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PubMed1982

Tuberculosis in patients with systemic lupus erythematosus.

Tuberculosis associated with systemic lupus erythematosus (SLE) was studied in a cohort of 311 patients seen between 1963 to 1979. There were 16 such patients, giving rise to a prevalence rate of 5%. The characteristics of SLE-associated tuberculosis include a high incidence of miliary and far-advanced pulmonary disease, delay in establishing diagnosis, especially the extrapulmonary form, and tendency to attribute symptoms like fever, malaise, and weight loss to the lupus process. Treatment was successful in 9 patients. Of the 7 death 5 were attributed directly to the mycobacterial infection and 2 to complications of SLE.

Adolescent↗

PubMed1984

Amyloidosis and systemic lupus erythematosus.

A patient with systemic lupus erythematosus who developed reactive amyloidosis associated with high levels of serum amyloid-A protein (SAA) is reported. The possible relevance of elevated SAA levels in the aetiology of amyloidosis is discussed.

Amyloidosis↗

PubMed2003

Mycophenolate mofetil prevents a clinical relapse in patients with systemic lupus erythematosus at risk.

BACKGROUND: Systemic lupus erythematosus (SLE) is characterised by the presence of antibodies to double stranded DNA (dsDNA), which are involved in the pathogenesis of SLE. Previous studies showed that at least two thirds of patients develop a clinical relapse within six months after a significant rise in the anti-dsDNA level, and most relapses were prevented by the administration of corticosteroids at the time of the rise. OBJECTIVE: To determine whether mofetil mycophenolate (MMF) can prevent a clinical relapse without the side effects associated with corticosteroids. METHODS: 36 patients with SLE were examined monthly to determine whether a rise in anti-dsDNA level had occurred. A rise was defined as an increase of 25% of the level of the previous sample of at least 15 IU/ml within a four month period. After a rise patients were treated with MMF 2000 mg daily for six months. Patients were monitored monthly for the occurrence of a clinical relapse and to assess the serological activity and state of activation of CD4+, CD8+, and CD19+ lymphocyte subsets. RESULTS: Anti-dsDNA rose in 10 patients. Treatment with MMF was started in all these patients, and after six months no clinical relapse had occurred. Side effects were minimal. Antibodies to dsDNA decreased during the treatment (p<0.001), associated with a decrease in the state of activation of CD19+ lymphocytes. No changes were found in the state of activation of CD4+ or CD8+ lymphocyte subsets. CONCLUSION: Administration of MMF after a rise in antibodies to dsDNA is well tolerated, decreases anti-dsDNA and B cell activation, and seems to prevent the occurrence of a clinical relapse in patients with SLE.

Adult↗

PubMed1979

HLA-linked C2 deficiency in a Dutch patient with systemic lupus erythematosus.

A patient with systemic lupus erythematosus was studied whose blood serum on repeated occasions showed undetectable levels of haemolytic omplement (C). A detailed investigation of individual C components in the serum of the proposita and her family revealed the absence of functional C2 in the patient and half-normal values in the relatives. C4 levels in the family, but not in the patient, were above normal, whereas the levels of factor B were low in all cases. No abnormalities were noted in C3, C9, or C1INH. Tissue typing showed linkage of the C2-deficiency gene with the HLA-A10/B18 and A9/B18 haplotypes. No linkage with red cell antigens and no relationship with plasma kallikrein levels was found.

Adolescent↗

PubMed1976

Unilateral cataplexy associated with systemic lupus erythematosus.

A patient with systemic lupus erythematosus (SLE) developed attacks of unilateral cataplexy precipitated by laughter. Unilateral cataplexy has not been described previously in detail and its association with SLE is unique. The clinical details, investigations, and diagnostic criteria are discussed and a causal relationship between cataplexy and SLE is suggested.

Adult↗

PubMed2005

[Systemic lupus erythematosus in children].

Pediatric systemic lupus erythematosus (pSLE) is a chronic mutisystemic autoimmune disease with complex clinical manifestations. Although the presentation, clinical manifestations, immunological findings and treatment issues of pSLE are similar to those of adult SLE patients, there are special issues which need to be considered when dealing with SLE in children. During the last decade survival has improved remarkably as a result of earlier diagnosis, recognition of milder disease and better approaches to therapy. However, pSLE remains a potentially serious condition. Although the pathogenesis of SLE remains poorly understood, susceptibility involves a combination of environmental, hormonal and genetic factors. Better understanding of SLE pathogenesis will hopefully lead to more specific and less toxic therapies for this disease.

Child↗

PubMed1995

Minimal-change nephrotic syndrome associated with systemic lupus erythematosus.

A case of systemic lupus erythematosus (SLE) associated with minimal-change nephrotic syndrome (MCNS) is described. A 41-year-old woman with SLE presented with symptoms of nephrotic syndrome. Renal biopsy revealed minor glomerular abnormalities without the deposition of immune complexes. The initial heavy proteinuria promptly decreased after the prednisolone dosage was increased and disappeared 4 weeks later. The patient had a relapse of nephrotic syndrome without exacerbation of immunoserological reactions when the prednisolone dose was subsequently decreased. Remission was achieved 5 days after methylprednisolone pulse therapy. T cell dysfunction, which is present both in SLE and MCNS, might have triggered MCNS during the course of SLE.

Adult↗

PubMed1984

Tubular dysfunction in systemic lupus erythematosus.

20 patients with systemic lupus erythematosus undergoing renal biopsies had their tubular function assessed by maximal concentrating ability, maximal urinary acidification and fractional urinary excretion of beta 2-microglobulin. 80% of patients showed disturbances in one or more of the parameters tested with fractional beta 2-microglobulin excretion being most frequently abnormal. No correlation was found between the histological changes and functional disturbances.

Adolescent↗

PubMed1993

Interleukin-3 immunoassay in systemic lupus erythematosus patients: preliminary data.

Systemic lupus erythematosus (SLE) may be associated with thrombocytopenia on one hand and lymphoma on the other. Interleukin-3 (IL-3) may contribute to both conditions. IL-3 is a pleotrophic growth factor affecting the proliferation and differentiation of stem cells to committed progenitors of several hematopoietic lineages including megakaryocytes and lymphocytes. The serum level of IL-3 determined by ELISA was found to be higher in a cohort of 16 patients with SLE in comparison to health controls. The IL-3 levels were highest in 2 patients with SLE and lymphoma. Interestingly, low serum levels were detected in SLE patients with thrombocytopenia. Our preliminary results may point to the role of IL-3 in the hematopoietic changes observed in SLE.

Enzyme-Linked Immunosorbent Assay↗

PubMed1993

Involvement of the local immune response in a case of advanced cervical cancer in a patient with systemic lupus erythematosus.

Although patients with systemic lupus erythematosus (SLE) have frequently accompanying malignancies, there are few documented cases in the literature of advanced cervical cancer patients with SLE. This report describes a case of advanced cervical cancer in a 39-year-old patient with a 20-year history of SLE (FIGO stage IIIb) and evaluates the immunological response of the tumor. The clinical course of this patient with SLE, with rapid growth of cervical cancer and a poor prognosis, may suggest that T cells play a key role in the growth of cancer.

Adult↗

PubMed1990

A conserved idiotype and antibodies to retroviral proteins in systemic lupus erythematosus.

22 of 61 systemic lupus erythematosus (SLE) patients produced antibodies to the p24 gag protein of HIV-1 demonstrated by Western blotting. 20 of these 22 patients (91%) also express the 4B4 idiotype (Id 4B4) previously identified on a human anti-Sm monoclonal antibody called 4B4. This represents an enrichment for this Id (seen in only 52% of SLE patients generally). Eight of these 22 SLE patients also have anti-Sm antibody activity. Sm partially inhibits the antibody binding of p24 gag suggesting immunologic cross-reactivity between the retroviral antigen p24 gag and the autoantigen Sm. Anti-Id 4B4 also inhibits p24 gag antibody binding by as much as 40%. Finally the monoclonal antibody 4B4 showed cross-reactivity to Sm and p24 gag. The following points emerge from our studies: (a) SLE patients make antibodies to p24 gag of HIV-1, (b) there is a relationship between immunity to p24 gag and a conserved idiotype, and (c) anti-Sm antibodies can cross-react with p24 gag.

Autoantigens↗

PubMed1995

Population and family studies of three disease-related polymorphic genes in systemic lupus erythematosus.

The contribution to systemic lupus erythematosus (SLE) of three lupus-associated polymorphisms (involving the C4A2 complement component, Humhv3005 and the T cell antigen receptor alpha chain gene) are investigated in 81 individuals from 14 multiplex SLE families, 41 unrelated lupus patients, and 88 unrelated healthy controls. The results show a strong association between C4A deletion and SLE in these families. While the current study confirms the previously reported association between hv3005 deletion and sporadic SLE, the study fails to support this association in familial SLE patients. Moreover, no correlation is detected between the occurrence of hv3005 deletion and C4A null alleles in lupus patients, suggesting that the effects of these genetic polymorphisms on predisposition to lupus are independent. The previously reported lupus-associated T cell receptor (TCR) alpha chain polymorphism is not detected in any of the individuals studied here. The combined data suggest that C4A null alleles predispose strongly to development of lupus, whereas the influence of hv3005 deletion is relatively weak. The results also suggest that contributions of weak susceptibility genes such as hv3005 to disease predisposition may be obscured by the effects of stronger genetic factors and thus need to be examined in patients lacking these factors.

Base Sequence↗

PubMed1997

Elevated anticardiolipin antibodies in autoimmune haemolytic anaemia irrespective of underlying systemic lupus erythematosus.

In patients with systemic lupus erythematosus (SLE) and concomitant Coombs positive autoimmune haemolytic anaemia (AIHA) anticardiolipin antibodies (aCL) are found more frequently and at higher titres than in SLE patients without AIHA. In order to assess if aCL elevation is primarily associated with the underlying SLE, or with AIHA itself, we examined AIHA patients with and without underlying SLE for the presence of aCL. aCL (IgG and IgM) were determined by ELISA in 74 SLE patients without AIHA, 22 SLE patients with AIHA, 50 patients with idiopathic AIHA (warm-reactive autoantibodies), 52 patients with idiopathic AIHA (cold-reactive autoantibodies) and 50 healthy controls. The mean IgG and IgM aCL titres in SLE patients without AIHA (IgG 37.0 U/ml, IgM 8.9 U/ml) were significantly elevated compared with the values in healthy controls (IgG 9.1 U/ml, IgM 3.2 U/ml; P < 0.005). The mean aCL levels in SLE patients with AIHA (IgG 53.2 U/ml, IgM 28.2 U/ml) were higher than in SLE patients without AIHA (P = 0.09 for IgG, P < 0.005 for IgM). Interestingly, the mean aCL levels of patients with idiopathic AIHA (warm-reactive autoantibody type: IgG 29.2 U/ml, IgM 19.3 U/ml; cold-reactive autoantibody type: IgG 27.4 U/ml, IgM 18.9 U/ml) were also significantly elevated compared with healthy controls P < 0.001). As aCL are elevated not only in SLE (with and without concomitant AIHA) but also in idiopathic AIHA it can be speculated that aCL are involved in the pathomechanism of autoantibody-induced erythrocyte destruction per se irrespective of an underlying SLE.

Anemia, Hemolytic, Autoimmune↗

PubMed2006

The spliceosomal autoantigen heterogeneous nuclear ribonucleoprotein A2 (hnRNP-A2) is a major T cell autoantigen in patients with systemic lupus erythematosus.

A hallmark of systemic lupus erythematosus (SLE) is the appearance of autoantibodies to nuclear antigens, including autoantibodies directed to the heterogeneous nuclear ribonucleoprotein A2 (hnRNP-A2), which occur in 20% to 30% of SLE patients as well as in animal models of this disease. To investigate the underlying cellular reactivity and to gain further insight into the nature and potential pathogenic role of this autoimmune response we characterized the T cell reactivity against hnRNP-A2 in patients with SLE in comparison to healthy controls. Cellular proliferation of peripheral blood T cells to hnRNP-A2 was determined by [3H]thymidine incorporation and T cell clones (TCCs) specific for hnRNP-A2 were grown by limiting dilution cloning; IFNgamma, IL-4 and IL-10 in culture supernatants were measured by ELISA. Bioactivity of culture supernatants was determined by incubation of anti-CD3/anti-CD28 stimulated peripheral blood CD4+ T cells with supernatants of TCCs. Stimulation assays performed with peripheral blood mononuclear cells of 35 SLE patients and 21 healthy controls revealed pronounced proliferative responses in 66% of SLE patients and in 24% of the controls, which were significantly higher in SLE patients (p < 0.00002). Furthermore, hnRNP-A2 specific TCCs generated from SLE patients (n = 22) contained a relatively high proportion of CD8+ clones and mostly lacked CD28 expression, in contrast to TCCs derived from healthy controls (n = 12). All CD4+ TCCs of patients and all control TCCs secreted IFNgamma and no IL-4. In contrast, CD8+ TCCs of patients secreted very little IFNgamma, while production of IL-10 did not significantly differ from other T cell subsets. Interestingly, all CD8+ clones producing IL-10 in large excess over IFNgamma lacked expression of CD28. Functional assays showed a stimulatory effect of the supernatants derived from these CD8+ CD28- hnRNP-A2 specific TCCs that was similar to that of CD4+ CD28+ clones. Taken together, the pronounced peripheral T cell reactivity to hnRNP-A2 observed in the majority of SLE patients and the distinct phenotype of patient-derived CD8+ TCCs suggest a role for these T cells in the pathogenesis of SLE.

Adult↗

PubMed2001

Assessing depression in systemic lupus erythematosus: determining reliable change.

Systemic lupus erythematosus (SLE) can follow an unpredictable course. Clinicians and researchers use various self-report inventories to track aspects of the patient's functioning during the course of the illness (e.g. health status, pain, fatigue, quality of life and psychological status). These self-report inventories are used to measure improvement or deterioration as a function of the natural history of the disease process, or as a function of response to treatment. Proper interpretation of scores derived from these inventories requires an understanding of their psychometric properties, in particular, their reliability. It is important to calculate reliable change difference scores for tests commonly used in rheumatology so clinicians can determine if a change score is a reliable indicator of improvement or deterioration in individual patients (i.e. the change score is not likely to be due to measurement error). The purpose of this article is to illustrate the use of the reliable change difference scores when assessing depression in patients with SLE using the Beck Depression Inventory (BDI).

Depression↗

PubMed2004

Classification criteria for systemic lupus erythematosus: a review.

The Systemic Lupus International Collaborating Clinics, in preparation for revising the ACR classification criteria for systemic lupus erythematosus, reviewed the current classification criteria. These critical reviews, discussed at the Lund, Sweden, meeting in 2003, will be useful to the clinician and to the researcher. This paper reviews and critiques previous classification attempts.

Classification↗

PubMed2005

Theory, targets and therapy in systemic lupus erythematosus.

The treatment of systemic lupus erythematosus (SLE) has been refined over the years, with the recognition that a fine balance lies between aggressive and prompt therapy and attendant complications brought upon by immunosuppressive therapy itself. However, there has been limited change to the repertoire of drugs available to treat this challenging disease. The current standard therapy for severe manifestations of SLE includes the use of high-dose corticosteroids and cytotoxic agents such as cyclophosphamide (CYC), which have been associated with an increased risk of serious and opportunistic infections. The need for safer, more targeted therapies has been recognized and now, with the exponential increase in the understanding of immunopathogenic mechanisms in SLE, the way has been paved for the development of biologic or targeted therapies in SLE. Although the potential immunosuppression, long-term safety issues and cost-effectiveness remain unclear. These targeted therapies may range from small molecules that specifically inhibit inflammatory processes at an intracellular, cell-cell or cell-matrix level to monoclonal antibodies, soluble receptors or natural antagonists that interfere with cytokine function, cellular activation and inflammatory gene transcription.

Animals↗

PubMed2006

Efficacy of cyclosporin-A in the long-term management of thrombocytopenia associated with systemic lupus erythematosus.

Thrombocytopenia frequently complicates systemic lupus erythematosus (SLE), and its long-term management may be problematic. Intravenous immunoglobulins and high doses of steroids are often effective as induction therapy, but thrombocytopenia frequently relapses during steroid tapering. Several immunosuppressive agents have been evaluated as induction or maintenance therapy in small series or in case reports. We describe six consecutive unselected SLE patients where cyclosporin-A (CyA) was effective and safe in the long-term management of thrombocytopenia and allowed steroid tapering. One relapse occurred during CyA reduction and responded to CyA dose adjustment. Steroids could be stopped in three out of six patients, and were maintained at very low doses in the remaining patients. CyA was stopped in one patient after one year of treatment, without relapse at month 11+ from discontinuation. No severe side effects were documented. Overall, these data suggest that CyA may prove to be an effective and safe therapeutic option for SLE-related thrombocytopenia.

Adrenal Cortex Hormones↗