RESUMO
La hidatidosis es una zoonosis producida por el parásito Echinococcus granulosus. En el ciclo zoonótico del parásito, el hombre es un huésped intermediario y sufre la enfermedad tras la ingesta de alimentos y agua contaminados por la materia fecal de animales infectados. En Argentina, la enfermedad constituye un problema importante de salud pública. Suele manifestarse con compromiso hepático y pulmonar. La afectación de otros órganos, que incluyen el corazón, es infrecuente.
Hydatidosis is a parasitic infection caused by the Echinococcus granulosus larvae, transmitted by the ingestion of infected food, characterized by the formation of cysts in vital organs. In Argentina, the disease is spread throughout the territory, constituting an important public health issue. The disease usually affects the liver and lungs. The affection of other organs is rare, and even more uncommon the affection of the heart. We present the case of a disseminated hydatidosis in a pediatric patient, whose initial clinical manifestation was an acute arterial embolism of the right limb caused by the rupture of a hydatidic cardiac cyst.
Assuntos
Humanos , Masculino , Adolescente , Equinococose/diagnóstico , Embolia/etiologia , Cardiopatias/diagnóstico , Doença Aguda , Equinococose/complicações , Embolia/parasitologia , Cardiopatias/complicações , Cardiopatias/parasitologiaRESUMO
Hydatidosis is a parasitic infection caused by the Echinococcus granulosus larvae, transmitted by the ingestion of infected food, characterized by the formation of cysts in vital organs. In Argentina, the disease is spread throughout the territory, constituting an important public health issue. The disease usually affects the liver and lungs. The affection of other organs is rare, and even more uncommon the affection of the heart. We present the case of a disseminated hydatidosis in a pediatric patient, whose initial clinical manifestation was an acute arterial embolism of the right limb caused by the rupture of a hydatidic cardiac cyst.
La hidatidosis es una zoonosis producida por el parásito Echinococcus granulosus. En el ciclo zoonótico del parásito, el hombre es un huésped intermediario y sufre la enfermedad tras la ingesta de alimentos y agua contaminados por la materia fecal de animales infectados. En Argentina, la enfermedad constituye un problema importante de salud pública. Suele manifestarse con compromiso hepático y pulmonar. La afectación de otros órganos, que incluyen el corazón, es infrecuente. Se presenta un caso de embolia arterial aguda como manifestación clínica inicial de una hidatidosis diseminada en un paciente pediátrico, a partir de la ruptura de un quiste hidatídico cardíaco.
Assuntos
Equinococose/diagnóstico , Embolia/etiologia , Cardiopatias/diagnóstico , Doença Aguda , Adolescente , Equinococose/complicações , Embolia/parasitologia , Cardiopatias/complicações , Cardiopatias/parasitologia , Humanos , MasculinoRESUMO
During infection with the hepatitis A virus (HAV), most patients develop mild or asymptomatic disease. However, a small number of patients develop serious, life-threatening hepatitis. We investigated this variability in disease severity by examining 30 Argentinean patients with HAV-induced acute liver failure in a case-control, cross-sectional, observational study. We found that HAV-induced severe liver disease was associated with a 6-amino-acid insertion in TIM1/HAVCR1 (157insMTTTVP), the gene encoding the HAV receptor. This polymorphism was previously shown to be associated with protection against asthma and allergic diseases and with HIV progression. In binding assays, the TIM-1 protein containing the 157insMTTTVP insertion polymorphism bound HAV more efficiently. When expressed by human natural killer T (NKT) cells, this long form resulted in greater NKT cell cytolytic activity against HAV-infected liver cells, compared with the shorter TIM-1 protein without the polymorphism. To our knowledge, the 157insMTTTVP polymorphism in TIM1 is the first genetic susceptibility factor shown to predispose to HAV-induced acute liver failure. Furthermore, these results suggest that HAV infection has driven the natural selection of shorter forms of the TIM-1 protein, which binds HAV less efficiently, thereby protecting against severe HAV-induced disease, but which may predispose toward inflammation associated with asthma and allergy.