Treatment of Crohn’s disease with infliximab

Garnett, William R.; Yunker, Nancy S.

doi:10.1093/ajhp/58.4.307

Cited by 16 publications

(9 citation statements)

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“…Finally, the interaction between the MMR and either MPO or iMPO may not be exclusive to RA. Tumour necrosis factor‐α appears to be involved in a number of other inflammatory diseases including Crohn's and multiple sclerosis 48 , 49 , 50 . Because other investigators have reported that alveolar Mφ ingested MPO in the lungs of animals with pulmonary inflammation, 51 studies completed by us using alveolar Mφ and either MPO or iMPO, have also indicated that iMPO induces more cytokine secretion than MPO.…”

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confidence: 99%

Macrophage–neutrophil interaction: A paradigm for chronic inflammation revisited

Lefkowitz

2001

Immunol Cell Biol

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Summary Macrophages have been described as 'factories' of pro-inflammatory cytokines. Several years ago the present investigators reported that binding of inactive myeloperoxidase (iMPO) to the macrophage-mannose receptor resulted in the induction of TNF and other cytokines. Also, if endothelial cells were incubated with iMPO, but not enzymatically active myeloperoxidase (MPO), upregulation of cytokine mRNA and cytokines was observed. Taken in their entirety, the data suggest a dichotomy of function for myeloperoxidase; that is, enzymatically active MPO functions primarily in cell killing through the 'cytotoxic triad' and iMPO functions as an immunoregulatory molecule through the induction of numerous cytokines. These studies underscore a previously unrecognized interaction among neutrophils, endothelial cells and macrophages, resulting in the induction of TNF and perpetuation of inflammation. The inflammation induced could be relevant in a number of diseases in which neutrophils play a prominent role. The importance of this interaction in the pathogenesis of rheumatoid arthritis is currently under investigation.

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confidence: 99%

Macrophage–neutrophil interaction: A paradigm for chronic inflammation revisited

Lefkowitz

2001

Immunol Cell Biol

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“…The patient was suffering from severe gastrointestinal manifestations of BD and was given infliximab 5 mg/kg IV at weeks zero, two, seven and twenty three, similar to the protocol for Crohn's disease. 5 The patient did not require maintenance therapy. Two other patients, reported by Travis et al, were given infliximab for BD on an 'as required' basis.…”

Section: Discussionmentioning

confidence: 92%

Infliximab in Refractory Behcet's Disease

Maxwell

2002

Pharmacy Practice and Res

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Objective: To describe the use of infliximab in a patient with refractory Behcet's disease (BD). Clinical features: The patient, a 39‐year‐old woman, had been suffering from BD for over 15 years. Previous therapy, including cyclophosphamide, methotrexate, interferon alpha‐ 2a and steroids, was not controlling her symptoms of severe cutaneous/oral/genital ulcers, uveitis, iritis, chronic sinusitis, diarrhoea, abdominal cramps and severe joint pain. A trial of infliximab, an anti‐tumour necrosis factor alpha (TNFα) monoclonal antibody, was commenced to control the symptoms. Outcome: A course of IV infliximab at 3 mg/kg was administered at weeks zero, two and six. During this period progress was measured using various indices, including the Health Assessment Questionnaire (HAQ) Disability Index and the Arthritis Impact Measurement Scale (AIMS) Anxiety Score, as well as a personal diary. The patient described almost immediate relief from diarrhoea and abdominal cramps. At the end of the six week treatment period, both the HAQ Disability Index and AIMS Anxiety score had decreased from 2.1 and 4.6 respectively, to zero, and the patient reported relief from joint pain, and healing of oral and genital ulcers. Six weeks after treatment finished the patient suffered a relapse of ulcers, joint pain and abdominal symptoms. Maintenance infliximab was commenced at 3 mg/kg IV every eight weeks. Discussion: This case, and other published reports describing short‐term use of infliximab in BD, suggest that infliximab may be suitable for the treatment of refractory BD. However maintenance therapy may be required to achieve long‐term symptom control in some patients, such as the one described in this report.

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“…The binding epitope for TNF is of murine origin while the IgG fragment is of human origin [21]. It is composed of human constant and murine variable regions.…”

Section: Symptoms and Pathophysiology Of Rheumatoid Arthritismentioning

confidence: 99%

Discovery of Selective Small Molecular TACE Inhibitors for the Treatment of Rheumatoid Arthritis

Shi²,

Tang³

et al. 2012

CMC

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Rheumatoid arthritis (RA) is a chronic, inflammatory disease that afflicts 1-2% of the world population, characterized by an immune mediated inflammatory synovitis that leads to joint destruction, functional impairment, and reduced quality of life. The treatment goals of RA should be longterm substantial relief of pain, arrested joint inflammation and damage, and improved function. Current treatment can be divided into four classes, namely general analgesics and non-steroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, disease modifying anti-rheumatic drugs (DMARDs) and biological agents (tumor-necrosis factor modifiers). However, gastrointestinal (GI) side effects of NSAIDs cannot be neglected, direct joint injections of glucocorticoids cannot be injected more than once every 3 months, synthetic DMARDs is far from optimal and only minority of patients achieved longterm remission, the biologics are very expensive to manufacture, need to be injected, and can cause allergic reactions. An alternative and good approach to the treatment of this disease is to lower the levels of tumour necrosis factor-α (TNF-α) in RA, which can be achieved by selectively inhibiting the tumour necrosis factor-α converting enzyme (TACE) that generate these cytokines using cheaper small molecules. This review focuses on the current status of selective small molecule inhibitors of TACE, with respect to lead compound search, inhibitors design approach, structure-activity relationship (SAR) and pharmacological studies in animals and humans. Through these methods, new hope is emerging for the treatment of RA through selective inhibition of TACE.

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Treatment of Crohn’s disease with infliximab

Cited by 16 publications

References 0 publications

Macrophage–neutrophil interaction: A paradigm for chronic inflammation revisited

Macrophage–neutrophil interaction: A paradigm for chronic inflammation revisited

Infliximab in Refractory Behcet's Disease

Discovery of Selective Small Molecular TACE Inhibitors for the Treatment of Rheumatoid Arthritis

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