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PubMedDate not supplied

[The role of anti-nucleosome antibodies in systemic lupus erythematosus. Results of a study of patients with systemic lupus erythematosus and other connective tissue diseases].

OBJECTIVE: The aim of our study was to investigate the prevalence and the disease specificity of anti-nucleosome antibodies in systemic lupus erythematosus and their association with disease activity and renal involvement. METHODS: Anti-nucleosome antibodies were measured by ELISA in the sera of patients with systemic lupus erythematosus (SLE) (47), rheumatoid arthritis (RA) (22), mixed connective tissue disease (MCTD) (19), systemic sclerosis (SSc) (11) and Sjögren's syndrome (SS) (10). Anti-dsDNA antibodies were measured by IIF on Crithidia luciliae. In the patients with SLE serum levels of C3 and C4 complement components were also measured. Sera of 22 healthy individuals were assayed as controls. SLE activity was evaluated by the ECLAM score. RESULTS: Anti-nucleosome antibodies were found in 40 patients with SLE (85.1%), in 10 with RA (45.4%), in 8 with MCTD (42.1%), in 4 with SSc (36.3%), in 1 with SS (10%) and in none of the healthy controls. Anti-dsDNA antibodies were found in 23 patients with SLE and were absent in the patients with other CTD and in controls. All the patients with SLE and renal involvement were positive both for anti-dsDNA antibodies and anti-nucleosome antibodies. No significant correlation was observed between anti-nucleosome antibodies and disease activity and renal involvement. CONCLUSION: Anti-nucleosome antibodies are present in a high percentage of the patients with SLE but they don't seem to be specific markers of the disease. Our data don't support a clear correlation between anti-nucleosome antibodies and disease activity and renal involvement.

Adolescent↗
PubMedDate not supplied

The pathogenesis of systemic lupus erythematosus.

Systemic lupus erythematosus is an autoimmune disease that causes inflammation in the tissues of the brain, endothelial cells, gastrointestinal/genitourinary (GI/GU), joints, kidneys, muscles, and skin. Lupus comprises a range of multisystem disorders involving the deposition of aberrant immune complexes into tissues. Inflammation occurs as a result of autoantibodies attacking organ systems. The pathogenesis of systemic lupus erythematosus is presented.

Antigen-Antibody Complex↗
PubMed2005

The role of host CD4 T cells in the pathogenesis of the chronic graft-versus-host model of systemic lupus erythematosus.

Systemic lupus erythematosus is characterized by production of autoantibodies and glomerulonephritis. The murine chronic graft-vs-host (cGVH) model of systemic lupus erythematosus is induced by allorecognition of foreign MHC class II determinants. Previous studies have shown that cGVH could not be induced in CD4 knockout (CD4KO) mice. We have further explored the role of host CD4 T cells in this model. Our studies now show that B cells in CD4KO mice have intrinsic defects that prevent them from responding to allohelp. In addition, B cells in CD4KO mice showed phenotypic differences compared with congeneic C57BL/6 B cells, indicating some degree of in vivo activation and increased numbers of cells bearing a marginal zone B cell phenotype. The transfer of syngeneic CD4 T cells at the time of initiation of cGVH did not correct these B cell abnormalities; however, if CD4 T cells were transferred during the development and maturation of B cells, then the B cells from CD4KO mice acquire the ability to respond in cGVH. These studies clearly indicate that B cells need to coexist with CD4 T cells early in their development to develop full susceptibility to alloactivation signals.

Adoptive Transfer↗
PubMed1989

The lupus anticoagulant in systemic lupus erythematosus.

The lupus anticoagulant was found in six of 41 unselected patients with systemic lupus erythematosus (14%). Three of these six patients had episodes of thrombosis. Thrombosis occurred in only one patient in the remainder of the series without the lupus anticoagulant. The lupus anticoagulant should be considered as one of the criteria for the diagnosis of systemic lupus erythematosus, and it may be a useful marker for those patients at risk from thromboembolism. It should be looked for in young adults with thrombotic episodes.

Adolescent↗
PubMed2004

Global cerebral edema and subarachnoid hemorrhage in a patient with systemic lupus erythematosus.

Systemic lupus erythematosus is a multifactorial autoimmune disease of complex etiology, which may be associated with cognitive dysfunction, seizures, and headache. The authors present an unusual presentation of systemic lupus erythematosus complicated by global cerebral edema and subarachnoid hemorrhage secondary to rupture of a cerebral aneurysm. The complicated patient management issues are discussed.

Adolescent↗
PubMed2001

Genetic epidemiology: systemic lupus erythematosus.

Systemic lupus erythematosus is the prototype multisystem autoimmune disease. A strong genetic component of susceptibility to the disease is well established. Studies of murine models of systemic lupus erythematosus have shown complex genetic interactions that influence both susceptibility and phenotypic expression. These models strongly suggest that several defects in similar pathways, e.g. clearance of immune complexes and/or apoptotic cell debris, can all result in disease expression. Studies in humans have found linkage to several overlapping regions on chromosome 1q, although the precise susceptibility gene or genes in these regions have yet to be identified. Recent studies of candidate genes, including Fcgamma receptors, IL-6, and tumour necrosis factor-alpha, suggest that in human disease, genetic factors do play a role in disease susceptibility and clinical phenotype. The precise gene or genes involved and the strength of their influence do, however, appear to differ considerably in different populations.

Animals↗
PubMed2003

Apoptosis in systemic lupus erythematosus.

Systemic lupus erythematosus is a complex, multisystem autoimmune disease characterized by production of high-titer autoantibodies directed against ubiquitously expressed self-antigens. Autoantigens in systemic lupus erythematosus are highly diverse in terms of structure and location in control cells, but become clustered in and on the surface blebs of apoptotic cells. The past several years have provided significant evidence that the apoptotic cell plays a central role in tolerizing B cells and T cells to both tissue-specific and ubiquitously expressed self-antigens, and may drive the autoimmune response in systemic autoimmune disease. The authors review the significant recent advances in this area. Recent studies suggest that predisposing factors to subsequent development of systemic autoimmunity may be the incomplete induction of tolerance to apoptotic antigens, potentially through abnormal apoptotic signaling and effector pathways, decreased apoptotic cell clearance, or abnormal signaling thresholds on responding lymphocytes. In such genetically susceptible hosts, proinflammatory events at the host-environment-immune system interface that lead to the binary change in the response to apoptotic material from tolerance to immunity may be responsible for initiation of autoimmunity and subsequent disease amplification. Such pathways may be amenable to therapeutic and preventive interventions.

Apoptosis↗
PubMedDate not supplied

Treating systemic lupus erythematosus.

Systemic lupus erythematosus is one of the more common rheumatic complaints, affecting mainly women of child-bearing age. It is a life-threatening condition that affects the immune system and causes damage to the main organs of the body. To coincide with Lupus Awareness Week (10-17 April), this article reviews the symptoms, causes, diagnosis and treatment of systemic lupus erythematosus and examines ways in which research is improving management of the condition.

Female↗
PubMed1997

[Neuropsychiatric symptoms and findings in systemic lupus erythematosus ].

Systemic lupus erythematosus (SLE) frequently involves the central nervous system. The clinical presentation is highly variable and heterogeneous. The involvement of the central nervous system is often reflected in minor or major neuropsychiatric symptoms. We describe three cases of this neuropsychiatric lupus erythematosus. A variety of laboratory tests are essential in order to establish the correct diagnosis of neuropsychiatric SLE. We discuss the usefulness of magnetic resonance imaging in both a diagnostic setting and as a tool for improving the understanding of the pathogenesis of neuropsychiatric SLE.

Adult↗
PubMed2004

[Diagnosis, therapy and prognosis in systemic autoimmune disorders like lupus erythematosus].

Systemic lupus erythematosus (SLE) is the prototype of a systemic autoimmune disorder, in which immune complexes or cytotoxic antibodies give rise to tissue damage and organ failure, which often results in death. Due to more sensitive diagnostic tools and more sufficient therapeutic methods, the five-year survival rate in patients with systemic lupus erythematosus has improved dramatically during the past decades from less than 50% to 95%. Mortality is still 4 to 5 times higher and is mostly caused by uncontrolled disease flares, infections, and thromboses. Risk factors influencing the course of SLE and favouring the higher mortality are serum antibodies (anti-dsDNA, anticardiolipin, lupus anticoagulant), infections, hypertension, osteoporosis with fractures, cytopenia, renal involvement, higher age at onset, and genetic factors. Morbidity and social consequences are conducted by individual multisystemic disease manifestations.

Anti-Inflammatory Agents↗
PubMed1994

Epidemiology, genetics, etiology, and environment relationships of systemic lupus erythematosus.

Systemic lupus erythematosus continues to provide a major etiologic challenge. Current investigation is focusing on the possibilities of environmental factors, including infection. How these factors are related to genetic factors, including the major histocompatibility complex and more recently observed defects in apoptosis genes, remains unclear. Ethnic and geographic studies of systemic lupus erythematosus are providing important clues, as are continued clinical observations on the various subsets of disease and the patterns of therapeutic response. Different pathogenic mechanisms are constantly being uncovered and in turn need to be related to the various etiologies.

Contraceptives, Oral↗
PubMed2005

Intravenous immunoglobulin therapy and systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease with diverse manifestations. We suggest that intravenous immunoglobulin (IVIg) therapy may be beneficial and safe for various manifestations in SLE. A structured literature search of articles published on the efficacy of IVIg in the treatment of SLE between 1983 and 2005 was conducted. We searched the terms "IVIg," "intravenous immunoglobulin," "lupus," "SLE," and "systemic lupus erythematosus." The various clinical manifestations of SLE that were reported to be successfully treated by IVIg in case reports include autoimmune hemolytic anemia, acquired factor VIII inhibitors, acquired von Willebrand disease, pure red cell aplasia, thrombocytopenia, pancytopenia, myelofibrosis, pneumonitis, pleural effusion, pericarditis, myocarditis, cardiogenic shock, nephritis, end-stage renal disease, encephalitis, neuropsychiatric lupus, psychosis, peripheral neuropathy, polyradiculoneuropathy, and vasculitis. The most extensive experience is with lupus nephritis. There are only a few case series of IVIg use in patients with SLE with various manifestations, in which the response rate to IVIg therapy ranged from 33 to 100%. We suggest that IVIg devoid of sucrose, at a dose of 2 g/kg over a 5-d period given uniformly and at a slow infusion rate in patients without an increased risk for thromboembolic events or renal failure, is a safe and beneficial adjunct therapy for cases of SLE that are resistant to or refuse conventional treatment. The duration of therapy is yet to be established. Controlled trials are warranted.

Adult↗
PubMed1990

Identification of human immunodeficiency virus hybridizing sequences in the peripheral blood of a patient with systemic lupus erythematosus.

Systemic lupus erythematosus, a multisystemic disorder, is considered a prototype of the autoimmune diseases. Although its cause remains unknown, a viral etiology has been proposed. We report that a rapid and sensitive messenger RNA in situ hybridization technique detected hybridizing sequences to the human immunodeficiency virus type in the peripheral blood cells of a woman with systemic lupus erythematosus in whom the presence of acquired immuno-deficiency syndrome was reasonably excluded.

Adult↗
PubMed1990

[Central nervous symptoms and findings in patients with systemic lupus erythematosus].

Systemic lupus erythematosus is a disease characterized by multiple autoimmune phenomena, and a broad clinical spectrum. Involvement of the central nervous system is common, and in the majority of patients occurs mainly as an organic brain syndrome or as migraineous headache. Cerebral atrophy as judged by CT scan is common. Cerebral infarction occurs in a minority of patients, mainly those with high disease activity and a high titer of anti-phospholipid antibodies. Systemic lupus erythematosus should be considered as a possible diagnosis in patients with certain central nervous system aberrations, especially young females.

Adult↗
PubMed2000

Neonatal lupus erythematosus.

Neonatal lupus erythematosus (NLE) is a rare disease characterized by the transplacental passage from the mother to the fetus of autoantibodies, in particular anti-Ro(SS-A), anti-La(SS-B), or both. The majority of infants with NLE exhibit isolated congenital heart block, cutaneous lesions analogous to those of adult subacute cutaneous lupus erythematosus, or both. We report a case of NLE in a 3-month-old male infant, born to a clinically asymptomatic mother, presenting small, annular, erythematous plaques with sharp, hyperkeratotic borders and central clearing localized at the eyebrow region. Both the infant and the mother were positive for anti-Ro(SS-A).

Adult↗
PubMed2003

Lupus headaches in childhood-onset systemic lupus erythematosus: relationship to disease activity as measured by the systemic lupus erythematosus disease activity index (SLEDAI) and disease damage.

The Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) is the most commonly used measure of disease activity for children with systemic lupus erythematosus (SLE). For headaches to be scored in the SLEDAI as a symptom of active disease, they have to be nonresponsive to narcotic analgesia. This may affect the overall estimation of disease activity, especially because headaches are common among children with SLE and narcotic analgesia is rarely used for headache therapy in paediatrics. Moreover, the importance of headaches for the development of damage and their relation to other clinical parameters and outcomes has not been well described for children with SLE. We reviewed the medical charts of an inception cohort of children (n = 63) who were newly diagnosed with SLE. Information on headaches and other disease parameters was obtained. Disease activity and damage were measured using the SLEDAI and the Systemic Lupus International Collaboration Clinics/American College of Rheumatology Damage Index (SDI), respectively. It has been shown that the accumulated burden of active disease as measured by serial SLEDAI scores over time is one of the best predictors of eventual damage to children with SLE. New-onset or significant increase of severe and/or persistent headaches (LHA) were reported in 43% of the patients during a mean follow-up of 3.6 years. LHA occurred preferentially among patients with elevated levels of antiphospholipid antibodies (aPL) (P < 0.02) and only 6% of all LHA episodes were treated with narcotics and thus considered for the measurement of disease activity in the SLEDAI. LHA were unrelated to proxy-measures of disease activity, such as the need to intensify therapies. When used in children, the insensitivity of the SLEDAI to capture LHA did not seem to decrease the responsiveness of the SLEDAI to detect clinically important worsening of disease, or negatively impact on its ability to predict damage.

Adolescent↗