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PubMed1978

Serologic studies in patients with systemic lupus erythematosus and central nervous system dysfunction.

Serologic studies were performed on 25 patients with systemic lupus erythematosus (SLE) during 29 acute episodes of central nervous system (CNS) disease. Increased anti-DNA antibody and decreased total serum hemolytic complement activity were observed only in those patients with associated extra-CNS disease manifestations. Patients with isolated CNS disease were otherwise in apparent clinical and serological remission regarding these two indices. No special association of cold-reactive IgM antilymphocyte antibodies was demonstrable in patients with ongoing CNS injury. Of special interest was an increased incidence of anti-Sm antibodies in the patients with CNS dysfunction relative to that in a large group of patients without neuropsychiatric disease. The incidence of anti-RNP was not increased. The data do not support direct involvement in SLE brain injury of either DNA/anti-DNA complexes or of lymphocytotoxic antibodies cross-reactive with brain cells, but do suggest an association of anti-Sm with CNS disease in this disorder.

Antibodies↗

PubMed2006

Heart involvement in systemic lupus erythematosus, anti-phospholipid syndrome and neonatal lupus.

Cardiac involvement is one of the main complications substantially contributing to the morbidity and mortality of patients suffering from systemic autoimmune diseases. All the anatomical heart structures can be affected, and multiple pathogenic mechanisms have been reported. Non-organ-specific autoantibodies have been implicated in immune complex formation and deposition as the initial triggers for inflammatory processes responsible for Libman-Sacks verrucous endocarditis, myocarditis and pericarditis. Anti-phospholipid antibodies have been associated with thrombotic events in coronary arteries, heart valve involvement and intra-myocardial vasculopathy in the context of primary and secondary anti-phospholipid syndrome. Antibodies-SSA/Ro and anti-SSB/La antigens play a major pathogenic role in affecting the heart conduction tissue leading to the electrocardiographic abnormalities of the neonatal lupus syndrome and have been closely associated with endocardial fibroelastosis.

Antibodies, Antiphospholipid↗

PubMed1986

Total lymphoid irradiation in refractory systemic lupus erythematosus.

In two patients with systemic lupus erythematosus, conventional therapy was considered to have failed because of persistent disease activity and unacceptable side effects. Both were treated with total lymphoid irradiation without clinical benefit, despite adequate immunosuppression as documented by markedly reduced numbers of circulating T lymphocytes and T-lymphocyte-dependent proliferative responses in vitro. The first patient developed herpes zoster, gram-negative septicemia, neurologic symptoms, and deterioration of lupus nephritis. The second patient developed massive bronchopneumonia, necrotic cutaneous lesions, and progressive nephritis and died 2 weeks after completion of radiotherapy. These observations, although limited to two patients, indicate that total lymphoid irradiation in patients with severe systemic lupus erythematosus should be regarded as strictly experimental.

Adult↗

PubMed1996

[Cardiac tamponade disclosing systemic lupus erythematosus].

Cardiac tamponade secondary to systemic lupus erythematosus is rare and has a very serious prognosis. The authors report a case of cardiac tamponade confirmed by echocardiography, which constituted the presenting sign of systemic lupus erythematosus in a 20-year-old patient, who required emergency pericardial aspiration. The diagnosis of systemic lupus erythematosus was established on the basis of the combination of pericardial involvement, non-erosive arthritis, leukopenia with lymphopenia, presence of LE cells and anti-native DNA antibodies and positive antinuclear antibody titre of 1/2560. The clinical course was favourable in response to 3 months of corticosteroid treatment. The possibility of SLE should be considered in any case of cardiac tamponade in a young patient in which the aetiology is not explained.

Adult↗

PubMed2003

[Apoptosis in systemic lupus erythematosus].

In autoimmune diseases including systemic lupus erythematosus (SLE), the immune system attacks various autoantigens and causes damage in target organs. Recently, it was found that dead cells serve as a repertoire for autoantigens which can stimulate an autoimmune response in sensitive persons. The mechanisms which lead to induction and progress of apoptosis include extra-cellular stimuli, intra-cellular signals, and cleavage of proteins. During apoptosis, several events occur including migration of intra-cellular components to the cell membrane, removal of apoptotic cells by specific proteins and complement systems, and phagocytosis of apoptotic cells by macrophages. In recent years, evidence has accumulated that the autoimmune response can be initiated as a result of defects in apoptosis and/or removal of apoptotic material. In this article, the association of apoptosis to the pathogenesis of systemic lupus erythematosus is discussed.

Apoptosis↗

PubMedDate not supplied

[Hemorrhagic pericarditis and cardiac tamponade in systemic lupus erythematosus. A case report].

Systemic lupus erythematosus is a chronic inflammatory autoimmune disorder that can affect any organ or system. Although pericarditis is the most frequent cardiac manifestation of this entity, usually is not a life threatening situation. Pericardial effusion causing cardiac tamponade is a very rare complication in lupus, with an incidence less than 2%. We report a case of pericardial tamponade due to SLE with severe hemodynamic involvement in a 21-year-old woman associated to rapidly progressive glomerulonephritis, acute pancreatitis, acute acalculous cholecystitis, pleural effusion, hematologic, cutaneous and neurologic lupus activity. Recognition of this rare manifestation of SLE may be life saving.

Adult↗

PubMed1976

Coronary arteritis in systemic lupus erythematosus.

Acute myocardial infarction in systemic lupus erythematosus may be due to an atheromatous or arteritic process. Confirmation of the latter etiology has previously been made only at postmortem examination. A 45-year-old white woman with known systemic lupus erythematosus developed anginal pain and multiple episodes of acute myocardial infarction. During this period, there was serologic but no other clinical evidence of active systemic lupus erythematosus. Serial coronary angiographic studies were strongly suggestive of an arteritic process based upon (1) a saccular aneurysm with no obstructive lesions in a coronary artery supplying an area of recent transmural myocardial infarction and (2) the development of significant obstructive lesions in a previously normal coronary artery over a period of 18 days. This case illustrates the difficulties in distinguishing between atherosclerosis and arteritis using a single coronary angiographic study. The distinction is significant because of the different therapeutic interventions required.

Acute Disease↗

PubMedDate not supplied

Primary biliary cirrhosis and systemic lupus erythematosus. A new case report.

Systemic lupus erythematosus and primary biliary cirrhosis are two autoimmune disorders that rarely occur in the same patient. Ten well-documented cases have been reported to date. We add the case of a woman who was diagnosed with systemic lupus erythematosus at 54 years of age then with primary biliary cirrhosis 18 years later. Interestingly, primary biliary cirrhosis antedated the systemic lupus erythematosus in all the other reported cases. The possibility that a patient may develop more than one autoimmune disorder should be borne in mind.

Autoimmunity↗

PubMedDate not supplied

Pleural effusion in systemic lupus erythematosus.

Three cases of systemic lupus erythematosus (SLE) with pleural effusion are reviewed. The characteristics of the effusions are presented, and the literature pertaining to lupus-related effusions is reviewed. There is great heterogeneity in lupus pleural effusions. The presence of polymorphonuclear neutrophils as the predominant white cell, while consistent with SLE, should raise the possibility of complicating bacterial infection. The presence of lupus erythematosus (LE) cells in the fluid seems to be the most specific diagnostic criterion.

Complement System Proteins↗

PubMed2002

Presentation and prognosis of the shrinking lung syndrome in systemic lupus erythematosus.

BACKGROUND AND OBJECTIVES: Systemic lupus erythematosus (SLE) may affect all the components of the respiratory system, including upper airways, lung parenchyma, pulmonary vasculature, pleura, and respiratory muscles. The shrinking lung syndrome (SLS) is a rare complication of SLE. This study describes the presenting features, investigation findings, treatment measures, and outcome of 7 patients with SLE and SLS. METHODS: Five patients with SLE/SLE were chosen retrospectively by examination of patient records, and 2 patients were chosen prospectively. All patients attended St. Thomas' Hospital or the Royal London Hospital between 1984 and 2001, with a total population of 2650 patients with SLE. RESULTS: Clinical features included dyspnea and pleuritic chest pain. Chest x-ray films showed small but clear lung fields, or basal atelectasis, with diaphragmatic elevation. No evidence of major parenchymal lung or pleural disease was found on the computerized tomography scan. Lung volumes were reduced on pulmonary function testing (PFT) in a restrictive pattern. Treatment of SLS included theophylline, increase in corticosteroid dosage, and intensification of immunosuppressive medication to include methotrexate or cyclophosphamide. During follow-up, 5 of 7 patients showed objective evidence on PFT of stabilization or improvement. CONCLUSIONS: The long-term prognosis of our SLS patients was reasonable, highlighting the importance of establishing a correct diagnosis and in particular differentiating it from fibrosing lung disease. Immunosuppressive therapy was helpful in stabilizing SLS and improving respiratory symptoms and PFT in some cases. RELEVANCE: SLS represents a rare complication of SLE, and it is important to be aware of its presenting features and prognosis.

Adolescent↗

PubMed1977

Retinal arterial occlusive disease in systemic lupus erythematosus.

Four patients with systemic lupus erythematosus (SLE) developed an unusual form of occlusive retinal arterial disease. The most prominent clinical features of this disorder were deposition of yellow-white material in retinal arterial walls and evidence of multifocal retinal arterial occlusion. Fluorescein angiographic findings included nonperfusion of the obstructed arteries and the retinal capillary beds fed by them, and fluorescein leakage at the sites of involvement of the retinal arteries. This ocular complication of SLE is presumably a manifestation of the widespread systemic vascular problems seen in this disorder. It may be more common in patients with lupus involving the CNS.

Adult↗

PubMed1995

Active systemic lupus erythematosus is associated with depletion of the natural generic anti-idiotype (anti-F(ab')2) system.

OBJECTIVE: To study the relationship of serum IgG anti-F(ab')2 and clinical disease activity in 108 patients with systemic lupus erythematosus (SLE) and to determine whether low serum anti-F(ab')2 with active renal disease is accompanied by deposition of anti-F(ab')2 in renal immune complex lesions. METHODS: We studied 108 patients with definite SLE over a 5 yr period and assayed serum anti-F(ab')2 levels in relation to degree of clinical disease activity. Renal biopsy eluates of 26 patients with SLE were examined by enzyme linked immunosorbent assay (ELISA) for relative amounts of IgG, anti-DNA, and IgG anti-F(ab')2. RESULTS: Active SLE was strongly associated with low serum anti-F(ab')2. SLE renal biopsy eluates frequently contained high levels of IgG and IgG anti-DNA and lower, but definite, IgG anti-F(ab')2 activity. When specific activity of IgG anti-DNA and IgG anti-F(ab')2 was compared between kidney biopsy eluates and concomitant serum, marked relative renal concentration was found for both anti-DNA (19-fold) and anti-F(ab')2 (74-fold). Some biopsy eluates contained IgG antibodies bearing apparent double specificity for both DNA and F(ab')2. CONCLUSION: Active SLE is often associated with low serum anti-F(ab')2. Relative enrichment over specific activity in serum of both IgG anti-F(ab')2 and anti-DNA in SLE kidney biopsy eluates may indicate participation of both reactants in the glomerular disease process. Low serum anti-F(ab')2 in active SLE may reflect down modulation of failure of idiotypic control mechanisms associated with disease progression.

Adolescent↗

PubMed1981

Severe retinal vascular lesions in systemic lupus erythematosus.

Retinal lesions in systemic lupus erythematosus (SLE) are usually closely related to the patient's general condition and occur frequently in severe states such as renal or central nervous system involvement. However, improved treatment of SLE has reduced retinal involvement, and it is rare today to observe severe retinal lesions in patients with SLE. We report two cases of severe retinal vascular lesions in SLE patients who developed otherwise unremarkable systemic manifestations and laboratory findings.

Adult↗

PubMed2006

Vascular changes of the retina and choroid in systemic lupus erythematosus: pathology and pathogenesis.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder that affects multiple organ systems. When eyes are involved, the principle manifestations are hemorrhage, retinal cotton wool spots, microangiopathy and vaso-occlusion. Research in the past two decades has significantly contributed to our understanding about this disease in general and its therapeutic management, although knowledge about the mechanism of ocular involvement and pathogenesis in SLE is limited. This is an important issue, because the ocular symptoms in this disease could be potentially sight threatening in acute cases. Here, we present an overview of the clinical and histopathologic features of retinal and choroidal vascular changes, as seen in patients with SLE. We discuss the role of immune complex deposition in vascular pathogenesis in the eye. Reports indicated an involvement of antiphospholipid antibodies (APAs) in the retinal and choroidal vasculopathy in SLE, although their precise role in this process is uncertain. It is important to look for mechanisms of immune complex-mediated vasculopathy and role of inflammatory mediators in this process in SLE. For this, established animal models can be utilized in research to learn about the precise role of various autoantibodies and complements involved in disease pathogenesis. A clear knowledge about the immunopathogenesis is warranted, and the rationale for the future therapy should be based on reducing vascular inflammation as well as ameliorating autoimmunity in this disease.

Autoantibodies↗

PubMed2006

Nonmyeloablative hematopoietic stem cell transplantation for systemic lupus erythematosus.

CONTEXT: Manifestations of systemic lupus erythematosus (SLE) may in most patients be ameliorated with medications that suppress the immune system. Nevertheless, there remains a subset of SLE patients for whom current strategies are insufficient to control disease. OBJECTIVE: To assess the safety of intense immunosuppression and autologous hematopoietic stem cell support in patients with severe and treatment-refractory SLE. DESIGN, SETTING, AND PARTICIPANTS: A single-arm trial of 50 patients with SLE refractory to standard immunosuppressive therapies and either organ- or life-threatening visceral involvement. Patients were enrolled from April 1997 through January 2005 in an autologous nonmyeloablative hematopoietic stem cell transplantation (HSCT) study at a single US medical center. INTERVENTIONS: Peripheral blood stem cells were mobilized with cyclophosphamide (2.0 g/m2) and granulocyte colony-stimulating factor (5 microg/kg per day), enriched ex vivo by CD34+ immunoselection, cryopreserved, and reinfused after treatment with cyclophosphamide (200 mg/kg) and equine antithymocyte globulin (90 mg/kg). MAIN OUTCOME MEASURES: The primary end point was survival, both overall and disease-free. Secondary end points included SLE Disease Activity Index (SLEDAI), serology (antinuclear antibody [ANA] and anti-double-stranded (ds) DNA), complement C3 and C4, and changes in renal and pulmonary organ function assessed before treatment and at 6 months, 12 months, and then yearly for 5 years. RESULTS: Fifty patients were enrolled and underwent stem cell mobilization. Two patients died after mobilization, one from disseminated mucormycosis and another from active lupus after postponing the transplantation for 4 months. Forty-eight patients underwent nonmyeloablative HSCT. Treatment-related mortality was 2% (1/50). By intention to treat, treatment-related mortality was 4% (2/50). With a mean follow-up of 29 months (range, 6 months to 7.5 years) for patients undergoing HSCT, overall 5-year survival was 84%, and probability of disease-free survival at 5 years following HSCT was 50%. Secondary analysis demonstrated stabilization of renal function and significant improvement in SLEDAI score, ANA, anti-ds DNA, complement, and carbon monoxide diffusion lung capacity adjusted for hemoglobin. CONCLUSIONS: In treatment-refractory SLE, autologous nonmyeloablative HSCT results in amelioration of disease activity, improvement in serologic markers, and either stabilization or reversal of organ dysfunction. These data are nonrandomized and thus preliminary, providing the foundation and justification for a definitive randomized trial. Clinical Trial Registration ClinicalTrials.gov Identifier: NCT00271934.

Adult↗

PubMed1986

Increased intrathecal immunoglobulin synthesis of both kappa and lambda types in patients with systemic lupus erythematosus and central nervous system involvement.

The concentration of immunoglobulins in paired serum and cerebrospinal fluid (CSF) specimens from 15 patients with systemic lupus erythematosus (SLE) and central nervous system (CNS) involvement (CNS-SLE) were determined based on their light chain properties. Eight patients with SLE without CNS involvement and 20 patients with noninflammatory neurological diseases were also studied for comparison. We found that both of the CSF Ig-k (immunoglobulin kappa) and Ig-1 (immunoglobulin lambda) indices were significantly elevated, indicating the increased intrathecal immunoglobulin synthesis of both kappa and lambda types in patients with CNS-SLE. Moreover, the CSF Ig-k and Ig-1 indices correlated well with each other, and both indices were found to decrease remarkably when the CNS manifestations subsided after successful treatment. In 4 of 15 patients, intrathecal synthesis of free light chains in addition to Ig bound light chains seemed to be increased. These observations provide substantial evidence for polyclonal B lymphocyte activation within the CNS.

Adolescent↗

PubMed2001

Alveolar hemorrhage and renal microangiopathy in systemic lupus erythematosus.

CONTEXT: Acute alveolar hemorrhage in systemic lupus erythematosus usually occurs as a pulmonary-renal syndrome. In most cases, the lungs show "bland" alveolar hemorrhage with little or no inflammation. Whether this alveolar injury is similar to the better-defined noninflammatory renal lupus vasculopathy is unresolved. OBJECTIVES: To investigate the relationships and the mechanisms of small vascular injury in the lung and kidney of 2 lupus patients who died of diffuse AH. METHODS: We investigated the relationship of AH to immune complex deposition in the lungs of 6 patients with systemic lupus erythematosus and correlated the findings with glomerular and vascular disease in the kidney. Lung and kidney were studied by light, immunofluorescence, and/or electron microscopy; apoptosis was investigated using in situ nick-end labeling. RESULTS: The clinical course of 2 patients was complicated by alveolar hemorrhage, and the lungs of these patients revealed alveolar wall immune complex deposits and bland alveolar hemorrhage. These 2 patients had World Health Organization class IV lupus nephritis and renal arterioles involved by a noninflammatory lupus vasculopathy. Apoptosis was identified in the lupus microangiopathy and in alveolar walls within areas of alveolar hemorrhage. Alveolar wall immune complex deposits were not found in 4 patients who had a lupus glomerulonephritis but did not have renal lupus vasculopathy. Apoptosis was not seen in renal arterioles or lungs of these 4 cases, except in areas of diffuse alveolar damage or herpesvirus pneumonia. CONCLUSIONS: Our findings indicate that alveolar hemorrhage in systemic lupus erythematosus, characterized by bland alveolar wall changes, is pathogenetically similar to the lupus microangiopathy of the kidney. In both lung and kidney, the pathogenesis of the microvascular injury appears to be related to immune complex deposition and the induction of apoptosis.

Adult↗

PubMed1990

Functional asplenia in systemic lupus erythematosus.

A patient with inactive systemic lupus erythematosus was successfully treated for pneumococcal sepsis complicated by disseminated intravascular coagulation, shock, renal failure, and functional asplenia. Functional asplenia was diagnosed from the total absence of uptake of intravenously administered 99mtechnetium-labeled sulfur colloid. Ten similar cases of functional asplenia occurring in patients with systemic lupus erythematosus were noted in a review of the literature. Six of these cases, including the current report, were complicated by pneumococcal (5) or salmonella (1) sepsis. The patient presented here had an excellent antibody response to pneumococcal vaccination. Spleen scan abnormalities fully reversed at 1 year. Although functional asplenia is a rare event in systemic lupus erythematosus, it appears to predispose to severe septic complications.

Acute Kidney Injury↗