2000
DOI: 10.1093/rheumatology/39.4.399
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A prospective study of survival and prognostic indicators of systemic lupus erythematosus in a southern Chinese population

Abstract: The survival of SLE in our southern Chinese patients is similar to that of the Caucasian series reported in the 1990s. Although nephritis contributes to organ damage, it is not a major determinant for survival. Infection remains the commonest cause of death. High-dose steroid treatment and thrombocytopenia are independent risk factors for mortality. Judicious use of immunosuppressive agents is necessary to improve the short-term survival of SLE.

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Cited by 183 publications
(163 citation statements)
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“…A PubMed search revealed 6 studies of SMRs in SLE patients, 12 in RA patients, 3 in PsA patients, 3 in SSc patients, and 3 in SV patients (9,. There was only one study on SMR in AS patients, published in 1993 (39).…”
Section: Life Expectancy Smrs and Causes Of Death In Rheumatic Disementioning
confidence: 99%
“…A PubMed search revealed 6 studies of SMRs in SLE patients, 12 in RA patients, 3 in PsA patients, 3 in SSc patients, and 3 in SV patients (9,. There was only one study on SMR in AS patients, published in 1993 (39).…”
Section: Life Expectancy Smrs and Causes Of Death In Rheumatic Disementioning
confidence: 99%
“…Among many organs affected in SLE, the kidney may be most frequent and severely injured. The incidence of lupus nephritis (LN) is 40%~80%, and LN remains a major cause of morbidity and mortality in patients with SLE (1). Treatment of SLE is difficult as it is hard to balance the efficacy and safety of drugs.…”
Section: Introductionmentioning
confidence: 99%
“…[13][14][15] Familial subphenotypes of SLE may be the result of fewer genes compared with overall disease susceptibility, and stratifying by subphenotypes may reduce heterogeneity and facilitate the identification of gene polymorphisms associated with SLE. One such subphenotype, thrombocytopenia, is an independent marker for severe and deadly SLE, [16][17][18][19] and stratification for thrombocytopenia found evidence for linkage to 1q23, a region involving the FasL gene, as well as suggestive linkage to a region on 10q24 in close proximity to FAS. 20 The Fas and FasL genes are considered possible candidate genes in human SLE, since evidence from animal models of lupus with defective Fas and FasL expression point to a role for FasL-mediated apoptosis in the pathogenesis of SLE.…”
Section: Introductionmentioning
confidence: 99%