J Korean Surg Soc.  2011 Feb;80(2):157-160. 10.4174/jkss.2011.80.2.157.

Acute Hepatic Failure Associated with Stevens-Johnson Syndrome Induced by Carbamazepine Treatment in a Patient with Transverse Myelitis

Affiliations
  • 1Department of Surgery, Kyung Hee University School of Medicine and the Kyung Hee University Hospital at Gangdong, Seoul, Korea. sunhyung@chol.com
  • 2Department of Neurology, Kyung Hee University School of Medicine and the Kyung Hee University Hospital at Gangdong, Seoul, Korea.

Abstract

Carbamazepine-induced liver injury is less common, but the consequences of the side effects can be very serious leading to death or a need for liver transplantation. We report a case of a 60-year-old female transverse myelitis patient with fulminant hepatic failure and Stevens-Johnson syndrome induced by carbamazepine who successfully underwent deceased donor liver transplantation. The patient, a 60-year-old female, was admitted to our service due to acute liver insufficiency and a drowsy mental state attributable to carbamazepine. She had been treated with carbamazepine to control transverse myelitis. Fifty days after the use of carbamazepine, she developed jaundice, erythematous papules and bullae, and decreased consciousness. The diagnosis of Stevens-Johnson syndrome was considered. She underwent deceased donor liver transplantation. She was discharged with normal graft functions 5 months after transplantation. Thus, liver transplantation can be a feasible therapy for patients with carbamazepine-induced hepatic failure associated with Stevens-Johnson syndrome.

Keyword

Carbamazepine; Stevens-Johnson syndrome; Fulminant hepatic failure; Liver transplantation; Transverse myelitis

MeSH Terms

Blister
Carbamazepine
Consciousness
Female
Hepatic Insufficiency
Humans
Jaundice
Liver
Liver Failure
Liver Failure, Acute
Liver Transplantation
Middle Aged
Myelitis, Transverse
Stevens-Johnson Syndrome
Tissue Donors
Transplants
Carbamazepine

Figure

  • Fig. 1 The spinal magnetic resonance imaging (MRI) demonstrated diffuse, ill-defined high signal intensities at the T8-10 level on a T2 sagittal image.

  • Fig. 2 (A) Macular rash in the lower limb (B) skin exfoliation.

  • Fig. 3 The histopathology shows massive hepatic necrosis with widespread inflammation and canalicular cholestasis. Hematoxylin and eosin staining. Original magnification, ×40.


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