Mostrando entradas con la etiqueta REUMATOLOGIA. Mostrar todas las entradas
Mostrando entradas con la etiqueta REUMATOLOGIA. Mostrar todas las entradas
sábado, 7 de mayo de 2011
miércoles, 19 de enero de 2011
ARTRITIS REACTIVA
TIPO: REVISION
FORMATO: PDF
IDIOMA: INGLES
DESCARGA DIRECTA: DESCARGAR
jueves, 16 de diciembre de 2010
ACTUALES, NUEVOS Y FUTUROS TRATAMIENTOS PARA LA OSTEOPOROSIS
TIPO: REVISION
FORMATO: PDF
IDIOMA: INGLES
DESCARGA DIRECTA: DESCARGAR
TRATAMIENTO DE LA ARTRITIS REUMATOIDEA DURANTE EL AMBARAZO
TIPO: REVISION
FORMATO: PDF
IDIOMA: INGLES
DESCARGA DIRECTA: DESCARGAR
martes, 14 de diciembre de 2010
MANEJO DE LA ARTRITIS REUMATOIDEA: CONSENSO
TIPO: GUIA
FORMATO: PDF
IDIOMA: INGLES
DESCARGA DIRECTA: DESCARGAR
sábado, 11 de diciembre de 2010
ENFERMEDAD SISTEMICA Y EL PULMON
Revisión publicada en PAEDIATRIC RESPIRATORY REVIEWSTIPO: REVISION
FORMATO: PDF
IDIOMA: INGLESDESCARGA DIRECTA; DESCARGAR
miércoles, 8 de diciembre de 2010
MANIFESTACIONES PULMONARES DEL SINDROME DE SJOGREN PRIMARIO
TIPO: REVISION
FORMATO: PDF
IDIOMA: INLGES
DESCARGA DIRECTA: DESCARGAR
lunes, 6 de diciembre de 2010
ARTRITIS REUMATOIDEA: NUEVOS CRITERIOS 2010
Rheumatology y la European League Agains Rheumatism collaborative initiative
TIPO: GUIAS
FORMATO: PDF
IDIOMA: INGLES
DESCARGA DIRECTA: DESCARGAR
miércoles, 1 de diciembre de 2010
CLINICA MAYO: REVISIONES EN MEDICINA INTERNA III
CONTENIDO: PARTE III
Reumatologia I
Reumatologia II
TIPO: REVISION
FORMATO: PDF
DESCARGA DIRECTA: DESCARGAR
domingo, 28 de noviembre de 2010
ACTUALIZACION EN LA PATOGENESIS DEL SINDROME ANTIFOSFOLIPIDO
TIPO: REVISION
TIPO: PDF
DESCARGA DIRECTA: DESCARGAR
martes, 29 de julio de 2008
ENFERMEDAD DE KAWASAKI
Revision publicada en el 2007 en Cardiology in Review.
INTRODUCCION
Kawasaki disease (KD) is an acute inflammatory vasculitis of childhood which was initially described more than 4 decades ago, yet the specific etiology remains unknown. It has become the most common cause of acquired cardiovascular disease in children in the United States. Advances in clinical therapies have reduced, but not eliminated, the incidence of coronary artery abnormalities in affected children. Pathophysiology seems to include an intense elaboration of cytokines, endothelin, and other vasoactive mediators resulting in the development of vascular endothelial changes that may leave a permanent impact on vascular integrity. Treatment with intravenous immune globulin and aspirin remains the primary management strategy and steroid therapy remains contoversial. In severe circumstances, coronary reperfusion strategies are required, and coronary artery surgery in children with KD has been required, albeit infrequently. KD may be a harbinger for early onset coronary artery disease in adults. Recently developed AHA recommendations have amended diagnostic strategies and indicated a stratified approach to the long-term follow up of this enigmatic yet widespread disease.
TIPO: REVISION
FORMATO: PDF
DESCARGAR DIRECTA: DOWNLOAD
Kawasaki disease (KD) is an acute inflammatory vasculitis of childhood which was initially described more than 4 decades ago, yet the specific etiology remains unknown. It has become the most common cause of acquired cardiovascular disease in children in the United States. Advances in clinical therapies have reduced, but not eliminated, the incidence of coronary artery abnormalities in affected children. Pathophysiology seems to include an intense elaboration of cytokines, endothelin, and other vasoactive mediators resulting in the development of vascular endothelial changes that may leave a permanent impact on vascular integrity. Treatment with intravenous immune globulin and aspirin remains the primary management strategy and steroid therapy remains contoversial. In severe circumstances, coronary reperfusion strategies are required, and coronary artery surgery in children with KD has been required, albeit infrequently. KD may be a harbinger for early onset coronary artery disease in adults. Recently developed AHA recommendations have amended diagnostic strategies and indicated a stratified approach to the long-term follow up of this enigmatic yet widespread disease.
TIPO: REVISION
FORMATO: PDF
DESCARGAR DIRECTA: DOWNLOAD
sábado, 26 de julio de 2008
LUPUS ERITEMATOSO SISTEMICO
Revision publicada en febrero del 2008 en THE NEW ENGLAND JOURNAL OF MEDICINE.
INTRODUCCION
To the clinician, systemic lupus erythematosus is important because it is a potentially fatal disease that is easily confused with many other disorders. To the immunologist, lupus is intriguing because all the key components of the immune system are involved in the underlying mechanisms of the disease. This review describes these mechanisms and shows how knowledge of the pathogenesis of lupus facilitates its treatment.
The prevalence of lupus ranges from approximately 40 cases per 100,000 persons among Northern Europeans to more than 200 per 100,000 persons among blacks.1 In the United States, the number of patients with lupus exceeds 250,000. The life expectancy of such patients has improved from an approximate 4-year survival rate of 50% in the 1950s2 to a 15-year survival rate of 80% today. Even so, a patient in whom lupus is diagnosed at 20 years of age still has a 1 in 6 chance of dying by 35 years of age, most often from lupus or infection. Later, myocardial infarction and stroke become important causes of death. This bimodal pattern of mortality in lupus was recognized more than 30 years ago.
The diverse presentations of lupus range from rash and arthritis through anemia and thrombocytopenia to serositis, nephritis, seizures, and psychosis. Lupus should be part of the differential diagnosis in virtually any patient presenting with one of these clinical problems, especially in female patients between 15 and 50 years of age.
TIPO: REVISION
FORMATO: PDF
DESCARGAR DIRECTA: DOWNLOAD
To the clinician, systemic lupus erythematosus is important because it is a potentially fatal disease that is easily confused with many other disorders. To the immunologist, lupus is intriguing because all the key components of the immune system are involved in the underlying mechanisms of the disease. This review describes these mechanisms and shows how knowledge of the pathogenesis of lupus facilitates its treatment.
The prevalence of lupus ranges from approximately 40 cases per 100,000 persons among Northern Europeans to more than 200 per 100,000 persons among blacks.1 In the United States, the number of patients with lupus exceeds 250,000. The life expectancy of such patients has improved from an approximate 4-year survival rate of 50% in the 1950s2 to a 15-year survival rate of 80% today. Even so, a patient in whom lupus is diagnosed at 20 years of age still has a 1 in 6 chance of dying by 35 years of age, most often from lupus or infection. Later, myocardial infarction and stroke become important causes of death. This bimodal pattern of mortality in lupus was recognized more than 30 years ago.
The diverse presentations of lupus range from rash and arthritis through anemia and thrombocytopenia to serositis, nephritis, seizures, and psychosis. Lupus should be part of the differential diagnosis in virtually any patient presenting with one of these clinical problems, especially in female patients between 15 and 50 years of age.
TIPO: REVISION
FORMATO: PDF
DESCARGAR DIRECTA: DOWNLOAD
CONCEPTOS ACTUALES SOBRE LA PATOGENESIS DEL SINDROME ANTIFOSFOLIPIDO
Revision publicada en septiembre del 2007 en la revista BLOOD de la American Society of Hematology.
INTRODUCCION
The antiphospholipid syndrome (APS) is an important cause of acquired thrombophilia. It is characterized by the core clinical manifestations of thrombosis, either venous or arterial, and in women it can also be associated with recurrent fetal loss. The detection of persistently elevated levels of antiphospholipid antibodies (aPL Abs) is a requisite laboratory feature for the diagnosis to be made. The dominant antigenic targets in APS are beta 2-glycoprotein I (2-GPI) and prothrombin. There is an accumulating body of experimental evidence that suggests that specific subgroups of aPL Abs may directly contribute to disease pathogenesis. This review critically examines the experimental evidence underlying the various propositions made to explain how these antibodies may predispose to disease in humans. Furthermore, it also examines the evidence relating to the immunologic mechanisms that may contribute to the breakage of peripheral tolerance in this disorder. Delineating the strengths and limitations of the experimental evidence accumulated thus far will hopefully stimulate further experimentation toward achieving the ultimate goal of precisely defining the dominant pathogenic mechanisms operational in APS. This may pave the way for the development of improved therapies. (Blood. 2007;109:422-430)
TIPO: REVISION
FORMATO: PDF
DESCARGAR DIRECTA: PATOGENESIS DEL SIND ANTIFOSFOLIPIDO.PDF
The antiphospholipid syndrome (APS) is an important cause of acquired thrombophilia. It is characterized by the core clinical manifestations of thrombosis, either venous or arterial, and in women it can also be associated with recurrent fetal loss. The detection of persistently elevated levels of antiphospholipid antibodies (aPL Abs) is a requisite laboratory feature for the diagnosis to be made. The dominant antigenic targets in APS are beta 2-glycoprotein I (2-GPI) and prothrombin. There is an accumulating body of experimental evidence that suggests that specific subgroups of aPL Abs may directly contribute to disease pathogenesis. This review critically examines the experimental evidence underlying the various propositions made to explain how these antibodies may predispose to disease in humans. Furthermore, it also examines the evidence relating to the immunologic mechanisms that may contribute to the breakage of peripheral tolerance in this disorder. Delineating the strengths and limitations of the experimental evidence accumulated thus far will hopefully stimulate further experimentation toward achieving the ultimate goal of precisely defining the dominant pathogenic mechanisms operational in APS. This may pave the way for the development of improved therapies. (Blood. 2007;109:422-430)
TIPO: REVISION
FORMATO: PDF
DESCARGAR DIRECTA: PATOGENESIS DEL SIND ANTIFOSFOLIPIDO.PDF
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