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PubMed2004

Clinical mini-review: systemic lupus erythematosus and the eye.

Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease, the exact etiology of which is unknown. It is characterized by the production of pathological autoantibodies which adhere to cellular surfaces or form immune complexes which deposit in tissue, leading to end-organ damage via inflammatory mechanisms including complement activation. SLE may manifest itself in any organ system. In the eye, keratoconjunctivitis sicca is the most common finding. Other ophthalmic sites of involvement include the cornea, conjunctiva, episclera, sclera, uveal tract, retina, vasculature, optic nerve, and orbit. Therapy varies based on the disease manifestation and severity.

Eye Diseases↗
PubMed2005

Immune cells and cytokines in systemic lupus erythematosus: an update.

PURPOSE OF REVIEW: Systemic lupus erythematosus is characterized by overactive B cells that differentiate into autoantibody-forming cells, aberrant T cell function that provides help to B cells, and the production of pro-inflammatory cytokines. This article reviews recent studies unraveling the complex interplay between cytokines and lymphocytes in systemic lupus erythematosus. RECENT FINDINGS: In systemic lupus erythematosus, T cells are characterized by heightened calcium responses early after activation of their surface receptor. Alterations of the T cell receptor/CD3 complex, namely the substitution of the FcepsilsonRgamma for the T cell receptor zeta chain, and increased mitochondrial potentials can account for this 'overexcitable' phenotype. At the same time, this heightened calcium signal leads to a block of the transcription of the IL-2 gene, a pivotal cytokine for the immune response. The end result is increased spontaneous apoptosis and decreased activation-induced cell death of T cells in systemic lupus erythematosus that in turn leads to enhanced help to B cells and potentially decreased regulatory function. The B cells, on the other hand, are shown to be directly activated by immune complexes by way of Toll-like receptors independently of T cells. Finally, recent studies have tried to elucidate the role of cytokines such as interferon-alpha in systemic lupus erythematosus and, following the paradigm of rheumatoid arthritis, to establish targets for treatment. SUMMARY: The increased apoptosis and aberrant T cell activation coupled with nonspecific activation of B cells lead to the production of auto-antigen: auto-antibody complexes that are the hallmark of systemic lupus erythematosus. Future treatments aiming at correcting the intracellular and intercellular signaling abnormalities may prove effective in restoring immune tolerance in systemic lupus erythematosus.

B-Lymphocytes↗
PubMed1996

[Systemic lupus erythematosus and antiphospholipid syndrome].

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by the synthesis of antinuclear antibodies. Nucleosomes- the disc-like structural units of chromatin, composed of histones and DNA-are the primary antigenic structure that induces the formation of complement-activating antigen-antibody complexes in basement membranes. The autoreactivity in SLE has been elucidated in drug-induced SLE: hypomethylation of DNA leads to overexpression of integrin CD11a/ CD18, increased binding of T-cells to macrophages and B-cells, a higher rate of apoptosis of macrophages, and elevated B-cell activity with consecutive production of autoantibodies. Disturbances of apoptosis (e.g. mutation of Fas gene) are relevant also in non-drug-induced SLE. The morphologic diagnosis-by light microscopy, immunohistology and electron microscopy-of skin and renal biopsies can confirm the diagnosis and help in prognostic assessment as well as therapeutic decisions in SLE. The value of the morphologic diagnosis in SLE is enhanced by reporting semiquantitative scores of disease activity and chronicity. The antiphospholipid syndrome (APS) is characterized by thrombosis, thrombocytopenia, recurrent fetal loss and antiphospholipid antibodies. APS associated with SLE or other systemic autoimmune diseases has been termed secondary APS. Antibodies in APS are directed against phospholipids and phospholipid-protein complexes. One of these proteins is beta 2-glycoprotein 1. An important mechanism of the increased rate of thrombosis in APS is probably the inhibition of the protein C-catalyzed inactivation of clotting factors V and VIII. Venous thrombosis with recurrent pulmonary emboli and arterial thrombi in brain, heart and kidney (thrombotic microangiopathy) can lead to divergent clinical manifestations in APS.

Antibodies, Antinuclear↗
PubMed1996

[Systemic lupus erythematosus and antiphospholipid syndrome].

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by the synthesis of antinuclear antibodies. Nucleosomes-the disc-like-structural unit of chromatin being composed of histones and DNA-are the primary antigenic structure that induces the formation of complement-activating antigen-antibody complexes in basement membranes. The autoreactivity in SLE has been elucidated in drug-induced SLE: Hypomethylation of DNA leads to overexpression of integrin CD 11a/CD 18, increased binding of T-cells to macrophages and B-cells, a higher rate of apoptosis of macrophages and elevated B-cell activity with consecutive production of autoantibodies. Disturbances of apoptosis (e.g. mutation of Fas gene) are relevant also in non drug-induced SLE. The morphologic diagnosis-by light microscopy, immunohistology and electron microscopy-of skin and renal biopsies can confirm the diagnosis and help in prognostic assessment as well as therapeutic decisions in SLE. The value of the morphologic diagnosis in SLE is enhanced by reporting semiquantitative scores of disease activity and chronicity. The antiphospholipid syndrome (APS) is characterized by thrombosis, thrombocytopenia, recurrent fetal loss and antiphospholipid antibodies. APS associated with SLE or other systemic autoimmune diseases has been termed secondary APS. Antibodies in APS are directed against phospholipids and phospholipid-protein complexes. One of these proteins is beta 2-glycoprotein 1. An important mechanism of the increased rate of thrombosis in APS is probably the inhibition of the protein C catalyzed inactivation of clotting factors V and VIII. Venous thrombosis with recurrent pulmonary emboli and arterial thrombi in brain, heart and kidney (thrombotic microangiopathy) can lead to divergent clinical manifestations in APS.

Animals↗
PubMed2002

Neuropsychiatric involvement in systemic lupus erythematosus.

The correct diagnosis of central and peripheral nervous system manifestations in patients with systemic lupus erythematosus (SLE) can be challenging because of many SLE-related and non-SLE-related processes that can be present in a patient. The American College of Rheumatology (ACR) has published case definitions for 19 neuropsychiatric SLE (NPSLE) syndromes, with careful attention to important exclusion criteria. These criteria were developed for research purposes but can be helpful to clinicians with a patient who has nervous system dysfunction. This report reviews the data regarding the application of the ACR NPSLE criteria and the influence of ethnicity and disease duration on the development of NPSLE syndromes. Cognitive dysfunction and psychiatric disorders are the two most common manifestations. The work-up and treatment of nervous system syndromes are also discussed.

Angiography↗
PubMed1992

Anti-Ro/SS-A and anti-La/SS-B autoantibody levels in relation to systemic lupus erythematosus disease activity and congenital heart block. A longitudinal study comprising two consecutive pregnancies in a patient with systemic lupus erythematosus.

OBJECTIVE: To analyze the anti-Ro/SS-A and anti-La/SS-B autoantibody responses, both quantitatively and qualitatively, in relation to the occurrence of congenital heart block (CHB) and disease activity in a patient with systemic lupus erythematosus. METHODS: The patient's course was carefully documented for a period of 80 months. Specific enzyme-linked immunosorbent assays, a HeLa cell immunoblotting test, and an RNA precipitation assay were used to determine autoantibody levels and fine specificities. RESULTS: Anti-Ro/SS-A and anti-La/SS-B antibody did not disappear. Levels of anti-Ro/SS-A appeared to fluctuate more frequently than levels of anti-La/SS-B. Fluctuations were unrelated to disease activity or immunosuppressive treatment. There was no characteristic relationship between levels of these antibodies and the occurrence of CHB. CONCLUSION: The occurrence of CHB cannot be predicted by frequent measurement of anti-Ro/SS-A and anti-La/SS-B levels. The immunoregulatory control of anti-Ro/SS-A and anti-La/SS-B antibodies differs from that of anti-DNA and anti-tetanus toxoid antibodies.

Adult↗
PubMed1984

Renal cortical necrosis in systemic lupus erythematosus.

A patient with active systemic lupus erythematosus had acute and irreversible renal failure after an uncomplicated cholecystectomy, and renal biopsy established the diagnosis of acute cortical necrosis. Patients with lupus have a diathesis for intravascular coagulation, and the interactive effects of immune complex or endotoxin-induced vascular injury, change in platelet dynamics, impairment of fibrinolysis, alterations in the mononuclear phagocytic system, and/or concomitant use of corticosteroids may have singularly or in combination been important in generating this rare renal complication of systemic lupus erythematosus in our patient.

Acute Disease↗
PubMed2002

Juvenile parkinsonism as a manifestation of systemic lupus erythematosus: case report and review of the literature.

Involvement of the central nervous system in systemic lupus erythematosus (SLE) has been well described. It usually includes psychiatric disturbance, seizures, and cranial nerve disorders. Movement disorders are less common, chorea being the one most frequently described. A parkinsonian syndrome may be an extremely rare manifestation of cerebral lupus. We report on a case of juvenile parkinsonism as a manifestation of SLE and review the literature.

Adult↗
PubMed1993

A secondary amyloidosis associated with systemic lupus erythematosus.

Secondary amyloidosis associated with systemic lupus erythematosus has rarely been reported. A 57-year-old female had been diagnosed as having possible systemic lupus erythematosus, although her clinical course was not typical. About one year after the diagnosis, treatment was begun with prednisolone because of progressive renal dysfunction, thrombocytopenia and low serum levels of complements. Recurrent diarrhea and gastrointestinal bleeding soon developed, then amyloidosis was revealed in the stomach and duodenum. Postmortem examination confirmed systemic amyloidosis. We discuss the significance of this rare association of systemic lupus erythematosus and secondary amyloidosis.

Amyloidosis↗
PubMed1989

[Antiphospholipid antibodies in systemic lupus erythematosus: incidence, significance and relation to lupus nephritis].

The prevalence of three different types of antiphospholipid antibody in 88 consecutive patients with systemic lupus were 27.2% for lupus anticoagulant (LAC), 31.8% for anticardiolipin antibody (aCL), and 13.6% for falsely positive serologic tests for syphilis (FPSTS). The three tests were correlated, thus confirming the overlapping specificities of this family of antibodies. Although FPSTS was not associated with any particular manifestation of systemic lupus, aCL correlated with thrombosis (p = 0.0001), thrombopenia (p = 0.009), neuropsychiatric features (p = 0.02) and membranous nephropathy (p = 0.001), while LAC correlated with thrombosis (p = 0.001) and hemolytic anemia (p = 0.04). The previously unreported association between membranous nephropathy and aCL might explain some features of the former, particularly the higher incidence of thromboembolic complications and the poorly known relation with renal vein thrombosis.

Adolescent↗
PubMed1990

Elevated levels of interleukin-6 in cerebrospinal fluid from patients with systemic lupus erythematosus and central nervous system involvement.

Paired serum and cerebrospinal fluid (CSF) specimens from 14 patients with systemic lupus erythematosus (SLE) and central nervous system (CNS) involvement were studied for interleukin-6 (IL-6) activity using the IL-6-dependent murine hybridoma, MH60.BSF2. We also studied 23 patients with noninflammatory neurologic diseases, and 9 SLE patients without CNS involvement. CSF IL-6 activity was elevated only in SLE patients with CNS involvement, although there was no significant difference in serum IL-6 activity among the 3 groups. CSF IL-6 activity was not correlated with either the CSF-serum albumin quotient (Q albumin; an indicator of blood-brain barrier function) or serum IL-6 activity in SLE patients with CNS involvement. The CSF IL-6 activity decreased significantly when CNS manifestations subsided after successful treatment. These results indicate that determination of CSF IL-6 activity may be useful in the evaluation of CNS disease activity in SLE. Moreover, the data confirm the presence of immune system activation within the CNS in patients with SLE-associated CNS disease.

Antibodies, Monoclonal↗
PubMed2004

Intrathecal levels of matrix metalloproteinases in systemic lupus erythematosus with central nervous system engagement.

Symptoms originating from the central nervous system (CNS) occur frequently in patients with systemic lupus erythematosus (SLE), and CNS involvement in lupus is associated with increased morbidity and mortality. We recently showed that neurones and astrocytes are continuously damaged during the course of CNS lupus. The matrix metalloproteinases (MMPs) are a group of tissue degrading enzymes that may be involved in this ongoing brain destruction. The aim of this study was to examine endogenous levels of free, enzymatically active MMP-2 and MMP-9 in cerebrospinal fluid from patients with SLE. A total of 123 patients with SLE were evaluated clinically, with magnetic resonance imaging of brain and cerebrospinal fluid (CSF) analyses. Levels of free MMP-2 and MMP-9 were determined in CSF using an enzymatic activity assay. CSF samples from another 22 cerebrally healthy individuals were used as a control. Intrathecal MMP-9 levels were significantly increased in patients with neuropsychiatric SLE as compared with SLE patients without CNS involvement (P < 0.05) and healthy control individuals (P = 0.0012). Interestingly, significant correlations between MMP-9 and intrathecal levels of neuronal and glial degradation products were noted, indicating ongoing intrathecal degeneration in the brains of lupus patients expressing MMP-9. In addition, intrathecal levels of IL-6 and IL-8--two cytokines that are known to upregulate MMP-9--both exhibited significant correlation with MMP-9 levels in CSF (P < 0.0001), suggesting a potential MMP-9 activation pathway. Our findings suggest that proinflammatory cytokine induced MMP-9 production leads to brain damage in patients with CNS lupus.

Adolescent↗
PubMedDate not supplied

Prospective measure of serum 3-nitrotyrosine levels in systemic lupus erythematosus: correlation with disease activity.

Systemic lupus erythematosus (SLE) is a prototypical autoimmune disease. Overproduction of nitric oxide (NO) has been implicated in its pathogenesis. Several retrospective studies have indicated a correlation between serum nitrate and nitrite (NOx) and disease activity. This measure of NO production can be falsely elevated by exogenous dietary and medication sources of NOx and variably reduced by serum thiols. These variables can make NOx a less reliable tool for studying the role of NO in SLE. Peroxynitrite, a by-product of NO and superoxide, nitrates tyrosine moieties. The resulting 3-nitrotyrosine (3NT) serves as a long-term indicator of NO-mediated protein modifications that is not affected by exogenous sources of NOx or serum thiols. We hypothesized that for these reasons serum 3NT levels would correlate with lupus disease activity more significantly than serum NOx. To address this hypothesis, we prospectively evaluated lupus disease activity, serum protein 3NT levels, and NOx levels in a cohort of lupus patients at 3-month intervals. Serum 3NT correlated with disease activity among African-Americans, while NOx correlated with disease activity among Caucasians. Subjects with active lupus nephritis had higher levels of serum 3NT than those without renal disease. Immunohistochemical analysis of renal biopsies from subjects with active proliferative lupus nephritis revealed renal expression of inducible NO synthase. The results of this study suggest that overproduction of NO may play a pathogenic role in SLE and lupus nephritis. Serum 3NT may be a useful, new tool for studying the contributions of NO to the pathogenesis of SLE.

Autoantibodies↗
PubMedDate not supplied

Pregnancy course and complications in patients with systemic lupus erythematosus.

Among 165 patients with systemic lupus erythematosus (SLE), we observed 21 pregnancies in 19 patients since 1987. The mean duration of disease at the time of pregnancy was 4.5 +/- 3 years. All but three patients required immunosuppressive treatment before and during pregnancy. The effect of pregnancy on the course of SLE was studied. Severe disease exacerbations were rare and largely confined to patients with renal involvement. Most patients showed elevated titers of dsDNA antibodies during pregnancy but clinical activity of disease was usually mild. Complement C3 decrease appeared to be the most sensitive marker for pregnancy-related complications. The detection of antibodies to phospholipids was frequent during pregnancy in contrast to a low prevalence before and after pregnancy. Their presence could be associated with intrauterine growth retardation. Preterm delivery before the 37th week of pregnancy had to be performed in the majority of patients. None of the patients experienced abortion although three patients had to delivered in the 29th week of pregnancy because of increasing symptoms of pre-eclampsia. Two of these children died and the third child suffered from intracranial hemorrhage in the early postpartum period. Our data demonstrate that successful pregnancy outcome was related to a gestational age of more than 32 weeks, making careful monitoring and appropriate therapeutic management necessary.

Adult↗
PubMedDate not supplied

Cardiac abnormalities in children with systemic lupus erythematosus.

Children and adolescents with systemic lupus erythematosus (SLE, n = 14) with no cardiac symptoms were examined for cardiac involvement by physical examination, electrocardiography (ECG) and echocardiography. The indexes of left ventricular (LV) systolic and diastolic function were compared with the findings of 20 healthy, age-matched control subjects. Echocardiographic examination revealed mild tricuspid valve regurgitation in three, and moderate tricuspid and mitral valve regurgitation in two patients. Pericardial thickening was found in one patient. Indexes of LV systolic and diastolic function of SLE patients differed significantly from control subjects, with marked reduced ejection fraction (EF) and fractional shortening (FS) as well as reduced peak early diastolic filling velocity (E) and ratio of early-to-late diastolic filling velocity (E/A). Deceleration time (DT) was longer in the patients than in the control group. Late filling velocity (A) and isovolumic relaxation time (IRT) did not differ between the two groups. Valvular and pericardial involvement was found to be lower than previous reports. We conclude that asymptomatic diastolic and systolic dysfunction is common in children with SLE, most likely representing myocardial involvement. Routine cardiac evaluation by echocardiography can be recommended in the follow-up of children with SLE in order to detect silent cardiac abnormalities.

Adolescent↗
PubMed1987

Antibodies to Ro(SSA) and the heterogeneity of systemic lupus erythematosus.

The clinical heterogeneity of systemic lupus erythematosus (SLE) is associated with a multiplicity of autoimmune responses to both cellular and soluble antigens. At least part of the clinical heterogeneity is associated with serological heterogeneity and this is particularly striking among patients with SLE who produce anti-Ro(SSA) and anti-La(SSB). Certain subsets within the lupus spectrum are closely associated with the anti-Ro(SSA) response. These include subacute cutaneous lupus erythematosus, the lupus like syndrome associated with homozygous C2 and C4 deficiency, and neonatal lupus erythematosus. Moreover, among the patients with SLE who produce anti-Ro(SSA) are 2 stable groups, on which produces anti-Ro(SSA) alone and one which produces both anti-Ro(SSA) and anti-La(SSB). Clear clinical and serological differences distinguish these groups and it is hypothesized that these differences are due to genetic differences in the HLA-D region. Exact identification of the genes involved and how they control immune responses should lead to a clearer understanding of the clinical phenomena seen in these patients.

Adolescent↗
PubMed1994

[Cyclosporin therapy of patients with systemic lupus erythematosus].

Seven patients suffering from systemic lupus erythematosus (SLE) were treated by cyclosporin A (CSA) plus corticosteroids. The indications for treatment were: lupus nephritis refractory to treatment with corticosteroids and cyclophosphamide (one patient), nephrosis syndrome or lupus nephritis associated with severe cytopenia and refractory to corticosteroid treatment (5 patients), severe thrombocytopenia refractory to conventional treatments (one patient). The treatment for 6 months of this latter patient resulted in complete remission, lasting for at least 1.5 years. Patients with kidney involvement also responded to therapy. The response manifested within 1 month. Treatment lasted for a mean of 5.1 months (the treatment of one patient was interrupted after 1 month because of lack of cooperation). There were no side effects. CSA treatment in combination with corticosteroids, when properly indicated, may be beneficial in SLE.

Adrenal Cortex Hormones↗