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Leo B A van de Putte

Researcher at Radboud University Nijmegen

Publications -  44
Citations -  4783

Leo B A van de Putte is an academic researcher from Radboud University Nijmegen. The author has contributed to research in topics: Rheumatoid arthritis & Placebo. The author has an hindex of 22, co-authored 44 publications receiving 4663 citations. Previous affiliations of Leo B A van de Putte include Harvard University.

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Cyclooxygenase in biology and disease

TL;DR: The current understanding of the role of cyclooxygenase‐1 and ‐2 in different physiological situations and disease processes ranging from inflammation to cancer is summarized.
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Basic biology and clinical application of specific cyclooxygenase-2 inhibitors

TL;DR: Clinical trials demonstrate the potential for clinically meaningful reductions in the incidence of the most serious GI complications found with nonselective NSAIDs, i.e., ulcer, perforation, and GI bleeding.
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Methotrexate in Rheumatoid Arthritis: An Update With Focus on Mechanisms Involved in Toxicity

TL;DR: An update of the current knowledge of the mechanism of action of low-dose methotrexate (MTX) in the treatment of patients with rheumatoid arthritis (RA), with an emphasis on the mechanisms involved in toxicity.
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A single dose, placebo controlled study of the fully human anti-tumor necrosis factor-alpha antibody adalimumab (D2E7) in patients with rheumatoid arthritis.

TL;DR: Treatment with the fully human Mab adalimumab was safe and well tolerated when administered as a single intravenous injection at doses up to 10 mg/kg, and was associated with a clinically significant improvement in the signs and symptoms of active RA.
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The C677T mutation in the methylenetetrahydrofolate reductase gene: a genetic risk factor for methotrexate-related elevation of liver enzymes in rheumatoid arthritis patients.

TL;DR: The C677T mutation is the first identified genetic risk factor for elevated alanine aminotransferase values duringMTX treatment in patients with RA and it is postulate that the incidence of clinically important elevation of liver enzyme levels during MTX treatment is mediated by homocysteine metabolism.