Thesis statement: A scrutiny of genetic polymorphisms predisposing to Systemic Lupus Erythematosus (SLE). Is there a possibility that SLE will mostly occur in members of the same genetic makeup? Is there any validation that the disease is a family disease as it is purported?
In the diagnosis of the disease, most of the medical experts rely on genetics since there seems to be a hereditary component in the disease. The generalizations of SLE being a "family disease" are not actually anecdotal. Based on research done on genetics over the last five years, discoveries have shown that genes do play a role in affecting the development of the disease. The empirical genetic research that has been conducted might in one day give doctors the ability to check on the genetic profile of a person, do a prediction of a possibility of getting SLE and possibly control the disease before it begins. Studies show that there is a high likelihood for the development of lupus in members of the same family especially children and siblings as compared to a family who does not have a member affected by lupus. The reason for this is that genes are passed from the parents to children and that there is a similarity of genes among the siblings and therefore if there is a variation between the genes, then the variation is passed along as well.
A genetic research done in 2010, showed that about 30 genetic variations were linked to lupus and overtime in the research, the number has grown nearly to 100. The factor responsible for all this is the DNA code, which is essentially the recipe for making a living creature. The code is responsible for instructing the immune system to carry a certain function in a certain way. For the case of the emergence of lupus, it means that a misprint occurs because of the failure of the DNA code to do the right instruction leading to something different. According to Courtney Montgomery, an associate member of Oklahoma Medical Research Foundation in Oklahoma City, the DNA of a human being is composed of 23 chromosomes (Wallace, 2008, p. 20). He says that the specific genetic variant that is linked to lupus is called TNFAIP3 which is a gene located on chromosome pair number six. Courtney adds that many other gene variations exist that are of the same type with TNFAIP3 and hence just like any other gene they can as well be passed from one generation to the next. The statement, therefore, attests the generalization that lupus will be prevalent in members of the same genetic makeup.
Talking about the predisposition towards lupus, the genes known to be responsible for this are DR genes, the complement genes, the X chromosome, and race. DR genes being a set of polymorphic sequences located on chromosome 6 play an important role in the presentation of antigen to responding T cells. Based on epidemiological studies conducted, there is an association between lupus and DR and the patients having DR3 have defective clearances of immune complexes. Complement genes, on the other hand, has a big role in the pathogenesis of lupus. There is a high frequency of lupus among patients with homozygous complement deficiencies.
Genetic factors have been cited as the ones that increase the tendency for the development of autoimmune diseases such as lupus. It has been observed that autoimmune disorders are more common among relatives of people with lupus than the general population. The first genetic association that has been described concerning SLE based on of case-control methodology was with human leucocyte antigen (HLA) region at chromosome 6p21.3. It is observed that there is a significant association between Seven HLA Class II alleles with SLE and Lupus Nephritis (LN). A strong association was as well observed to exist between HLA-DR2 and DR3 alleles with SLE susceptibility among the Asians, European, African and Southern American populations (Wiener, Fauci, Braunwald, Kasper, Hauser, Longo & Brown, 2012, pg. 12). The available reliable hypothesis suggests the influence of HLA-DR on the selection and the enrichment of autoreactive T cells through the presentation of molecular mimics. These associations are what aids the development of SLE in people and therefore becomes an explanation to the prevalence of SLE among family people due to genetic linkage.
Based on the above demonstration, there seems to be an absolute proof that genetic factors play a pivotal role in the pathogenesis of SLE. Evidence also not only shows the role of genetic factors in the susceptibility of this disease but also in the development of the phenotype of the specific disease. It can therefore generally be concluded that Systemic Lupus Erythematosus is a family disease that is transferred from one generation to the next due to the similarity in the makeup of the genes.
Murkoff, Heidi E, and Sharon Mazel. What to Expect When You're Expecting. New York: Workman Pub, 2008. Internet resource.
Wallace, Daniel J. The Lupus Book: A Guide for Patients and Their Families. , 2009. Print.
Wiener, Charles M, Cynthia D. Brown, Anna R. Hemnes, and Tinsley R. Harrison. Harrison's Principles of Internal Medicine: Self-assessment and Board Review. New York: McGraw-Hill Medical, 2012. Internet resource.
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