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Nathan Goodyear

Systemic lupus erythematosus and hormone repla... [Menopause Int. 2007] - PubMed - NCBI - 0 views

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    Women with SLE enter menopause earlier.  This study comments on the need for hormone testing in women with SLE and appropriate therapy as indicated.  This study recommended against estrogen therapy due to studies revealing increased flares.  The problem with those studies is that they looked at OCPs and synthetic HRT.
Nathan Goodyear

Dehydroepiandrosterone in systemic lupus erythemat... [Arthritis Rheum. 1995] - PubMed ... - 0 views

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    DHEA aids in SLE treatment for mild/moderat SLE
Nathan Goodyear

Dehydroepiandrosterone treatment of women with mil... [Arthritis Rheum. 2002] - PubMed ... - 0 views

  • CONCLUSION: The overall results confirm that DHEA treatment was well-tolerated, significantly reduced the number of SLE flares, and improved patient's global assessment of disease activity.
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    DHEA reduces SLE flares
Nathan Goodyear

Inadequate production of progesterone in wome... [Br J Rheumatol. 1992] - PubMed - NCBI - 0 views

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    Low progesterone found to be associated with SLE in women.
Nathan Goodyear

Ovarian function and disease acti... [Clin Exp Rheumatol. 2008 May-Jun] - PubMed - NCBI - 0 views

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    imbalanced sex hormones in women links to SLE. 
Nathan Goodyear

Arthritis Research & Therapy | Abstract | Restoration of regulatory and effector T cell... - 0 views

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    Vitamin D supplementation in those individuals with SLE found to benefit these patients.   Vitamin D found to reduce TH1 and Th17 activity.  It also was found to decrease memory B cells and auto-antibodies.  Also of note is the level of vitamin D after therapy-only at 51.4 at 2 months and 41.5 at 6 months.
Nathan Goodyear

Modulation of autoimmune rheumatic diseases by oestrogen and progesterone : Nature Revi... - 0 views

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    only abstract available here, but estradiol increases inflammatory pathways in SLE; in contrast, progesterone decreases these pathways.
Nathan Goodyear

The Complex Role of Estrogens in Inflammation - 0 views

  • These studies suggest inflammation-dependent up-regulation of ERβ relative to ERα.
  • up-regulation of ERβ relative to ERα under hypoxic conditions, which might lead to a preponderance of signaling through ERβ pathways
  • it seems that E2 at periovulatory to pregnancy levels inhibited proinflammatory cytokines from PBMCs
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  • it is clear that E2 can stimulate antibody production by B cells, probably by inhibiting T cell suppression of B cells
  • In cycling women, the largest quantities of Ig were detected before ovulation
  • In contrast, E2 at high concentrations leads to a suppression of B-lymphocyte lineage precursors
  • E2 at periovulatory to pregnancy serum levels is able to stimulate antibody secretion under healthy conditions but also in autoimmune diseases, whereas similar serum levels of E2 lead to a suppression of bone marrow B cell lineage precursors
  • In chronic inflammatory disorders, where B cells play a decisive role, E2 would promote the disease when autoaggressive B cells are already present, whereas chronically elevated E2 would inhibit initiation of an autoimmune disease when no such B cells are available. This might be a good reason why particularly B cell-dependent diseases such as SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis appear in women in the reproductive years, predominantly, in the third or fourth decades of life
  • Th17 cells are thought to be the main responsible cells for chronic inflammatory tissue destruction in autoimmune diseases
  • IFN-γ, IL-12, and TNF were allocated to Th1 reactions
  • IL-4, IL-5, and IL-10 to Th2 responses
  • antiinflammatory T regulatory cells producing TGF-β and proinflammatory T helper type 17 cells (Th17) producing IL-17
  • no direct effects of estrogens on Th17 cells or IL-17 secretion have been described until now.
  • So-called Th17 cells producing IL-17 are the main T cells responsible for chronic inflammation.
  • Because IFN-γ has been allocated a Th17-inhibiting role (Fig. 1⇑), its increase by E2 at pregnancy doses and the E2-mediated inhibition of TNF must be viewed as a favorable effect in chronic inflammation
  • in humans and mice, E2 at periovulatory to pregnancy levels stimulates IL-4, IL-10, and IFN-γ but inhibits TNF from CD4+ T cells
  • In humans and mice, E3 and E2, respectively, at pregnancy levels inhibit T cell-dependent delayed type hypersensitivity
  • increased IL-4, IL-10, and IFN-γ in the presence of low TNF support an antiaggressive immune response
  • secretion of IL-1β is increased at periovulatory/proestrus to early pregnancy levels, whereas IL-1 secretion is inhibited at high pregnancy levels
  • The dichotomous effect of E2 on IL-1β and TNF at high and low concentrations is most probably due to inhibition of NF-κB at high concentrations
  • experiments with mouse and rat macroglial and microglial cells demonstrate that E2 at proestrus to pregnancy levels exerts neuroprotective effects by increasing TGF-β and by inhibiting iNOS and NO release, and reducing expression of proinflammatory cytokines and prostaglandin E2 production.
  • E2 at periovulatory to pregnancy levels inhibits NF-κB activation, which must be viewed as an antiinflammatory signal
  • It was shown that E2 concentrations equal to or above 10−10 m are necessary to inhibit NF-κB activation
  • important proinflammatory cytokines are typically inhibited at periovulatory (proestrus) to pregnancy levels of E2, which is evident for IL-6, IL-8, and TNF
  • low E2 concentrations were demonstrated to have no or even stimulatory effects
  • This renders a woman in the postmenopausal phase to a more proinflammatory situation
  • most in vitro studies demonstrated a stimulatory effect of E2 on secretion of IL-4, IL-10, and TGF-β typically at periovulatory to pregnancy levels
  • E2 at periovulatory to pregnancy levels has an ameliorating effect on chronic inflammatory diseases as long as B cell-dependent immunity or an overshooting fibrotic tissue repair process do not play a crucial pathogenic role. However, when the B cell plays an important role, E2 might even stimulate the disease process as substantiated by flare-ups in SLE during pregnancy
    • Nathan Goodyear
       
      SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis
  • Short-term administration of E2 at pregnancy levels was shown to induce an inflammatory response specific to the lateral prostate of the castrated male rat
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    great review of the complex interaction between Estrogens and inflammation.  Reference here is in females.
Nathan Goodyear

Molecular mechanisms involved in the estrogen-d... [Clin Immunol. 2000] - PubMed - NCBI - 0 views

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    Another abstract only, but this abstract points out that ER signaling is altered in those with SLE.  No discussion as to whether this was ER alpha or beta or both.
Nathan Goodyear

JAMA Network | JAMA Dermatology | Sex Hormones and the Genesis of Autoimmunity - 0 views

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    Hormones and autoimmune disease.  This article specifically touches on SLE.  Good discussion on the biochemical signaling of hormones and their contribution to the increased autoimmunity found in women.
Nathan Goodyear

A double-blind, placebo-controlled, clinical trial... [Lupus. 1999] - PubMed result - 0 views

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    DHEA beneficial in mild/moderate SLE
Nathan Goodyear

An open study of dehydroepiandrosterone in systemi... [Arthritis Rheum. 1994] - PubMed ... - 0 views

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    DHEA improves SLE symptom score and reduces Corticosteroid requirments
star yu

La Diálisis es el Mejor Tratamiento para Curar la Etaopa 5 de SLE - 0 views

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    Alrededor del 60% de los pacientes con SLE (lupus eritematoso sistémico) tiene daño renal. Cuando el SLE causa la inflamación del riñón, que se traduce en la nefritis lúpica que puede conducir a insuficiencia renal, aunque la etapa 5 de insuficiencia renal. La diálisis es una de las más tratamiento para el tratamiento de esta enfermedad, pero no es la mejor.
fnfdoc

How Lupus Affects The Health? - 0 views

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    SLE or Lupus is an autoimmune disease that causes inflammation of the organs and swelling of the joints. It has vast effects on the renal, skeletal, gastrointestinal and blood systems. It affects mostly people of Chinese and African origin and presents in a capricious and unpredictable manner.
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    10 May Is Lupus Day We Must Know About Lupus
Nathan Goodyear

Dehydroepiandrosterone in systemic lupus erythematosus - 0 views

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    DHEA therapy has provided benefit in autoimmune disease.  IN this study they review the previous articles and physiology behind DHEA's proposed benefit in autoimmune disease.
Nathan Goodyear

The effect of combined estrogen and progester... [Ann Intern Med. 2005] - PubMed - NCBI - 0 views

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    HRT, particularily estrogen therapy, is shown to increase mild to moderate flares of lupus.
Nathan Goodyear

Clinical Utility of Common Serum Rheumatologic Tests - American Family Physician - 0 views

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    older, but good review on autoimmune testing.
Nathan Goodyear

[Hormonal changes in fertile women with quiescent systemic lupus erythematosus] - Abstr... - 0 views

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    Abstract suggests that low progesterone plays a role in Lupus.
Nathan Goodyear

Sex hormones and systemic lupus eryt... [Rheum Dis Clin North Am. 2000] - PubMed - NCBI - 0 views

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    older study and only the abstract.  However, sex hormones play role in inflammation and autoimmune disease.
Nathan Goodyear

Sex hormones as immunomodulators in heal... [Int Immunopharmacol. 2001] - PubMed - NCBI - 0 views

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    Estradiol in mice predisposed to Lupus have increased inflammation and characteristics of Lupus.  In contrast, Estradiol in those without predisposition, do not.  Clearly this is an inflammatory signaling problem.  Studies have shown an Interferon gamma signaling deficit in those with Lupus.  Testosterone decreases the above inflammation signaling.
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