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FRI0299 N-terminal pro-brain natriuretic peptide (NT-PROBNP) level in patients with untreated systemic lupus erythematosus
  1. T Panafidina,
  2. M Sokhova,
  3. T Popkova,
  4. D Novikova,
  5. E Alexandrova,
  6. E Nasonov
  1. V.A.Nasonova Research Institute of Rheumatology, Moscow, Russian Federation

Abstract

Objectives The aim of this study was to determine NT-proBNP serum levels in patients with untreated SLE, thus ruling out any potential effect of SLE therapy: to analyze any possible correlation between NT-proBNP values and traditional risk factors (TRF), inflammatory markers and myocardial function parameters.

Methods The study included 28 pts (82% females, aged 28,5 [25,0–32,0] years (median [interquartile range 25%>75%]) with untreated SLE (ACR criteria, 1997) and 27 healthy controls (89% females, age 30,0 [23,0–49,0] years). None of SLE pts was treated either with prednisone or cytotoxic drugs at the moment of inclusion, 5 (18%) pts received hydroxychloroquine 200 mg/day. SLE-related factors, including disease duration, clinical features, SLE Disease Activity Index (SLEDAI 2K) and Systemic Lupus International Collaborating Clinics damage index (SLICC/DI) were evaluated in parallel with relevant laboratory findings (blood and urine tests, CRP, IL-6, INF-α, immunoglobulins G, A and M, C3 and C4 complement fragments and others), autoantibodies (ANA, antiDNA, ENA-SSA, -SSB, -Sm, -RNP-70, aPL), echocardiography was performed using standard techniques. Serum levels of NT-proBNP (pg/ml) were measured using electrochemiluminescence method Elecsys proBNP II (Roche Diagnostics, Switzerland). Normal NT-proBNP levels should vary within ≤125,0 pg/mL.

Results Mean SLE duration was 21,0 [5,0–60,0] months, SLEDAI 2K score - 11 [8–9], SLICC/DI score - 0 [0–0]. SLE pts had higher levels of NT-proBNP vs control (160,7 [88,6–335,4] vs 55,2 [36,6–70,3] pg/ml, p<0,001). Elevated levels of NT-proBNP (>125,0 pg/ml) was detected in 18 (64%) SLE pts. In SLE pts NT-proBNP serum levels showed positive correlation with creatinine (r=0,480, p<0,01), uric acid (r=0,427, p<0,05), ACL IgG (r=0,710, p<0,001), antiDNA (r=0,395, p<0,05), ANA levels (r=0,256, p<0,05), left ventricle (LV) end-systolic dimension (r=0,442, p<0,05), mean pulmonary artery pressure (r=0,486, p<0,05); and negative correlation with hemoglobin level (r=-0,493, p<0,01), C4 complement component (r=-0,475, p<0,05), glomerular filtration rate (r=-0,558, p<0,01) and LV ejection fraction (r=-0,505, p<0,01); left ventricular diastolic dysfunction (DDLV) was only in pts with NT-proBNP levels >125,0 pg/ml. Mean NT-proBNP concentration in verified DDLV cases (n=5 (18%)) considerably exceeded normal values, reaching up to 799,2 [276,6–1777,0] pg/ml.

Conclusions Untreated SLE patients without a history of myocardial infarction, coronary procedure or any evidence of heart failure demonstrated higher NT-proBNP concentration as compared to healthy controls (p<0,001). NT-proBNP levels showed correlation with numerous SLE markers (ACL IgG, ANA, antiDNA, C4 fragment of complement), kidney function (creatinine, uric acid, glomerular filtration rate) and myocardial function (end-systolic dimension of the LV, mean pulmonary artery pressure, LV ejection fraction). No correlation was documented between NT-proBNP concentration and TRF or inflammatory markers (CRP, IL-6, INF-α). All abovementioned data suggest presumable SLE-associated autoimmune damage of cardiomyocytes and/or mediated decrease of myocardial function caused by kidney disease.

Disclosure of Interest None declared

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