Dataset Information

Postchemoembolisation syndrome--tumour necrosis or hepatocyte injury?

ABSTRACT: Transarterial chemoembolisation of liver tumours is typically followed by elevated body temperature and liver transaminase enzymes. This has often been considered to indicate successful embolisation. The present study questions whether this syndrome reflects damage to tumour cells or to the normal hepatic tissue. The responses to 256 embolisations undertaken in 145 patients subdivided into those with hepatocyte-derived (primary hepatocellular carcinoma) and nonhepatocyte-derived tumours (secondary metastases) were analysed to assess the relative effects of tumour necrosis and damage to normal hepatocytes in each group. Cytolysis, measured by elevated alanine aminotransferase, was detected in 85% of patients, and there was no difference in the abnormalities in liver function tests measured between the two groups. Furthermore, cytolysis was associated with a higher rate of postprocedure symptoms and side effects, and elevated temperature was associated with a worse survival on univariate analysis. Multivariate analysis demonstrated that there was no benefit in terms of survival from having elevated temperature or cytolysis following embolisation. Cytolysis after chemoembolisation is probably due to damage to normal hepatocytes. Temperature changes may reflect tumour necrosis or necrosis of the healthy tissue. There is no evidence that either a postchemoembolisation fever or cytolysis is associated with an enhanced tumour response or improved long-term survival in patients with primary or secondary liver cancer.

SUBMITTER: Wigmore SJ

PROVIDER: S-EPMC2394347 | biostudies-other | 2003 Oct

REPOSITORIES: biostudies-other

ACCESS DATA

Similar Datasets

Project description:Cystic white matter injury is highly associated with severe neurodevelopmental disability and cerebral palsy in preterm infants, yet its pathogenesis remains poorly understood and there is no established treatment. In the present study, we tested the hypothesis that slowly evolving cystic white matter injury after hypoxia-ischaemia is mediated by programmed necrosis initiated by tumour necrosis factor. Tumour necrosis factor blockade was begun 3 days after hypoxia-ischaemia to target the tertiary phase of injury, when most secondary cell death is thought to be complete. Chronically instrumented preterm foetal sheep (0.7 gestation) received 25 min of hypoxia-ischaemia induced by complete umbilical cord occlusion or sham-umbilical cord occlusion (controls, n = 10), followed by intracerebroventricular infusion of the soluble TNF inhibitor, Etanercept, at 3, 8 and 13 days after umbilical cord occlusion (n = 9) or vehicle (n = 9). Foetal brains were processed for histology at 21 days after umbilical cord occlusion. Umbilical cord occlusion with vehicle was associated with a spectrum of macroscopic white matter degeneration, including white matter atrophy, ventriculomegaly and overt temporal lobe cystic white matter injury. Oligodendrocyte maturational arrest and impaired labelling of myelin proteins, characteristic of diffuse white matter injury, was observed in the parietal lobe and surrounding the cystic lesions in the temporal lobe. Etanercept markedly attenuated cystic white matter injury on the side of the intracerebroventricular infusion, with partial contralateral protection. Further, Etanercept improved oligodendrocyte maturation and labelling of myelin proteins in the temporal and parietal lobes. The present study shows that cystic white matter injury reflects late-onset tertiary cell death mediated by delayed neuroinflammation through the tumour necrosis factor pathway. Delayed tumour necrosis factor blockade markedly attenuated cystic white matter injury and restored oligodendrocyte maturation and deficits in myelin protein expression. These data suggest that delayed tumour necrosis factor blockade may represent a viable therapeutic strategy to reduce the risk of cystic and diffuse white matter injury and potentially cerebral palsy after preterm birth, with a surprisingly wide therapeutic window.

Dataset Information

Postchemoembolisation syndrome--tumour necrosis or hepatocyte injury?

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets