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      Actividad sérica de la acetilhidrolasa del factor activador de plaquetas en pacientes afrodescendientes y mestizos con dengue, Colombia Translated title: Serum platelet-activating factor acetylhydrolase activity in dengue patients of African or mestizo descendency


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          Introducción. El dengue grave se caracteriza por el aumento de la permeabilidad vascular inducida por citocinas y mediadores químicos; uno de estos es el factor activador de plaquetas. La acetilhidrolasa del factor activador de plaquetas es la enzima responsable de su degradación, y su deficiencia o aumento se ha relacionado con varias enfermedades. Sin embargo, su papel en la infección por dengue es poco conocido, como tampoco se sabe si existe diferente actividad según el grupo étnico. Objetivo. Comparar la actividad en suero de la acetilhidrolasa del factor activador de plaquetas en dos grupos étnicos con infección por el virus del dengue. Materiales y métodos. Se llevó a cabo un estudio descriptivo, longitudinal, prospectivo, en dos departamentos de Colombia, Antioquia y Chocó. A 43 pacientes mestizos y a 33 pacientes afrodescendientes con diagnóstico de dengue, se les tomó una muestra de suero por cinco días consecutivos en la fase aguda y una muestra en la de convalecencia. Resultados. Se observó mayor frecuencia de casos de dengue hemorrágico en los pacientes mestizos que en los afrodescendientes (23,3 % Vs. 12,1 %, p=0,248). La actividad sérica de la acetilhidrolasa del factor activador de plaquetas (mediana, percentil 25 y percentil 75) fue más elevada en afrodescendientes que en mestizos (0,89 (0,72-1,10) Vs. 0,76 (0-1,03), p=0,000). Este comportamiento se conserva en el dengue clásico (0,89 (0,73-1,10) Vs. 0,73 (0-1,05), p=0,000) y en el hemorrágico (0,88 (0,69-1,12) Vs. 0,83 (0,71-1,08), p=0,893). Conclusiones. Se encontró mayor producción de acetilhidrolasa del factor activador de plaquetas en los pacientes afrodescendientes. Sin embargo, es necesario hacer estudios de polimorfismos de esta enzima que permitan obtener resultados concluyentes.

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          Dengue viruses occur as four antigenically related but distinct serotypes transmitted to humans by Aedes aegypti mosquitoes. These viruses generally cause a benign syndrome, dengue fever, in the American and African tropics, and a severe syndrome, dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS), in Southeast Asian children. This severe syndrome, which recently has also been identified in children infected with the virus in Puerto Rico, is characterized by increased vascular permeability and abnormal hemostasis. It occurs in infants less than 1 year of age born to dengue-immune mothers and in children 1 year and older who are immune to one serotype of dengue virus and are experiencing infection with a second serotype. Dengue viruses replicate in cells of mononuclear phagocyte lineage, and subneutralizing concentrations of dengue antibody enhance dengue virus infection in these cells. This antibody-dependent enhancement of infection regulates dengue disease in human beings, although disease severity may also be controlled genetically, possibly by permitting and restricting the growth of virus in monocytes. Monoclonal antibodies show heterogeneous distribution of antigenic epitopes on dengue viruses. These epitopes serve to regulate disease: when antibodies to shared antigens partially neutralize heterotypic virus, infection and disease are dampened; enhancing antibodies alone result in heightened disease response. Further knowledge of the structure of dengue genomes should permit rapid advances in understanding the pathogenetic mechanisms of dengue.
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            The recent emergence and spread of dengue hemorrhagic fever in the Americas have been a major source of concern. Efforts to control this disease are dependent on understanding the pathogenicity of dengue viruses and their transmission dynamics. Pathogenicity studies have been hampered by the lack of in vitro or in vivo models of severe dengue disease. Alternatively, molecular epidemiologic studies which associate certain dengue virus genetic types with severe dengue outbreaks may point to strains with increased pathogenicity. The comparison of nucleotide sequences (240 bp) from the E/NS1 gene region of the dengue virus genome has been shown to reflect evolutionary relationships and geographic origins of dengue virus strains. This approach was used to demonstrate an association between the introduction of two distinct genotypes of dengue type 2 virus and the appearance of dengue hemorrhagic fever in the Americas. Phylogenetic analyses suggest that these genotypes originated in Southeast Asia and that they displaced the native, American genotype in at least four countries. Vaccination and other control efforts should therefore be directed at decreasing the transmission of these "virulent" genotypes.
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              Dengue fever, a very old disease, has reemerged in the past 20 years with an expanded geographic distribution of both the viruses and the mosquito vectors, increased epidemic activity, the development of hyperendemicity (the cocirculation of multiple serotypes), and the emergence of dengue hemorrhagic fever in new geographic regions. In 1998 this mosquito-borne disease is the most important tropical infectious disease after malaria, with an estimated 100 million cases of dengue fever, 500,000 cases of dengue hemorrhagic fever, and 25,000 deaths annually. The reasons for this resurgence and emergence of dengue hemorrhagic fever in the waning years of the 20th century are complex and not fully understood, but demographic, societal, and public health infrastructure changes in the past 30 years have contributed greatly. This paper reviews the changing epidemiology of dengue and dengue hemorrhagic fever by geographic region, the natural history and transmission cycles, clinical diagnosis of both dengue fever and dengue hemorrhagic fever, serologic and virologic laboratory diagnoses, pathogenesis, surveillance, prevention, and control. A major challenge for public health officials in all tropical areas of the world is to develop and implement sustainable prevention and control programs that will reverse the trend of emergent dengue hemorrhagic fever.

                Author and article information

                Instituto Nacional de Salud (Bogotá, Cundinamarca, Colombia )
                December 2011
                : 31
                : 4
                : 599-607
                [02] Medellín orgnameUniversidad de Antioquia orgdiv1Grupo Malaria Colombia
                [01] Medellín orgnameInstituto Colombiano de Medicina Tropical-Universidad CES Colombia
                S0120-41572011000400015 S0120-4157(11)03100415

                This work is licensed under a Creative Commons Attribution 4.0 International License.

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