Refractory ascites in systemic lupus erythematosus: further biological support of intraperitoneal steroid treatment as a suitable therapeutical option

Clinical Rheumatology - The objective of this report was to evaluate the ascitic fluid of a patient with refractory lupus ascites (proband) at different time points—pre- and...     

C-reactive protein (CRP) polymorphisms and haplotypes are associated with SLE susceptibility and activity but not with serum CRP levels in Mexican population

To evaluate the association of C-reactive protein (CRP) polymorphisms with risk of development SLE in a group of Mexican individuals. Five CRP polymorphisms (rs3093059, rs3093062, rs1800947, rs1130864, and rs1205) were determined by PCR-restriction fragment length polymorphism and SNP rs3093061 by refractory mutation system PCR assay in 126 SLE patients and 131 controls. Four of the polymorphisms showed differences between patients and controls. rs3093061 polymorphism was associated with a lower risk of developing lupus principally in the codominant 2 (OR?=?0.219, 95% CI 0.108–0.785, P =?0.015) model. rs1130864 was associated with decreased risk mainly under codominant 1 (OR?=?0.288, 95% CI 0.143–0.581, P =?0.001) model. rs1205 was associated under the over-dominant model (OR?=?0.504, 95% CI 0.270–0.942, P =?0.032). The rs3091244 polymorphism was associated with decreased risk of SLE mostly under additive (OR?=?0.605, 95% CI 0.393–0.931. P =?0.022) model. Our study establishes that rs3093061, rs1130864, rs1205, and rs3091244 polymorphisms are associated with decreased risk of developing SLE.     

Tuberculosis and systemic lupus erythematosus: a case-control study in Mexico City

To determine, among systemic lupus erythematosus patients, factors associated with active tuberculosis. We performed a case-control study, in a tertiary-care center in Mexico City. We defined cases as systemic lupus erythematosus patients with active tuberculosis and matched them 1:1 with systemic lupus erythematosus patients without tuberculosis (controls) by age, date of systemic lupus erythematosus diagnosis, and disease duration. We analyzed clinical variables, lupus disease activity (SLEDAI-2K), and accumulated damage (SLICC/ARC-DI). We performed a nonconditional logistic regression to determine factors associated with tuberculosis. We identified 72 tuberculosis cases among systemic lupus erythematosus patients, 58% were culture confirmed. Thirty-three percent (24/72) were pulmonary only, 47.2% (34/72) extrapulmonary only, and 19.4% both. After adjustment for age, gender, and socioeconomic status, SLEDAI-2K and SLICC/ARC-DI, a 1-year cumulative dose of prednisone ≥?3 g (odds ratios (OR), 18.85; 95% confidence interval (95% CI), 6.91–51.45) was associated with tuberculosis, and the antimalarial treatment was protective (OR, 0.13; 95% CI, 0.04–0.36). Among systemic lupus erythematosus patients, cumulative dose of prednisone is associated with tuberculosis. Further research is required to elucidate the protective effect of antimalarial drugs for tuberculosis. Preventive strategies must be implemented in patients at risk.     

MCP-1, RANTES, and SDF-1 polymorphisms in Mexican patients with systemic lupus erythematosus

Chemokines and cytokines play an important role in the inflammatory development and progression of autoimmune diseases. The aim of the present study was to evaluate the role of MCP-1, SDF-1, and RANTES polymorphisms as susceptibility markers for systemic lupus erythematosus (SLE) in a group of Mexican patients. MCP-1-2518, SDF-1 G801A, and RANTES-28 polymorphisms were determined in 242 patients with SLE and 220 ethnically matched healthy controls by the polymerase chain reaction–restriction fragment length polymorphism technique. The differences between patients and healthy controls were evaluated by χ², Fisher’s exact test, and Woolf method for odds ratio. A moderately increased frequency of MCP-1-2518 A allele (p = 0.033, pC = NS) and AA genotype (p = 0.017, pC = NS) existed in SLE patients compared with healthy controls. There was a relationship between polymorphisms and some clinical and laboratory characteristics. SLE patients with and without antiphospholipid syndrome demonstrated different distribution of SDF-1 G801A genotype frequencies. On the other hand, patients with leukopenia, anti-dsDNA, and antiphospholipid autoantibodies demonstrated different MCP-1-2518 genotype distribution compared with patients without these features. Our results suggest that MCP-1 polymorphism is moderately associated with the genetic susceptibility to SLE in Mexican individuals. The polymorphisms could be related to specific clinical and laboratory characteristics in these patients.     

Meant to B: B cells as a therapeutic target in systemic lupus erythematosus

B cells have a prominent role in the pathogenesis of systemic lupus erythematosus (SLE). They are mediators of inflammation through the production of pathogenic antibodies that augment inflammation and cause direct tissue and cell damage. Multiple therapeutic agents targeting B cells have been successfully used in mouse models of SLE; however, these preclinical studies have led to approval of only one new agent to treat patients with SLE: belimumab, a monoclonal antibody targeting B cell–activating factor (BAFF). Integrating the experience acquired from previous clinical trials with the knowledge generated by new studies about mechanisms of B cell contributions to SLE in specific groups of patients is critical to the development of new treatment strategies that will help to improve outcomes in patients with SLE. In particular, a sharper focus on B cell differentiation to plasma cells is warranted.     

Systemic lupus erythematosus in Hispanics

Systemic lupus erythematosus is a serious autoimmune disease that causes significant morbidity and mortality. It is also a disease for which several clinical differences among ethnic groups have been documented. Until recently, Hispanics, as separate patient cohort, had not been included in these studies. As a result, there is currently little information concerning its characteristics both at the clinical and at the molecular levels. With the currently available data, we can ascertain that this population exhibits considerable heterogeneity, in which some genetic mutations have been detected that may confer greater susceptibility and/or protection against the disease. The important differences in the clinical manifestations include a higher rate of renal complications as well as greater mortality. The latter may be due, at least in part, to lower socio-economic levels and inappropriate access to health care. However, given the limited data available that have focused on potential molecular mechanisms that may affect the Hispanic population affected with lupus, we cannot conclude that all the differences in disease outcome, complications, and severity that affect this patient population may be due to sociological factors. We conclude that more research is required to evaluate potential genetic and molecular factors that affect Hispanic lupus patients.     

Loss of an IgG plasma cell checkpoint in patients with lupus

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