RESUMO
A 2-year-old girl was diagnosed as having acute gastroenteritis with severe diarrhoea, for which she was prescribed a loperamide solution. Following this she developed paralytic ileus. She was then treated conservatively and was administered fluid and electrolytes parenterally. She started to recover after 48 hours. In young children with acute diarrhoea there usually is no place for medicinal treatment, and certainly not with antimotility drugs such as loperamide.
Assuntos
Antidiarreicos/efeitos adversos , Obstrução Intestinal/induzido quimicamente , Loperamida/efeitos adversos , Antidiarreicos/uso terapêutico , Pré-Escolar , Diarreia/tratamento farmacológico , Eletrólitos/administração & dosagem , Feminino , Hidratação , Gastroenterite/tratamento farmacológico , Humanos , Obstrução Intestinal/terapia , Loperamida/uso terapêuticoAssuntos
Doença Celíaca/complicações , Síndrome de Fadiga Crônica/etiologia , Adolescente , Adulto , Estudos de Casos e Controles , Doença Celíaca/imunologia , Síndrome de Fadiga Crônica/imunologia , Feminino , Humanos , Imunoglobulinas/sangue , Masculino , Pessoa de Meia-Idade , Testes Sorológicos/métodosRESUMO
Celiac disease is a common severe intestinal disease resulting from intolerance to dietary wheat gluten and related proteins. The large majority of patients expresses the HLA-DQ2 and/or DQ8 molecules, and gluten-specific HLA-DQ-restricted T cells have been found at the site of the lesion in the gut. The nature of peptides that are recognized by such T cells, however, has been unclear so far. We now report the identification of a gliadin-derived epitope that dominantly is recognized by intestinal gluten-specific HLA-DQ8-restricted T cells. The characterization of such epitopes is a key step toward the development of strategies to interfere in mechanisms involved in the pathogenesis of celiac disease.
Assuntos
Doença Celíaca/imunologia , Gliadina/imunologia , Intestino Delgado/imunologia , Fragmentos de Peptídeos/imunologia , Linfócitos T/imunologia , Sequência de Aminoácidos , Doença Celíaca/etiologia , Doença Celíaca/patologia , Células Clonais , Gliadina/química , Gliadina/genética , Antígenos HLA-DQ , Humanos , Epitopos Imunodominantes/química , Epitopos Imunodominantes/genética , Mucosa Intestinal/imunologia , Mucosa Intestinal/patologia , Intestino Delgado/patologia , Ativação Linfocitária , Dados de Sequência Molecular , Pepsina A , Fragmentos de Peptídeos/química , Fragmentos de Peptídeos/genética , Linfócitos T/patologiaRESUMO
Celiac disease (CD) is caused by gluten ingestion in susceptible individuals. Tissue transglutaminase (tTG)-specific Abs are characteristic of CD, and increased tTG activity has been observed in the jejunal biopsies of patients. Here we demonstrate that tTG selectively deamidates gluten peptides, which results in strongly enhanced T cell-stimulatory activity. To our knowledge, this is the first example of an enzymatic modification of a food protein that affects T cell recognition. Moreover, these modifications may lead to the amplification of gluten-specific T cell responses in the gut and consequently may be important for the development of CD.
