Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The numerous clinical and experimental data suggesting a lupus-induced modulation of sex hormones prompted the study of sex hormone metabolism in these patients. Some hormonal abnormalities were reported in female patients: a) over production of 16-alpha-hydroxylated estradiol derivatives with potent peripheral estrogenic activities; b) under production of the following androgens: testosterone, dihydrotestosterone, dihydroandrosterone, dihydroandrosterone sulfate, delta 4-androstenedione. Moreover, some observations suggest an excessive transformation of androgens into estrogens: increased oxidation of testosterone on C17, skin lesions, abnormal skin, aromatase activity responsible for estradiol synthesis.
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PMID:[Sex hormone metabolism in acute systemic lupus erythematosus]. 236 14

The prevalence of autoimmune diseases in women may be the consequence of a bidirectional signaling network between hormones and the immune system that regulates female reproductive life. Two prototypical autoimmune diseases, rheumatoid arthritis and systemic lupus erythematosus, arise from 2 different immune responses that generate mutually exclusive signals in response to different inflammatory triggers. Certain estrogens may ameliorate the rheumatoid-arthritis-like TH1 response while exacerbating the lupus-like TH2 response. Studies of sex hormone metabolism in lupus patients reveal increased 16-hydroxylation of estrone in some patients and decreased levels of androgens as a result of increased oxidation at C17. These occurrences result in low serum levels of dehydroepiandrosterone (DHEA). Both the increase of 16-hydroxylation of estrone and the depletion of DHEA have immune effects that would tend to exacerbate a lupus-like TH2 response. This theoretical framework provides a rationale for ongoing initial clinical trials of exogenous hormones in autoimmune diseases.
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PMID:Autoimmunity: The Female Connection. 974 57

Brain atrophy, neurologic and psychiatric (NP) manifestations are common complications in the systemic autoimmune disease, lupus erythematosus (SLE). Here we show that the cerebrospinal fluid (CSF) from autoimmune MRL-lpr mice and a deceased NP-SLE patient reduce the viability of brain cells which proliferate in vitro. This detrimental effect was accompanied by periventricular neurodegeneration in the brains of autoimmune mice and profound in vivo neurotoxicity when their CSF was administered to the CNS of a rat. Multiple ionic responses with microfluorometry and protein peaks on electropherograms suggest more than one mechanism of cellular demise. Similar to the CSF from diseased MRL-lpr mice, the CSF from a deceased SLE patient with a history of psychosis, memory impairment, and seizures, reduced viability of the C17.2 neural stem cell line. Proposed mechanisms of cytotoxicity involve binding of intrathecally synthesized IgG autoantibodies to target(s) common to different mammalian species and neuronal populations. More importantly, these results indicate that the viability of proliferative neural cells can be compromised in systemic autoimmune disease. Antibody-mediated lesions of germinal layers may impair the regenerative capacity of the brain in NP-SLE and possibly, brain development and function in some forms of CNS disorders in which autoimmune phenomena have been documented.
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PMID:Proliferating brain cells are a target of neurotoxic CSF in systemic autoimmune disease. 1619 28