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Reduction in plasma homocysteine level in patients with rheumatoid arthritis given pulsed glucocorticoid treatment
  1. P E Lazzerini1,
  2. P L Capecchi1,
  3. S Bisogno2,
  4. M Galeazzi2,
  5. R Marcolongo2,
  6. F Laghi Pasini1
  1. 1Clinical Immunology Unit, Department of Clinical Medicine and Immunological Sciences, University of Siena, Policlinico “Le Scotte”, 53100, Siena, Italy
  2. 2Institute of Rheumatology, Department of Clinical Medicine and Immunological Sciences, Policlinico “Le Scotte”, 53100, Siena, Italy
  1. Correspondence to:
    Professor F Laghi Pasini;
    laghi{at}unisi.it

https://doi.org/10.1136/ard.62.7.694

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    High levels of homocysteine are commonly found in patients with rheumatoid arthritis (RA), thus accounting, at least in part, for the high rate of mortality for cardiovascular events in these subjects.1–5 The mechanisms responsible for hyperhomocysteinaemia in RA are not clear. However, drugs such as methotrexate and sulfasalazine affect homocysteine metabolism, interfering with vitamin metabolism and absorption.1,3,5 Furthermore, an increased use or accelerated catabolism of vitamin B6 has been shown in chronic inflammatory diseases, particularly RA.2,6–8

    Recently, it has been shown that rats treated with cortisol have plasma homocysteine levels lower than controls.9 Glucocorticoids increase the activity of betaine-homocysteine methyltransferase, which transforms homocysteine in methionine with consumption of betaine as methyl donor coenzyme.10 Moreover, steroids may produce genomic inhibition of several cytokines, …

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