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PubMed1996

Protein losing enteropathy as the initial manifestation of childhood systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a multisystem organ disease, and involvement of the gastrointestinal system is relatively rare. We describe a 13-year-old girl who presented initially with abdominal pain, diarrhea, edema, and hypoalbuminemia. She was diagnosed with protein losing enteropathy (PLE) based on the significant increase of alpha 1-antitrypsin clearance in the stool. Two weeks after admission she developed clinical and serological findings that fulfilled the ACR criteria for SLE. Over 22 cases of lupus associated PLE have now been reported, but only 3 in children. Children with PLE should be evaluated for SLE. In addition, PLE should be suspected as a possible cause of unexplained edema and/or hypoalbuminemia in SLE.

Adolescent↗

PubMed2005

Quality of life in children with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) in children is a chronic multi-system disease with wide ranging effects on their quality of life (QOL). While SLE's impact on different arenas of life and well-being has been extensively examined in the adult population, its effect on children has not received adequate attention. This paper briefly discusses the multidimensional aspect of QOL, the biopsychosocial implications of SLE, factors complicating QOL measurement in the affected population, and the different generic and disease-specific scales used for measuring QOL and related constructs, and it also highlights the need for SLE-specific pediatric QOL instruments.

Adaptation, Physiological↗

PubMed1998

Central nervous system nitric oxide formation in cerebral systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is an inflammatory disease in which up to two thirds of the patients present neurological symptoms. The diagnosis of the disease is based on clinical findings and the presence of autoantibodies, and the pathogenesis is unclear. The purpose of this study was to determine if the pathogenesis was partly mediated via nitric oxide (NO) formation. Cerebrospinal fluid (CSF) samples from 15 patients with cerebral SLE were analyzed for the NO metabolites nitrite and nitrate using capillary electrophoresis. The severity of neurological symptoms was scored by dividing the patients into two groups with either mild or moderate/severe CNS involvement. All patients with cerebral SLE showed increased levels of NO metabolites. In CSF, there was a relationship between signs of NO production and clinical results showing that increased levels of nitrite and nitrate were associated with more severe neurological symptoms. These findings may shed new light on the pathogenesis of cerebral SLE, and analysis of nitrate and nitrate may prove to be of value in monitoring the activity of the disease.

Brain Diseases↗

PubMedDate not supplied

Posture in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a connective autoimmune disease that may involve many organ systems and neural function impairment. Postural apparatus dysfunction in SLE may develop in the case of central and peripheral neural involvement. We studied the presence of postural abnormalities in SLE patients with different degrees of disease activity. Twenty-eight subjects (18 SLE patients and 10 normal controls) underwent postural evaluation by means of Static Computerised Posturography. Disease severity or specific clinical problems did not form selection criteria. Lupus activity was assessed using the Systemic Lupus Activity Measure (SLAM). A statistically significant (p < 0.05) increase in the parameters of trace length, trace surface, trace velocity, standard deviation in velocity, and Fast Fourier trX and Y (FET), were found in both the closed and opened eyes tests, when lupus patients were compared to controls subjects. No significant pattern variation in posture was observed between more active and less active SLE patients. Postural control alterations in SLE may be considered a complication of the chronic autoimmune inflammatory process, independent of disease activity as evaluated by the SLAM index. The site of the neuropathy remains uncertain, although we believe it to be peripheral rather than central in origin due to the absence of symptoms or clinical signs of CNS involvement or vascular degeneration.

Adult↗

PubMed1999

Cardiac involvement in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE), a connective tissue disease characterized by the production of autoantibodies, can affect all organ systems. Cardiac involvement in patients with SLE has been described since the early 20th century. The manifestations are numerous and can involve all components of the heart, including the pericardium, conduction system, myocardium, valves, and coronary arteries. In recent years, echocardiography has yielded additional information about the heart in patients who have SLE with and without clinical cardiac involvement. Moreover, antiphospholipid antibodies have been linked to several cardiac manifestations in patients with SLE, including valvular abnormalities and possibly coronary artery disease. This updated, comprehensive review summarizes the new literature on SLE and the heart.

Antibodies, Antiphospholipid↗

PubMed2001

Orthopaedic manifestations of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease of unknown origin. It affects multiple organ systems, but most frequently the musculoskeletal system. Highly variable manifestations include small and large joint involvement, spinal involvement, periarticular tissue symptoms, and complications associated with chronic steroid use such as osteonecrosis, osteoporosis, and stress fractures. The following review summarizes the common orthopaedic manifestations of SLE.

Humans↗

PubMed2002

Ocular manifestations of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic, immunologic disorder that may affect multiple organ systems. Keratoconjunctivitis sicca is the most common ocular manifestation, but visual morbidity is usually due to retinal and neuro-ophthalmic manifestations of the disease. Ocular manifestations of lupus are a reflection of systemic disease. The presence of ocular manifestations should alert the clinician to the likely presence of disease activity elsewhere. Therefore, all patients with ocular lupus should be carefully evaluated for systemic involvement to detect potentially treatable and preventable complications of the disease. In addition, the ophthalmologist should include SLE in the differential diagnosis of many retinal vascular and neuro-ophthalmic disorders. The ophthalmologist may play an important role in the care of patients with SLE, since ocular inflammatory lesions may precede potentially serious extraocular disease.

Diagnosis, Differential↗

PubMed2004

Apoptosis and mitochondrial dysfunction in lymphocytes of patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is characterized by abnormal activation and cell death signaling within the immune system. Activation, proliferation, or death of cells of the immune system are dependent on controlled reactive oxygen intermediate (ROI) production and ATP synthesis in mitochondria. The mitochondrial transmembrane potential (Delta(Psi)m) reflects the energy stored in the electrochemical gradient across the inner mitochondrial membrane, which in turn is used by F0F1-ATPase to convert adenosine 5'-diphosphate to ATP during oxidative phosphorylation. Mitochondrial hyperpolarization and transient ATP depletion represent early and reversible steps in T-cell activation and apoptosis. By contrast, T lymphocytes of patients with SLE exhibit elevated Delta(Psi)m, that is, persistent mitochondrial hyperpolarization, cytoplasmic alkalinization, increased ROI production, as well as diminished levels of intracellular glutathione and ATP. Oxidative stress affects signaling through the T-cell receptor as well as the activity of redox-sensitive caspases. ATP depletion may be responsible for diminished activation-induced apoptosis and sensitize lupus T cells to necrosis. Mitochondrial dysfunction is identified as a key mechanism in the pathogenesis of SLE.

Adenosine Triphosphate↗

PubMed2001

A case of hypothermia combined with systemic lupus erythematosus.

Systemic lupus erythematosus(SLE) is a prototypic autoimmune disease affecting various organ systems. Hypothermia is a rare manifestation of SLE. We experienced a case of SLE combined with hypothermia. A 36-year-old woman, who had been diagnosed as SLE 3 days before admission, admitted complaining of mental confusion. After admission, her body temperature, initially 36.1 degrees C, became 32.6 degrees C. Her core body temperature was less than 35.0 degrees C. Despite of warming with heating lamp and blankets, her core temperature did not reach 35.0 degrees C during 18 hours. Ten days later, her temperature exceeded 36.0 degrees C.

Adrenal Cortex Hormones↗

PubMed1998

Association of an insertion polymorphism of angiotensin-converting enzyme gene with the activity of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) shows various clinical manifestations, which are characterized by inflammation in many different organ systems. The cause of SLE is still unclear; however, the immunological abnormalities are considered to be responsible for the pathogenesis of SLE. As angiotensin I-converting enzyme (ACE) has been reported to be associated with various immunological phenomena, we investigated the correlation between insertion (I)/deletion (D) polymorphism of the ACE gene and the disease activity of SLE. Ninety-three patients with newly diagnosed SLE were enrolled in this study. ACE genotype was determined by the polymerase chain reaction (PCR). We measured serum levels of anti-double-stranded (ds) DNA antibody (Ab) and serum levels of total complements (CH50) as the parameter for lupus activity. Moreover, we evaluated the clinical disease activity by calculating SLE disease activity index (SLEDAI). Individuals with II genotype showed a significant increase in SLE activity. Patients with the ACE II genotype showed a higher serum level of anti-dsDNA Ab (14.3 IU/ml (5.475, 74.6, median (25th centile, 75th centile)) than those with the DD genotype (4.65IU/ml (4.05, 6.8)) (P<0.01). Moreover, patients with the 11 genotype also showed lower levels of serum CH50 than those with the DD genotype (P < 0.01). Patients with the II1 or DI genotype had significantly higher SLEDAI score than those with the DD genotype (P < 0.01). These results suggest that the ACE genotype could be associated with the disease activity of SLE. ACE insertion polymorphism might be used as one of predictive factors for the activity of lupus.

Adult↗

PubMed1993

Pathophysiology and pharmacology of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is the classical example of an immune complex (IC) associated systemic autoimmune disease. Although an important part of SLE etiopathogenesis has yet to be discovered, it is generally accepted that genetic factors, sex hormones, alternations in T- and B-lymphocyte activity and defects in RES-function contribute to the development of SLE. In an SLE patient, symptoms and severity of the disease are linked to the pattern of autoantibodies expressed, referring to some pathophysiological importance of antibodies found in SLE. In addition, the interindividually variable expression of antibodies to ds-DNA, Ro or anticardiolipin, for example, permit a subtyping of SLE and indicate SLE as collective concept of heterogeneous systemic connective tissue diseases with overlapping, e.g. to dermatomyositis, progressive systemic sclerosis or Sjögren's syndrome. In view of the variable, heterogeneous disease manifestations, it is obvious that the strategy in SLE therapy is to treat manifestations and not just SLE per se. Using this concept together with pathophysiologically related control parameters and standard clinical investigations, 90 to 95% of SLE patients are adequately treated with NSAID, steroids, antimalarials and immunosuppressiva. Only 5-10% need experimental therapy, and this kind of treatment should be strictly limited to this group.

Autoantibodies↗

PubMed2000

Molecular aberrations in human systemic lupus erythematosus.

Systemic lupus erythematosus is an autoimmune disorder that predominantly affects women during the childbearing years. Clinically, major organ systems are affected, including the skin, kidneys and nervous system. Genetic, hormonal, environmental and immunoregulatory factors contribute to the highly variable expression of the disease. Impaired cellular and humoral immune responses reflect disordered biochemical and molecular functions that might be determined genetically. Enhanced understanding of these molecular abnormalities should enable development of new, effective therapeutic agents in the near future.

Apoptosis↗

PubMed2004

High-dose immunosuppression with autologous stem cell transplantation in severe refractory systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is an immune-mediated disease that is responsive to suppression or modulation of the immune system. Patients with SLE who experience persistent multiorgan dysfunction, despite standard doses of intravenous cyclophosphamide (Cy), represent a subset of patients at high risk of early death. We investigated the efficacy and toxicity of high-dose immunosuppression and autologous hematopoietic stem cell transplantation (SCT) to treat such patients. Six patients (all female, age 15-29 years) with severe refractory SLE were enrolled in the clinic of our institution from 1998 to 2003. All patients were seriously ill, with SLE disease activity indices (SLEDAI) of 6-30, including two cases with central nervous system lupus, one case with lung vasculitis, and three cases with nephritis and nephrotic syndrome. All patients were registered in the European Group for Blood and Marrow Transplantation (EBMT)/European League Against Rheumatism (EULAR) database. Previous immunosuppression included pulse Cy intravenous, prednisolone (standard doses and pulse therapy), oral Cy and azathioprine, with little or no effect on disease progression. Autologous hemopoietic stem cells were collected from bone marrow (n = 4) or mobilized from peripheral blood with Cy and granulocyte colony-stimulating factor (G-CSF) (n = 2). Pre-transplant conditioning regimens included BEAM +/- ATG (n = 2), melphalan 140 mg/m2 + etoposid 1600 mg/m2 (n = 2) and Cy 200 mg/kg +/- ATG (n = 2). Median time to an absolute neutrophil count (ANC) greater than 0.5 x 10(9)/L and platelet count greater than 50 x 10(9)/L was 13 and 15 days, respectively. Three patients died on days 11, 22 and 63 due to transplant-related complications. The follow-up is now 60 and six months for two patients (complete remission), and 42 months for one other patient (partial response). All patients had experienced multiple and severe episodes of infections pre-SCT and long-term history of corticosteroid therapy (3-14 years). We conclude that achievement of prolonged, corticosteroid-free remissions is a reality. Judicious selection of patients earlier in disease or in remission, but with a high risk of relapse or further progression, will diminish transplantation-related mortality.

Adolescent↗

PubMed2005

Premature atherosclerosis and acute coronary syndrome in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a vasculitic disorder with potential for multisystem organ dysfunction. Among the organ systems affected is the cardiovascular system. Patients with SLE are prone to premature atherosclerosis; this premature atherosclerosis places the patient at risk for myocardial infarction with onset at a relatively young age. We present 4 patients with SLE who experienced myocardial infarction; these patients also experienced diagnostic and treatment delays because of their relatively young age at presentation. Relevant pathophysiology and diagnostic strategies are discussed.

Adult↗

PubMed2003

Managing organ-threatening systemic lupus erythematosus.

Systemic lupus erythematosus is a chronic, usually life-long, and potentially fatal autoimmune musculoskeletal condition. The involvement of the heart, lungs, kidneys, and central nervous system, and hematologic complications increase morbidity and mortality. Consequently, the medical-surgical nurse must understand the disease process and treatment modalities when assessing and developing a plan of care for the patient and family.

Adolescent↗

PubMed1991

Soluble interleukin 2 receptor levels in serum and its relationship to T cell abnormality and clinical manifestations of the disease in patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is associated with alterations in immune regulation that results in T cell activation and release of the soluble interleukin 2 receptors (sIL-2R) in serum. SLE, a disease with varied clinical manifestations also has regulatory T cell subset abnormalities in blood. Levels of sIL-2R in serum of patients with active SLE were higher than in those with other common rheumatic diseases. Patients with active SLE and an increased percentage of CD4+ CDw29+ helper inducer (memory) and decreased percentage of CD4+ CD45R+ suppressor inducer (virgin) T cell subsets in blood demonstrated elevated levels of sIL-2R in serum. When compared with clinical manifestations of the disease, the sIL-2R levels in the sera of the patients with active SLE and thrombocytopenia were higher (mean 1710 units/ml) than those in active SLE with nephrotic syndrome (mean 1230 units/ml) or in active SLE with central nervous system disease (mean 1157 units/ml). However, patients with active SLE with humoral immunodeficiency (hypogammaglobulinemia) had highly elevated levels of sIL-2R in serum as compared to other patients with active SLE. The highly elevated levels of sIL-2R in serum may indicate that in vivo T cell activation plays an important role in this disease.

Adolescent↗

PubMed1992

Genetics of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease in which multiple genes appear to play important roles in pathogenesis. Hereditary deficiencies, both complete and partial, of several components of the complement system clearly predispose to lupus. HLA class II alleles appear to mediate specific autoantibodies, many of which are pathogenic. Modern molecular techniques are now providing insight into the specific major histocompatibility complex class II polymorphisms that are associated with different autoantibodies in SLE. Other genetic systems also may be important.

Complement System Proteins↗

PubMed2000

Impairment of genomic DNA binding to a putative dysfunctional receptor on erythrocytes independent of complement and antibodies in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is characterized by a variety of autoantibodies and other immune abnormalities indicative of an immunological hyperactivity. Antibodies against native DNA, however, are a disease-specific marker and play a major role in the pathogenesis of systemic or organ-specific disease manifestations. Nevertheless, the mechanisms causing the appearance of autoantibodies and immune complexes in SLE are not yet understood. Here, we report that chromosomal DNA and other forms of nucleic acids are usually cleared from circulation by binding to a yet unidentified receptor-like protein on the surface membrane of erythrocytes, independently from complement or antibodies. The binding kinetics of DNA and other nucleic acids to erythrocytes are significantly altered in SLE patients, showing an overall reduced binding capability and presaturated binding kinetics. Significant amounts of chromosomal DNA can be isolated from erythrocytes of SLE patients but not from normal controls. Electron microscopy shows electron-dense particles on the surface of SLE erythrocytes (approximate size 20-40 nm). Comparative genomic hybridization reveals that the nucleic acid isolated from erythrocytes of SLE patients is of genomic and random origin, leading to an accumulation of "free" nucleic acids in the periphery, which eventually induces a B-cell immune response.

Antibodies↗