RESUMEN
Diverticulitis and diverticular abscesses are rare and potentially serious complications of duodenal diverticulum. These conditions often lead to perforation of the diverticulum, necessitating surgical treatment. There have been few reported cases of duodenal diverticulitis with or without perforation treated by endoscopic drainage. Here, we present a case of duodenal diverticulitis accompanied by abscess formation that was treated successfully with an endoscopic nasobiliary drainage catheter. We suggest this treatment could be an acceptable option for selected patients with a localized abscess that is resistant to conservative treatment.
Asunto(s)
Absceso/complicaciones , Catéteres de Permanencia , Diverticulitis/complicaciones , Drenaje/métodos , Enfermedades Duodenales/complicaciones , Absceso/diagnóstico por imagen , Absceso/terapia , Adulto , Diverticulitis/diagnóstico por imagen , Diverticulitis/terapia , Enfermedades Duodenales/diagnóstico por imagen , Enfermedades Duodenales/terapia , Femenino , Humanos , Tomografía Computarizada por Rayos XRESUMEN
Adult T-cell leukemia (ATL) is an aggressive type of leukemia, originating from T-cells infected with human T-cell leukemia virus type 1. Accumulating evidence suggests the aberrant activation of NF-kappaB to be a causative factor mediating the abnormal proliferation of leukemic cells, thus resulting in the development of ATL. A rearranged NF-kappa B2/p100 gene was isolated from an ATL-derived cell line, which was generated by a chromosomal translocation. The isolated NF-kappa B2 mutant is fused with the with no (lysine) deficient protein kinase 1 gene, coding for a 58 kDa protein that retains the DNA binding Rel homology domain, but it lacks the entire ankyrin repeat inhibitory domain, thus suggesting its constitutive activation. This rearranged NF-kappa B2 gene product (p58) was localized in the nucleus, and formed a complex with NF-kappaB p65 or RelB. Moreover, a T-cell line expressing p58 increased the amount of an NF-kappa B2-inducible gene, NF-kappa B2/p100 by itself. These results suggest that such NF-kappa B2 gene rearrangement may therefore be a factor in the constitutive activation of NF-kappaB in ATL, and thereby playing a role in the ATL pathogenesis.