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Exploring new territory: the move towards individualised treatment.

Abstract

The main goal of therapy for lupus nephritis is to achieve remission, as this has a major impact on patient and renal survival. Furthermore, early treatment success has been shown to improve long-term prognosis. This has traditionally been achieved with intravenous cyclophosphamide, but recent data show that mycophenolate mofetil is equally effective and causes fewer adverse effects. Research is ongoing to find new treatment targets. Possible future therapies include monoclonal antibodies against CD20 (rituximab), CD22 (epratuzumab) and CD40, and therapies targeted at cytokine secretion, immunoglobulin secretion, B-cell maturation and T-cell proliferation and differentiation. Rituximab has shown promise in patients with active proliferative lupus nephritis, which suggests that B-cell depletion may be successful. Anti-double-stranded DNA antibodies correlate with flares of lupus nephritis and may represent another therapeutic target. Therapy with LIP 394, which crosslinks anti-double-stranded DNA antibodies in solution or on the B-cell surface, has been shown to reduce flares. Cardiovascular disease is a major cause of mortality in systemic lupus erythematosus, and this must also be addressed if long-term outcomes are to be improved. Many patients with systemic lupus erythematosus have subclinical atherosclerosis quite early in the disease course, and the risk of coronary artery disease at any level of traditional cardiovascular risk factors is higher than in the general population. Specific lupus-associated risk factors include the inflammatory process itself and anticardiolipin antibodies. Possible strategies to reduce the risk include reduction of disease activity to improve endothelial function and reduction of steroid dose whenever possible. Therapy with aspirin or statins may be another possibility. Thus treatment of lupus nephritis is evolving from standardised therapy to individualised therapy based on analysis of organ involvement, risk factors and cytokine, antibody or cell profiles.

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  • Publisher Full Text
  • Authors+Show Affiliations

    Department of Nephrology, Medical School Hannover, Hannover, Germany. Haubitz.Marion@MH-Hannover.de

    Source

    Lupus 16:3 2007 pg 227-31

    MeSH

    Antibodies, Monoclonal
    Antibodies, Monoclonal, Murine-Derived
    Atherosclerosis
    Humans
    Immunologic Factors
    Immunosuppressive Agents
    Lupus Erythematosus, Systemic
    Lupus Nephritis
    Mycophenolic Acid
    Oligonucleotides
    Rituximab
    Time Factors

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    17432112

    Citation

    Haubitz, M. "Exploring New Territory: the Move Towards Individualised Treatment." Lupus, vol. 16, no. 3, 2007, pp. 227-31.
    Haubitz M. Exploring new territory: the move towards individualised treatment. Lupus. 2007;16(3):227-31.
    Haubitz, M. (2007). Exploring new territory: the move towards individualised treatment. Lupus, 16(3), pp. 227-31.
    Haubitz M. Exploring New Territory: the Move Towards Individualised Treatment. Lupus. 2007;16(3):227-31. PubMed PMID: 17432112.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Exploring new territory: the move towards individualised treatment. A1 - Haubitz,M, PY - 2007/4/17/pubmed PY - 2007/5/11/medline PY - 2007/4/17/entrez SP - 227 EP - 31 JF - Lupus JO - Lupus VL - 16 IS - 3 N2 - The main goal of therapy for lupus nephritis is to achieve remission, as this has a major impact on patient and renal survival. Furthermore, early treatment success has been shown to improve long-term prognosis. This has traditionally been achieved with intravenous cyclophosphamide, but recent data show that mycophenolate mofetil is equally effective and causes fewer adverse effects. Research is ongoing to find new treatment targets. Possible future therapies include monoclonal antibodies against CD20 (rituximab), CD22 (epratuzumab) and CD40, and therapies targeted at cytokine secretion, immunoglobulin secretion, B-cell maturation and T-cell proliferation and differentiation. Rituximab has shown promise in patients with active proliferative lupus nephritis, which suggests that B-cell depletion may be successful. Anti-double-stranded DNA antibodies correlate with flares of lupus nephritis and may represent another therapeutic target. Therapy with LIP 394, which crosslinks anti-double-stranded DNA antibodies in solution or on the B-cell surface, has been shown to reduce flares. Cardiovascular disease is a major cause of mortality in systemic lupus erythematosus, and this must also be addressed if long-term outcomes are to be improved. Many patients with systemic lupus erythematosus have subclinical atherosclerosis quite early in the disease course, and the risk of coronary artery disease at any level of traditional cardiovascular risk factors is higher than in the general population. Specific lupus-associated risk factors include the inflammatory process itself and anticardiolipin antibodies. Possible strategies to reduce the risk include reduction of disease activity to improve endothelial function and reduction of steroid dose whenever possible. Therapy with aspirin or statins may be another possibility. Thus treatment of lupus nephritis is evolving from standardised therapy to individualised therapy based on analysis of organ involvement, risk factors and cytokine, antibody or cell profiles. SN - 0961-2033 UR - https://www.unboundmedicine.com/medline/citation/17432112/Exploring_new_territory:_the_move_towards_individualised_treatment_ L2 - http://journals.sagepub.com/doi/full/10.1191/0961203306075616?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -