ABSTRACT
The cause of systemic lupus erythematosus (SLE) remains rather poorly understood. Accumulating reported evidence suggests that both environmental and genetic factors play a part. They somehow create an abnormal CD4 T-cell driving force which results in autoantibody production. We present a synthesis of previously published study. The objective of our original study was to examine the role of genetic and environmental factors in 26 families having two or more members of SLE. The role of genetic factors was examined by determining the HLA of each individual in the study. No association between SLE and HLA-A, B, C antigens was found. There was however, a significant association with HLA-DR2 in white subjects with SLE. The most striking finding was that HLA sharing was increased among the affected members, suggesting genetic similarities. Seven of 14 sib pairs (50%) who had concordant SLE were HLA identical as opposed to an expected 25%. The role of environmental factors was examined by determining lymphocytotoxic antibodies (LCA) in patients and their consanguineous and non-consanguineous relatives. Interestingly 15/18 (83%) patients with SLE and 11/22 (50%) consanguineous relatives had LCA, while 1/9 (11%) spouses and 2/42 (5%) healthy controls had these antibodies. We conclude that genetic factors have a role in the development and expression of SLE. Environmental factors may trigger the disease in genetically susceptible individuals.
La causa del lupus eritematoso sistémico (LES) continúa con deficiente comprensión hasta el momento actual. Abundan los datos publicados en el sentido de que tanto los factores ambientales como los genéticos cumplen cierta función en su desarrollo. De algún modo actúan induciendo la producción de células T tipo CD4 anormales, responsables a su vez de la producción de un autoanticuerpo. Presentamos la síntesis de un estudio que hemos publicado recientemente. El objetivo de nuestra investigación original fue examinar el papel de los factores genéticos y ambientales en 26 familias con dos o más miembros enfermos de LES. La participación del componente genético fue analizada a través de la determinación del HLA de cada individuo incluido en el estudio. No se encontró relación alguna entre LES y los antígenos HLA-A, B, C. Sin embargo, hubo una asociación significativa con HLA-DR2 en individuos de raza blanca con esta enfermedad del tejido conectivo. El hallazgo más notorio fue que la participación del HLA era mayor entre los miembros afectados, señal de la existencia de similitudes genéticas. Siete de 14 pares de allegados consanguíneos (50%) que poseían LES concordante eran HLA idénticos, a diferencia del 25% que en realidad se esperaba. El papel de los factores ambientales se analizó determinando los anticuerpos antilinfocitotóxicos (ALT) en los pacientes y en sus familiares consanguíneos y no consanguíneos. En forma llamativa, 15 de 18 individuos con LES (83%) y 11 de 22 familiares consanguíneos (50%) tenían ALT, mientras que sólo 1 de 9 cónyuges (11%) y 2 de 42 controles sanos (5%) eran portadores de estos anticuerpos. Concluimos que los factores genéticos desempeñan un papel en el desarrollo y la expresión del LES. Los factores ambientales pueden actuar como desencadenantes de la enfermedad en individuos genéticamente susceptibles.
Subject(s)
Causality , Lupus Erythematosus, Systemic , Play and Playthings , T-Lymphocytes , HLA-A Antigens , CD4 Antigens , HLA-DR2 Antigen , Connective Tissue , Racial Groups , Antibodies , Antigens , Antilymphocyte SerumABSTRACT
BACKGROUND: Asthma mortality rates have been increasing despite our improved understanding of the pathophysiology of asthma and advanced methods of treatment. Although there are many national studies of asthma mortality rates, few studies have concentrated on subnational regions such as individual states. OBJECTIVES: We sought to determine the trends in asthma mortality in children and young adults during the last 15 years in Louisiana. METHODS: Asthma mortality data were acquired from the Louisiana State Center for Health Statistics for the years 1983 through 1997. All asthma deaths coded International Classification of Disease, Ninth Revision 493 were included in the data set along with year, sex, and rate characteristics. State population estimates obtained from the United States Bureau of Census for three 5-year periods (1983 to 1987, 1988 to 1992, and 1993 to 1997) were used to calculate crude and adjusted mortality rates. These time periods were compared with one another and with the period 1983 to 1987, which was used as a baseline. RESULTS: For all residents, the mortality rate increased from 0.41 deaths per 100,000 persons during the 1983 to 1987 time period to 0.49 and 0.63 deaths per 100,000 persons during 1988 to 1992 and 1993 to 1997 time periods, respectively. Mortality rates have increased in both the white and non-white populations over the 15-year study period, with the most pronounced increases among the non-white population. CONCLUSION: Asthma mortality rates in Louisiana have increased, particularly among the non-white population, over the last 15 years, although the results are not statistically significant. When compared with other states, asthma mortality in Louisiana is lower than in the northeast and central north states.
