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CS-01 Differential expression of the FSTL-1 protein among patients with systemic lupus erythematosus
  1. Adriana Carlomagno1,2,
  2. Fiorella Cavalleri3,
  3. Paola Contreras1,4,
  4. José Badano3,
  5. Álvaro Danza2,
  6. José Mario Sabio5 and
  7. Carlos Escande1
  1. 1Laboratory of Metabolic Diseases and Aging – Institut Pasteur de Montevideo. Montevideo – Uruguay
  2. 2Clinical Medical ‘2’ Faculty of Medicine – Hospital Pasteur – Montevideo – Uruguay
  3. 3Laboratory of Human Molecular Genetics – Institut Pasteur de Montevideo. Montevideo – Uruguay
  4. 4Department of Physiology, Faculty of Medicine – Montevideo – Uruguay
  5. 5Unit of Autoimmune diseases, Virgen de las Nieves Hospital – Granada – Spain


Background There is an increasing prevalence of insulin resistance and metabolic syndrome in Systemic Lupus Erythematosus (SLE). Follistatin-like 1 (FSTL-1) is a secreted glycoprotein recently identified as a proinflammatory cytokine and emerging as a potential mediator of inflammation. Its plasma levels are elevated in rheumatoid arthritis and correlate with disease activity. In fact, FSTL-1 has been proposed as a marker of autoimmune diseases. However, it is not clear whether this protein plays a role in SLE. We aimed to evaluate the plasma FSTL-1 value of patients with SLE and the interactions between their plasma concentration, metabolic syndrome variables, markers of activity and disease damage.

Methods Plasma concentration of FSTL-1 of 40 female SLE patients and 20 healthy controls was measured by enzyme-linked immunosorbent assay (ELISA). Metabolic variables, activity and disease damage were measured and analyzed. The activity of SLE was determined by Systemic Lupus Erythematosus Disease Activity Index (SLEDAI-2K). Damage accumulated was calculated by the Index of Damage SLICC/ACR (SDI Damage index). A one-way ANOVA test was performed to assess the difference between the mean FSTL-1 values in different groups. Interactions between variables of the database and their effect on FSTL-1 was evaluated using a regression tree technique.

Results Healthy controls and SLE females attended on an outpatient basis had a mean of 38±16 and 40±13 years old respectively. SLE patients had low levels of activity and damage measured both by the scores and by the individual parameters of inflammatory activity. The mean value of FSTL-1 was 12213±1424 pg/ml for healthy individuals. Of the SLE patients 57% had a mean value of 4855±662.8 pg/ml and 43% had a mean of 68000±4789 pg/ml. There was a significant difference between the subgroup of SLE with high value of FSTL-1 compared to the control (p-value<0.001) and the subgroup with low value of FSTL-1 (p-value<0.001) (figure 1). From the regression analysis, we found a correlation between increasing plasma concentrations of FSTL-1 and presence of variables of metabolic syndrome (insulin, cholesterol and leptin) in patients with SLE. No correlation was found between FSLT-1 value and the activity or damage of the disease.

Conclusions FSTL-1 is significantly elevated in patients with SLE compared to controls. Moreover, elevated levels were observed in SLE patients with elevated leptin, cholesterol or insulin. More studies are needed to determine if there is a pathogenic role, and if this population have a worse long-term cardiovascular prognosis.

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