THU0302 Hepcidin, Interleukin-6 and Anemia of Chronic Inflammation in Systemic Lupus Erythematosus (SLE). (23rd January 2014)

• Record Type: Journal Article
• Authors: Mok, C. C.; Birmingham, D.; Ho, L. Y.; Hebert, L.; Rovin, B.
• Is Part Of: Annals of the rheumatic diseases. Volume 72:Supplement 3(2013)
• Page Start: A268
• Page End: A268
• Publication Date: 2014-01-23
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2013-eular.830
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: Hepcidin is an acute phase reactant produced by hepatocytes that has been linked to anemia of chronic inflammation. Objectives: To evaluate the serum hepcidin and interleukin (IL)-6 levels in patients with SLE and their relationship with hemoglobin, disease activity and organ damage. Methods: Consecutive patients who fulfilled ³4 ACR criteria for SLE were recruited. Those with obvious cause(s) of anemia such as active hemolysis, iron deficiency, clinical evidence of chronic or acute blood loss, thalassemia trait and nutritional deficiency were excluded. Blood was taken from the participants at 9am in the morning for the assay of hepcidin (peptide enzyme immunoassay; Peninsula Lab, USA), IL-6 (Meso Scale Discovery, USA), high-sensitivity C-reactive protein (hsCRP) (Siemens Healthcare Diagnostics, Inc., USA) and hemoglobin level. SLE disease activity was assessed by the SELENA-SLEDAI and physician's global assessment (PGA) scores. Organ damage of SLE was assessed by the ACR/SLICC damage index (SDI). Correlation among hepcidin, IL-6, hsCRP, disease activity and damage score of SLE was performed by Pearson's correlation and linear regression. Results: 289 SLE patients were invited but 72 were excluded because of obvious causes of anemia (renal insufficiency N=46; active hemolysis N=4; iron deficiency N=4; thalassemia N=18). Finally, 217 patients were studied (94% women). The mean age at SLE onset was 32.1±13 years and the mean disease duration was 7.3±6.1 years. At the time of venepuncture, the mean SLEDAI score was 4.3±4.7 (median 3.5) and the mean PGA score was 0.70±0.7 (median 0.5). 85 (39%) patients had clinically active SLE and 80 (37%) other patients had active SLE serology (elevated anti-dsDNA or depressed complements, or both) without clinical signs or symptoms. Anemia, defined as a hemoglobin level of <11.6g/dL in women and <13.4g/dL in men, was present in 74 (34%) patients who did not have any obvious cause(s) other than anemia of inflammation. Among patients with anemia, clinical SLE activity was present in 40 (54%) patients and serological activity was present in 33 (45%) patients. The mean serum hepcidin, IL-6 and hsCRP levels were 20.7±28.1 (median 11.5) ng/ml, 1.60±3.91 (median 0.30) pg/ml and 4.49±11.0 (median 0.94) mg/L, respectively. Hepcidin level correlated significantly with the total SLEDAI score (r=0.14, p=0.046), clinical SLEDAI score (total SLEDAI scores minus those contributed by lupus serology) (r=0.16; p=0.02), PGA score (r=0.23; p=0.001), as well as IL-6 (r=0.26; p<0.001) and hsCRP level (r=0.47, p<0.001). Moreover, hepcidin level correlated negatively and significantly with the hemoglobin level (r=-0.21, p=0.002). The levels of hepcidin, IL-6 and hsCRP were significantly higher in patients with anemia than those without (28.4±33.6 vs 16.7±24 ng/ml, p=0.009; 2.76±5.5 vs 1.00±2.6ng/ml, p=0.01; and 8.53±17 vs 2.39±5.0 mg/L, p=0.003, respectively). However, hepcidin level did not correlate significantly with anti-dsDNA titer, complement levels or SLE damage SDI scores. Conclusions: In patients with SLE, the serum hepcidin, IL-6 and hsCRP levels are elevated in relation with clinic disease activity. This acute phase response to systemic inflammation is associated with the development of anemia of chronic inflammation. Disclosure of Interest: None Declared