作者: Jing Li , Warren May , Robert W. McMurray
DOI: 10.1002/ART.21436
关键词: Hormone 、 Peptide hormone 、 Internal medicine 、 Testosterone 、 Dehydroepiandrosterone 、 Endocrinology 、 Prolactin 、 Sex hormone-binding globulin 、 Luteinizing hormone 、 Adrenocorticotropic hormone 、 Medicine
摘要: Systemic lupus erythematosus (SLE) is known for its predominant occurrence in women and peak incidence during the reproductive years. The increased ratio of female to male SLE patients implies that sex-associated genetic and/or endocrine factors modulate disease proclivity development. While chromosome differences or metabolic environmental may underlie women, no relationship with has proven stronger than those sex female/male hormones. This concept been supported not only by epidemiologic studies, but also substantial evidence immunoregulatory actions 17 -estradiol (estradiol), testosterone, progesterone, dehydroepiandrosterone (DHEA)/ DHEA sulfate, prolactin (1–4). A recent review meta-analysis data examining hormone abnormalities revealed had significantly depressed concentrations androgens elevated estradiol compared their counterparts healthy controls (5). In addition, both abnormally serum concentrations, patients, elevation was aberration clearly identified meta-analyses Elevated (4,5), regulation steroids pituitary gonadotropins (6,7), interdependence neuroendocrine immune systems (8), effects inflammatory cytokines on function (9,10) evoke possibility contribute synergize altered contributing expression. Investigations hormones have relatively uniform enrollment appropriately matched controls. However, small numbers study participants, variability interand intrastudy results, long time intervals over which comparisons reported, absence sufficient statistical power test respective hypotheses limited conclusions possibly obscured identification important relationships between hormonal immunomodulation. Furthermore, peptide hormone/steroid/cytokine feedback loops, interconversions (e.g., testosterone estradiol), superimposed hourly, daily, monthly chronobiologic variations menses, pregnancy, administration complicate a simple interpretation these cause-and-effect as well successful application immunotherapy. We herein investigations adenohypophyseal hormones—follicle-stimulating (FSH), luteinizing (LH), adrenocorticotropic (ACTH), thyroid-stimulating (TSH), growth (GH), prolactin—in SLE. These anterior are peptides various molecular weights bind surface receptors stimulate variety (6,7). They can affect system directly (11) indirectly through synthesis immunomodulatory capacity Moreover, manipulation shown be immunoregulatory, especially animal models (11–15). order better understand associations SLE, sex, hormones, clinical studies measuring FSH, LH, ACTH, TSH, GH (as prolactin) nonpregnant adult men were computSupported Mississippi Lupus Association. Jing Li, MD, Warren May, PhD, Robert W. McMurray, MD: University Medical Center, Jackson. Address correspondence reprint requests Division Rheumatology Molecular Immunology, L525 Clinical Sciences Building, 2500 North State Street, Jackson, MS 39216. E-mail: Robert.McMurray@medicine.umsmed.edu. Submitted publication March 9, 2005; accepted revised form August 25, 2005.