Systemic Lupus Erythematosus Essay
INTRODUCTION:
- Systemic lupus erythematosus (SLE) is an autonomous disorder with variety of autoantibodies (double stranded DNA [dsDNA], ANA). It causes inflammation diffusely through the body (skin, brain, kidneys, and joints) and also the blood. Lupus has varied abnormal blood tests related to it (anemia, anti-Sm, anti-phospholipid antibodies), however this is often not a similar issue as knowing what causes lupus. Its cause could be a mystery. The etiology of lupus is unknown, however multiple genetic, epigenetic, and environmental risk factors are involved. The inheritance of genes alone isn't enough for developing lupus, suggesting the influence of environmental triggers on unwellness expression. Despite the numerous role of the surroundings …show more content…
in modulating response pathologic process, the precise mechanisms by that it acts stay poorly understood.
ARTICLE 1: Environmental Influences on Systemic Lupus Erythematosus Expression
This article discusses varied environmental factors that play a vital role within the etiology of systemic lupus erythematosus.
Over fifty genes found to play a job in lupus, however none found to be shown the exact/firm phenomena (Webb R, 2011). Though alterations in diet will cut back the danger of associated conditions like plaques in the artery and metabolic syndrome, definitive proof is lacking that dietary factors influence lupus illness development or disease activity (Absher DM, 2013). Conflicting results are found with bound dietary factors, a number of which can have had supporting proof from animal models or case reports. Some studies have shown an association between vitamin D and lupus, however they're self-reported cases and that we would like a real bit of vitamin D in our body (limitation)(Costenbader KH,2008). We cannot accurately predict if vitamin D is related to SLE (Hiraki LT, 2012). Total antioxidant intake, as well as vitamins A, C, and E, α-carotene, β-carotene, β-cryptoxanthin, lycopene, lutein, and carotenoid, wasn't related to the chance of developing SLE (Costenbader KH, 2010). Silica was the sole exposure found to be related to lupus in three case management illness. Exposure to particulate silica (crystalline silica or quartz) most ordinarily comes from mining and “dusty trades” like sandblasting, granite cutting, construction work, cement work, brick and tile laying (Parks CG, 2002). The high dose exposure is related to the additional prevalence of the disease (Brown lm, 1997). Smoking is also one in every of the contributors. Smoking will have an effect on through genetic pathway and inflammatory reactor pathway (Costenbader KH, 2004). Epstein Barr Virus (EBV) that causes Infectious Mononucleosis(IM) shares clinical options with active lupus and leads to antinuclear antibody (ANA) positivity and production of SLE-related autoantibodies like anti-Sm (ANA and anti-Sm are the autoantibodies that we tend to use to see if the disease is
present)(James JA,2001). Alternative exposures are worth investigation, however with presently very little information on lupus associations embodies asbestos, industrial chemicals and solvents, care merchandise (e.g., cosmetics), UV radiation, and air pollution. The sole exposure deemed by the National Institute of Environmental Health Sciences (NIEHS) Panel to be “unlikely” to contribute to disease was the utilization of hair dyes and development of lupus, of that multiple case-control studies haven't found an association (James JA, 2001).
The one revealed study thus far of occupational and avocational metal exposures in lupus cases compared to controls found that exposure to mercury within the activity setting a minimum of once per week was related to a with modesty (but not statistically significant) higher risk of lupus (OR 3.1; 95th CI 0.8 – 12.7)(Cooper GS,2010). Exposure to 5 or additional days of stained or leaded glass as a hobby was also highly common among systemic lupus erythematosus cases than controls, however the rarity of those exposures led to an inaccurate result estimate (OR 3.0; 95th CI 0.8 – 11.6)(Cooper GS,2010). In an analysis of the Women’s Health Initiative cohort, 50- to 79-year-old ladies who reported in person mixing/applying pesticides (mostly in a very residential setting) had higher risks of developing systemic lupus erythematosus throughout the study follow-up, with trends of accelerating risk by frequency and period of use. There are few epidemiologic studies of Persistent organic pollutants (POPs) in relevance systemic lupus erythematosus. One study of U.S. electrical employees (typically exposed to PCBs) reported half-hour considerable additional mortality from musculoskeletal system and four-hundredth additional mortality, classifications that embody the ICD-9 code for SLE (Tsai pc, 2007). One cohort study with twenty four years of follow-up in a very Taiwanese population that was accidentally exposed to high levels of PCBs and furans through consumption of contaminated rice found higher mortality from systemic lupus erythematosus, with PCB-related deaths beginning ten years after the exposure. A current study of environmental triggers of systemic lupus erythematosus among Gullah African Americans found ANA positive controls (48% at baseline) had higher mean levels compared to ANA negative controls for PFOS (75.1 vs. 48.2 ng/ml, p=0.06), PFOA (7.0 vs. 5.8, p=NS) and PFNA (3.2 vs. 2.1, p=0.04)(Kamen decilitre,2012). A meta-analysis, including those selfsame three studies of systemic lupus erythematosus, found a major association between organic solvent exposure and development of illness once multiple autoimmune diseases were combined as the outcome (OR 1.54, 95% CI 1.25 – 1.92) (Barragan-Martinez C,2012).
- All black females between 15-45 , history of SLE in the family, taking medicine causing SLE, exposure to ultraviolet, smokers, EBV,CMV infection, chemical and metal exposure are at a higher risk.
- Strengths of this study include all the details provided in this study is backed up with some sort of research study. They have to take so many different factors into account that can contribute to SLE like genetic, diet, silica, smoking, EBV, metals, pesticides.
- Weakness for this study would be meta-analysis. They need to perform a meta-analysis to increase power for the studies that have been done already. There are few other factors that need to be considered like alcohol, radiation, and other infectious diseases that may play a role in causing the disease. This study doesn't show how to prevent the disease. This is important because 16000 new cases diagnosed every year in the United States.
- Lots of research needs to be done. What should be done when you see someone with genes causing SLE? What is the high risk vs. low risk factor causing SLE? How does the dietary factor affect our immune system in causing SLE? How can we prevent them? I understand that experimental study is not possible in environmental science. Observational studies can be done to prove above questions. Increasing dialog and collaboration between epidemiologists, biostatisticians, bioinformatics experts, laboratory and environmental scientists, and lupus clinical researchers will advance our collective contributions to an understanding of the causes of SLE. We need to find answers to all of the above questions.
- Systemic lupus erythematosus (SLE) is an autonomous disorder with variety of autoantibodies (double stranded DNA [dsDNA], ANA). It causes inflammation diffusely through the body (skin, brain, kidneys, and joints) and also the blood. Lupus has varied abnormal blood tests related to it (anemia, anti-Sm, anti-phospholipid antibodies), however this is often not a similar issue as knowing what causes lupus. Its cause could be a mystery. The etiology of lupus is unknown, however multiple genetic, epigenetic, and environmental risk factors are involved. The inheritance of genes alone isn't enough for developing lupus, suggesting the influence of environmental triggers on unwellness expression. Despite the numerous role of the surroundings …show more content…
in modulating response pathologic process, the precise mechanisms by that it acts stay poorly understood.
ARTICLE 1: Environmental Influences on Systemic Lupus Erythematosus Expression
This article discusses varied environmental factors that play a vital role within the etiology of systemic lupus erythematosus.
Over fifty genes found to play a job in lupus, however none found to be shown the exact/firm phenomena (Webb R, 2011). Though alterations in diet will cut back the danger of associated conditions like plaques in the artery and metabolic syndrome, definitive proof is lacking that dietary factors influence lupus illness development or disease activity (Absher DM, 2013). Conflicting results are found with bound dietary factors, a number of which can have had supporting proof from animal models or case reports. Some studies have shown an association between vitamin D and lupus, however they're self-reported cases and that we would like a real bit of vitamin D in our body (limitation)(Costenbader KH,2008). We cannot accurately predict if vitamin D is related to SLE (Hiraki LT, 2012). Total antioxidant intake, as well as vitamins A, C, and E, α-carotene, β-carotene, β-cryptoxanthin, lycopene, lutein, and carotenoid, wasn't related to the chance of developing SLE (Costenbader KH, 2010). Silica was the sole exposure found to be related to lupus in three case management illness. Exposure to particulate silica (crystalline silica or quartz) most ordinarily comes from mining and “dusty trades” like sandblasting, granite cutting, construction work, cement work, brick and tile laying (Parks CG, 2002). The high dose exposure is related to the additional prevalence of the disease (Brown lm, 1997). Smoking is also one in every of the contributors. Smoking will have an effect on through genetic pathway and inflammatory reactor pathway (Costenbader KH, 2004). Epstein Barr Virus (EBV) that causes Infectious Mononucleosis(IM) shares clinical options with active lupus and leads to antinuclear antibody (ANA) positivity and production of SLE-related autoantibodies like anti-Sm (ANA and anti-Sm are the autoantibodies that we tend to use to see if the disease is
present)(James JA,2001). Alternative exposures are worth investigation, however with presently very little information on lupus associations embodies asbestos, industrial chemicals and solvents, care merchandise (e.g., cosmetics), UV radiation, and air pollution. The sole exposure deemed by the National Institute of Environmental Health Sciences (NIEHS) Panel to be “unlikely” to contribute to disease was the utilization of hair dyes and development of lupus, of that multiple case-control studies haven't found an association (James JA, 2001).
The one revealed study thus far of occupational and avocational metal exposures in lupus cases compared to controls found that exposure to mercury within the activity setting a minimum of once per week was related to a with modesty (but not statistically significant) higher risk of lupus (OR 3.1; 95th CI 0.8 – 12.7)(Cooper GS,2010). Exposure to 5 or additional days of stained or leaded glass as a hobby was also highly common among systemic lupus erythematosus cases than controls, however the rarity of those exposures led to an inaccurate result estimate (OR 3.0; 95th CI 0.8 – 11.6)(Cooper GS,2010). In an analysis of the Women’s Health Initiative cohort, 50- to 79-year-old ladies who reported in person mixing/applying pesticides (mostly in a very residential setting) had higher risks of developing systemic lupus erythematosus throughout the study follow-up, with trends of accelerating risk by frequency and period of use. There are few epidemiologic studies of Persistent organic pollutants (POPs) in relevance systemic lupus erythematosus. One study of U.S. electrical employees (typically exposed to PCBs) reported half-hour considerable additional mortality from musculoskeletal system and four-hundredth additional mortality, classifications that embody the ICD-9 code for SLE (Tsai pc, 2007). One cohort study with twenty four years of follow-up in a very Taiwanese population that was accidentally exposed to high levels of PCBs and furans through consumption of contaminated rice found higher mortality from systemic lupus erythematosus, with PCB-related deaths beginning ten years after the exposure. A current study of environmental triggers of systemic lupus erythematosus among Gullah African Americans found ANA positive controls (48% at baseline) had higher mean levels compared to ANA negative controls for PFOS (75.1 vs. 48.2 ng/ml, p=0.06), PFOA (7.0 vs. 5.8, p=NS) and PFNA (3.2 vs. 2.1, p=0.04)(Kamen decilitre,2012). A meta-analysis, including those selfsame three studies of systemic lupus erythematosus, found a major association between organic solvent exposure and development of illness once multiple autoimmune diseases were combined as the outcome (OR 1.54, 95% CI 1.25 – 1.92) (Barragan-Martinez C,2012).
- All black females between 15-45 , history of SLE in the family, taking medicine causing SLE, exposure to ultraviolet, smokers, EBV,CMV infection, chemical and metal exposure are at a higher risk.
- Strengths of this study include all the details provided in this study is backed up with some sort of research study. They have to take so many different factors into account that can contribute to SLE like genetic, diet, silica, smoking, EBV, metals, pesticides.
- Weakness for this study would be meta-analysis. They need to perform a meta-analysis to increase power for the studies that have been done already. There are few other factors that need to be considered like alcohol, radiation, and other infectious diseases that may play a role in causing the disease. This study doesn't show how to prevent the disease. This is important because 16000 new cases diagnosed every year in the United States.
- Lots of research needs to be done. What should be done when you see someone with genes causing SLE? What is the high risk vs. low risk factor causing SLE? How does the dietary factor affect our immune system in causing SLE? How can we prevent them? I understand that experimental study is not possible in environmental science. Observational studies can be done to prove above questions. Increasing dialog and collaboration between epidemiologists, biostatisticians, bioinformatics experts, laboratory and environmental scientists, and lupus clinical researchers will advance our collective contributions to an understanding of the causes of SLE. We need to find answers to all of the above questions.