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PubMed2005

The bioavailability of oral methotrexate in children with inflammatory bowel disease.

OBJECTIVES: Methotrexate is used to treat patients with inflammatory bowel disease. Although no available pharmacologic data support the assumption that the bioavailability of methotrexate is diminished in patients with inflammatory bowel disease, most such patients receive methotrexate parenterally. METHODS: The oral bioavailability of methotrexate was determined in 11 pediatric patients being treated with methotrexate for inflammatory bowel disease. Serial plasma methotrexate concentrations were determined after equal subcutaneous and oral doses of methotrexate. RESULTS: The mean bioavailability of methotrexate in patients with inflammatory bowel disease was 84% +/- 38%. Interpatient variability in drug exposure was similar after oral and subcutaneous administration. CONCLUSIONS: The bioavailability of methotrexate in patients with inflammatory bowel disease is no different from that observed in other disease states. Subcutaneous administration of methotrexate does not appear to decrease the interpatient variability in drug exposure. There is no sound pharmacologic basis for favoring administration of methotrexate via the subcutaneous route for patients with inflammatory bowel disease.

Administration, Oral↗
PubMed2001

Nutrition in inflammatory bowel disease: impact on disease and therapy.

Nutritional derangements are frequent in inflammatory bowel disease. In the last year, significant work was published examining the mechanisms of impaired food intake in animal models of inflammatory bowel disease, which allow a better understanding of these processes. These data have shed new light on the relative role of underfeeding and inflammation on the growth retardation associated with intestinal inflammation. Other studies have provided further information on the risk factors and predictive biomarkers of bone loss in patients with inflammatory bowel disease. The potential role of enteral nutrition as primary therapy for Crohn disease is particularly addressed in the present review. Recent contributions emphasized the special importance of this therapeutic modality in pediatric patients, but the possible mechanisms for such therapeutic effect are still not well understood. Other nutrients may have a therapeutic potential in inflammatory bowel disease. In particular, recent data on the in vivo antiinflammatory action of butyrate merit special mention. Finally, novel nutritional therapeutic strategies for inflammatory bowel disease, such as transforming growth factor-beta2-enriched enteral feeding or hydrothermally processed cereals, have recently been explored.

Journal Article↗
PubMed2007

Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease.

BACKGROUND: Mouse models of inflammatory bowel diseases (IBD) are used to unravel the pathophysiology of IBD and to study new treatment modalities, but their relationship to Crohn's disease (CD) or ulcerative colitis (UC) is speculative. METHODS: Using Agilent mouse TOX oligonucleotide microarrays, we analyzed colonic gene expression profiles in three widely used models of experimental colitis. In 2 of the models (TNBS and DSS-induced colitis), exogenous agents induce the colitis. In the third model the colitis is induced after transfer of a T-cell population (CD4(+)CD45RB(high) T cells) that lacks regulatory cells into an immunodeficient host. RESULTS: Compared with control mice, in DSS, TNBS, and the CD45RB transfer colitis mice, 387, 21, and 582 genes were more than 2-fold upregulated in the intestinal mucosa. Analyses of exclusively shared gene expression profiles between the different models revealed that DSS/transfer colitis share 69 concordantly upregulated genes, DSS/TNBS 6, and TNBS/transfer colitis 1. Seven genes were upregulated in all three models. The CD45RB transfer model expression profile included the most genes that are known to be upregulated in IBD. Of 32 genes that are known to change transcriptional activity in IBD (TNF, IFN-gamma, Ltbeta, IL-6, IL-16, IL-18R1, IL-22, CCR2, 7, CCL2, 3, 4, 5, 7, 11, 17, 20, CXCR3, CXCL1, 5, 10, Mmp3, 7,9, 14, Timp1, Reg3gamma, and Pap, S-100a8, S-100a9, Abcb1, and Ptgs2), 2/32 are upregulated in TNBS, 15/32 are upregulated or downregulated in DSS and 30/32 are upregulated or downregulated in the CD45RB transfer colitis. CONCLUSION: The pattern of gene expression in the CD45RB transfer model most closely reflects altered gene expression in IBD.

Animals↗
PubMed2002

Treatment with neurokinin-1 receptor antagonist reduces severity of inflammatory bowel disease induced by Cryptosporidium parvum.

Inflammatory bowel disease (IBD) is a chronic, debilitating disorder of uncertain and perhaps multiple etiologies. It is believed to be due in part to disregulation of the immune system. Neuroimmune interactions may be involved in induction or maintenance of IBD. In the present study, we examined the potential role of a neurotransmitter, substance P, in a mouse model of IBD. We found that binding sites for substance P, and more specifically, neurokinin-1 receptors, were upregulated in intestinal tissue of mice with IBD-like syndrome. Dosing of mice with LY303870, a neurokinin-1 receptor antagonist, reduced the severity of IBD, and treatment of mice with preexisting IBD allowed partial healing of lesions. We hypothesize that blocking the binding of substance P to the neurokinin-1 receptor interrupts the inflammatory cascade that triggers and maintains intestinal lesions of IBD.

Animals↗
PubMed2001

Prothrombotic inherited abnormalities other than factor V Leiden mutation do not play a role in venous thrombosis in inflammatory bowel disease.

OBJECTIVES: Because the incidence of thromboembolism is increased in patients with inflammatory bowel disease, we attempted to assess the role of prothrombotic inherited coagulation abnormalities in the development of thrombosis. METHODS: Four populations were compared: 15 patients with inflammatory bowel disease and a previous venous thrombosis, 58 control patients with inflammatory bowel disease but without thrombosis, 110 patients without inflammatory bowel disease but with previous deep venous thrombosis, and 84 healthy subjects. Inherited and acquired risk factors of venous thrombosis, e.g., factor V Leiden and prothrombin 20210A mutations, C677T methylenetetrahydrofolate reductase polymorphism, a polymorphism located in exon 13 of factor V gene, inflammatory and hypercoagulability markers were studied in each population. RESULTS: In the study, 14.3% of thrombotic patients with inflammatory bowel disease had factor V Leiden mutation versus 0% of control patients with inflammatory bowel disease (p = 0.04), 15.5% of thrombotic patients without inflammatory bowel disease (NS) and 3.6% of the healthy controls. A total of 14% of thrombotic patients with inflammatory bowel disease and 11.8% of thrombotic patients without inflammatory bowel disease carried prothrombin 20210A mutation, compared to 1.7% of control patients with inflammatory bowel disease; however, the difference was just below significance. Other inherited coagulation abnormalities were not statistically significantly different among the four populations. CONCLUSIONS: Our study confirms that factor V Leiden mutation increases the risk for thrombotic events but is not more frequent in patients with inflammatory bowel disease. Our results do not support the role of other thrombotic risk factors.

Adult↗
PubMed2002

Homing of mucosal lymphocytes to the liver in the pathogenesis of hepatic complications of inflammatory bowel disease.

Primary sclerosing cholangitis is strongly linked to inflammatory bowel disease, but any model to explain the development of primary sclerosing cholangitis must take into account the fact that it usually runs a course independent from inflammation in the bowel, illustrated by the fact that this disease can develop many years after proctocolectomy. Thus, liver disease can develop in the absence of a diseased colon and cannot be explained solely by release of toxic factors from the inflamed gut. We propose the existence of an enterohepatic circulation of lymphocytes, whereby some mucosal lymphocytes generated in the gut during active inflammatory disease subsequently persist as longlived memory cells capable of recirculation through the liver. Under the right conditions, these dual-homing lymphocytes might become activated in the liver resulting in hepatic inflammation that is independent from inflammation in the gut. Recent reports that some lymphocyte homing-receptors are shared by the liver and gut provide a molecular basis for this hypothesis and explain the distribution of extraintestinal disease in inflammatory bowel disease.

Cell Adhesion Molecules↗
PubMed1994

Sonography of inflammatory bowel disease: findings and value in differential diagnosis.

OBJECTIVE: Inflammatory bowel diseases produce segmental or diffuse mural thickening of the intestine that can be detected and evaluated by using sonography. The purpose of this study was to evaluate the sonographic findings and determine their diagnostic value in patients with inflammatory bowel diseases. MATERIALS AND METHODS: We reviewed sonograms of 81 patients with inflammatory bowel diseases. The findings were compared with those of barium study, colonoscopy, and surgery. Forty-five patients had tuberculous enterocolitis, 13 had ulcerative colitis, eight had Crohn's disease, five had ischemic colitis, two had Behçet's syndrome, and eight had unspecified colitis. Diagnosis was based on surgical and pathologic findings in 23; results of barium study and endoscopic biopsy in 20; and results of barium study, colonoscopic findings, and clinical findings in 38. RESULTS: Seventy-two patients (89%) had sonograms that showed segmental or diffuse mural thickening and a paucity of luminal content in the involved bowel. Involved areas were the ileocecal region in the cases of tuberculous enterocolitis and Behçet's syndrome, the left side of the colon in ulcerative colitis, and the colon and terminal part of the ileum in Crohn's disease. In ischemic colitis, the distribution of involved bowel was nonspecific. Sonographic findings correlated well with the findings of barium enema or colonoscopy in terms of the involved segments of the bowel. Mesenteric lymphadenitis, omental thickening, and ascites were frequently observed in cases of tuberculous enterocolitis. CONCLUSION: Sonographic evidence of mural thickening of the bowel with a paucity of luminal content may be helpful in the detection of inflammatory bowel diseases. However, the findings are nonspecific, and the differential diagnosis must be related to the specific segment of the bowel involved.

Barium Sulfate↗
PubMed1998

Myeloperoxidase concentrations in the stool as a new parameter of inflammatory bowel disease.

Neutrophils play a predominant role in inflammatory and immune reactions in inflammatory bowel disease. It is well established that the level of myeloperoxidase, a constituent of neutrophil azurophil granules, reflects the number of neutrophil. We examined the usefulness of determining stool levels of myeloperoxidase in patients with inflammatory bowel disease. Myeloperoxidase levels in stool extracts were measured using a radio-immunoassay in 33 patients with ulcerative colitis, 32 with Crohn's disease, 9 inflammatory disease controls and 15 normal controls. Stool levels of myeloperoxidase in active inflammatory bowel disease patients increased significantly, and correlated with laboratory parameters and endoscopic grade of inflammation. A paired analysis showed a decrease in myeloperoxidase levels after the resolution of disease exacerbation. These results suggest that stool myeloperoxidase is a simple, noninvasive, and relevant marker of disease activity.

Adolescent↗
PubMed1996

Current medical therapy for inflammatory bowel disease.

Traditional medical therapy for inflammatory bowel disease (IBD) includes corticosteroids and sulfasalazine. In recent years, several mesalamine derivatives of sulfasalazine have become available. These allow delivery of increased dosages of active medication with minimal side effects. Newer steroid preparations, all investigational at this point, likely will offer efficacy similar to that of prednisone but with an improved side effect profile. Immunosuppressive agents, including 6-mercaptopurine, azathioprine, and likely also methotrexate, are beneficial in treating refractory IBD, particularly in patients with chronic steroid dependence. Cyclosporine has been shown to be remarkably effective in delaying colectomy for severe ulcerative colitis, but its long-term role remains uncertain.

Administration, Topical↗
PubMed2003

Cytokine and anti-cytokine therapies for inflammatory bowel disease.

Although the pathogenesis of inflammatory bowel disease (IBD) remains elusive, it appears that there is chronic activation of the immune and inflammatory cascade in genetically susceptible individuals. Current disease management guidelines have therefore focused on the use of anti-inflammatory agents, aminosalicylates and corticosteroids. These conventional therapies continue to be a first choice in the management of IBD. Immunomodulators, such as azathioprine, 6-mercaptopurine, methotrexate or cyclosporin, are demonstrating increasing importance against steroid-resistant and steroid-dependent patients. However, some patients are still refractory to these therapies. Recent advances in the understanding of the pathophysiological conditions of IBD have provided new immune system modulators as therapeutic tools. Other immunosuppressive agents including FK506 and thalidomide have expanded the choice of medical therapies available for certain subgroups of patients. Furthermore, biological therapies have begun to assume a prominent role. Studies with chimeric monoclonal anti-TNF-alpha antibody treatment have been reported with dramatic successes. However, observations in larger numbers of treated patients are needed to explicate fully the safety of or risks posed by this agent such as developing lymphoma, or other malignancies. Another anti-inflammatory cytokine-therapy includes anti anti-IL-6R, anti-IL-12 or toxin-conjugated anti IL-7R, recombinant cytokines (IL-10 or IL-11). Given the diversity of proinflammatory products under its control, NF-kappaB may be viewed as a master switch in lymphocytes and macrophages, regulating inflammation and immunity. Although some of them still need more confirmatory studies, those immune therapies will provide new insights into cell-based and gene-based treatment against IBD in near future.

Adjuvants, Immunologic↗
PubMedDate not supplied

Therapeutic potential of infliximab in inflammatory bowel disease.

Traditional treatment approaches for patients with inflammatory bowel disease involve 1) pharmacologic management with aminosalicylates, corticosteroids, immunomodulatory agents, and antibiotics; and 2) nonpharmacologic management by surgical and dietary means. Complications and inadequate responses to current treatment modalities have resulted in the development of new and more specific biologic therapies. The proinflammatory cytokine tumor necrosis factor alpha (TNF alpha) is present in elevated concentrations in patients with inflammatory bowel disease; therefore, it has been targeted for treatment approaches. Infliximab is a chimeric, monoclonal antibody to TNF alpha developed to inhibit the interaction of TNF alpha with its receptor, to result in amelioration of inflammation. This biologic agent has received the most attention and is the most studied of those for the treatment of patients with Crohn's disease. This article reviews the symptoms of inflammatory bowel disease, the traditional treatment approaches used, the role of TNF alpha in disease pathogenesis, and the value of infliximab in treatment.

Antibodies, Monoclonal↗
PubMed2002

[Changes in cell kinetics and clinical course in inflammatory bowel diseases].

INTRODUCTION: The pathogenesis of inflammatory bowel diseases is still unknown, but is accessible from several ways. One possibility is the immunohistochemical analysis of cellular changes in the intestinal mucosa. The increased epithelial cell turnover is connected with false immunological pathways in the subepithelial layer. Behind these disturbances which can lead to chronic remitting inflammatory processes the imbalance of apoptosis and proliferation plays a key role. AIM: Of this study is to summarize our current knowledge of the cell kinetical alterations considering histological activity of disease. CONCLUSIONS: On the basis of current understanding it is known that the apoptosis and proliferation of epithelial cells increase in active inflammation compare to normal, although an uniform standpoint of evaluating is still missing. Some alterations of apoptosis and antigen presentation are described in the mononuclear cells of the subepithelial layer. Getting acquainted with and describing the changes of cell kinetics provide facilities to develop new and effective diagnostical methods and therapies.

Apoptosis↗
PubMed2002

Allium sativum (garlic) suppresses leukocyte inflammatory cytokine production in vitro: potential therapeutic use in the treatment of inflammatory bowel disease.

BACKGROUND: Cytokines involved in inflammatory bowel disease (IBD) direct a predominantly cell-mediated T- helper-1 (Th1) immune response. The nonspecific anti-inflammatory treatment being used in the management of patients with IBD has not changed much since the 1970s and new therapeutic agents are keenly sought. Several compounds isolated from Allium sativum (garlic) modulate leukocyte cell proliferation and cytokine production. METHODS: To investigate the possible therapeutic effects of garlic in the treatment of patients with IBD, whole blood and peripheral blood mononuclear cells (PBMCs) were stimulated in the presence of various concentrations of garlic extract and the effect on leukocyte cytokine production was determined in vitro using multiparameter flow cytometry. RESULTS: Monocyte interleukin (IL)-12 production was inhibited significantly in the presence of low concentrations of garlic extract (>or=0.1 microg/ml total protein). Monocyte IL-10 production increased significantly and monocyte tumor necrosis factor-alpha (TNF-alpha), IL-1alpha, IL-6, IL-8, T-cell interferon-gamma (IFN-gamma), IL-2, and TNF-alpha decreased significantly in the presence of >or=10 microg/ml garlic extract. Twenty to fifty percent of the immunomodulatory activity of garlic extract on cytokine production was acid labile. The inhibitory activity of methylprednisolone, a commonly used anti-inflammatory in IBD, with garlic on leukocyte cytokine production was additive. CONCLUSIONS: By inhibiting Th1 and inflammatory cytokines while upregulating IL-10 production, treatment with garlic extract may help to resolve inflammation associated with IBD. An in vivo animal model study needs to be undertaken to determine the significance of these in vitro findings.

Anti-Inflammatory Agents↗
PubMed2004

Gene expression in mononuclear cells from patients with inflammatory bowel disease.

OBJECTIVES: Discovery of Nod2 as the inflammatory bowel disease 1 (IBD1) susceptibility gene has brought to light the significance of mononuclear cells in inflammatory bowel disease pathogenesis. The purpose of this study was to examine changes in gene expression in peripheral blood mononuclear cells in patients with untreated Crohn's disease (CD) and ulcerative colitis (UC) as compared to patients with other inflammatory gastrointestinal disorders and to healthy controls. METHODS: We used a 2400 gene cDNA glass slide array (MICROMAX) to examine gene expression in peripheral blood mononuclear cells from seven patients with Crohn's disease, five patients with ulcerative colitis, 10 patients with other inflammatory gastrointestinal disorders, and 22 age- and sex-matched controls. Results. Novel categories of genes differentially expressed in Crohn's disease and ulcerative colitis patients included genes regulating hematopoietic cell differentiation and leukemogenesis, lipid raft-associated signaling, the actin cytoskeleton, and vesicular trafficking. CONCLUSIONS: Altered gene expression in mononuclear cells may contribute to inflammatory bowel disease pathogenesis.

Colitis, Ulcerative↗
PubMed2001

Hydrocolonic sonography for evaluating inflammatory bowel disease.

OBJECTIVE: The purpose of our study was to compare the usefulness of hydrocolonic sonography and (99m)Tc-hexamethylpropyleneamine oxime (HMPAO)--labeled leukocyte scintigraphy in the examination of patients with inflammatory bowel disease, using precise sonographic criteria of bowel involvement. SUBJECTS AND METHODS: Sixty-eight consecutive patients with active inflammatory bowel disease (34 ulcerative colitis and 34 Crohn's disease), 12 with inactive inflammatory bowel disease, and 10 control subjects were prospectively studied. Patients with active disease underwent clinical assessment, hydrocolonic sonography, scintigraphy, and colonoscopy within 72 hr, whereas patients with inactive disease and control subjects underwent clinical examination and hydrocolonic sonography. RESULTS: Involvement of a colonic segment by active inflammatory bowel disease was best defined by mucosal thickness greater than 1.5 mm, bowel wall thickness greater than 4 mm, mucosal irregularity, or the absence of haustra; and involvement of the terminal ileum by bowel wall thickness greater than 4 mm. Using these criteria, hydrocolonic sonography had 100% sensitivity for identifying patients with active inflammatory bowel disease and a greater overall accuracy (87%) than scintigraphy (77%) in the assessment of disease extension. In addition, strong correlation was shown between a hydrocolonic sonography activity index and clinical and endoscopic activity indexes. CONCLUSION: This prospective study provides precise sonographic criteria for the definition of bowel involvement by active inflammatory bowel disease. Hydrocolonic sonography has a greater accuracy than scintigraphy for assessing disease extension and activity. Therefore, hydrocolonic sonography should be considered a first-choice technique to complete the study of inflammatory bowel disease after confirmation of the diagnosis by histology.

Adolescent↗
PubMed2003

Haemostasis in inflammatory bowel diseases: clinical relevance.

BACKGROUND: In inflammatory bowel disease (IBD), many alterations of haemostasis have been reported. Furthermore. IBD is associated with thromboembolic disease. METHODS: Literature on new insights into the physiology of haemostasis. the interaction between haemostasis and inflammation, plasmatic and mucosal changes in haemostasis in IBD, and haemostasis-interfering therapy in patients with IBD are reviewed. RESULTS: Haemostasis is a vascular-bed-specific, locally regulated, physiological phenomenon aimed at the maintenance of fluidity of blood, and not a simple cascade-shaped chain of reactions. Coagulation activation is part of the inflammatory response, but coagulation activation induces pro-inflammatory effects at the same time. Coagulation and fibrinolysis are activated in the course of IBD. but sometimes in a misbalanced way. Overall, this may induce a state of plasmatic hypercoagulation, irrespective of disease activity. Thromboembolic disease is a common extra-intestinal manifestation of IBD. Established treatment of thromboembolism is similarly useful in IBD patients: concurrent aggressive treatment of exacerbations is recommended. Intractable gastrointestinal bleeding seldom occurs, and has mainly been reported in patients with untreated active IBD. Thrombophilic genetic background does not seem to be responsible for either the increased risk of thromboembolism, or the prevalence of IBD. Haemostasis-interfering therapy to alter the course of IBD is experimental. CONCLUSION: Thromboembolism is an extraintestinal manifestation of IBD, partly because of the associated state of plasmatic hypercoagulation. Thrombophilic genetic background does not contribute to prevalence or course of IBD: genetic investigations may be restricted to patients with clinically proven thrombophilia. Anticoagulant therapy can normally be given to patients. but not as an established therapy against IBD.

Anticoagulants↗
PubMed2004

Embracing complexity: what determines quality of life in inflammatory bowel disease?

A subset of patients with inflammatory bowel disease have markedly impaired quality of life. In this issue, Mussell et al. report that patients' self-rated health status and disease-related concerns were determined at least as strongly by their habitual use of depressive coping patterns as by their disease activity. Although past disease severity may have confounded these results, the finding that quality of life is better for patients armed with a positive approach to problem-handling suggests that psychologically oriented interventions could have far-reaching benefits for selected patients. Since evidence is accumulating that stress and distress can worsen tissue inflammation and clinical course in animal models and in clinical populations with inflammatory bowel disease, we may dare to hope that interventions aimed at improving patients' stress tolerance, depressive symptoms, and coping capacities might not only improve perceived quality of life but could potentially decrease bowel inflammation and reduce some patients' need for toxic medications or surgery. Designing, applying, and evaluating such interventions should be a major item on the agenda of psychosomatic medicine in gastroenterology, and biological reductionism should be replaced by the biopsychosocial model.

Adaptation, Psychological↗
PubMed1998

Review article: The management of inflammatory bowel disease during pregnancy.

The management of inflammatory bowel disease during pregnancy is a particular challenge because adequate disease control before and during gestation is essential for both maternal and foetal health. As a practical problem this situation arises frequently, because a quarter of patients conceive after the diagnosis of their disease. Many of the clinical, biochemical, radiological and endoscopic investigations that are used to monitor and assess disease activity are difficult to use and interpret during pregnancy. Furthermore, patients and clinicians often have concerns about the safety of medical and surgical treatments for the foetus. This review is designed for the practising clinician, to guide the management of patients with inflammatory bowel disease before and during pregnancy. The literature is at times conflicting and data on some issues are scanty, therefore recommendations are based on the balance of evidence including, if necessary, extrapolation from other conditions.

Breast Feeding↗