(warning could be TMI)
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| In summary, we found in this controlled clinical trial that the increase of E2 levels in serum was highly correlated with improved BMD. We have tried to elucidate possible ways, in the network of proinflammatory cytokines and IGF-1, by which HRT exerts its effects on the skeleton in long-lasting active RA. We found that HRT reduces serum levels of sIL-6R, whereas IGF-1 levels were observed to be increased. Both of these results – the effects on the IL-6/ sIL-6R pathway and on IGF-1 in the endocrine system – may be involved in the mechanisms mediating the beneficial effects of HRT. There is a need for larger, controlled, long-term studies of combined treatment in RA – estrogen plus progestogen, and estrogen alone – to support our results and to investigate the effects of the various hormones. |
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| Hormonal Factors: A third theory is that RA may be affected by hormones. Researchers have found that hormones, like estrogen and progesterone, increase during pregnancy but decrease afterward. This may explain why onset of RA often occurs following child birth or why women with RA who become pregnant often experience significant symptom improvement during pregnancy but have flare ups of RA once they have given birth. |
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Scientists are studying the complex relationships among the hormonal, nervous, and immune systems in rheumatoid arthritis. For example, they are exploring whether and how the normal changes in the levels of steroid hormones (such as estrogen and testosterone) during a person’s lifetime may be related to the development, improvement, or flares of the disease. Scientists are also looking at how these systems interact with environmental and genetic factors. Results from these studies may suggest new treatment strategies. Researchers are exploring why so many more women than men develop rheumatoid arthritis. In hopes of finding clues, they are studying female and male hormones and other elements that differ between women and men, such as possible differences in their immune responses. To find clues to new treatments, researchers are examining why rheumatoid arthritis often improves during pregnancy. Results of one study suggest that the explanation may be related to differences in certain special proteins between a mother and her unborn child. These proteins help the immune system distinguish between the body’s own cells and foreign cells. Such differences, the scientists speculate, may change the activity of the mother’s immune system during pregnancy. |
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Estrogen deficiency is known to increase bone remodeling and resorption, which subsequently leads to an increased risk of osteoporosis. Hormone replacement therapy (HRT) is known to restore this imbalance. Receptors for the sex steroids estrogen, androgen, and progesterone have been shown to be expressed in the osteoblasts and osteoclasts.[2] Estrogen, besides having direct effects on bone cells, also acts indirectly, by modulating the production of osteoclast-stimulating and -inhibiting factors by paracrine substances from bone marrow cells and by the osteoblasts.[2] Estrogen also influences the skeleton through the endocrine system, increasing the production of insulin-like growth factor 1 (IGF-1), which has anabolic effects on bone.[3,4] The effects of sex hormones on rheumatic diseases are controversial. Some data suggest that estrogens and HRT may be beneficial in RA,[5-7] whereas other findings did not show amelioration of disease activity by HRT.[8] The peak incidence of RA in women coincides with the perimenopausal age, suggesting a connection with hormonal alterations.[9] Furthermore, type-II-collagen-induced arthritis in female mice is exacerbated by ovariectomy and is ameliorated by subsequent treatment with estradiol (E2).[10] In a recent trial exploring the effects of HRT in RA, we found ameliorating effects on clinical measures of disease activity and inflammation, improved bone mineral density (BMD), and also results pointing towards retardation of joint damage.[11] The aim of this study was to assess the effects of HRT on serum levels of the osteoclast-stimulating cytokines, tumor necrosis factor (TNF-), IL-I, IL-6, on their modifiers IL-1-receptor antagonist (IL-1Ra |