Popisujeme případ 49leté pacientky s akutním selháním jater způsobeným akutní halotanovou hepatitidou. Selhání jater bylo natolik závažné, že pacientka byla indikována k transplantaci jater. Provedení úspěšné transplantace jater bylo umožněno i podpůrnou terapií na podkladě frakcionované plazmatické separace a adsorpce (FPSA) na přístroji Prometheus®.
We describe a case of a 49 years old female patient with acute liver failure caused by halothan induced hepatitis. The liver failure was so severe that she was indicated for liver transplantation. The successful outcome of liver transplantation was facilitated also by supportive treatment with fractionated plasma separation and adsorption (FPSA) on Prometheus® device.
- MeSH
- Liver Failure, Acute etiology complications therapy MeSH
- Anesthetics, Inhalation adverse effects therapeutic use toxicity MeSH
- Chemical Phenomena MeSH
- Dialysis methods instrumentation utilization MeSH
- Adult MeSH
- Halothane analogs & derivatives adverse effects toxicity MeSH
- Chemical and Drug Induced Liver Injury etiology complications therapy MeSH
- Humans MeSH
- Liver Transplantation methods utilization MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Female MeSH
- Publication type
- Case Reports MeSH
Although the inhalation anaesthetics are commonly used in clinical practice, their toxic effects on the lung cells have not yet been well studied. Previous studies indicated strong genotoxic effect of some inhalation anaesthetics, applied at clinically relevant concentrations. The aim of the present study was to assess the extent of DNA damage, nuclear abnormalities and possibility of human A549 cells to recover after treatment with halothane at lower concentrations. The data obtained demonstrate that even lower halothane concentrations could induce DNA damage although the anaesthetic does not interact directly with DNA. We have found that irreversible impairment of the cell genome is initiated at a concentration as low as 1.5 mM. Part of the cell population displays some characteristics of stress-induced apoptosis, defining this concentration as threshold for cell survival. We suggest that the intracellular signalling pathway triggers the toxic effects of halothane.
