RESUMO
It is thought that many of the idiopathic pancreatitis could have a genetic base. Approximately 50% of them correspond to CFTR (cystic fibrosis transmembrane conductance regulator gene) and SPINK-1 (serine protease inhibitor Kazal type 1) mutations. A recent study compares patients with acute pancreatitis and SPINK-1 mutation with patients with idiopathic acute pancreatitis. The study highlights a 12-fold increased risk of developing pancreatic cancer with SPINK-1 mutation versus the control group. Nonetheless, authors conclude that only specific pN34s mutation is related to pancreatic cancer. This relation is controversial, and international consensus guidelines for the follow-up in chronic pancreatitis with pancreatic cancer still do not recommend follow-up in SPINK-1 p. N34S mutation. We believe that developing prospective studies in which subgroups of patients with SPINK-1 mutation benefit from closer follow-ups would be necessary.
Assuntos
Pancreatite , Inibidor da Tripsina Pancreática de Kazal , Humanos , Doença Aguda , Proteínas de Transporte/genética , Predisposição Genética para Doença , Mutação , Neoplasias Pancreáticas/genética , Pancreatite/genética , Estudos Prospectivos , Inibidor da Tripsina Pancreática de Kazal/genéticaRESUMO
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Assuntos
Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Pancreatite/diagnóstico , Doenças Autoimunes/diagnóstico , Diagnóstico Diferencial , Carcinoma Ductal Pancreático/diagnóstico , Neoplasias Pancreáticas/diagnóstico , Pancreatite/classificaçãoRESUMO
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No disponible
