Mar 10

Infantile case of early manifestation of SLE-like symptoms in complete C1q deficiency.

Infantile case of early manifestation of SLE-like symptoms in complete C1q deficiency.

J Nihon Med Sch. 2011;78(5):322-8

Authors: Hayakawa J, Migita M, Ueda T, Itoh Y, Fukunaga Y

Abstract
C1q deficiency is a rare complement deficiency in the early part of the complement cascade. Patients with C1q deficiency have severe recurring life-threatening infections and systemic lupus erythematosus (SLE)-like symptoms. We report on a boy with recurrent life-threatening infections and SLE-like recurrent skin conditions before 2 years of age. Immunological studies revealed an undetectable level of C1q. No abnormality was observed in the urine, but renal biopsy showed segmental granulonephritis. However, the changes observed were atypical for SLE nephritis. This case of C1q deficiency was unusual because the SLE-like symptoms appeared earlier than that normally seen in complement deficiency. Therefore, this case provides insights into the development of autoimmune disease, particularly in the early phase of component deficiency, and in managing renal disease that may develop in the future.

PMID: 22041880 [PubMed - indexed for MEDLINE]

Mar 01

Blacks in Illinois Urged to Donate Blood to Help Others with Diseases Like Lupus

A Legislative Black Caucus campaign in Illinois is encouraging Blacks to donate blood, particularly to help patients with diseases like lupus that disproportionately affect this population.  While at the Illinois state level, the need for blood donations from Blacks is widespread nationwide.

Feb 27

New Targets For Lupus Treatment Inspired By Natural Method For Clearing Cellular Debris

Main Category: Lupus
Article Date: 27 Feb 2012 – 0:00 PST

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Cells that die naturally generate a lot of internal debris that can trigger the immune system to attack the body, leading to diseases such as lupus.

Now Georgia Health Sciences University researchers report that an enzyme known to help keep a woman’s immune system from attacking a fetus also helps block development of these autoimmune diseases that target healthy tissues, such as DNA or joints.

The findings point toward new treatment strategies for autoimmune diseases, which are on the rise in light of a germ-conscious society that regularly destroys many of the previously pervasive microbes that made the immune system more tolerant.

“The basic premise of lupus is you have lost normal tolerance to yourself, your own proteins and DNA,” said Dr. Tracy L. McGaha, GHSU immunologist and corresponding author of the study published in Proceedings of the National Academy of Sciences.

They found that IDO, or indoleomine 2,3-dioxegenase, helps promote tolerance to debris generated by natural cell death and that when IDO is removed from the mix, the debris spurs an immune response that can trigger autoimmune disease. In mice genetically programmed to develop lupus, blocking IDO resulted in earlier, more aggressive disease.

“This connects IDO and macrophages. It’s a newly described role for IDO in regulation of tolerance toward self,” McGaha said. Consequently, increasing IDO production or its downstream effects might be a way to regain lost tolerance, he said.

They studied activity in the spleen, a hard-working immune organ, that constantly filters blood. In a perfectly orchestrated defense, the entrance to the spleen is surrounded by immune cells that scour blood for viruses, bacteria, even fat and cholesterol floating by.

A nearby subset of macrophages, which are essentially scavengers, then capture and consume the undesirables, McGaha said. Interestingly, a lot of what macrophages consume is dead immune cells.

Macrophages also appear to help keep the peace by preventing the immune system from joining the fray. McGaha earlier found that if he destroyed macrophages, then fed the spleen dead cells, there was inflammation instead of calm. “That tells us there is something inherent in this subset of macrophages that is important for the suppressive process,” McGaha said referencing the paper published in 2011 in the journal Blood.

The new paper shows IDO is part of that “something.” Efficient elimination of cell debris while keeping nearby immune cells quiet is important because some debris is known to grab the attention of the immune system, McGaha said. He noted that it’s normal – and healthy – for damaged cells to become targets.

“We are really interested in this process of normal cell debris removal because in lupus, it’s thought to be one of the main drivers of inflammation,” he said.

The immune system has points of expansion and regulation where it decides whether or not to act. Knowing key points, such as IDO’s regulatory role, provides treatment targets that can interrupt a destructive cascade of immune activity, McGaha said. Previous studies have shown evidence of self-attack is present many years before disease symptoms appear, he said.

Environmental assaults, such as a bad sunburn, can be the initial trigger of the abnormal immune response in diseases like lupus. In healthy individuals, the immune system rises to the occasion of an infection then goes back to baseline. In autoimmune disease, patients tend not to return to normal levels.

GHSU’s Drs. Andrew Mellor and David Munn reported in 1998 in the journal /i>Science that the fetus expresses IDO to help avoid rejection by the mother’s immune system. Subsequent studies have shown tumors also use it and that it could help transplanted organs escape rejection. They suggested that McGaha look at IDO as a regulatory mechanism used by macrophages.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our lupus section for the latest news on this subject.
Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Georgia Health Sciences University. “New Targets For Lupus Treatment Inspired By Natural Method For Clearing Cellular Debris.” Medical News Today. MediLexicon, Intl., 27 Feb. 2012. Web.
27 Feb. 2012. <http://www.medicalnewstoday.com/releases/242141.php>


APA
Georgia Health Sciences University. (2012, February 27). “New Targets For Lupus Treatment Inspired By Natural Method For Clearing Cellular Debris.” Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/242141.php.

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Feb 18

Inflammatory cytokines in systemic lupus erythematosus.

Inflammatory cytokines in systemic lupus erythematosus.

J Biomed Biotechnol. 2011;2011:432595

Authors: Ohl K, Tenbrock K

Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown origin affecting virtually all organ systems. Beyond genetic and environmental factors, cytokine imbalances contribute to immune dysfunction, trigger inflammation, and induce organ damage. The key cytokine that is involved in SLE pathogenesis is interferon alpha. Interferon secretion is induced by immune complexes and leads to upregulation of several inflammatory proteins, which account for the so-called IFN signature that can be found in the majority of SLE PBMCs. Additionally IL-6 and IFN-y as well as T-cell-derived cytokines like IL-17, IL-21, and IL-2 are dysregulated in SLE. The latter induce a T-cell phenotype that is characterized by enhanced B-cell help and enhanced secretion of proinflammatory cytokines but reduced induction of suppressive T cells and activation-induced cell death. This paper will focus on these cytokines and highlights pathophysiological approaches and therapeutic potential.

PMID: 22028588 [PubMed - indexed for MEDLINE]

Feb 18

Women With Rheumatoid Arthritis And Lupus Give Birth To Fewer Children

Main Category: Arthritis / Rheumatology
Also Included In: Lupus;  Fertility
Article Date: 18 Feb 2012 – 0:00 PST

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New research shows that more than half of women with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) have fewer children than desired. While patient choice has some influence on the smaller family size, findings published in Arthritis Care & Research, a journal of the American College of Rheumatology (ACR), suggest that higher rates of infertility and miscarriage may also impact the number of offspring born to women with these chronic conditions.

According to the ACR up to 322,000 U.S. adults have systemic lupus – a disease in which the body’s immune system becomes overactive and attacks healthy cells, tissues, or organs. Roughly 1.3 million adult Americans suffer from RA, a chronic autoimmune disease that causes painful joint inflammation. Medical evidence reports that both RA and SLE are more common in women, and onset often occurs during reproductive years which can lead to challenges in family-building.

To further understand the role of infertility, pregnancy loss and family size choice in women with RA and SLE, Megan Clowse, M.D., Kaleb Michaud, Ph.D. and colleagues from institutes across the U.S. surveyed 1,017 female participants in the National Data Bank for Rheumatic Diseases. Respondents to the reproductive-health questionnaire included 578 women with RA and 114 with SLE, who based upon their responses, were then categorized as: those interested in having children at symptom onset who had either fewer children than planned (group A) or the same number as planned (group B), and those no longer interested in having children at diagnosis (group C).

Study findings reveal that over 60% of respondents were in group C. Researchers found that 55% of women with RA and 64% with SLE had fewer children than originally planned. Women with RA who were in group A had an infertility rate 1.5 times higher than those in group B, but both groups had similar rates of miscarriage. Women with SLE in group A had a similar number of pregnancies as those in group B, but a 3-fold higher miscarriage rate.

Overall the infertility rate among participants with RA was 42% in women who had fewer children than desired. In women diagnosed with RA during childbearing years the infertility rate was higher than in those diagnosed after childbearing was complete. For participants with SLE no significant increase in infertility was noted. However, among women with lupus having fewer children than desired was associated with pregnancy loss. The authors suggest that patient education to enhance awareness of safe medical options during pregnancy and effective control of these autoimmune diseases will assist women with achieving their childbearing goals.

“Our study highlights important reproductive-health concerns for women with RA and lupus,” said Dr. Clowse. Study findings reported that concerns about inability to care for their children, adverse effects from medications taken during pregnancy, and genetic transmission of their disease to offspring lead to fewer pregnancies in women with RA and SLE. “Further study of the underlying causes of infertility and pregnancy loss in women with RA and SLE is needed to help fulfill their desire for children,” concludes Dr. Clowse.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our arthritis / rheumatology section for the latest news on this subject.
Full citation: “The Effects of Infertility, Pregnancy Loss, and Patient Concerns on Family Size of Women with Rheumatoid Arthritis and Systemic Lupus Erythematosus.” Megan E. B. Clowse, Eliza Chakravarty, Karen H. Costenbader, Christina Chambers, Kaleb Michaud. Arthritis Care & Research; Published Online: February 16, 2012 (DOI: 10.1002/acr.21593).
Wiley-Blackwell
Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Wiley-Blackwell. “Women With Rheumatoid Arthritis And Lupus Give Birth To Fewer Children.” Medical News Today. MediLexicon, Intl., 18 Feb. 2012. Web.
18 Feb. 2012. <http://www.medicalnewstoday.com/releases/241788.php>


APA
Wiley-Blackwell. (2012, February 18). “Women With Rheumatoid Arthritis And Lupus Give Birth To Fewer Children.” Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/241788.php.

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Feb 17

Lupus Research Institute Applauds Formation of Congressional Lupus Caucus

Extends Support and Assistance through LRI’s Coalition of Lupus Advocacy Groups Nationwide

NEW YORK, NY – February 16, 2012. The Lupus Research Institute (LRI) and its National Coalition of lupus patient advocacy organizations congratulate U.S. Representatives Tom Rooney (R-FL), William Keating (D-MA), Ileana Ros-Lehtinen (R-FL), and Jim Moran (D-VA) on co-chairing a new Congressional Lupus Caucus to apprise Members of Congress of the critical issues impacting lupus sufferers.
 

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Feb 16

Association of NCF2, IKZF1, IRF8, IFIH1, and TYK2 with systemic lupus erythematosus.

Association of NCF2, IKZF1, IRF8, IFIH1, and TYK2 with systemic lupus erythematosus.

PLoS Genet. 2011 Oct;7(10):e1002341

Authors: Cunninghame Graham DS, Morris DL, Bhangale TR, Criswell LA, Syvänen AC, Rönnblom L, Behrens TW, Graham RR, Vyse TJ

Abstract
Systemic lupus erythematosus (SLE) is a complex trait characterised by the production of a range of auto-antibodies and a diverse set of clinical phenotypes. Currently, ~8% of the genetic contribution to SLE in Europeans is known, following publication of several moderate-sized genome-wide (GW) association studies, which identified loci with a strong effect (OR>1.3). In order to identify additional genes contributing to SLE susceptibility, we conducted a replication study in a UK dataset (870 cases, 5,551 controls) of 23 variants that showed moderate-risk for lupus in previous studies. Association analysis in the UK dataset and subsequent meta-analysis with the published data identified five SLE susceptibility genes reaching genome-wide levels of significance (P(comb)<5×10(-8)): NCF2 (P(comb) = 2.87×10(-11)), IKZF1 (P(comb) = 2.33×10(-9)), IRF8 (P(comb) = 1.24×10(-8)), IFIH1 (P(comb) = 1.63×10(-8)), and TYK2 (P(comb) = 3.88×10(-8)). Each of the five new loci identified here can be mapped into interferon signalling pathways, which are known to play a key role in the pathogenesis of SLE. These results increase the number of established susceptibility genes for lupus to ~30 and validate the importance of using large datasets to confirm associations of loci which moderately increase the risk for disease.

PMID: 22046141 [PubMed - indexed for MEDLINE]

Feb 15

Lupus Research Institute Awards $3.6 Million for Novel Studies Driving Wide-Ranging New Science in Lupus

NEW YORK, NY – February 15, 2012 – The Lupus Research Institute (LRI) today awards 12 "Novel Research Grants" to jumpstart discovery in lupus by supporting original, highly promising ideas from some of the country’s most creative scientists. Studies will look at why lupus turns the body’s immune system against itself and pioneer strategies for new treatment development.

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Feb 09

Pregnancy outcomes and appropriate timing of pregnancy in 183 pregnancies in Korean patients with SLE.

Pregnancy outcomes and appropriate timing of pregnancy in 183 pregnancies in Korean patients with SLE.

Int J Med Sci. 2011;8(7):577-83

Authors: Ko HS, Ahn HY, Jang DG, Choi SK, Park YG, Park IY, Lee G, Park SH, Shin JC

Abstract
This study was undertaken to investigate the pregnancy outcomes in patients with systemic lupus erythematosus (SLE) and the appropriate timing of pregnancy. We performed a retrospective evaluation of 183 pregnancies with SLE at Catholic University Medical Center during the 13-year period from 1998 to 2010. Pregnancy outcomes were compared according to SLE characteristics. The predictive value of the different cut-off points of the stable period before conception on adverse pregnancy outcomes was calculated by ROC (Receiver operating characteristics) curve analysis. In multivariate analysis, the presence of antiphospholipid antibodies (aPLs) increased the risk of pregnancy loss (p<0.0001) and premature birth (p=0.0040). Active disease at conception increased the risk of premature birth (p< 0.0001) and complications (IUGR, PIH, or both) (p= 0.0078). The other predictor of complications was found to be lupus flare (p=0.0252). At a cut-off level of stable period of 4 months before conception, sensitivity and specificity were 70.8% and 53.2%, 71.4% and 61.5%, and 63.6 % and 59.8 %, respectively on reducing pregnancy loss, premature birth, and complications. Pregnancies with aPLs, active disease at conception and SLE flares are at a higher risk of adverse outcomes. It is essential that disease activity remains stable at least 4 months before conception, for favorable pregnancy outcomes.

PMID: 22022210 [PubMed - indexed for MEDLINE]

Feb 09

Deranged bioenergetics and defective redox capacity in patients with systemic lupus erythematosus.

Deranged bioenergetics and defective redox capacity in T lymphocytes and neutrophils are related to cellular dysfunction and increased oxidative stress in patients with active systemic lupus erythematosus.

Clin Dev Immunol. 2012;2012:548516

Authors: Li KJ, Wu CH, Hsieh SC, Lu MC, Tsai CY, Yu CL

Abstract
Urinary excretion of N-benzoyl-glycyl-Nε-(hexanonyl)lysine, a biomarker of oxidative stress, was higher in 26 patients with active systemic lupus erythematosus (SLE) than in 11 non-SLE patients with connective tissue diseases and in 14 healthy volunteers. We hypothesized that increased oxidative stress in active SLE might be attributable to deranged bioenergetics, defective reduction-oxidation (redox) capacity, or other factors. We demonstrated that, compared to normal cells, T lymphocytes (T) and polymorphonuclear neutrophils (PMN) of active SLE showed defective expression of facilitative glucose transporters GLUT-3 and GLUT-6, which led to increased intracellular basal lactate and decreased ATP production. In addition, the redox capacity, including intracellular GSH levels and the enzyme activity of glutathione peroxidase (GSH-Px) and γ-glutamyl-transpeptidase (GGT), was decreased in SLE-T. Compared to normal cells, SLE-PMN showed decreased intracellular GSH levels, and GGT enzyme activity was found in SLE-PMN and enhanced expression of CD53, a coprecipitating molecule for GGT. We conclude that deranged cellular bioenergetics and defective redox capacity in T and PMN are responsible for cellular immune dysfunction and are related to increased oxidative stress in active SLE patients.

PMID: 22007252 [PubMed - indexed for MEDLINE]

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