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PubMed2006

Relationship of plasma interleukin-18 concentrations to traditional and non-traditional cardiovascular risk factors in patients with systemic lupus erythematosus.

OBJECTIVES: Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis. Recent studies indicated that the concentrations of circulating interleukin (IL)-18, a novel proinflammatory T helper-1 cytokine, in SLE patients were significantly higher than those in healthy control subjects. The objective of this study was to examine the relationship between IL-18 and cardiovascular risk factors in patients with SLE. METHODS: Both traditional and non-traditional cardiovascular risk factors including body mass index (BMI), systolic blood pressure, diastolic blood pressure (DBP), fasting insulin and glucose, plasma lipid profile, plasma homocysteine, thiobarbituric acid-reactive substances, titres of autoantibodies against oxidized low-density lipoprotein, and brachial-ankle pulse wave velocity (baPWV) were determined in a total of 72 female SLE patients. All patients were further classified into subgroups based on tertiles of plasma IL-18 concentrations. RESULTS: Plasma concentrations of IL-18 were significantly higher in SLE patients than age-matched healthy controls. SLE patients with IL-18 concentration in the top tertile compared with the bottom tertile had significantly higher plasma levels of insulin, triglyceride, homocysteine and values of homeostasis model assessment insulin resistance (HOMA IR) and HOMA beta-cell. In addition, plasma concentrations of IL-18 correlated positively and significantly with BMI, insulin, HOMA IR, HOMA beta-cell, triglyceride, homocysteine, DBP and baPWV in all SLE patients. CONCLUSIONS: This is th first report showing the relationship between IL-18 and cardiovascular risk factors in SLE. In patients with SLE, the synergistic effects of hyperinsulinaemia, insulin resistance, hyperhomocysteinaemia, and vascular stiffness most likely contribute to the elevation of plasma IL-18 concentrations.

Adult↗
PubMed2000

Neurologic, ophthalmic, and neuropsychiatric manifestations of pediatric systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is an autoimmune, multisystem disorder with diverse manifestations. There are limited reports on the neuro-ophthalmic and neuropsychiatric findings in childhood SLE. CASE REPORT: An 8-year-old patient with suspected SLE with a history of skin rash, joint pain, transient hematologic abnormality, headaches, seizures, and psychosis, presented with papilledema secondary to acquired, obstructive hydrocephalus. DISCUSSION: SLE-related ocular and neuropsychiatric findings are reviewed. Proposed mechanisms for ocular and cerebral lupus include immune complex deposition, vascular thrombosis, and postinflammatory lesions. CONCLUSION: The prevalent neurologic and neuropsychiatric complications of pediatric SLE require close follow-up and interdisciplinary management.

Child↗
PubMed1993

Presence of anti-La(SS-B) is associated with binding to the 13-kD carboxyl terminus of 60-kD Ro(SS-A) in systemic lupus erythematosus.

In systemic lupus erythematosus (SLE) clinical manifestations, autoantibody production, and immunogenetics are inter-related. The ability to study parts of the autoimmune response may allow a more detailed understanding of these relationships. We undertook this study to determine whether the fine specificity of the autoimmune response to 60-kD Ro(SS-A) was related to the presence of other autoantibodies. We screened 74 patients with SLE for antibodies to the carboxyl 13-kD terminal of 60-kD Ro(SS-A) (13 kD). Twenty-five sera had such antibodies. This reactivity was distinguished by the presence of not only anti-Ro(SS-A) but also other antibodies. All nine sera with Ro(SS-A) and La(SS-B) Ouchterlony immunodiffusion precipitins bound 13-kD (p = 0.01), whereas 10 of 11 sera with both anti-Ro(SS-A) and anti-La(SS-B) as determined by immunosorbent assay bound 13-kD (p = 0.002). Inhibition studies demonstrated that antibodies binding the 13-kD fragment bound the 60-kD Ro(SS-A) protein but did not bind the La(SS-B) protein. Thus, anti-La(SS-B) was found in those sera that bound epitopes within the 13-kD carboxyl terminal of 60-kD Ro(SS-A). These data suggest a structural basis by which anti-Ro(SS-A) and anti-La(SS-B) are coupled in SLE.

Antibodies, Antinuclear↗
PubMed1987

Platelet antibodies in systemic lupus erythematosus.

In systemic lupus erythematosus (SLE), the precise cause of the thrombocytopenia is unknown. Since platelet associated IgG is increased in many patients, it has been suggested that the destruction of platelets might be dependent on specific antibodies. In nine patients with SLE, platelet associated immunoglobulins were found together with free serum antibody which bound to platelets from all normal subjects. Using an immunoblotting technique with membrane proteins from normal platelets incubated with patient sera, target antigens were localized on a band of mol wt 108,000 in two cases (B. and N.) and on a band of mol wt 66,000 in a third (M.). When the same technique was applied to autologous platelets of patient N., autoantibody binding to the protein of mol wt 108,000 was demonstrated. The antigenic determinants were not removed from the platelets by enzyme treatment or by disulphide bond reduction, and were localized in the cytoplasmic fraction of the platelets.

Autoantibodies↗
PubMed1986

Current concepts in the etiopathogenesis and treatment of systemic lupus erythematosus (SLE).

Systemic lupus erythematosus is an autoimmune disorder that occurs spontaneously in humans and mice. Genetic factors play an important role in the predisposition to and expression of disease. Environmental factors augment the expression of illness and in the absence of normal control mechanisms may provide the stimulus to autoimmunity. Sex hormones modulate the immune response and tend to modify disease expression. Disordered immune regulation may be due to a primary or secondary abnormality in cellular, cytokine, and/or humoral function. Therapy for SLE is directed towards suppression of exaggerated immunological and inflammatory activity. This review will re-evaluate current therapy and describe newer approaches including the use of pharmacological, hormonal, immunological, dietary, and physical modalities.

Humans↗
PubMed2006

Traditional risk factor assessment does not capture the extent of cardiovascular risk in systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is associated with accelerated atherosclerosis. However, the degree of endothelial dysfunction and its relationship to traditional and novel cardiovascular risk factors have not been examined in SLE. METHODS: In a case-control design, 35 patients with clinically stable SLE and 35 control subjects matched for age, sex, body mass index and smoking status were studied. Arterial elasticity, lipid profile, homocysteine, measures of inflammation and oxidative stress were determined. RESULTS: Among traditional vascular risk factors, there was a nonsignificant trend towards lower blood pressure in the control subjects, whereas low-density lipoprotein (LDL) cholesterol levels were significantly lower in the SLE group (2.5 vs 3.3 mmol/L, P < 0.001). Patients with SLE had significantly lower small artery elasticity (SAE; 4.9 vs 7.0 ml/mmHg x 100, P < 0.001) and higher plasma homocysteine (11.4 vs 8.3 mmol/L, P = 0.002) than control subjects. Levels of serum sVCAM-1 (614 vs 494 ng/mL, P = 0.002), oxidized LDL (144 vs 97, P < 0.001) and CD40 ligand (4385 vs 1373 pg/ml, P = 0.001) were significantly higher in SLE. Oxidized LDL levels, older age at SLE diagnosis and higher disease damage scores correlated inversely with SAE but not traditional risk factors. CONCLUSION: Impaired endothelial function as shown by decreased SAE, and an adverse profile of novel proatherogenic and prothrombotic vascular disease risk factors were prevalent in clinically quiescent SLE. These findings show the vulnerability of patients with SLE for atherosclerosis, and emphasize that assessments based on traditional risk factors alone may be inadequate.

Adult↗
PubMed1993

Resistance of MHC class I-deficient mice to experimental systemic lupus erythematosus.

Experimental systemic lupus erythematosus (SLE) can be induced in mice by immunization with a human monoclonal antibody to DNA that bears a common idiotype (16/6Id). These mice generate antibodies to 16/6Id, antibodies to DNA, and antibodies directed against nuclear antigens. Subsequently, manifestations of SLE develop, including leukopenia, proteinuria, and immune complex deposits in the kidney. In contrast, after immunization with 16/6Id, mice lacking major histocompatibility complex (MHC) class I molecules generated antibodies to 16/6Id but did not generate antibodies to DNA or to nuclear antigen. Furthermore, they did not develop any of the above clinical manifestations. These results reveal an unexpected function of MHC class I in the induction of autoimmune SLE.

Animals↗
PubMed1988

Cerebral systemic lupus erythematosus.

Cerebral systemic lupus erythematosus is uncommon in childhood. Three further cases are presented to draw attention to the unusual and varied clinical manifestations of this condition.

Brain Diseases↗
PubMed2002

Increased lung uptake of technetium-99m hexamethylpropylene amine oxime in systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) can affect every organ. Involvement of the lungs in this disease is a significant cause of morbidity and mortality. OBJECTIVES: To assess pulmonary vascular endothelium damage in SLE by lung uptake of technetium-99m hexamethylpropylene amine oxime ((99m)Tc-HMPAO). METHODS: Lung uptake of (99m)Tc-HMPAO was measured in 20 SLE patients and for comparison in 25 controls without SLE, referred for brain imaging due to dementia or stroke. Of the 20 SLE patients, 10 had significant clinical pulmonary manifestations. However, all SLE patients had normal chest X-ray findings. Anterior lung image, including a large part of the liver, was taken 10 min after intravenous injection of 20-25 mCi of (99m)Tc-HMPAO. Regions of interest were calculated over the liver and lung. RESULTS: The mean lung/liver uptake ratio in patients without SLE was 0.36 +/- 0.1. The mean lung/liver uptake ratio in SLE patients was 0.79 +/- 0.58. The difference was significant. CONCLUSIONS: Our results indicated that determining the ratio of lung/liver uptake of (99m)Tc-HMPAO may be a useful complementary method to assess pulmonary injury in SLE patients.

Adult↗
PubMed2003

The VH gene repertoire of splenic B cells and somatic hypermutation in systemic lupus erythematosus.

In systemic lupus erythematosus (SLE) it has been hypothesized that self-reactive B cells arise from virgin B cells that express low-affinity, nonpathogenic germline V genes that are cross-reactive for self and microbial antigens, which convert to high-affinity autoantibodies via somatic hypermutation. The aim of the present study was to determine whether the VH family repertoire and pattern of somatic hypermutation in germinal centre (GC) B cells deviates from normal in SLE. Rearranged immunoglobulin VH genes were cloned and sequenced from GCs of a SLE patient's spleen. From these data the GC V gene repertoire and the pattern of somatic mutation during the proliferation of B-cell clones were determined. The results highlighted a bias in VH5 gene family usage, previously unreported in SLE, and under-representation of the VH1 family, which is expressed in 20-30% of IgM+ B cells of healthy adults and confirmed a defect in negative selection. This is the first study of the splenic GC response in human SLE.

B-Lymphocytes↗
PubMed2001

Prolactin in murine systemic lupus erythematosus.

Murine systemic lupus erythematosus (SLE) manifests several autoimmune perturbations that resemble human SLE, including cytokine aberrations, lymphoproliferation, hypergammaglobulinemia, autoantibody formation, and immune complex glomerulonephritis. In multiple studies, elevated serum prolactin concentrations (hyperprolactinemia) stimulated appearance or progression of murine lupus. Autoimmune disease acceleration by prolactin appears to be accentuated by estrogen stimulation of prolactin secretion and independent of immunosuppressive effects of androgens such as testosterone. Conversely, suppression of serum prolactin concentrations by bromocriptine inhibits development of murine SLE. These data clearly support the concept that prolactin is immunostimulatory in autoimmune disease and that the therapeutic goal of lowering serum prolactin concentrations may be beneficial to patients. Further utilization of murine SLE models will facilitate dissection of the actions and interactions of prolactin with estrogen, progesterone and testosterone and lead to a better understanding of hormonal immunomodulation and therapy of autoimmune disease.

Animals↗
PubMed2004

Targeting interferon-alpha: a promising approach for systemic lupus erythematosus therapy.

System lupus erythematosus (SLE) is an autoimmune disease with multicellular pathogeneic components. Recent studies suggest an important role for interferon-alpha (IFN) in the immunopathogenesis of SLE. Data demonstrating a correlation between IFN-alpha and SLE disease severity range from elevated IFN-alpha levels in patients' serum and induction of IFN-regulated genes in peripheral blood mononuclear cells, to drug induced lupus disease in hepatitis C or cancer patients treated with recombinant IFN-alpha. In addition, mouse models of lupus in which the IFNR is deleted fail to develop disease manifestations. Thus, targeting IFN-alpha promises to be therapeutically efficacious for SLE.

Animals↗
PubMed2004

Double-blind, randomized, placebo-controlled pilot study of leflunomide in systemic lupus erythematosus.

Twelve systemic lupus erythematosus (SLE) patients with mild to moderate disease activity (SLEDAI of > or = 6 and on prednisolone < 0.5 mg/kg/day) were included in a prospective, randomized, double-blind, placebo-controlled pilot study for 24 weeks. Six were randomized to receive oral leflunomide and six received placebo. Primary outcome of this study included the mean change of SLEDAI at 24 weeks. Secondary outcomes included the changes in proteinuria, complement levels, anti ds-DNA binding, and prednisolone dosage. The mean age of the 12 patients was 41+/-9 years, and the mean disease duration was 8.5+/-5.8 years. All were female except one patient. The disease activity of both groups of patients decreased significantly after six months of treatment (14.7+/-6.0 to 3.7+/-2.3 in leflunomide group, P = 0.028, and 9.7+/-3.4 to 5.2+/-4.1 in placebo group, P = 0.027). Reduction in the SLEDAI from baseline to 24 weeks was significantly greater in the leflunomide group than the placebo group (11.0+/-6.1 in the leflunomide group and 4.5+/-2.4 in the placebo group respectively, P = 0.026). Minor adverse events included transient elevation in ALT, hypertension and transient leucopenia. In summary, leflunomide was more effective than placebo in treating SLE patients with mild to moderate disease activity and was safe and well-tolerated.

Adult↗
PubMed2005

QT-interval parameters are increased in systemic lupus erythematosus patients.

Systemic lupus erythematosus (SLE) patients have increased cardiovascular morbidity and mortality. QT-interval parameters are presumed markers of cardiovascular risk and have not been previously evaluated in SLE. Standard 12-lead ECGs were obtained from 140 female SLE outpatients and 37 age and body mass index-matched controls. QT interval was measured in each lead and heart rate-corrected maximum QT-interval duration (QTcmax) and QT-interval dispersion (QTd) were calculated. Risk factors for cardiovascular disease and lupus clinical features, disease treatment, disease activity and damage index were recorded. SLE patients have increased QT-interval parameters when compared to controls (QTcmax: 427.91 +/- 31.53 ms(1/2) versus 410.05 +/- 15.45 ms(1/2), P < 0.001; QTd: 52.38 +/- 22.21 ms versus 37.12 +/- 12.88 ms, P < 0.001). These differences persisted after excluding those patients with arterial hypertension, diabetes and with ECG abnormalities (QTcmax: 419.90 +/- 28.78 ms(1/2) versus 409.15 +/- 15.85 ms(1/2), P = 0.041; QTd: 54.74 +/- 26.00 ms versus 37.96 +/- 13.05 ms, P = 0.001). Multivariate linear regression for factors associated with QTcmax selected the presence of electrocardiographic left ventricular hypertrophy (ECG-LVH) (P = 0.003), nonspecific ST-T-wave abnormalities (P = 0.022) and left atrial enlargement (P = 0.044). Multivariate associates with QTd were age (P = 0.018), ECG-LVH (P = 0.022) and ST-T abnormalities (P = 0.031). In conclusion, SLE patients have increased QT interval parameters when compared to controls. This prolongation may lead to an increased cardiovascular risk. This finding might be due to subclinical atherosclerotic cardiovascular disease.

Adult↗
PubMed1999

Immunological and clinical differences between juvenile and adult onset of systemic lupus erythematosus.

INTRODUCTION: Systemic lupus erythematosus (SLE) in children usually follows a more severe course than in adults, but sometimes in the previous studies reported there are many confounding factors. OBJECTIVE: To analyse the immunological and clinical characteristics of SLE juvenile onset and SLE adult onset. METHODS: We studied 179 patients with SLE, 49 patients were aged 6-18 yrs at onset of disease. Anti-dsDNA antibodies were detected by radioimmunoassay and antibodies to extractable nuclear antigens (ENA): anti-nRNP, anti-Sm, anti-Ro/SS-A and anti-La/SS-B antibodies by ELISA, counterimmuno-electrophoresis and immunoblotting. RESULTS: Juvenile-onset SLE shows a higher frequency of cutaneous vasculitis (44.8% vs 27.6%; P < 0.05), seizures (18.3% vs 7.6%; P < 0.05) nephropathy (67.3% vs 48.4%; P < 0.025), and discoid lupus erythematosus (26.5% vs 13.8%; P < 0.05). The incidence of articular manifestations is lower than in adults (85.7% vs 96.1%; P < 0.025). No significant differences were found between the two groups in relation with the prevalence of antinuclear antibodies. CONCLUSIONS: Juvenile-onset SLE has more frequent neurological and renal manifestations than adult-onset SLE, but immunological markers are similar in both groups. These features suggest the most severe clinical manifestations in the juvenile-onset SLE group are not related with the presence of studied antibodies by different methods.

Adolescent↗
PubMedDate not supplied

Outpatient management of systemic lupus erythematosus.

SUMMARY: Systemic lupus erythematosus (SLE) is often managed by primary care practitioners, who must coordinate the care with the support of subspecialists. The management of patients with such a serious and chronic disease can be both rewarding and challenging. This article reviews common problems and suggests management strategies. KEY POINTS: Measurement of serum antinuclear antibodies can lead to an erroneous diagnosis if used as the sole basis for diagnosis. Infections are the leading cause of death in lupus patients, and immunizations and antibiotic prophylaxis need to be considered. Acute cutaneous SLE is exacerbated by exposure to ultraviolet light. Patients should avoid sun exposure. Specific treatment of cutaneous SLE includes topical corticosteroids and antimalarial agents. Some of the most perplexing problems seen in SLE relate to neuropsychiatric features. NSAIDs, corticosteroids, and antimalarials are the most commonly used medications for SLE.

Adrenal Cortex Hormones↗
PubMed1998

Lack of evidence of active lytic replication of Epstein-Barr and cytomegaloviruses in patients with systemic lupus erythematosus.

OBJECTIVES: Systemic lupus erythematosus (SLE) is a multifactorial disease. Environmental factors such as viral infection(s) have been proposed as pathaetiological factors. There are particular interests in studying lymphotropic viruses such as the Epstein-Barr virus (EBV) and cytomegalovirus (CMV). Although previous case reports and in vitro studies suggested that they may have a role, there is no direct evidence that onset of SLE or disease exacerbation is associated with active infection by these viruses. Using the very sensitive polymerase chain reaction (PCR) technique, we tried to find out evidence of active replication of these viruses in patients with SLE. METHODS: Thirty-four patients with SLE were compared with matched normal controls. Eleven patients were newly diagnosed to have SLE and 18 of the 34 patients had active disease as determined by a SLE Disease Activity Index (SLEDAI) score of > or = 10 at the time of study. RESULTS: Our results showed no evidence of active replication or reactivation of EBV in the leucocytes amongst the newly diagnosed SLE patients, established SLE patients, patients with SLEDAI > or = 10, patients with SLEDAI < 10, and control subjects. There was no evidence of CMV infection in any of the subjects studied. The IgG and IgA responses against EBV early antigen (EA) and viral capsid antigen (VCA) were also studied. The IgG and IgA responses against VCA of EBV were increased in patients with SLE when compared with controls. However, there were no differences in these responses among different subgroups of patients. The mechanism of these responses was not apparent but may represent non-specific hyperimmune responses in these patients. There were no differences in the titre of IgG and IgA against EBV EA between the patient groups and controls. CONCLUSION: There is no direct evidence that either EBV or CMV plays a direct role in the onset and/or exacerbation of SLE.

Antibodies, Viral↗