The role of neuroendocrine system in the pathogenesis of rheumatic diseases (minireview).
Interactions between the neuroendocrine and immune system play an important role in maintaining and restoring homeostasis. In susceptible individuals a dysfunction of the neuroendocrine system may be one of the risk factors involved in the pathogenesis of rheumatic diseases. Specific causes of altered neuroendocrine function are still not fully elucidated. Accumulation of genetical, environmental, behavioral and other risk factors during long preclinical period may result in chronic imbalances in homeostatic mechanisms maintained by neuroendocrine, microvascular and immune systems. Chronic inflammatory stress mediated by humoral and neural signals during active stages of the disease and autoantibodies against the structures of the neuroendocrine system may further participate in the neuroendocrine dysfunction. In a subset of patients with rheumatoid arthritis (RA), an assumed defect of the hypothalamic-pituitary-adrenocortical axis may be implicated in the pathogenesis. Results of some studies support the concept of adrenal dysfunction in women with premenopausal onset of the RA. Significantly lower levels of dehydroepiandrosterone sulfate (DHEAS) plasma levels of women who subsequently developed RA indicate that neuroendocrine dysfunction may be present already in preclinical period and thus are not only secondary due to ongoing inflammatory process. These findings are sketching the new prospects of possible primary prevention of RA in the future. The role of some other hormones including prolactin, growth hormone, sex hormones and involvement of autonomic nervous system in relation with the rheumatic diseases is also reviewed in the paper. Further research concerning their role in the pathogenesis of other rheumatic diseases will possibly provide new prospects in optimizing their therapy.
Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, 933 06 Bratislava, Slovak Republic. ueenmri@savba.sk
Richard
R
Imrich
D001341:Autonomic Nervous System / Q000503:physiopathology; D005260:Female; D019382:Human Growth Hormone / Q000378:metabolism; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D007249:Inflammation / Q000503:physiopathology; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D009490:Neurosecretory Systems / Q000502:physiology* / Q000503:physiopathology; D010913:Pituitary-Adrenal System / Q000503:physiopathology; D011247:Pregnancy; D011248:Pregnancy Complications; D011388:Prolactin / Q000378:metabolism; D012216:Rheumatic Diseases / Q000209:etiology* / Q000378:metabolism; D013312:Stress, Physiological / Q000503:physiopathology
D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D011388:Prolactin