Complications in patients with neurological impairment after gastrostomy.

BACKGROUND: Neurological impairment (NI) is responsible for most conditions that require a permanent gastrostomy tube. The present study assessed the occurrence of short- and long-term complications after video-assisted gastrostomy (VAG) in patients with NI. METHODS: The incidence of short- (<6 months) and long-term (over 2 years) complications of VAG were analyzed in a retrospective study. The differences between the incidence of the complications of VAG according to the age at surgery (≤15 years vs. ≥16 years) were also evaluated. The short- and long-term complications observed were granulation tissue formation, infection requiring antibiotic treatment, skin problems, perigastrostomy leakage, vomiting, accidental tube dislodgement, dumping syndrome, ileus, and peritonitis. RESULTS: Eighty-two patients were evaluated for short- and long-term complications. The long-term complication rate was significantly lower than the short-term complication rate (P = 0.0026). Onodera's prognostic nutritional index before VAG in patients with long-term complications was significantly lower than in patients without such complications (P = 0.046). The incidence of long-term granulation tissue formation, infection, and vomiting were significantly lower than those of similar short-term complications. Long-term skin problems were associated with short-term skin problems (odds ratio: 18.95; 95% confidence interval: 4.53-92.98; P < 0.001). The number of patients ≥16 years old with short- and long-term skin problems was significantly higher than in patients ≤15 years old (P = 0.0014 and P = 0.0073, respectively). CONCLUSIONS: The incidence rate of granulation tissue formation and infection after VAG were lower in the long term than in the short term. However, patients ≥16 years old presented with persistent complications.

UBC9 regulates the stability of XBP1, a key transcription factor controlling the ER stress response.

XBP1 is a key transcription factor regulating the mammalian endoplasmic reticulum (ER) stress response, which is a cytoprotective mechanism for dealing with an accumulation of unfolded proteins in the ER (ER stress). The expression of XBP1 is regulated by two different mechanisms: mRNA splicing and protein stability. When ER stress occurs, unspliced XBP1 mRNA is converted to mature mRNA, from which an active transcription factor, pXBP1(S), is translated and activates the transcription of ER-related genes to dispose of unfolded proteins. In the absence of ER stress, pXBP1(U) is translated from unspliced XBP1 mRNA and enhances the degradation of pXBP1(S). Here, we analyzed the regulatory mechanism of pXBP1(S) stability, and found that a SUMO-conjugase, UBC9, specifically bound to the leucine zipper motif of pXBP1(S) and increased the stability of pXBP1(S). Suppression of UBC9 expression by RNA interference reduced both the expression of pXBP1(S) and ER stress-induced transcription by pXBP1(S). Interestingly, overexpression of a UBC9 mutant deficient in SUMO-conjugating activity was able to increase pXBP1(S) expression as well as wild-type UBC9, indicating that UBC9 stabilizes pXBP1(S) without conjugating SUMO moieties. From these observations, we concluded that UBC9 is a novel regulator of the mammalian ER stress response.