REVIEW - Estrogens and autoimmune diseases

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Ann N Y Acad Sci. 2006 Nov;1089:538-47.

Estrogens and autoimmune diseases.

Cutolo M, Capellino S, Sulli A, Serioli B, Secchi ME, Villaggio B, Straub RH.

Research Laboratory and Division of Rheumatology, Department of

Internal Medicine, University of Genova, Viale Benedetto XV, 6, 16132

Genova, Italy.

Sex hormones are implicated in the immune response, with estrogens as

enhancers at least of the humoral immunity and androgens and

progesterone (and glucocorticoids) as natural immune-suppressors .

Several physiological, pathological, and therapeutic conditions may

change the serum estrogen milieu and/or peripheral conversion rate,

including the menstrual cycle, pregnancy, postpartum period,

menopause, being elderly, chronic stress, altered circadian rhythms,

inflammatory cytokines, and use of corticosteroids, oral

contraceptives, and steroid hormonal replacements, inducing altered

androgen/estrogen ratios and related effects. In particular, cortisol

and melatonin circadian rhythms are altered, at least in rheumatoid

arthritis (RA), and partially involve sex hormone circadian synthesis

and levels as well. Abnormal regulation of aromatase activity (i.e.,

increased activity) by inflammatory cytokine production (i.e.,

TNF-alpha, IL-1, and IL-6) may partially explain the abnormalities of

peripheral estrogen synthesis in RA (i.e., increased availability of

17-beta estradiol and possible metabolites in synovial fluids) and in

systemic lupus erythematosus, as well as the altered serum sex-hormone

levels and ratio (i.e., decreased androgens and DHEAS). In the

synovial fluids of RA patients, the increased estrogen concentration

is observed in both sexes and is more specifically characterized by

the hydroxylated forms, in particular 16alpha-hydroxyestrone, which is

a mitogenic and cell proliferative endogenous hormone. Local effects

of sex hormones in autoimmune rheumatic diseases seems to consist

mainly in modulation of cell proliferation and cytokine production

(i.e., TNF-alpha, Il-1, IL-12). In this respect, it is interesting

that male patients with RA seem to profit more from anti-TNFalpha

strategies than do female patients.

PMID: 17261796

http://www.ncbi.nlm.nih.gov/pubmed/17261796

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