Systemic lupus erythematosus

Systemic lupus erythematosus is a prototypic autoimmune disease characterized by antinuclear antibody production. In recent investigations, the contributions of various polymorphic immune response gene systems to disease pathogenesis have been analyzed. Unique cellular and molecular studies have also established the role of 'autoantigen drive' in autoantibody induction and its relationship to polyclonal B-cell activation.     

Systemic lupus erythematosus.

Recent investigations in systemic lupus erythematosus (SLE) have disclosed the presence of paramyxo-virus-like nucleocapsids in the cytoplasm of renal endothelial cells of patients with this disease. Elaborate techniques have failed to demonstrate conclusively that these are indeed viruses. Concomitantly, there is increasing evidence that SLE patients have defective cell-mediated-immunity. A 3-year-old child with SLE exhibited clinical evidence of defective cellular immunity. At postmortem, paramyxoviruslike tubular structures were demonstrated in her kidneys. Additional findings included the presence of intracytoplasmic viral particles consistent morphologically with herpes simplex virus in neurons from the lateral geniculate body and numerous "nuclear bodies" in neurons and glial cells. A dysplastic thymus gland demonstrated virtual absence of lymphocytes and was devoid of Hassall corpuscles, unlike the thymus usually seen in SLE.     

Systemic lupus erythematosus and hypertension

Systemic lupus erythematosus (SLE) is associated with a high burden of cardiovascular disease (CVD), which is in part imputed to classical vascular risk factors such as hypertension. Hypertension is frequent among patients with SLE and studies show it is more prevalent in SLE patients than in people without SLE. Despite the high frequency of hypertension in SLE patients, the pathophysiological mechanisms underlying the development of hypertension remain poorly understood. 24-h ambulatory blood pressure monitoring has emerged as a valuable tool in determining blood pressure (BP) in SLE patients in whom hypertension has been associated with damage accrual, stroke and cognitive dysfunction. Although prevalent, current guidelines neglect the specific management of hypertension in SLE patients in their recommendations. This review discusses the mechanisms that may lead to hypertension and the literature evaluating hypertension screening and management in SLE patients.     

Systemic lupus erythematosus and apoptosis

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the presence of autoantibodies directed against a range of intracellular nucleoprotein targets. SLE patients are believed to develop an autoimmune response triggered by surface-exposed intracellular macromolecules translocated to the cell surface during apoptosis. Apoptosis—or programmed cell death—is a genetically controlled process initiated by two principal pathways. The extrinsic pathway is activated by the ligation of death receptors, and the intrinsic pathway emerges from mitochondria. As shown in fas-deficient mice and humans, the inability of the immune system to eliminate self-reactive lymphocytes by apoptosis can cause persistence of autoreactive cells and autoimmunity. However, as shown in complement deficiencies, increased apoptotic material and altered clearance of apoptotic cells is found in patients with SLE. These results suggest that what is found in rare individuals with genetic deficiencies that develop SLE or SLE-like disease may be found in the larger population of SLE patients as a common end point pattern of unbalanced process of both apoptosis and clearance of apoptotic material.     

Systemic lupus erythematosus and human development

The symptoms of systemic lupus erythematosus (SLE) suggest that the manifestations of the disorder are related to known or plausible control mechanisms in embryogenesis. It is suggested that homo sapiens has, in the course of evolution, developed novel processes controlling development.     

Systemic lupus erythematosus in Hispanics

Systemic lupus erythematosus is a serious autoimmune disease that causes significant morbidity and mortality. It is also a disease for which several clinical differences among ethnic groups have been documented. Until recently, Hispanics, as separate patient cohort, had not been included in these studies. As a result, there is currently little information concerning its characteristics both at the clinical and at the molecular levels. With the currently available data, we can ascertain that this population exhibits considerable heterogeneity, in which some genetic mutations have been detected that may confer greater susceptibility and/or protection against the disease. The important differences in the clinical manifestations include a higher rate of renal complications as well as greater mortality. The latter may be due, at least in part, to lower socio-economic levels and inappropriate access to health care. However, given the limited data available that have focused on potential molecular mechanisms that may affect the Hispanic population affected with lupus, we cannot conclude that all the differences in disease outcome, complications, and severity that affect this patient population may be due to sociological factors. We conclude that more research is required to evaluate potential genetic and molecular factors that affect Hispanic lupus patients.     

Systemic lupus erythematosus in Hispanics

Systemic lupus erythematosus is a serious autoimmune disease that causes significant morbidity and mortality. It is also a disease for which several clinical differences among ethnic groups have been documented. Until recently, Hispanics, as separate patient cohort, had not been included in these studies. As a result, there is currently little information concerning its characteristics both at the clinical and at the molecular levels. With the currently available data, we can ascertain that this population exhibits considerable heterogeneity, in which some genetic mutations have been detected that may confer greater susceptibility and/or protection against the disease. The important differences in the clinical manifestations include a higher rate of renal complications as well as greater mortality. The latter may be due, at least in part, to lower socio-economic levels and inappropriate access to health care. However, given the limited data available that have focused on potential molecular mechanisms that may affect the Hispanic population affected with lupus, we cannot conclude that all the differences in disease outcome, complications, and severity that affect this patient population may be due to sociological factors. We conclude that more research is required to evaluate potential genetic and molecular factors that affect Hispanic lupus patients.     

Systemic lupus erythematosus and nucleosome]

The property of nucleosome in systemic lupus erythematosus (SLE) is reviewed. Nucleosome, complex of histone and DNA, is thought to have a pivotal role in pathogenesis of SLE. It is formed during apoptosis that is increased in peripheral lymphocytes of SLE. The concentration of nucleosome is elevated in SLE, probably related with disease activity. Nucleosome is speculated that the clearance from peripheral blood is decreased and that is modified by viral infection to become more immunogenic. Anti-nucleosome antibody is highly positive in majority of SLE, and is very specific for SLE except scleroderma and mixed connective tissue disease. This antibody is thought as a diagnostic marker and probably an activity marker for SLE. Anti-nucleosome antibody forms immune complex with nucleosome. As histone has strong positive charge, it is demonstrated that this nucleosome/anti-nucleosome complex is bound to negatively charged heparan sulfate of glomerular basement membrane in kidney. Then, complements bind to this antibody to generate lupus glomerulonephritis. Although main site of apoptosis in SLE is considered as lymphocytes, we experienced a case with SLE who had liver dysfunction with elevated soluble Fas ligand (sFasL) and apoptosis in her hepatocytes in the active stage of SLE. We measured serum sFasL, and found the relation of sFasL and liver involvement in active SLE. As major source of nucleosome should be apoptosis of lymphocytes in SLE, hepatocytes could be another candidate of apoptosis in some SLE.     

Systemic lupus erythematosus in children

Conclusions The special needs of children and adolescents afflicted with SLE are being recognized with increasing clarity. The development of pediatric rheumatology programs that are dedicated to caring for children and adolescents with SLE has been a vitally important development in heightening awareness of the special needs, characteristics and management strategies for the pediatric patient. While there has been substantial improvement in survival and quality of life as a result of earlier diagnosis and more effective and judicious therapy, it must be acknowledged that we are still fundamentally far away from understanding and optimally manageing SLE in children. Through collaborative research efforts improved understanding of SLE in children and adolescents can be achieved. The patients served will be the ultimate beneficiaries of such cooperative initiatives.     

Systemic lupus erythematosus in the elderly

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease, characterized by multisystemic involvement. Late onset SLE represents a specific sub-group of the disorder, beginning above 50-65 years of age. The incidence of late onset SLE ranges in the interval of 12-18% and the course of the disease is considered to be more benign. According to several authors, skin manifestations, photosensitivity, arthritis and nephritis, occur rarely in the elderly patients with late SLE onset; prevalence of serositis, lung involvement and Sj?gren's syndrome were observed more often. Late onset SLE patients manifested higher rate of positive findings of rheumatoid factors, as well as of anti-Ro and anti-La antibodies; and the lower occurrence of anti-RNP antibodies and hypocomplementaemia. A slow onset of the disorder, non-specific manifestations at the beginning of the illness and less frequent prevalence of SLE in the elderly often result in late diagnosis. Treatment of the disease depends on its clinical manifestations. NSAID's, antimalarials or low doses of glucocorticoids are used for the less severe forms. Immunosuppressives and higher doses of glucocorticoids are the treatments of choice for more severe organ involvements and complications. A multidisciplinary approach is recommended for the treatment of late onset SLE patients.