Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comparative Study
. 2016 Jul 21;11(7):e0159384.
doi: 10.1371/journal.pone.0159384. eCollection 2016.

Metabolic Profiling of Systemic Lupus Erythematosus and Comparison with Primary Sjögren's Syndrome and Systemic Sclerosis

Anders A Bengtsson  1 , Johan Trygg  2 , Dirk M Wuttge  1 , Gunnar Sturfelt  1 , Elke Theander  3 , Magdalena Donten  4 , Thomas Moritz  5 , Carl-Johan Sennbro  6 , Frida Torell  2 , Christian Lood  1 , Izabella Surowiec  2 , Stefan Rännar  4 , Torbjörn Lundstedt  4
Affiliations
Comparative Study

Metabolic Profiling of Systemic Lupus Erythematosus and Comparison with Primary Sjögren's Syndrome and Systemic Sclerosis

Anders A Bengtsson et al. PLoS One. .

Abstract

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease which can affect most organ systems including skin, joints and the kidney. Clinically, SLE is a heterogeneous disease and shares features of several other rheumatic diseases, in particular primary Sjögrens syndrome (pSS) and systemic sclerosis (SSc), why it is difficult to diagnose The pathogenesis of SLE is not completely understood, partly due to the heterogeneity of the disease. This study demonstrates that metabolomics can be used as a tool for improved diagnosis of SLE compared to other similar autoimmune diseases. We observed differences in metabolic profiles with a classification specificity above 67% in the comparison of SLE with pSS, SSc and a matched group of healthy individuals. Selected metabolites were also significantly different between studied diseases. Biochemical pathway analysis was conducted to gain understanding of underlying pathways involved in the SLE pathogenesis. We found an increased oxidative activity in SLE, supported by increased xanthine oxidase activity and an increased turnover in the urea cycle. The most discriminatory metabolite observed was tryptophan, with decreased levels in SLE patients compared to control groups. Changes of tryptophan levels were related to changes in the activity of the aromatic amino acid decarboxylase (AADC) and/or to activation of the kynurenine pathway.

PubMed Disclaimer

Conflict of interest statement

Competing Interests: JT, TM, and TL are shareholders and managers of AcureOmics AB. Magdalena Donten is employed by AcureOmics AB. Carl-Johan Sennbro is employed by Leo Pharma A/S. There are no patents, products in development, or marketed products to declare. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials.

Figures

Fig 1
Fig 1. PCA model overview of the three different clinical SLE phenotypes.
PCA model parameters: R2X(cum) = 0.522, Q2(cum) = 0.138, 4 components.
Fig 2
Fig 2. PCA model overview SLE and control group (HV), and the two related disease groups (pSS, SSc).
PCA model parameters: R2X(cum) = 0.602, Q2(cum) = 0.158, 8 components.
Fig 3
Fig 3
Cooman's plot was used to assess specificity and sensitivity of metabolic profiles to distinguish between A) SLE and control group (HV). B) The same model was used to predict SSc and pSS groups.
Fig 4
Fig 4. P(corr) profile for the metabolites significant for the separation (p < 0.05) between SLE and control group (HV).
Fig 5
Fig 5. Metabolic profiles (p(corr) values) from OPLS-DA models between SLE versus healthy volunteers (HV) (blue),SSc versus HV (red) and pSS versus HV (gray).
See this image and copyright information in PMC

Comment in

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Stahl-Hallengren C, Jonsen A, Nive O, Sturfelt G. Incidence studies of systemic lupus erythematosus in Southern Sweden: increasing age, decreasing frequency of renal manifestations and good prognosis. J Rheumatol. 2000; 27(3): 685–691. - PubMed
    1. Rahman A, Isenberg DA. Systemic lupus erythematosus. New Engl J Med. 2008; 358: 929–939. 10.1056/NEJMra071297 - DOI - PubMed
    1. Liu CC, Ahearn JM. The search for lupus biomarkers. Best Practice Res. 2009; 23: 507–523 - PMC - PubMed
    1. Fries J. F, Holman, H. R. Systemic lupus erythematosus: a clinical analysis. Major Probl Intern Med. 1975; 6: v–199. - PubMed
    1. Sturfelt G, Sjöholm AG. Complement components, complement activation, and acute phase response in systemic lupus erythematosus. Int Arch Allergy Appl Immunol. 1984; 75: 75–83. - PubMed

Publication types

Grants and funding

This research was supported by Medical Faculty at Lund University (AB, DMW), The Craford Foundation (AB, DMW), Greta and Johan Kock’s Foundation (AB, DMW), King Gustaf V’s 80th Birthday Foundation (AB), Lund University Hospital (AB), the Swedish Rheumatism Association (AB), Österlund’s Foundation (AB), the Biology of Liver and Pancreatic Development and Disease (BOLD) Marie Curie Initial Training Network (MCITN) within EU’s FP7 program (TL, JT, SC), and Swedish Research Council grant no. 2011-6044 (JT, FT). AcureOmics AB and Leo Pharma A/S provided support in the form of salaries for authors MD and CJS. The specific roles of these authors are articulated in the "author contributions" section. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.