This paper discusses the tissue disease of systemic lupus erythematosus.
Written in 2007; 750 words; 4 sources; MLA; $ 26.95
Paper Summary:
In this article, the writer looks at systemic lupus erythematosus (SLE) that is also simply called lupus. The writer explains that this is an inflammatory connective tissue disease which is manifested in variable signs and symptoms. The writer notes that this condition may affect multiple organ systems with immune complexes and a large array of auto antibodies, particularly antinuclear antibodies. Further, the writer points out that there are also genetic factors that play a role in the development and expression of SLE and environmental factors may also trigger the disease in genetically susceptible hosts.
From the Paper:
"The cause of SLE is still unknown. This is an immunologic disorder with the production of auto antibodies. There are different triggering factors of this disease which includes sunlight exposure. Specific medications could also trigger SLE. They initiate immune response in individuals who are susceptible to develop SLE. The two most common of these are Hydralazine and Procainamide. Some anticonvulsants, antiemetics, antituberculars and antibiotics could be among those that trigger this disease."
"The pathophysiology of this disease is not completely known. Studies show that the production of abnormal antibodies by B cells remains the hallmark sign of lupus erythematosus. Such auto antibodies like anti double-stranded DNA and anti-Smith, are very specific for systemic lupus erythematosus. Anti-RNP, anti-Rho and anti-La, are also present in other autoimmune diseases. Whether the B cells themselves are intrinsically abnormal is a subject of current research. One of the underlying deficiencies in SLE may be emphasized on apoptosis, or programmed cell death; cellular antigens exposed during apoptosis incite an immune response."
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