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Acute liver failure caused by occupational exposure to HCFC-123: Two case reports

RATIONALE: Hydrochlorofluorocarbon 123 (HCFC-123, Freon123; 2,2-dichloro-1,1,1-trifluoroethane) has been widely used in refrigeration and heat-transfer applications as a substitute for chlorofluorocarbons due to its lower ozone-depleting potentials. Occupational exposure to HCFC-123 may cause mild r...

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Detalles Bibliográficos
Autores principales: Choe, Hun Jee, Ahn, Soomin, Jung, Kwangrok, Kim, Jin-Wook
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer Health 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6831264/
https://www.ncbi.nlm.nih.gov/pubmed/30817569
http://dx.doi.org/10.1097/MD.0000000000014522
Descripción
Sumario:RATIONALE: Hydrochlorofluorocarbon 123 (HCFC-123, Freon123; 2,2-dichloro-1,1,1-trifluoroethane) has been widely used in refrigeration and heat-transfer applications as a substitute for chlorofluorocarbons due to its lower ozone-depleting potentials. Occupational exposure to HCFC-123 may cause mild reversible hepatoxicity, but no fatal cases have been reported yet. PATIENT CONCERNS: In this report, we present cases of severe hepatitis with fatal outcome by HCFC-123. Two industrial workers from a manufacturing factory of fire extinguishers which use HCFC-123 were presented with diarrhea, fever, myalgia, and jaundice. Patients had been repeatedly exposed to the liquid form of HCFC-123 for the past three weeks before flare of symptoms. DIAGNOSIS: The blood biochemistry tests showed acute cholestatic hepatitis and liver biopsy findings indicated inflammatory hepatocellular injury. The diagnosis of HCFC-123 induced hepatitis was made. INTERVENTIONS: The treatment for both patients were generally supportive. The second patient went through hemodialysis, ventilatory care, and artificial liver support therapy (molecular adsorbent recirculating system) at intensive care unit. OUTCOMES: One patient recovered uneventfully, whereas the other patient showed rapid deterioration leading to acute liver failure complicated with cerebral edema, subdural hemorrhage, and death on hospital day 10. LESSONS: The HCFC-123-induced hepatitis showed similarities with halothane hepatitis, both of which may share pathophysiologic mechanisms. Exposure to HCFC-123 needs to be listed as a potential cause of acute liver failure, and to be considered in patients with acute hepatitis of uncertain etiology and negative viral serology.