Jan 26

Pericardial effusion and systemic lupus erythematosus

Pericardial effusion in a young patient with newly diagnosed systemic lupus erythematosus and a mediastinal mass.

Hellenic J Cardiol. 2011 Sep-Oct;52(5):448-51

Authors: Lazaros G, Aggelis A, Tsiachris D, Iliadis K, Scarpidi E, Bratsas A, Komnou AA, Stefanadis C

Abstract
We present the case of a 32-year-old-woman who was admitted to the hospital for evaluation of pericardial effusion. The subsequent diagnostic workup revealed the presence of a mediastinal mass along with systemic lupus erythematosus (SLE). The patient underwent thymectomy, and histological evaluation of the resected mass revealed thymic follicular hyperplasia without evidence of malignancy. SLE disease activity was promptly controlled by corticoids. Clinicians should be aware of the occasional association of autoimmune disorders with focal thymic hyperplasia, which might be confused with thymomas or thymocarcinomas.

PMID: 21940294 [PubMed - indexed for MEDLINE]

Jan 20

Indian systemic lupus erythematosus (SLE) patients.

Fc γ R IIB gene polymorphisms in Indian systemic lupus erythematosus (SLE) patients.

Indian J Med Res. 2011 Aug;134(2):181-5

Authors: Pradhan V, Patwardhan M, Nadkarni A, Ghosh K

Abstract
BACKGROUND & OBJECTIVES: Receptors for the Fc fragment of immunoglobulin G (Fc γ Rs) represent the link between humoral and cellular immune responses. Polymorphisms in Fc γ Rs have been identified as genetic factors influencing susceptibility to various autoimmune diseases. This study was aimed to identify Fc γ R IIB genotypes in Indian systemic lupus erythematosus (SLE) patients and to correlate these with clinical presentation and autoantibody profile.
METHODS: Eighty consecutive clinically diagnosed SLE patients were included. SLE patients were classified according to the American College of Rheumatology (ACR) criteria. Disease activity was assessed by Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). PCR-RFLP method was used to detect Fc γ R IIB polymorphism.
RESULTS: Of the 80 SLE patients, 53 were LN and 27 were SLE without nephritis. The mean SLEDAI score at evaluation was 6.5 ± 5.8. Among SLE patients Fc γ R IIB genotype frequency was 61.2 per cent for Ile/Thr, 20.0 per cent for Thr/Thr and 18.8 per cent for Ile/Ile as compared to 65, 12.5 and 22.5 per cent respectively among normal population. There was no significant difference for Fc γ R IIB genotypes between SLE and normals. The allele frequency for Thr allele in SLE patients was slightly higher (0.51) than in normals (0.45). Thr allele frequency in LN patients was slightly higher (0.53) than in SLE patients without nephritis (0.49). Though a higher percentages of symptoms like renal manifestations (81.3%), arthritis (62.5%) and oral ulcer (56.3%) were noted in patients with Thr/Thr genotypes, no significant difference was noted when these patients were compared with Ile/Ile and Ile/Thr genotypes.
INTERPRETATION & CONCLUSIONS: The findings of this study indicate towards an involvement of Thr allele with SLE disease severity and clinical presentation in Indian SLE patients. Future study on a large sample is needed to support this finding to understand the association of Fc γ R IIB 232Thr/Thr genotype as a susceptibility factor in SLE.

PMID: 21911970 [PubMed - indexed for MEDLINE]

Jan 20

Porphyria cutanea tarda and systemic lupus erythematosus.

Porphyria cutanea tarda and systemic lupus erythematosus.

An Bras Dermatol. 2011 Feb;86(1):173-5

Authors: Haendchen L, Jordão JM, Haider O, Araújo F, Skare TL

Abstract
The co-existence of systemic lupus erythematosus and porphyria although rare has been known for a long time. This association forces the physician to make a careful differential diagnosis of the bullous lesions that might appear in such patients and to be careful when prescribing certain drugs such as chloroquine. This drug, when used in the regular doses for treating lupus, may cause hepatotoxicity in patients.suffering from porphyria. It is described here the case of a patient with lupus who developed bullous lesions compatible with porphyria cutanea tarda.

PMID: 21437551 [PubMed - indexed for MEDLINE]

Jan 18

DNA Sequence Discovered That Causes The Most Severe Cases Of Lupus

Main Category: Lupus
Also Included In: Genetics
Article Date: 18 Jan 2012 – 0:00 PST

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A “genetic accelerator” is responsible for the most severe cases of Lupus (systemic lupus erythemathosus), an autoimmune disease: the accelerator, called enhancer HS1.2, speeds up the activity of some critical genes of the immune system involved in the disease.

A team of Italian researchers at the Catholic University of Sacred Heart in Rome found that the enhancer HS1.2 is like the accelerator of the car and boosts the pathological immune response typical of the disease by enhancing the production of the pathological antibodies that attack the patient’s body instead of defending it (autoantibodies).

Professor Gianfranco Ferraccioli, Head of the Rheumatology Unit of Rheumatology and Internal Medicine of the Catholic University led the research in collaboration with Professor Domenico Frezza at Tor Vergata University of Rome and Professor Raffaella Scorza at University of Milan and they published their results in the Annals of the Rheumatic Diseases.

The discovery could lead to more targeted and effective therapies against this complex disease, in particular against the most severe cases, Professor Ferraccioli explained.

Systemic lupus erythematosus is an autoimmune disease, that is a condition in which the patient’s immune system goes haywire and begins to attack the body rather than defend it. Lupus affects about 60,000 people in Italy, with a major prevalence among females. Lupus affects several different organs and tissues and causes a variety of symptoms, including joint pain, fever, skin rashes, hair loss, Raynaud’s disease, anemia, nephritis.

The therapies currently used are based on cortisone, anti-malarial drugs and immunosuppressants (azathioprine, mycophenolate, cyclophosphamide) and biologic drugs (rituximab, Belimumab).

But in many cases Lupus is more aggressive and so far the origin of this particular severity was quite unclear.

Italian researchers discovered that the cause of the most severe cases is the accelerator HS1.2 enhancer. Enhancers are DNA sequences that accelerate the activation of neighboring genes and enhance their functioning, hence the name.

HS1.2 leads to enhanced activation of the “transcription factor NF-KB” (a transcription factor is a molecule that “reads” the genes to make them work), which in turn dramatically increases the aggressiveness of the inflammatory processes underlying the disease.

Italian researchers have discovered that over 30 per cent of the patients has the enhancer HS1.2 in their Dna and that it causes a more severe form of Lupus.

The researchers reached this finding after demonstrating that the enhancer HS1.2 promotes also other autoimmune diseases such as rheumatoid arthritis and identified how the enhancer causes increased susceptibility to autoimmune diseases.

“Our results suggest that new drugs that turn off the enhancer HS1.2, or inhibit its effect on NF-KB, can stop the disease without the need for immunosuppressive drugs or other therapies with many side effects,” Ferraccioli said. “Moreover the discovery of the role of this enhancer allows us to better classify patients and formulate a precise prognosis for each one moving toward more personalized care.”

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
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Catholic University of Rome. “DNA Sequence Discovered That Causes The Most Severe Cases Of Lupus.” Medical News Today. MediLexicon, Intl., 18 Jan. 2012. Web.
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Jan 13

Systemic lupus erythematosus and Graves’ disease in Thai population

Association between CTLA-4 polymorphisms and the susceptibility to systemic lupus erythematosus and Graves’ disease in Thai population.

Asian Pac J Allergy Immunol. 2011 Sep;29(3):229-35

Authors: Kimkong I, Nakkuntod J, Sae-Ngow S, Snabboon T, Avihingsanon Y, Hirankarn N

Abstract
BACKGROUND: Cytotoxic T-lymphocyte antigen-4 (CTLA-4) is a cell surface molecule involved in the regulation of T cells. Single nucleotide polymorphisms (SNPs) of CTLA-4 gene are known to be associated with susceptibility to several autoimmune diseases, including systemic lupus erythematosus (SLE) and Graves’ disease (GD).
OBJECTIVE: The aim of this study was to determine whether the common SNPs +49A/G on exon1 and CT60A/G in 3′UTR of the CTLA-4 gene are associated with susceptibility to SLE and GD in Thai population.
METHODS: Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to analyze these two SNPs in 151 patients with SLE, 132 patients with GD and 153 healthy controls.
RESULTS: Our study showed that there were no statistically significant differences in the allele and genotype frequencies of +49A/G and CT60A/G SNPs between patients with SLE and healthy controls as well as patients with GD vs. healthy controls (P > 0.05). However, the GG genotypes of +49A/G and CT60A/G were likely to be risk factors (OR >1) for GD but not in SLE. The effect of the +49G allele was similar to that of an autosomal recessive gene in the presence of the GG genotype, when compared to AA and AG, with an OR of 1.58 (95% CI = 0.95-2.61, p = 0.061) in GD. We also observed a dose response effect of the CT60G allele on GD susceptibility with an OR of 1.43 for GG homozygous and 1.17 for AG heterozygous subjects, when compared to the AA genotype, although these were not statistically significant (P > 0.05).
CONCLUSION: We found no association between two functional polymorphisms (+49A/G and CT60A/G) of the CTLA-4 gene and susceptibility to SLE and GD. However, the association study utilizing a larger sample size should be performed to confirm this.

PMID: 22053592 [PubMed - indexed for MEDLINE]

Jan 13

Phenotyping of P105-negative B cell subsets in patients with systemic lupus erythematosus.

Phenotyping of P105-negative B cell subsets in patients with systemic lupus erythematosus.

Clin Dev Immunol. 2012;2012:198206

Authors: Koarada S, Tada Y, Suematsu R, Soejima S, Inoue H, Ohta A, Nagasawa K

Abstract
This study aimed to investigate phenotype of RP105(-) B cell subsets in patients with systemic lupus erythematosus (SLE). Flow cytometry was used for phenotyping RP105-negaive B cell subsets. Based on CD19, RP105, and CD138 expression, RP105(-) B cells consist of at least 5 subsets of late B cells, including CD19(+)RP105(int), CD19(+) RP105(-), CD19(low) RP105(-) CD138(-), CD19(low) RP105(-)CD138(int), and CD19(low) RP105(-) CD138(++) B cells. Especially, CD19(+)RP105(int) and CD19(low) RP105(-)CD138(int) B cells are significantly larger than other RP105(-) B cell subsets in SLE. By comparison of RP105(-) B cell subsets between patients with SLE and normal subjects, these subsets were detectable even in normal subjects, but the percentages of RP105(-) B cell subsets were significantly larger in SLE. The phenotypic analysis of RP105(-) B cell subsets suggests dysregulation of later B cell subsets in SLE and may provide new insights into understanding regulation of B cells in human SLE.

PMID: 21961021 [PubMed - indexed for MEDLINE]

Jan 13

A proposed model for physiologic and pathologic regulation in systemic lupus erythematosus.

Adenosine inhibits the release of arachidonic acid in activated human peripheral mononuclear cells. A proposed model for physiologic and pathologic regulation in systemic lupus erythematosus.

ScientificWorldJournal. 2011;11:972-80

Authors: Sipka S

Abstract
In the current work, the pathways are presented and reviewed showing how adenosine acts on the production and release of arachidonic acid (AA) in activated human monocytes by the involvement of various phospholipase A2 (PLA2) and protein kinase C (PKC) enzymes in physiological (normal) conditions and in a pathologic state in systemic lupus erythematosus (SLE). Two molecules of activated monocytes mainly determine the actual amounts of AA released: (1) interleukin-1 beta (IL-1 beta) increasing and (2) adenosine (Ado) suppressing this process. The AA production of monocytes mainly depends on two (IV and VI) types of PLA2 enzymes. PKC alpha phosphorylates the cytosolic, Ca2+-dependent and steroid-sensitive PLA2 (type IV), whereas PKC delta phosphorylates the Ca2+-independent PLA2 (type VI). By the suppression of IL-1 beta production in the activated human monocytes, adenosine can decrease the release of AA causing a diminished phosphorylation of both PKC isoenzymes. In SLE monocytes, the disease-specific decreased release of AA that we found earlier could be related to the decreased expression of PKC delta. These pathways are summarized in a proposed model.

PMID: 21516291 [PubMed - indexed for MEDLINE]

Jan 12

Star Player from University of Alabama Going Pro – Plans to take care of mom with lupus and two daughters

Jan 12

S.L.E. Lupus Foundation and Lupus LA send our best wishes to Toni Braxton for continued recovery

Jan 12

Lupus Research Institute Launches Bold Global Research Initiative to Uncover the Root Causes of Lupus that Can Lead to a Cure

Call for Proposals for Distinguished Innovator Awards

NEW YORK, NY – January 12, 2012 – The Lupus Research Institute (LRI) launched today its new Distinguished Innovator Awards program inviting proposals for $1 million grants to conduct cutting-edge projects with the greatest promise for transforming the lives of people with lupus. The awards will be given to outstanding established scientists proposing innovative projects that pair unconventional creativity with sound science to discover the fundamental causes of lupus and unlock the potential for a cure.

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