RESUMO
We report a case of a previously healthy 52-year-old man who presented with fever and liver lesions suspicious for metastatic disease, which proved subsequently to be abscesses. Further workup revealed a gastrointestinal stromal tumor (GIST) in the gastric corpus as entry port to Streptococcus intermedius-associated bacteremia and liver abscesses. After antibiotic treatment and surgical resection of the tumor, the patient recovered well. This unusual case indicates that gastrointestinal stromal tumors can remain undetected until they cause a life threatening infection. A review of recent literature pertaining to GIST and liver abscesses follows.
Assuntos
Bacteriemia/microbiologia , Neoplasias Gastrointestinais/microbiologia , Tumores do Estroma Gastrointestinal/microbiologia , Abscesso Hepático Piogênico/microbiologia , Infecções Estafilocócicas/microbiologia , Staphylococcus intermedius/isolamento & purificação , Antibacterianos/administração & dosagem , Bacteriemia/tratamento farmacológico , Diagnóstico Diferencial , Neoplasias Gastrointestinais/diagnóstico , Tumores do Estroma Gastrointestinal/diagnóstico , Humanos , Abscesso Hepático Piogênico/prevenção & controle , Masculino , Pessoa de Meia-Idade , Penicilina G/administração & dosagem , Infecções Estafilocócicas/tratamento farmacológico , Staphylococcus intermedius/efeitos dos fármacos , Resultado do TratamentoRESUMO
Experimental autoimmune encephalomyelitis (EAE) is mediated by myelin-specific CD4(+) T cells secreting Th1 cytokines, while recovery from disease is associated with expression of Th2 cytokines. Investigations into the role of individual cytokines in disease induction have yielded contradictory results. Here we used animals with targeted deletion of the STAT4 or STAT6 genes to determine the role of these signaling molecules in EAE. The STAT4 pathway controls the differentiation of cells into a Th1 phenotype, while the STAT6 pathway controls the differentiation of cells into a Th2 phenotype. We found that mice deficient in STAT4 are resistant to the induction of EAE, with minimal inflammatory infiltrates in the central nervous system. In contrast, STAT6-deficient mice, which have a predominantly Th1 phenotype, experience a more severe clinical course of EAE as compared with wild-type or STAT4 knockout mice. In addition, adoptive transfer studies confirm the regulatory functions of a Th2 environment in vivo. These novel data indicate that STAT4 and STAT6 genes play a critical role in regulating the autoimmune response in EAE.
