We are the combination of four hospitals: the General Hospital, the Children’s Hospital, the Women’s Hospital and the Traumatology, Rehabilitation and Burns Hospital. We are part of the Vall d’Hebron Barcelona Hospital Campus: a world-leading health park where healthcare plays a crucial role.
Patients are the centre and the core of our system. We are professionals committed to quality care and our organizational structure breaks down the traditional boundaries between departments and professional groups, with an exclusive model of knowledge areas.
Would you like to know what your stay at Vall d'Hebron will be like? Here you will find all the information.
The commitment of Vall d'Hebron University Hospital to innovation allows us to be at the forefront of medicine, providing first class care adapted to the changing needs of each patient.
Prof. Mikko Seppänen, Chief Physician, Specialist in Internal Medicine and Infectious Diseases, Adjunct Professor HUS Helsinki University Hospital, Children and Adolescents, Rare Disease Center- and Inflammation Center, Adult Immunodeficiency Unit- Majakka, Helsinki
"Finnish PIDDs- unexpected autoinflammation in unexpected places"
Finns, a genetically-isolated population do to historical bottleneck events, carry relatively little genomic variation and enrichment of autosomal recessive “Finnish Disease Heritage” (FDH) genes. Some FDH PIDDs display features of inflammasome-mediated autoinflammation, potentially offering new therapeutic targets. Within CVID phenotype - also enriched in Finns - AD NFKB1 mutations cause autoinflammatory features that suggest long sought immunopathogenetic mechanisms of more common inflammatory diseases. A novel noncanonical inflammasomopathy “C/EBPε-associated autoinflammation and immune impairment of neutrophils” (CAIN) raises further interesting questionsFinns, a genetically-isolated population do to historical bottleneck events, carry relatively little genomic variation and enrichment of autosomal recessive “Finnish Disease Heritage” (FDH) genes. Some FDH PIDDs display features of inflammasome-mediated autoinflammation, potentially offering new therapeutic targets. Within CVID phenotype - also enriched in Finns - AD NFKB1 mutations cause autoinflammatory features that suggest long sought immunopathogenetic mechanisms of more common inflammatory diseases. A novel noncanonical inflammasomopathy “C/EBPε-associated autoinflammation and immune impairment of neutrophils” (CAIN) raises further interesting questions.
Host: Infection in Immunocompromised Pediatric Patients psoler@vhebron.net
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