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PubMed1976

[Headache in the pathology of small cerebral blood vessels: study of patients with systemic lupus erythematosus].

Seventy-two records of patients with systemic lupus erythematosus were reviewed retrospectively. Sixty-one fulfilled the criteria for the disease. Forty-six percent had clinical evidence of central nervous system involvement. The incidence of headache was compared in those with and without central nervous system lupus. No difference in the frequency of headache in the two groups was found and the incidence of hypertension, renal disease and steroid therapy was equally distributed among those with and without headache. A significantly higher incidence of hypertension was found in patients with central nervous system lupus erythematosus. We conclude that headache in systemic lupus erythematosus in the absence of neurologic symptoms or signs is no indication of central nervous system involvement by the process and that small vessel disease of the brain is not a cause of headache.

Adolescent↗

PubMed1982

Mode of inheritance of decreased C3b receptors on erythrocytes of patients with systemic lupus erythematosus.

The erythrocytes of patients with systemic lupus erythematosus have been shown to have a decreased number of receptors for the major cleavage fragment of the third component of complement (C3b). We studied the basis for this decreased number of C3b receptors by measuring the uptake of anti-C3b-receptor antibody on cells from 113 normal subjects, 38 patients with systemic lupus erythematosus, 14 of their spouses, and 47 of their relatives. The normal subjects had 5014 +/- (mean +/- S.E.M.) receptor sites per cell, but the patients and their relatives had significantly fewer sites--2809 +/- 241 and 3167 +/- 196, respectively (P less than 0.0005). The number of sites in the patients' spouses did not differ from normal (P greater than 0.3). Three phenotypes, indicated by the numbers of receptors, occurred in the normal population; a high phenotype (HH, with 5500 to 8500 sites per cell), an intermediate phenotype (HL, with 3000 to 5499), and a low phenotype (LL, less than 3000). These three phenotypes were present in 34, 54, and 12 percent, respectively, of the normal subjects; in contrast, 5, 42, and 53 per cent of patients had these respective phenotypes. Pedigree analyses indicated that these phenotypes were inherited in an autosomal codominant manner. We conclude that the decreased number of C3b receptors in lupus is inherited, not acquired.

Adult↗

PubMed1986

Livedoid vasculitis and central nervous system involvement in systemic lupus erythematosus.

Of 66 patients with systemic lupus erythematosus (SLE), 11 (16.7%) had livedoid vasculitis. The sites of predilection included the elbows, knees, fingers, soles, and back, which are not those of common livedoid vasculitis. Livedoid vasculitis developed in ten (90.9%) of the 11 patients with SLE who eventually developed central nervous system (CNS) lupus. In contrast, such preceding livedoid vasculitis occurred in only three (11.5%) of the 26 patients with severe nephrotic lupus nephritis. Livedoid vasculitis did not occur in any patient with neither CNS lupus nor severe lupus nephritis. These results indicate that livedoid vasculitis in SLE is a very important cutaneous manifestation that may possibly be prodromal to CNS lupus.

Adult↗

PubMed1986

High IgM antibody to human T-lymphotropic virus type I in systemic lupus erythematosus.

Twenty-six percent of 53 systemic lupus erythematosus sera had high levels of IgM antibody to human T-lymphotropic virus Type I, significantly more than the 5% of normal controls. Neither IgG antibodies to Type I virus nor IgM or IgG antibodies to Type II virus were increased in lupus. Further analysis using competition immunoassay and Western blot techniques also suggested that the IgM Type I antibodies in lupus sera were directed against viral antigens but did not completely exclude a nonviral reaction. Other studies also have not found IgG antibodies to the Type I virus but have not tested for IgM antibodies. Our study suggests that human T-lymphotropic virus Type I or a related virus may be involved in the pathogenesis of some cases of systemic lupus erythematosus.

Adolescent↗

PubMedDate not supplied

Nervous system involvement in systemic lupus erythematosus: report of three cases.

Central nervous system involvement in systemic lupus erythematosus is rather frequent whereas peripheral nervous system involvement is much less common. The three patients studied by us had isolated manifestations uncommon in nature. The first one developed a sensory-motor polineuropathy with signs of axonal degeneration. It responded to the therapeutic association of corticosteroids with an immunosuppressive agent. Satisfactory recovery took place over a time span of a year. The second patient had encephalic and cerebral trunk involvement from which an irreversible dementia resulted. The third patient, who had recurrent aseptic meningitis, is asymptomatic for six months now. Patients one and two had no systemic manifestations at the time of nervous system involvement. Suspicion of systemic lupus erythematosus was made on the basis of past inspecific articular symptoms. The neurological and systemic manifestations may be sometimes simultaneous; they are usually followed by serologic changes. Isolated nervous system involvement may be seen with and without sorologic changes, and there may be found antibodies reactive with phospholipids (anticardiolipin, antigangliosides and anticerebrosides). The employment of nonsteroid immunosuppressive drugs associated with corticosteroids in small doses seems to be useful in cases of systemic lupus erythematosus with nervous system involvement.

Adolescent↗

PubMed2004

Pulmonary disease in systemic lupus erythematosus and the antiphospholpid syndrome.

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by disturbances in innate and adaptive immune mechanisms. Multiple systems and organs may be involved. Tissue damage and dysfunction are mediated by autoantibodies and immune complex formation. The lungs are among the organ systems commonly involved. The pulmonary manifestations usually occur in patients with multisystem disease and include: pleural involvement, parenchymal disease, pulmonary vascular disease and diaphragmatic dysfunction. Manifestations may range from sub-clinical abnormalities to life threatening disorders. Many of the pulmonary manifestations characteristic of SLE are seen in the antiphospholipid syndrome (APS) as well, in both the primary and secondary syndrome. In this review the diverse pulmonary manifestations are described as well as the diagnostic modalities available, including the use of induced sputum evaluation for early diagnosis and follow up. New treatment modalities are referred to.

Antibodies, Antiphospholipid↗

PubMed2005

Serum free prolactin concentrations in patients with systemic lupus erythematosus are associated with lupus activity.

OBJECTIVE: To determine in patients with systemic lupus erythematosus (SLE) the relationships among serum total and free prolactin (PRL) levels, isoforms of PRL and lupus activity. METHODS: In a cross-sectional study, 259 patients with SLE were tested for serum total PRL, serum free PRL, and PRL in fractions obtained after gel filtration chromatography (in 70 sera taken at random) by immunoradiometric assay based on disease activity. RESULTS: A significant correlation between direct PRL and free PRL levels was found in patients with and without lupus activity (r = 0.475, P<0.001); however, this was less so for non-active patients than for active patients (r=0.433, P<0.001 and r=0.909, P<0.001, respectively). SLE Disease Activity Index (SLEDAI) scores correlated positively with serum free PRL levels (r=0.314, P<0.001) and percentage of little PRL (r=0.33, P=0.005) and negatively with percentage of big big PRL (r=-0.3, P=0.012). Patients with active disease had higher serum free PRL levels (median 12.6 vs 9.3 ng/ml, P<0.001), higher percentages of little PRL (83.1 +/- 21.2 vs 63.6 +/- 24.8%, P=0.011) and lower percentages of big big PRL (9.4 +/- 18.0 vs 25.2 +/- 24.3%, P=0.031). Different clinical manifestations and serological parameters of lupus disease activity were more frequent in patients with free hyperprolactinaemia than in patients with normal serum free PRL levels (such as neurological manifestations, renal involvement, serositis, haematological manifestations, anti-double-stranded DNA and hypocomplementaemia; P<0.021). CONCLUSION: An increase in serum free PRL levels, higher percentages of little PRL and lower percentages of big big PRL proved to be factors related to lupus activity in a subset of patients with SLE. These novel data must be taken into account in future studies aiming to establish a relationship between PRL and disease activity in SLE.

Adult↗

PubMed2001

Mortality and causes of death in systemic lupus erythematosus.

Cohort studies of survival in systemic lupus erythematosus (SLE) often have been limited by methodologic problems. In studies of inception cohorts of patients followed since 1980, survival at 5 years has exceeded 90%. These estimates are generally higher than survival estimates from earlier studies, suggesting that short-term survival in SLE has improved. There is less evidence to support major improvements over time in survival after 10 years or more of SLE. Infections, atherosclerotic disease, and active systemic lupus erythematosus or organ damage caused by SLE are the main causes of death in patients with SLE, but the proportion of early deaths caused by active SLE has decreased over time.

Bacterial Infections↗

PubMed1982

Suppression of the normal autologous mixed leukocyte reaction by sera from patients with systemic lupus erythematosus.

Sera from 15 patients with active systemic lupus erythematosus and 7 patients with inactive lupus were added to normal autologous mixed leukocyte reaction (MLR) cultures. Twelve of the 22 sera reduced autologous T cell proliferative responsiveness to B plus null (B + N) cells or macrophages by 50% or more. This inhibition correlated with defective autologous MLR in fresh mononuclear cells from those patients. When normal responding and stimulating cell populations were preincubated with suppressive lupus sera, then added to autologous MLR cultures that contained normal serum, proliferative responses were also reduced; inhibitors are directed against participating mononuclear cell subpopulations. The suppressive serum factors were directed variously against monocyte/macrophage (M phi), B + N, or T cell populations; M phi/T interactions were suppressed most frequently. The inhibitors were not removed by high-speed centrifugation or by depletion of antibodies to DNA, and they did not correlate with the presence of lymphocytotoxic antibodies. The presence of serum inhibitors of normal M phi/T and B + N/T autologous MLR may be an immunologic abnormality important in the initiation, perpetuation, or exacerbation of systemic lupus erythematosus.

Adult↗

PubMed1995

[Systemic lupus erythematosus and Salmonella enteritidis osteomyelitis].

Infections in systemic lupus erythematosus are frequent. However, osteoarticular Salmonella infections are rarely reported. We report a case of systemic lupus erythematosus diagnosed in a 15 year-old girl. Seven months later, she presented with fever and a localized collection of the upper extremity of the left tibia related to a Salmonella enteritidis acute osteomyelitis (sub periosteal abscess). The out-come was chronic and led to death. The authors emphasize the severity of non typhoidal salmonellosis in systemic lupus erythematosus.

Adolescent↗

PubMed1984

Complement components, complement activation, and acute phase response in systemic lupus erythematosus.

The investigation concerned 33 systemic lupus erythematosus (SLE) patients assigned to three groups representing mild SLE, more severe extra renal SLE, and SLE with significant renal involvement. In patients with extrarenal disease, the inflammatory plasma protein response was often pronounced during exacerbation, as evidenced by markedly increased concentrations of C-reactive protein (CRP), alpha 1-antichymotrypsin, alpha 1-antitrypsin, and orosomucoid. CRP responses were rare in patients with renal involvement, despite the increased concentrations of other acute-phase reactants in some of these patients. Superimposed bacterial infections were not clearly distinguished by raised CRP concentrations. The classical pathway of complement was activated in all patients during exacerbation, as indicated by increased concentrations of C1r-C1s-C1 inactivator complexes and C2a fragments. C1, C2, and probably also C3 activation varied according to the amounts of circulating C1q-binding immune complexes, as measured by solid-phase assay. Manifest hypocomplementemia was usually associated with glomerulonephritis. Participation of complement components in the inflammatory plasma protein response apparently counteracted the development of hypocomplementemia in many patients with extrarenal SLE. Circulating C3d was detected in all patients during exacerbation of renal disease and in most patients with severe extrarenal manifestations. Inverse relationships were found between immunochemical C2 concentrations and the percentage of cleaved C2 and between C3 and C3d. There was no appreciable consumption of factors B and D and properdin of the alternative pathway in the patients. High concentrations of factor D, a low molecular weight protein, were exclusively found in patients with renal involvement and could be ascribed to retention due to reduced glomerular filtration.

Antigen-Antibody Complex↗

PubMed2002

Characterization of CD3+ CD4- CD8- (double negative) T cells in patients with systemic lupus erythematosus: production of IL-4.

Systemic lupus erythematosus (SLE) is a chronic autoimmune rheumatic disease that may affect every organ or system in the body. We have shown previously that the TCR alphabeta+ subpopulation of CD3+ CD4- CD8-, DN T cells is expanded in patients with SLE and that double negative T cells express increased levels of activation markers compared both with healthy people and with patients with rheumatoid arthritis, (RA) as autoimmune controls. The aim of this study was to characterize these cells in terms of their ability to produce IL4, a Th2 cytokine, both spontaneously and after mitogen stimulation. It was found that a higher percentage of TCR alphabeta+ double negative T cells from patients with SLE contained IL4 constitutively than did the same population of cells from healthy people or from those with RA. After mitogen stimulation, there was no significant difference in the amount of IL4 produced by each of the three groups. Further study of patients producing high levels of IL4 (about one third of the patients) indicated that they had a lower percentage of alphabeta+ T cells in the double negative compartment than did patients with fewer IL4 containing cells.

Adolescent↗

PubMed2003

Systemic lupus erythematosus and the type I interferon system.

Patients with systemic lupus erythematosus (SLE) have ongoing interferon-alpha (IFN-alpha) production and serum IFN-alpha levels are correlated with both disease activity and severity. Recent studies of patients with SLE have demonstrated the presence of endogenous IFN-alpha inducers in such individuals, consisting of small immune complexes (ICs) containing IgG and DNA. These ICs act specifically on natural IFN-alpha-producing cells (NIPCs), often termed plasmacytoid dendritic cells (PDCs). Given the fact that the NIPC/PDC has a key role in both the innate and adaptive immune response, as well as the many immunoregulatory effects of IFN-alpha, these observations might be important for the understanding of the etiopathogenesis of SLE. In this review we briefly describe the biology of the type I IFN system, with emphasis on inducers, producing cells (especially NIPCs/PDCs), IFN-alpha actions and target immune cells that might be relevant in SLE. On the basis of this information and results from studies in SLE patients, we propose a hypothesis that explains how NIPCs/PDCs become activated and have a pivotal etiopathogenic role in SLE. This hypothesis also indicates new therapeutic targets in this autoimmune disease.

Antigen Presentation↗

PubMed1997

[Oral manifestations in patients with systemic lupus erythematosus].

Forty-six patients with systemic lupus erythematosus underwent thorough dental examination to determine the frequency and severity of oral lesions and periodontal diseases. According to clinical criteria, disease was classified as severe (n = 26) or less severe (n = 20). The overall rate of mucosal involvement in the studied patients was 48%-from 54% in patients with severe disease, 40% in those with less severe disease. Patients with severe disease were found to have a higher rate of tooth loss and an increased rate of gingival inflammation. The severity of periodontal lesions correlated with alterations in the immunoglobulin pattern, particularly with an increase in gamma-immunoglobulins. Thus it is suspected that complex immunodysregulation in combination with immunosuppressive therapy is responsible for the high rate of oral and periodontal lesions in patients with systemic lupus erythematosus.

Adult↗

PubMed2001

Lupus anticoagulant and history of thrombosis are not associated with persistent endothelial cell activation in systemic lupus erythematosus.

Antiphospholipid antibodies (aPL), especially lupus anticoagulant (LAC), characterize systemic lupus erythematosus (SLE) patients at increased risk for arterial and venous thromboembolic complications. It has been reported that purified human anti-phospholipid antibodies cause endothelial cell activation in in vitro experiments. In order to investigate whether increased endothelial cell activation is associated with thromboembolic events in SLE patients with LAC, we measured plasma levels of thrombomodulin (TM), von Willebrand factor (vWf), sP-selectin, vascular cell adhesion molecule-1 (sVCAM-1) and ED1-fibronectin in a study of 76 patients with SLE. Patients were subdivided on the basis of: no history of thrombosis and LAC-negative (n = 22) or LAC-positive (n = 17); positive history of thrombosis and LAC-negative (n = 16) or LAC-positive (n = 21). The median SLE disease activity index (SLEDAI) was 4. Although concentrations of sTM, vWf, sP-selectin and sVCAM-1 were significantly elevated in SLE compared with values in healthy controls, they did not differ between the four groups, between patients with or without history of thrombosis, and between patients with or without LAC. Presence of anticardiolipin antibodies could not explain these negative findings. Adjustment of the concentrations for significantly associated variables, such as age, hypertension, smoking, immunosuppressive treatment and concentrations of creatinine, cholesterol and homocysteine, did not change the main results of the study. Only sTM was significantly lower in patients with both LAC and thrombosis than in patients without both these features after adjustment for serum creatinine concentrations. In conclusion, we did not find an association between endothelial cell activation and presence of LAC or history of thrombosis in SLE.

Adult↗

PubMed2004

Myocarditis as a prognostic indicator in systemic lupus erythematosus.

Lupus myocarditis is a life threatening complication of systemic lupus erythematosus (SLE). A case of left ventricular failure secondary to myocarditis occurring in a patient with SLE is reported. Despite resolution of the cardiac failure with pulsed cyclophosphamide and steroids, she eventually died of non-cardiac complications 18 months later. The literature is also reviewed.

Adult↗

PubMed1991

Occlusive vasculopathy in systemic lupus erythematosus. Association with anticardiolipin antibody.

Patients with systemic lupus erythematosus and with antiphospholipid antibody are subject to sudden occlusion of multiple blood vessels. We describe two patients with systemic lupus erythematosus with acute, catastrophic, widespread non-inflammatory visceral vascular occlusions associated with high-titer antiphospholipid antibody. The histopathologic features clearly distinguished these patients from classic systemic lupus erythematosus vasculitis. We further suggest that, based on a probable pathogenesis related to the presence of antiphospholipid antibody, and based on the non-inflammatory vascular occlusion, steroids and other immunosuppressive medications are of limited value. Plasmapheresis along with anticoagulant therapy should be considered.

Adult↗

PubMed1985

Antibody-dependent cellular cytotoxicity of human vascular endothelium in systemic lupus erythematosus.

Sera from 35 patients with systemic lupus erythematosus were examined for a cytotoxic effect on human umbilical vein endothelium. Although none of these sera produced direct cytotoxicity of 51Cr-labelled endothelial cells, even with added complement, 3 sera regularly produced increased 51Cr release when co-cultured with endothelial cells and normal human peripheral blood mononuclear cells. The effector cells involved in this cytotoxicity possessed Fc-receptors but were non-T and non-adherent while fractionation studies indicated that the responsible serum factor(s) was IgG, probably in the form of immune complexes of small size. Control studies, using sera from both 27 normal controls and 19 patients with either diabetes or extensive atherosclerotic vascular disease failed to reveal any similar cytotoxicity. Two of the 3 patients, whose sera produced this antibody-dependent cellular cytotoxicity, had had clinical episodes of major vascular thrombosis, raising the possibility that the cytotoxicity might provide an additional pathogenic mechanism in certain patients with systemic lupus erythematosus.

Adult↗