Systemic lupus erythematosus (SLE)

Evidence of infectious cause

Familial aggregationOccurrence of a given trait shared by members of a family (or community) that cannot be readily accounted for by chance. 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), photosensitivityAbnormal sensitivity to sunlight and bright lights. Also referred to as "sun flare" or "light flare." (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. 1)

see also neuroscientistnews

Now, researchers at Temple University School of Medicine (TUSM) have shown that bacterial communities that form biofilms A structured community of microorganisms encapsulated within a self-developed protective matrix and living together. play a role in the development of the autoimmune disease systemic lupus erythematosus – a discovery that may provide important clues about several autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body ailments. 2) Sample PubMed cite3)


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.

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.


Side effects

Once you understand the immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed. resulting from killing these Th1 pathogensThe community of bacterial pathogens which cause chronic inflammatory disease - one which almost certainly includes multiple species and bacterial forms., all these so-called side-effects are shown up for what they are - Immunopathology - and they disappear as you get rid of he pathogens.


See also: 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 erythematosus 4)

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 vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory.. METHODOLOGY/PRINCIPAL FINDINGS: In this study, 25-OH vitamin D (25-DThe vitamin D metabolite widely (and erroneously) considered best indicator of vitamin D "deficiency." Inactivates the Vitamin D Nuclear Receptor. Produced by hydroxylation of vitamin D3 in the liver.) 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-DPrimary biologically active vitamin D hormone. Activates the vitamin D nuclear receptor. Produced by hydroxylation of 25-D. Also known as 1,25-dihydroxycholecalciferol, 1,25-hydroxyvitamin D and calcitirol.. 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 vivoA type of scientific study that analyzes an organism in its natural living environment. and, most importantly, improves clinical outcome.

Increased prevalence of vulnerable atherosclerotic plaques and low levels of natural IgM antibodies against phosphorylcholine in patients with systemic lupus erythematosus. 5)

Anania C, Gustafsson T, Hua X, Su J, Vikstroem M, de Faire U, Heimbuerger M, Jogestrand T, Frostegard J. Arthritis Res Ther. 2010 Nov 23;12(6):R214. [Epub ahead of print]

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.

Lupus Risk Linked To Staph Bacteria: Study

While the number of people diagnosed with lupus has more than tripled over the past four decades, researchers remain baffled, for the most part, as to what exactly causes the autoimmune disease. Previous studies have pointed to gender, ethnicity (lupus is two to three times more prevalent among women of color than it is among Caucasian women) and even the use of some prescription drugs as risk factors, but a recent study conducted at the Mayo Clinic has uncovered another possible risk – the bacteria staph, short for Staphylococcus aureus. In the study, published online this month in The Journal of Immunology, even small amounts of the pervasive bacteria caused mice to develop a lupus-like disease, with kidney disease and autoantibodies like those found in the blood of lupus patients. “We think this … could be an important clue to what may cause or exacerbate lupus in certain genetically predisposed patients,” said Vaidehi Chowdhary, M.D., a Mayo Clinic rheumatologist and co-author of the study. The next step, Dr. Chowdhary explains, is to study lupus patients to see if the staph protein in question plays a similar role in humans. “Our hope is to confirm these findings in lupus patients and hopefully prevent flares,” he said in a release. Lupus symptoms may come and go, but the times when a person is having symptoms are called flares, which can range from mild, such as dizzy spells or anemia, to severe, including pain or swelling in joints, red rashes and hair loss. Mayo Clinic researchers are also hoping to uncover whether eradicating staph among people who are at risk for lupus can help prevent onset of the disease altogether. Staph is commonly found on the skin or in the nose and can cause infections ranging from pneumonia to food poisoning. But skin infections are the most common, experts say, and are more likely to occur if you have a cut or scratch, or have contact with a person or surface that has staph bacteria.

Dr Chowdhary's studies 6) 7) 8) 9) 10) 11)

Patient interviews

Bonnie B.

lupus, Sjogren’s Syndrome

Read the interview

Interviews of patients with other diseases are also available.

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Notes and comments


Sandym,p marion villa, Yomi and Andreea Soare and others all have SLE or MCTD. Some MPeers have possible markers for it, or have suspected it and tested as something else


Familial aggregation of lupus and autoimmunity in an unusual multiplex pedigree.
Sestak AL, Shaver TS, Moser KL, Neas BR, Harley JB
J Rheumatol26p1495-9(1999 Jul)
Amyloid-DNA Composites of Bacterial Biofilms Stimulate Autoimmunity.
Gallo PM, Rapsinski GJ, Wilson RP, Oppong GO, Sriram U, Goulian M, Buttaro B, Caricchio R, Gallucci S, Tükel Ç
Immunity42p1171-84(2015 Jun 16)
Vitamin D discovery outpaces FDA decision making.
Marshall TG
Bioessays30p173-82(2008 Feb)
The impact of vitamin D on dendritic cell function in patients with systemic lupus erythematosus.
Ben-Zvi I, Aranow C, Mackay M, Stanevsky A, Kamen DL, Marinescu LM, Collins CE, Gilkeson GS, Diamond B, Hardin JA
PLoS One5pe9193(2010 Feb 16)
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, Vikström M, de Faire U, Heimbürger M, Jogestrand T, Frostegård J
Arthritis Res Ther12pR214(2010)
Liver involvement in systemic lupus erythematosus: case review of 40 patients.
Chowdhary VR, Crowson CS, Poterucha JJ, Moder KG
J Rheumatol35p2159-64(2008 Nov)
Chronic exposure to staphylococcal superantigen elicits a systemic inflammatory disease mimicking lupus.
Chowdhary VR, Tilahun AY, Clark CR, Grande JP, Rajagopalan G
J Immunol189p2054-62(2012 Aug 15)
Increased risk of systemic lupus erythematosus in 29,000 patients with biopsy-verified celiac disease.
Ludvigsson JF, Rubio-Tapia A, Chowdhary V, Murray JA, Simard JF
J Rheumatol39p1964-70(2012 Oct)
Epidemiology of systemic lupus erythematosus and cutaneous lupus erythematosus in a predominantly white population in the United States.
Jarukitsopa S, Hoganson DD, Crowson CS, Sokumbi O, Davis MD, Michet CJ Jr, Matteson EL, Maradit Kremers H, Chowdhary VR
Arthritis Care Res (Hoboken)67p817-28(2015 May)
Cancer risk in cutaneous lupus erythematosus: a population-based cohort study.
Singh AG, Crowson CS, Singh S, Davis MD, Maradit-Kremers H, Matteson EL, Chowdhary VR
Rheumatology (Oxford)55p2009-2013(2016 Nov)
Incidence of systemic lupus erythematosus in a population-based cohort using revised 1997 American College of Rheumatology and the 2012 Systemic Lupus International Collaborating Clinics classification criteria.
Ungprasert P, Sagar V, Crowson CS, Amin S, Makol A, Ernste FC, Osborn TG, Moder KG, Niewold TB, Maradit-Kremers H, Ramsey-Goldman R, Chowdhary VR
Lupus26p240-247(2017 Mar)
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