Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D02598 (Infliximab)
 1,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infliximab is a chimeric tumor necrosis factor-alpha (TNF-alpha) monoclonal antibody, which has been used extensively in patients with rheumatoid arthritis and inflammatory bowel disease. It also appears to be effective in other conditions such as psoriasis and ankylosing spondylitis. The major side effect of infliximab is infection. Renal complications are uncommon and not well recognized. This report describes a probable case of infliximab-induced membranous nephropathy.
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PMID:Infliximab and nephrotic syndrome. 1620 73

We report a case of heart failure after infusion of Remicade (infliximab) in a patient without heart insufficiency. The patient, a 25-year-old woman with inflammatory bowel disease, developed new-onset heart failure after receiving TNF antagonist therapy. After the treatment was discontinued and heart failure therapy was started, the patient improved significantly. The U.S. Food and Drug Administration has published 47 case reports of heart failure after therapy with a tumor necrosis factor antagonist, where 38 patients developed new-onset heart failure and 9 patients experienced heart failure exacerbation. There are no published reports of heart failure after TNF antagonist therapy in the Danish literature.
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PMID:[Dilated cardiomyopathy as a side effect of treatment with infliximab]. 1621 21

Crohn's disease is a chronic inflammatory bowel disease which affects mainly children and young adults, and its cause remains unknown so far. Infliximab, a monoclonal antibody to the pivotal cytokine tumor necrosis factor-alpha, has been approved as a drug for both induction and maintenance therapy for moderately to severely active, or fistula-complicated Crohn's disease. The authors report a 12-year-old male patient diagnosed as Crohn's disease complicated with a perianal fistula, which was refractory to the conventional therapy. After the 0, 2, and 6 week scheduled intravenous infusion of infliximab, the patient reached to clinical remission in both subjective symptoms and objective manifestations. For children or young adults who develop Crohn's disease in a refractory course, infliximab may serve as a drug which leads to a clinical improvement or even to an extent of remission.
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PMID:[A case of refractory pediatric Crohn's disease with a successful treatment by infliximab therapy]. 1624 74

We report the case of a 57-year old female patient with refractory to treatment pyoderma gangrenosum associated with clinically inactive Crohn's disease. Pyoderma gangrenosum was successfully treated with Infliximab, a chimeric monoclonal antibody that inhibits tumour necrosis factor alpha (TNF-alpha). Our case report suggests that Infliximab, a therapeutic agent for refractory and fistulizing Crohn's disease, may also be safe and effective in the treatment of Crohn's disease associated pyoderma gangrenosum, even though the inflammatory bowel disease is clinically inactive and repeated infusions may be required for successful treatment.
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PMID:Infliximab for treatment of pyoderma gangrenosum associated with clinically inactive Crohn's disease. A case report. 1640 Mar 59

Infliximab, the chimeric monoclonal IgG1 antibody to tumour necrosis factor, is indicated for refractory luminal and fistulizing Crohn's disease and extra-intestinal manifestations of inflammatory bowel disease. Recently, the active ulcerative colitis trials (ACT) studies have shown that infliximab is also efficacious to treat ulcerative colitis resistant to standard therapy. Induction with 5 mg/kg infliximab at weeks 0, 2 and 6 is advocated. The response to infliximab is improved when concomitant immunosuppressive therapy is given. As the majority of patients will relapse if not retreated, a long-term strategy is necessary. Although episodic therapy can be used, the optimal strategy is systematic maintenance treatment with 5 mg/kg intravenous (i.v.) every 8 weeks. Long-term maintenance therapy with infliximab results in a reduction of the rate of complications, hospitalizations and surgeries associated with Crohn's disease. Safety problems with the monoclonal antibody infliximab treatment mainly concern the formation of antibodies to infliximab, which may lead to infusion reactions, loss of response and serum sickness-like delayed infusion reactions. Latent tuberculosis needs to be screened for. The rate of other opportunistic infections is slightly increased mainly in patients treated concomitantly with immunosuppression. There is no evidence that malignancy rates in patients treated with antitumour necrosis factor strategies are increased.
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PMID:Review article: Infliximab therapy for inflammatory bowel disease--seven years on. 1644 65

The therapy of chronic inflammatory diseases like rheumatoid arthritis (RA) and inflammatory bowel disease (IBD) has recently been enriched by the successful launch of the anti-cytokine biologicals Etanercept (tumor necrosis factor (TNF) receptor-p75 Fc fusion protein), Infliximab (chimeric anti-human TNF-alpha monoclonal antibody), Adalimumab (recombinant human anti-human TNF-alpha monoclonal antibody) and Anakinra (recombinant form of human interleukin 1beta (IL-1) receptor antagonist). The success of these novel treatments has impressively demonstrated the clinical benefit that can be gained from therapeutic intervention in cytokine signalling, highlighting the central role of proinflammatory cytokine systems like IL-1alpha and TNF-alpha to be validated targets. However, all of the anti-cytokine biologicals available to date are proteins, and therefore suffering to a varying degree from the general disadvantages associated with protein drugs. Therefore, small molecular, orally active anti-cytokine agents, which target specific pathways of proinflammatory cytokines, would offer an attractive alternative to anti-cytokine biologicals. A number of molecular targets have been identified for the development of such small molecular agents but p38 mitogen-activated protein (MAP) kinase occupies a central role in the regulation of IL-1beta and TNF-alpha signalling network at both the transcriptional and translational level. Since the mid-1990s, an immense number of inhibitors of p38 MAP kinase has been characterised in vitro, and to date several compounds have been advanced into clinical trials. This review will highlight the correlation between effective inhibition of p38 MAP kinase at the molecular target and cellular activity in functional assays of cytokine, particularly TNF-alpha and IL-1beta production. SAR will be discussed regarding activity at the enzyme target, but also with regard to properties required for efficient in vitro and in vivo activity.
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PMID:New approaches to the treatment of inflammatory disorders small molecule inhibitors of p38 MAP kinase. 1645 63

Infliximab infusion is not yet FDA-approved for psoriasis but has been reported to be very effective for plaque psoriasis. We report 2 patients without a history of psoriasis who after administration of infliximab for their inflammatory bowel disease experienced new onset, biopsy confirmed psoriasis.
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PMID:Infliximab associated new-onset psoriasis. 1648 87

Patients with inflammatory bowel disease (IBD) are at increased risk for osteoporotic fracture. Bone density testing and osteoporosis management are recommended for IBD patients at greater risk for fracture (ie, postmenopausal women, men aged . 60 years, and those with low body mass indices, glucocorticoid use, family history of osteoporosis, and malabsorption). Patient management includes modification of osteoporosis risk factors, such as calcium and vitamin D supplementation, hormone deficiency correction, and smoking cessation. When indicated, bisphosphonates, such as risedronate and alendronate, have been shown to increase bone mass and reduce fracture risk in patients with glucocorticoid-induced osteoporosis. Infliximab, an anti-tumor necrosis factor a antibody, increases bone mineral density, but this effect has not as yet translated into reduced fracture risk.
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PMID:Osteoporosis in patients with inflammatory bowel disease: risk factors, prevention, and treatment. 1669 75

The better understanding of the mechanisms of inflammatory bowel disease has driven our progress into the development of new biological therapies targeting specific molecules. Anti-TNF-alpha biologic compounds have shown great efficacy particularly in Crohn's disease. Infliximab (an IgG1 mouse/human chimeric monoclonal anti-TNF-alpha antibody fragment) is the most efficacious compound in induction and maintenance therapy of active and fistulizing Crohn's disease, being at present the only biological compound approved for therapy, but with the limit of the immunogenicity; CDP-571 (a humanized anti-TNF-alpha antibody) and CDP-870 (a PEGylated anti-TNF-alpha antibody) are less immunogenic, showed some efficacy in induction therapy in Crohn's disease but a rapid loss of response in maintenance therapy. Etanercept and onercept (soluble human recombinant TNF-alpha receptors fusion proteins) seem not to be efficacious in Crohn's disease demonstrating no class-effect for anti-TNF-alpha compounds. In preliminary study, adalimumab (an IgG1 humanized monoclonal anti-TNF-alpha antibody) offers good perspective of efficacy and safety also in infliximab-resistant or allergic patients. Inhibition of lymphocyte trafficking to the gut, through anti-adhesion molecules specific therapies (natalizumab, MLN-02, alicaforsen), has shown promising results: unfortunately, natalizumab, the most effective drug of this class, has recently been suspected to favour serious neurological complications. Other biologic therapies are under evaluation but at present seem to be less promising than infliximab; they consist of antiinflammatory cytokines, inhibitors of proinflammatory cytokines, hormones and growth factors: anti-IL12-antibody, interferon-alpha, interferon-beta, G-CSF, GM-CSF, EGF, growth hormone, anti-interferon-gamma, anti-IL-18, anti-IL-2-receptor and anti-CD3 antibodies. The evaluation of other biological drugs has been suspended for severe side effects as happened for anti-CD40L antibody causing thromboembolism and anti-CD4 antibody causing ly.mphopenia. Other compounds as IL-10 and IL-11 have been proven to be ineffective even if an oral formulation of IL-11 is under evaluation. Among the MAP kinases inhibitors BIRB-796 and RDP58 showed to be ineffective while CNI-1493 is under evaluation. The effort in identifying specific patients features predicting therapy response and the possible combination of different biological therapies represent undoubtedly a very promising perspective. Aim of this article is to review the biological compounds and their efficacy in IBD.
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PMID:Biological therapies for inflammatory bowel disease: research drives clinics. 1684 27

Inflammatory bowel disease (IBD) is characterized by idiopathic chronic intestinal inflammation, due to abnormalities in gastrointestinal immunoregulation. Pediatric IBD has been rarely reported in Thailand. We describe eight children, five girls and three boys, who were diagnosed with IBD at Ramathibodi Hospital during 1999-2005 and had a follow-up of more than one year. Four cases had Crohn's disease (CD) and four cases had ulcerative colitis (UC). The ages at diagnosis ranged from 3.5 to 15.5 years. Diagnosis of IBD was delayed for more than 12 months in five patients. Five out of eight patients had early onset of disease, before 6 years of age. The manifestations included chronic diarrhea, abdominal pain, rectal bleeding and perianal lesions. The common extraintestinal manifestations were oral ulcer, anemia, weight loss and failure to thrive. Most patients had moderate to severe diseases and ileocolic fistula developed in one patient with CD. The disease was controlled with 5-aminosalicylic acid and corticosteroid in most patients. Four patients required additional therapy with azathioprine. Infliximab was used in two patients who were chronically steroid-dependent CD, one also had persistent ileocolic fistula and both patients responded well. During the follow-up period ranging from 1.1 to 5.8 years, three patients remained growth retardation; all had early onset of disease before 6 years of age, long duration of symptoms of more than 3 years before diagnosis and had multiple relapses. It is concluded that there is an increasing number of IBD in Thai children during the recent years. Most patients had moderate to severe diseases. Early onset of disease, delay in diagnosis and treatment are responsible for more complications, particularly persistent growth impairment. Early recognition of IBD and treatment are essential for a satisfactory long-term outcome.
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PMID:Inflammatory bowel disease in Thai children: presentations and outcomes of treatment. 1691 91


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