Elisabet Svenungsson

Elisabet Svenungsson

Senior Forskare | Docent
Besöksadress: D2:01, Karolinska Universitetssjukhuset, 17176 Stockholm
Postadress: K2 Medicin, Solna, K2 Reuma Antovic A, 171 77 Stockholm

Om mig

  • I studied medicine at Karolinska Institutet and did my internship at Örebro
    hospital. Thereafter, I worked at Karolinska University Hospital as a
    resident and became a specialist in Rheumatology and in Internal medicine in
    1994. I have since worked with Rheumatology with a special interest in
    systemic lupus erythematosus (SLE) and related systemic autoimmune diseases.
    I defended my thesis on “Cardiovascular Disease in Systemic lupus
    Erythematosus” in 2003.
    During many years I worked with medical responsibility for the inpatient
    rheumatology ward, and during that time I also organised the clinical
    education for medical students in Rheumatology. Presently, I hold a position
    as senior consultant and adjunct professor in Rheumatology. I split my time
    between clinical work and clinical/translational research.
    I have several international collaborations, and I am now the president of
    SLEuro and a member of the international Systemic Lupus Erythematosus
    International Collaborating Clinics (SLICC) group.


  • *My research is mainly focused on: *
    * Autoimmune mechanisms contributing to cardiovascular disease in SLE, in
    the antiphospholipid syndrome (APS) and in the general population.
    * Identifying sub-phenotypes in systemic lupus erythematosus (SLE)
    Together with colleagues I initiated the Karolinska SLE cohort in 1995 and
    the Karolinska APS cohort in 2009. Over the years we have collected
    detailed clinical information and stored samples and information regarding
    approximately 750 SLE patients, 200 APS patients and matched controls.
    *Major lines of research *
    We have studied why patients with systemic autoimmune diseases, primarily,
    SLE, but also Systemic sclerosis (SSc) and APS, are affected with premature
    cardiovascular disease. Our studies have demonstrated that pro-thrombotic
    antiphospholipid antibodies (aPL), nephritis/impaired renal function,
    systemic inflammation with endothelial activation as well as genetic
    predisposition are SLE associated risk factors, which predict cardiovascular
    mortality (CVM) and the first cardiovascular events in patients with SLE. In
    a more recent study we could show that in comparison to age and gender
    matched controls, it is only the SLE subgroup with nephritis (30-40%), which
    is affected with accelerated atherosclerosis, measured as carotid plaques
    with ultrasound. “Non-nephritis” SLE patients did not differ from
    controls regarding carotid plaques.
    We have also demonstrated that genetic susceptibility is important for SLE
    associated CVD. This work has identified STAT4, HLA-DRB1*04 and HLADRB1*13 as
    risk alleles for SLE associated CVD and the same risk alleles were also
    associated with pro-thrombotic (aPL) in SLE patients.
    A more recent research focus has been to identify more homogeneous sub-groups
    among patients with SLE. Using various types of cluster analyses we have
    demonstrated that there are several fairly distinct subgroups of SLE
    patients. In particular we have studied differences between patients with SLE
    and APS and patients with SLE and Sjögren’s syndrome. Notably there is
    very little overlap between these two groups.
    *Selected publications:*
    1) Svenungsson E, Gustafsson JT, Grosso G, Rossides M, Gunnarsson I,
    Jensen-Urstad K, et al. Complement deposition, C4d, on platelets is
    associated with vascular events in systemic lupus erythematosus.
    Rheumatology (Oxford). 2020.
    2) Grosso G, Sippl N, Kjellstrom B, Amara K, de Faire U, Elvin K, et al.
    Antiphospholipid Antibodies in Patients With Myocardial Infarction. Ann
    Intern Med. 2019(170):277-80.
    3) Idborg H, Eketjall S, Pettersson S, Gustafsson JT, Zickert A, Kvarnstrom
    M, et al. TNF-alpha and plasma albumin as biomarkers of disease activity
    in systemic lupus erythematosus. Lupus science &
  • medicine.
  • 5(1):e000260.
    4) Gustafsson JT, Herlitz Lindberg M, Gunnarsson I, Pettersson S, Elvin K,
    Ohrvik J, et al. Excess atherosclerosis in systemic lupus
    erythematosus, -A matter of renal involvement: Case control study of 281
    SLE patients and 281 individually matched population controls. PLoS One.
  • 12(4):e0174572.
    5) Gustafsson JT, Gunnarsson I, Kallberg H, Pettersson S, Zickert A,
    Vikerfors A, et al. Cigarette smoking, antiphospholipid antibodies and
    vascular events in Systemic Lupus Erythematosus. Ann Rheum Dis.
  • 74(8):1537-43.
    6) Lundstrom E, Gustafsson JT, Jonsen A, Leonard D, Zickert A, Elvin K, et
    al. HLA-DRB1*04/*13 alleles are associated with vascular disease and
    antiphospholipid antibodies in systemic lupus erythematosus. Annals of
    the rheumatic diseases. 2013
  • 72(6):1018-25.


Alla övriga publikationer


  • Senior Forskare, Medicin, Solna, Karolinska Institutet, 2024-

Examina och utbildning

  • Docent, Reumatologi, Karolinska Institutet, 2010
  • MEDICINE DOKTORSEXAMEN, Institutionen för medicin, Solna, Karolinska Institutet, 2003


  • Esin Ylmaz, The impact of female hormonal fluctuations on SLE features and damage, 2023
  • Sara Brolin, Educational needs, quality of life, and health care support in persons with systemic rheumatic disease, 2023
  • Natali Karandyszowska, Diagnostic and therapeutic challenges in patients with antiphospholipid syndrome, 2021

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