Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010346 (Crohn's disease)
 21,615 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apilimod is a small molecule that inhibits IL-12 and IL-23 production - cytokines that are involved in autoimmune diseases - through the prevention of nuclear translocation of c-Rel. Synta Pharmaceuticals Corp is developing apilimod for the potential treatment of Crohn's disease (CD) and other autoimmune diseases. Preclinical studies demonstrated the successful inhibition of IL-12 and IL-23 production by the drug. In the clinical setting, apilimod has been generally well tolerated, with mild-to-moderate side effects reported, including headaches and nausea. Patients with CD responded within 14 days of treatment with apilimod and, after 28 days, the drug significantly reduced the Crohn's disease activity index (CDAI). Apilimod is currently in phase II clinical trials for rheumatoid arthritis, common variable immunodeficiency and CD. From the data available to date, apilimod appears to be a promising treatment for CD, and the oral formulation of this compound provides an advantage for apilimod over injectable therapies.
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PMID:Drug evaluation: apilimod, an oral IL-12/IL-23 inhibitor for the treatment of autoimmune diseases and common variable immunodeficiency. 1718 16

In this case report we will describe a rare association between anhyrotic ectodermal dysplasia (AED) and immunodeficiency and autoimmunity [in our case: Idiopathic Thrombocytopenic Purpura (ITP) and Crohn disease]. AED is a rare congenital disorder characterized by sparse hair, abnormal teeth and anhidrosis due to lack of eccrine glands. The survey of 87 cases with (AED) revealed only one Irritable Bowel Disease (IBD). AED has only two relevancies with immunodeficiency: (EDA-ID: Ectodermal Dysplasia Anhyrotic with Immunodeficiency) and APE-CED (Autoimmune polyendocrinopathy, Candidiasis and Ectodermal Dysplasia) that in our case EDA-ID is strongly suspected.
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PMID:Crohn's disease and idiopathic thrombocytopenic purpura in a patient with ectodermal dysplasia and immunodeficiency. 1723 67

In 2005, a 24-year-old man with Crohn disease who had been treated with infliximab for several months was exposed to an individual with smear-positive tuberculosis. Soon after exposure, he complained of malaise, dry cough, and weight loss. Despite normal chest radiograph findings and negative tuberculin skin test results, tuberculosis was considered to be the most likely diagnosis. The results of a whole-blood assay for detection of interferon- gamma production in response to Mycobacterium tuberculosis-specific antigen were positive. Acid-fast staining and polymerase chain reaction of bronchoalveolar lavage fluid samples had negative results, but M. tuberculosis was cultured. After the initiation of 4 antitubercular drugs and the discontinuation of infliximab therapy, the patient developed an immune reconstitution syndrome accompanied by enlarged mediastinal lymph nodes and multiple intrapulmonary miliary lesions. This case of de novo tuberculosis during anti-tumor necrosis factor alpha treatment illustrates the uncharacteristic presentation of the disease and the elusiveness of the diagnosis, as well as the fact that discontinuation of anti-tumor necrosis factor alpha treatment can be accompanied by an immune reconstitution syndrome similar to that observed in human immunodeficiency virus-infected individuals with tuberculosis.
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PMID:A patient with de novo tuberculosis during anti-tumor necrosis factor-alpha therapy illustrating diagnostic pitfalls and paradoxical response to treatment. 1799 Feb 30

Crohn's disease arises from a defective interaction between the highly concentrated mass of bacteria in the gastrointestinal tract and the underlying tissues. It has generally been believed to result from an excessively exuberant inflammatory response or from 'autoimmunity'. Recent evidence has emerged that the problem is instead a failure of the way in which the body responds to the penetration of bacteria and other bowel contents through the intestinal mucosal barrier. Rather than Crohn's disease being caused by excessive inflammation, the primary mechanism is actually that of an immunodeficiency. Failure of inflammatory mediator production leads to insufficient recruitment of neutrophils, resulting in inadequate removal of bacteria and other debris. This impairment of acute inflammation can be compensated in some circumstances by signalling through NOD2. If not cleared, the foreign material in the bowel wall is taken up within macrophages, eliciting a granulomatous reaction and the local and systemic sequelae so characteristic of Crohn's disease.
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PMID:Innate immunity in inflammatory bowel disease: a disease hypothesis. 1816 47

Inflammatory bowel diseases are common chronic inflammatory disorders. The majority are idiopathic and can be broadly divided into Crohn's disease and ulcerative colitis. Their cause is unknown, but most hypotheses focus on a primary role for T-cell dysfunction. Conversely, there is a collection of congenital disorders of phagocyte function that result not only in immunodeficiency but also in noninfectious inflammatory bowel disease. In all cases, the latter is strikingly reminiscent of the clinical and pathological features of Crohn's disease. This coincides with recent work demonstrating that despite previous emphasis on adaptive immune dysfunction, patients with Crohn's disease actually possess an unusually weak acute innate inflammatory response. This review consolidates the literature on inflammatory bowel disease in congenital immunodeficiencies and considers the role of phagocyte dysfunction in Crohn's disease. Concepts about pathogenesis and treatment that can be carried across these disorders are also discussed.
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PMID:Phagocyte dysfunction and inflammatory bowel disease. 1842 61

The reactivation of latent tuberculosis (TB) is a major complication of tumor necrosis factor (TNF)-alpha inhibitors. Screening for TB infection is recommended before anti-TNF therapy is initiated; however, the use of tuberculin skin testing (TST) is controversial, due to the high rate of false-negative results in patients receiving immunosuppressive treatment. To compare the performance of two commercial interferon (IFN)-gamma release assays (IGRA), T-SPOT.TB (TS-TB) and QuantiFERON-TB Gold "In-tube" (QFT-GIT), with TST for the detection of TB infection in patients due to start anti-TNF therapy, 69 human immunodeficiency virus (HIV)-negative Italian patients (mean age: 45.2 +/- 12.6 years; male=39) were enrolled between September 2005 to August 2006. Patients affected by rheumatoid arthritis (n = 18), psoriatic arthritis (n = 26), ulcerous rectocolitis (n = 6), and Crohn's disease (n = 19) were tested simultaneously with TST, TS-TB, and QFT-GIT. Overall, 26% of patients were positive by TST, 30.4% by TS-TB, and 31.8% by QFT-GIT. Agreement with TST was similar (kappa = 0.21, p = 0.0002 and kappa = 0.26, p < 0.001, respectively). In 11 TST-negative cases, IFN-gamma release assays were positive. In addition, in seven Mantoux-positive cases with no TB risk factors, TST result agreement was achieved with at least one blood test. Indeterminate results were detected in 5.8% and 2.8% of cases, respectively, with TS-TB and with QFT-GIT (p = not significant [ns]). In conclusion, our results suggest that IGRAs may be helpful for screening purposes in patient candidates for anti-TNF therapy to confirm positive TST results and in selected cases when false-negative results are suspected. The utility of blood tests in patients with low or no TB risk remains to be assessed.
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PMID:Performance of two commercial blood IFN-gamma release assays for the detection of Mycobacterium tuberculosis infection in patient candidates for anti-TNF-alpha treatment. 1847 May 44

Inflammatory bowel disease (IBD) is uncommon in children younger than 2 years of age. The criteria for differentiating IBD from other diseases with similar clinical presentation is unclear. We describe 16 patients who, between 1984 and 2004, received a histological diagnosis of IBD during the first two years of life. Six patients presented with histological Crohn's disease, eight with ulcerative colitis and two with indeterminate colitis. The median age at diagnosis was 125 days (range 1 day to 18 months) and the medium follow up was 89 months (range 65 days to 20 years). The disease appeared to be very severe: four children (25%) underwent total parenteral nutrition (TPN), two received colectomy (12.5%) and three patients died. Many of the patients required an aggressive, multidrug, immunosuppressive approach (azathioprine [AZA], Infliximab, thalidomide, cyclosporine A). One child presented with a hypogammaglobulinaemia without any specific immunodeficiency, while in the other patients, Wiskott-Aldrich syndrome (WAS) (4 cases) and chronic granulomatous disease (CGD) (2 cases) were identified. In 6/16 cases, allergic colitis was first considered; these cases initially underwent cow's milk protein-free diet as the only therapy before IBD was finally diagnosed. In conclusion, early IBD has a severe prognosis and often needs an aggressive therapeutic approach. Furthermore, an improper diagnosis of allergic colitis might cause an important diagnostic delay. Some severe immunodeficiencies, such as WAS and CGD, may represent a problem in terms of differential diagnosis and might be wrongly diagnosed as very early onset IBD.
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PMID:IBD and IBD mimicking enterocolitis in children younger than 2 years of age. 1854 19

Colony-stimulating factors (CSFs) have an established role in oncology. This article reviews the advances in the pharmacology, pharmacotherapy, and expanded indications of CSFs outside oncology and the role of the infusion nurse. New pharmacologic formulations of CSFs allow for less frequent dosing, less nursing administration time, and increased adherence. Expanded uses in human immunodeficiency virus/acquired immunodeficiency syndrome, Crohn's disease, mucositis, wound healing, chronic kidney disease, Jehovah's Witnesses, illegal use in sports, and non-drug-induced thrombocytopenia are reviewed. The role of the infusion nurse in the minimization of CSF prescribing errors, administration, monitoring, and patient education are summarized.
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PMID:A review of the pharmacology and pharmacotherapy of colony-stimulating factors. 1880 40

Current treatments for Crohn's disease are aimed at suppressing excessive immune activation in the bowel walls. However, alternative strategies can be drawn. These involve the augmentation of the innate immune response, in the hypothesis that patients affected with Crohn's disease are characterized by a relative immunodeficiency, with failure of the defensive barrier to luminal microbes and microbial products, resulting in a chronic inflammatory process sustained by T-cells. Alternatively, therapy could act by enhancing the number or the activity of subpopulations of T regulatory cells, able to reduce T-cell activation. Colony-stimulating factors are substances that could be efficacious in these settings. In fact, besides in vitro and animal studies, some human studies have been conducted in recent years with both granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor, the results of which are reported here.
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PMID:Treatment of Crohn's disease with colony-stimulating factors: An overview. 1920 75

Probiotics are live microorganisms that produce a benefit to the host when provided in adequate amounts from food or supplements. There is an increased interest in the use of probiotics in the management and treatment of complex medical conditions. Recommendations for probiotic supplementation in the pediatric population are often conflicting due to limited research in many pediatric disease states. Research on single and multistrain probiotics has shown promise for some pediatric populations. This review discusses the research available for probiotic supplementation for children with irritable bowel syndrome, Crohn's disease, diarrhea, short bowel syndrome, human immunodeficiency virus, and food allergies. Probiotic safety also is discussed.
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PMID:Clinical use of probiotics in the pediatric population. 1924 49


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