous gene variants with inflammatory bowel disease, but most of these require further replication and functional validation. Dissection of the molecular events coupling CARD15 mutation to Crohn's disease has also been intensively investigated and, while not resolved as of yet, has significantly advanced understanding of the intestinal immune response to microbial challenge. SUMMARY: The application of genetic information to diagnosis and risk prediction in inflammatory bowel disease will require comprehensive knowledge of the relevant susceptibility alleles. However, the genetic data accrued in recent years have already provided major insight into the pathophysiology of inflammatory bowel disease and identified a number of potential molecular targets for therapeutic intervention.

Genetic Linkage↗
PubMed1996

Mediators of inflammation in chronic inflammatory bowel disease.

A distinguishing feature of inflammatory bowel disease (IBD) is its apparently spontaneous, chronic relapsing course. Despite extensive research over several decades the etiology of IBD remains unknown, but evidence has accumulated to suggest that the mucosal inflammatory response may be caused by (i) a defective mucosal barrier function resulting in an abnormally increased exposure to luminal antigens and toxins, (ii) an appropriate immunologic response to an unusual infection, antigen or toxin, or (iii) an inappropriate immunological response to ubiquitous antigens or stimuli. In recent years, the identification of established and potential mediators of inflammation has expanded to include eicosanoids, platelet activating factor, biogenic amines, kinins, complement-derived peptides, chemotactic peptides, cytokines, neuropeptides, and reactive metabolites of oxygen and nitrogen. Thus, the study of the inflammatory process has become ever more complex. Until the predisposing and trigger factors have been identified the achievement of a more rational and effective approach to therapy in IBD relies on interruption of the mechanisms responsible for excess mediator formation. As summarized in this review on the role of soluble mediators of inflammation, several Danish gastroenterologists have been profoundly engaged in basic and clinical research in the past 25 years to place some pieces of the confusing puzzle of IBD.

Colitis, Ulcerative↗
PubMed1983

111Indium autologous leucocytes in inflammatory bowel disease.

A non-invasive method of imaging and assessing inflammatory bowel disease is described. 111Indium labelled leucocyte scans were performed on 33 patients with a wide variety of inflammatory bowel diseases and 25 control patients. All patients with moderate or severe inflammatory bowel disease had positive scans with localisation of abnormal activity corresponding to the sites assessed to be diseased by radiology in either small or large bowel. No false positives were recorded in the control patients. Faecal excretion of 111In labelled leucocytes was increased in patients with inflammatory bowel disease according to disease severity and correlated with disease activity assessed by serum C-reactive protein levels (r = 0.74, p less than 0.001) or in those patients with Crohn's disease by Crohn's Disease Activity Index (r = 0.78, p less than 0.001). These data suggest that 111In labelled leucocytes may be used to provide a safe, non-invasive method of imaging diseased bowel and objectively assessing disease activity.

Colitis, Ulcerative↗
PubMedDate not supplied

Increasing rates and changing patterns of hospital admissions for patients with inflammatory bowel disease in Ireland: 1996-2001.

BACKGROUND: The inflammatory bowel diseases require frequent hospital visits. The literature suggests that the incidence of IBD may be increasing. AIM: To investigate the pattern of admissions of patients with inflammatory bowel disease (IBD) to hospital over a five-year period (between 1996 and 2001). METHODS: We obtained national data regarding admission rates for patients with IBD from the Economic and Social Research Institute (ESRI) during the years 1996 and 2001. Local data were gathered from the Hospital In-Patient Enquiry (HIPE) scheme for the same years. RESULTS: Over this five-year period, there has been a substantial increase in the rate of admission with IBD (58% for Crohn's disease and 25% for ulcerative colitis), in particular in the number of day-case admissions for patients with Crohn's disease (125%). There has been little change in the number of patients undergoing surgery for their disease (Crohn's disease; 24% vs 20% and Ulcerative colitis; 17% vs 16.6%) and in the length of hospital stay. CONCLUSION: Despite an increase in the rate of admission with IBD, there has been little change in the rates of surgical intervention and length of stay. The most dramatic increase was seen in the day-case admissions for patients with Crohn's disease and may reflect the use of anti-TNFalpha (infliximab) in the treatment of this disease.

Adolescent↗