Abstract
Objectives: Leukoencephalopathy syndrome is a neurologic complication after organ transplantation caused predominantly by the neurotoxic effects of immunosuppressive agents on cerebral white matter. We determined the incidence and features of leukoencephalopathy syndrome in recipients after living-donor liver transplantations. Materials and Methods: We retrospectively investigated 205 patients who had a living-donor liver transplantation performed at our institution between August 1998 and October 2008. Results: Leukoencephalopathy syndrome developed in 7 of 205 patients (3.9%) and in 4.7% of the 150 patients treated with tacrolimus-based immuno - suppression after their living-donor liver transplantation. The underlying diseases were alcoholic cirrhosis in 3 cases, viral cirrhosis in 2, biliary atresia in 1, and Wilson disease in 1. Time to clinical onset after tacrolimus medication was 15.6 days (range, 6-30 days). The neurologic symptoms included headache, confusion, myoclonus, seizures, and visual disturbances. The mean serum trough level of tacrolimus at clinical onset was not very high (11.7 ng/mL [range, 6.0-14.2 ng/mL]). T2-weighted magnetic resonance imaging in all cases showed diffuse high signal in the white matter of the frontal, parieto-occipital, and temporal lobes. Treatment with antihypertensives, anticonvulsants, and withdrawal of tacrolimus resulted in amelioration of symptoms and magnetic resonance imaging abnormalities. Six patients showed complete recovery, while the seventh had residual rigidity and cognitive impairment caused by hypoxia during a convulsion. Conclusions: Tacrolimus neurotoxicity can occur despite low trough levels; it depends on variations in pharmacokinetics, such as absorption and maximum concentration level. Early diagnosis and treatment of leukoencephalopathy syndrome should contribute to complete remission.
| Original language | English |
|---|---|
| Pages (from-to) | 139-144 |
| Number of pages | 6 |
| Journal | Experimental and Clinical Transplantation |
| Volume | 9 |
| Issue number | 2 |
| Publication status | Published - Apr 2011 |
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Keywords
- Complication
- Liver transplantation
- Neurotoxicity
- Tacrolimus
ASJC Scopus subject areas
- Transplantation
Cite this
Leukoencephalopathy syndrome after living-donor liver transplantation. / Umeda, Yuzo; Matsuda, Hiroaki; Sadamori, Hiroshi; Shinoura, Susumu; Yoshida, Ryuichi; Sato, Daisuke; Utsumi, Masashi; Yagi, Takahito; Fujiwara, Toshiyoshi.
In: Experimental and Clinical Transplantation, Vol. 9, No. 2, 04.2011, p. 139-144.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Leukoencephalopathy syndrome after living-donor liver transplantation
AU - Umeda, Yuzo
AU - Matsuda, Hiroaki
AU - Sadamori, Hiroshi
AU - Shinoura, Susumu
AU - Yoshida, Ryuichi
AU - Sato, Daisuke
AU - Utsumi, Masashi
AU - Yagi, Takahito
AU - Fujiwara, Toshiyoshi
PY - 2011/4
Y1 - 2011/4
N2 - Objectives: Leukoencephalopathy syndrome is a neurologic complication after organ transplantation caused predominantly by the neurotoxic effects of immunosuppressive agents on cerebral white matter. We determined the incidence and features of leukoencephalopathy syndrome in recipients after living-donor liver transplantations. Materials and Methods: We retrospectively investigated 205 patients who had a living-donor liver transplantation performed at our institution between August 1998 and October 2008. Results: Leukoencephalopathy syndrome developed in 7 of 205 patients (3.9%) and in 4.7% of the 150 patients treated with tacrolimus-based immuno - suppression after their living-donor liver transplantation. The underlying diseases were alcoholic cirrhosis in 3 cases, viral cirrhosis in 2, biliary atresia in 1, and Wilson disease in 1. Time to clinical onset after tacrolimus medication was 15.6 days (range, 6-30 days). The neurologic symptoms included headache, confusion, myoclonus, seizures, and visual disturbances. The mean serum trough level of tacrolimus at clinical onset was not very high (11.7 ng/mL [range, 6.0-14.2 ng/mL]). T2-weighted magnetic resonance imaging in all cases showed diffuse high signal in the white matter of the frontal, parieto-occipital, and temporal lobes. Treatment with antihypertensives, anticonvulsants, and withdrawal of tacrolimus resulted in amelioration of symptoms and magnetic resonance imaging abnormalities. Six patients showed complete recovery, while the seventh had residual rigidity and cognitive impairment caused by hypoxia during a convulsion. Conclusions: Tacrolimus neurotoxicity can occur despite low trough levels; it depends on variations in pharmacokinetics, such as absorption and maximum concentration level. Early diagnosis and treatment of leukoencephalopathy syndrome should contribute to complete remission.
AB - Objectives: Leukoencephalopathy syndrome is a neurologic complication after organ transplantation caused predominantly by the neurotoxic effects of immunosuppressive agents on cerebral white matter. We determined the incidence and features of leukoencephalopathy syndrome in recipients after living-donor liver transplantations. Materials and Methods: We retrospectively investigated 205 patients who had a living-donor liver transplantation performed at our institution between August 1998 and October 2008. Results: Leukoencephalopathy syndrome developed in 7 of 205 patients (3.9%) and in 4.7% of the 150 patients treated with tacrolimus-based immuno - suppression after their living-donor liver transplantation. The underlying diseases were alcoholic cirrhosis in 3 cases, viral cirrhosis in 2, biliary atresia in 1, and Wilson disease in 1. Time to clinical onset after tacrolimus medication was 15.6 days (range, 6-30 days). The neurologic symptoms included headache, confusion, myoclonus, seizures, and visual disturbances. The mean serum trough level of tacrolimus at clinical onset was not very high (11.7 ng/mL [range, 6.0-14.2 ng/mL]). T2-weighted magnetic resonance imaging in all cases showed diffuse high signal in the white matter of the frontal, parieto-occipital, and temporal lobes. Treatment with antihypertensives, anticonvulsants, and withdrawal of tacrolimus resulted in amelioration of symptoms and magnetic resonance imaging abnormalities. Six patients showed complete recovery, while the seventh had residual rigidity and cognitive impairment caused by hypoxia during a convulsion. Conclusions: Tacrolimus neurotoxicity can occur despite low trough levels; it depends on variations in pharmacokinetics, such as absorption and maximum concentration level. Early diagnosis and treatment of leukoencephalopathy syndrome should contribute to complete remission.
KW - Complication
KW - Liver transplantation
KW - Neurotoxicity
KW - Tacrolimus
UR - http://www.scopus.com/inward/record.url?scp=79955930903&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79955930903&partnerID=8YFLogxK
M3 - Article
C2 - 21453233
AN - SCOPUS:79955930903
VL - 9
SP - 139
EP - 144
JO - Experimental and Clinical Transplantation
JF - Experimental and Clinical Transplantation
SN - 1304-0855
IS - 2
ER -