Systemic lupus erythematosus (SLE)

http://pediatrics.aappublications.org/cgi/content/extract/101/5/926

Familial aggregation of lupus and autoimmunity in an unusual multiplex pedigree.

Sestak AL, Shaver TS, Moser KL, Neas BR, Harley JB. University of Oklahoma Health Sciences Center, Oklahoma Medical Research Foundation, Oklahoma City 73104, USA. OBJECTIVE: To evaluate an unusual pedigree with 8 members diagnosed with systemic lupus erythematosus (SLE) METHODS: Pedigree members were evaluated through questionnaires, interviews, and medical records. Sixty members contributed serum samples for autoantibody analysis. RESULTS: The 8 affected females shared several disease features, including arthritis (8/8), antinuclear antibodies (ANA) (8/8), pleuritis (6/8), malar rash (6/8), photosensitivity (5/8), and nephritis (4/8). A total of 15 of 51 (29%) blood relatives had autoantibodies; 9 had autoimmune disease, including 7 with SLE, one with psoriasis, and one with Sjögren's syndrome. Five of 11 (45%) nonconsanguineous spouses also had autoantibodies; one spouse had SLE, and 2 others had thyroid disease. Among 68 spouses of patients with SLE in other pedigrees, only 9 (13%) had autoantibodies, and none were symptomatic (p = 0.02). CONCLUSION: The high rate of autoimmunity among both blood relatives and nonconsanguineous mates in this unusual pedigree suggests a complex interaction of genetic and environmental factors contributing to disease. PMID: 10405936

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Does minocycline have side effects or cause lupus?

The reports that Minocycline can induce lupus are laughable. Exactly how does a complex immune disease arise from the actions of a bacteriostatic antibiotic? Such a suggestion is ridiculous. The same goes for the suggestion that minocycline induces autoimmune hepatitis. Show us the beef, please - the molecular mechanisms.

Remember that it was not too long ago that the majority of physicians agreed with the statement below. That consensus didn't make it any more correct…

In order to comprehend the discoveries springing from the cracking of the genome, today's physicians need to have a good understanding of modern science. It is tough for us to expect this, as many have not been even taught the basics of molecular biology. The alternative is for them to listen to those who are accepted as well grounded in science. Many physicians find that just as hard to swallow, as the profession trains them to present medicine, and its practitioners, to the public as infallible.

~Trevor

Side effects

Once you understand the immunopathology resulting from killing these Th1 pathogens, all these so-called side-effects are shown up for what they are - Immunopathology - and they disappear as you get rid of he pathogens.

..Trevor..

See also:

What should I know about Minocycline?

I'm allergic to an antibiotic on the Protocol. Is there a substitute?

Lupus In 'Overlap' With Other Connective Tissue Diseases

Antinuclear Antibody tests (ANA)

The impact of vitamin d on dendritic cell function in patients with systemic lupus erythematosus²

Ben-Zvi I, Aranow C, Mackay M, Stanevsky A, Kamen DL, Marinescu LM, Collins CE, Gilkeson GS, Diamond B, Hardin JA PLoS One 2010; 5(2) :e9193 Free full text via publisher | Download citation Affiliation Division of Autoimmune and Musculoskeletal Disease, Feinstein Institute for Medical Research, Manhasset, New York, United States of America. Abstract

BACKGROUND: Excessive activity of dendritic cells (DCs) is postulated as a central disease mechanism in Systemic Lupus Erythematosus (SLE). Vitamin D is known to reduce responsiveness of healthy donor DCs to the stimulatory effects of Type I IFN. As vitamin D deficiency is reportedly common in SLE, we hypothesized that vitamin D might play a regulatory role in the IFNalpha amplification loop in SLE. Our goals were to investigate the relationship between vitamin D levels and disease activity in SLE patients and to investigate the effects of vitamin D on DC activation and expression of IFNalpha-regulated genes in vitro. METHODOLOGY/PRINCIPAL FINDINGS: In this study, 25-OH vitamin D (25-D) levels were measured in 198 consecutively recruited SLE patients. Respectively, 29.3% and 11.8% of African American and Hispanic SLE patient had 25-D levels <10 ng/ml. The degree of vitamin D deficiency correlated inversely with disease activity; R = -.234, p = .002. In 19 SLE patients stratified by 25-D levels, there were no differences between circulating DC number and phenotype. Monocyte-derived DCs (MDDCs) of SLE patients were normally responsive to the regulatory effects of vitamin D in vitro as evidenced by decreased activation in response to LPS stimulation in the presence of 1,25-D. Additionally, vitamin D conditioning reduced expression of IFNalpha-regulated genes by healthy donor and SLE MDDCs in response to factors in activating SLE plasma. CONCLUSIONS/SIGNIFICANCE: We report on severe 25-D deficiency in a substantial percentage of SLE patients tested and demonstrate an inverse correlation with disease activity. Our results suggest that vitamin D supplementation will contribute to restoring immune homeostasis in SLE patients through its inhibitory effects on DC maturation and activation. We are encouraged to support the importance of adequate vitamin D supplementation and the need for a clinical trial to assess whether vitamin D supplementation affects IFNalpha activity in vivo and, most importantly, improves clinical outcome.

Arthritis Res Ther. 2010 Nov 23;12(6):R214. [Epub ahead of print] Increased prevalence of vulnerable atherosclerotic plaques and low levels of natural IgM antibodies against phosphorylcholine in patients with systemic lupus erythematosus. Anania C, Gustafsson T, Hua X, Su J, Vikstroem M, de Faire U, Heimbuerger M, Jogestrand T, Frostegard J. Abstract ABSTRACT: INTRODUCTION: The risk of cardiovascular disease (CVD) and atherosclerosis is reported to be increased in systemic lupus erythematosus (SLE). We recently reported a negative association between natural IgM-antibodies against phosphorylcholine (anti-PC) in the general population, high anti-PC levels leading to decreased atherosclerosis development and low levels to increased risk of CVD. Potential mechanisms include anti-inflammatory properties and inhibition of uptake of oxidized low density lipoprotein (LDL) in macrophages. The objective herein was to study atherosclerosis in SLE in detail and in relation to traditional and non-traditional risk factors. METHODS: 114 patients with SLE were compared with 122 age- and sex matched population-based controls. Common carotid intima-media thickness (IMT), calculated intima-media area (cIMa) and plaque occurrence were determined by B-mode ultrasound as a surrogate measure of atherosclerosis. Plaques were graded according to echogenicity and grouped as 1-4, with 1 being echoluscent, and considered most vulnerable. Anti-PC was studied by ELISA. RESULTS: Hypertension, triglycerides and insulin resistance (determined by homeostasis model assessment of insulin resistance) and C-reactive protein (CRP) were increased in SLE (P < 0.01) while smoking, LDL, high density lipoprotein (HDL) did not differ between groups. Low levels of anti-PC IgM (lowest tertile) were more common in SLE patients than in controls (P = 0.0022). IMT and cIMa did not differ significantly between groups. However, plaques were more often found in SLE patients (P = 0.029). Age, LDL and IgM anti-PC (lowest tertile) were independently associated with plaque occurrence in SLE. Further, in the left carotid arteries echoluscent plaques (grade 1) were more prevalent in SLE as compared to controls (P < 0.016). CONCLUSIONS: Plaque occurrence in the carotid arteries is increased in SLE and is independently associated with age, LDL and low anti-PC levels. Vulnerable plaques were more common in SLE. Anti-PC could be a novel risk marker also with a therapeutic potential in SLE. PMID: 21092251

Bonnie B.

lupus, Sjogren’s Syndrome

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