Human T-cell leukemia virus type I–associated myelopathy following living-donor liver transplantation
✍ Scribed by Akihiko Soyama; Susumu Eguchi; Mitsuhisa Takatsuki; Tatsuki Ichikawa; Masako Moriuchi; Hiroyuki Moriuchi; Tatsufumi Nakamura; Yoshitsugu Tajima; Takashi Kanematsu
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 95 KB
- Volume
- 14
- Category
- Article
- ISSN
- 1527-6465
- DOI
- 10.1002/lt.21414
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✦ Synopsis
This report describes a patient who developed human T-cell leukemia virus type I-associated myelopathy (HAM) following a living-donor liver transplantation (LDLT) for liver cirrhosis due to hepatitis C virus (HCV) infection. Both the recipient and the living donor (his sister) were human T-cell leukemia virus type I (HTLV-I) carriers. Since the LDLT, he had been treated with immunosuppressive drugs such as tacrolimus and steroids as well as interferon-␣ to prevent rejection and a recurrence of the HCV infection, respectively. Even though the HTLV-I proviral load had decreased upon interferon treatment, he developed a slowly progressive gait disturbance with urinary disturbance 2 years after the LDLT and was diagnosed with HAM. This appears to be the first report of HAM development in an HLTV-I-infected LDLT recipient.
📜 SIMILAR VOLUMES
## Abstract Human T‐cell lymphotropic virus type I (HTLV‐I) is the etiologic agent of HTLV‐I‐associated myelopathy/tropical spastic paraparesis (HAM/TSP). High HTLV‐I provirus load and __tax__ mRNA level have been suggested as predictors of disease progression in patients with HAM/TSP, but little i
## Abstract There is no effective therapy for human T‐cell lymphotropic virus type I (HTLV‐I)‐associated myelopathy/tropical spastic paraparesis (HAM/TSP). Glucocorticoids are effective to reduce the motor disability in these patients, but its role as anti‐spastic drugs is unknown. Here it is repor
Tropical spastic paraparesis/HTLV-I associated myelopathy (TSP/HAM), is characterized by infiltration of human T cell leukaemia virus type-I (HTLV-I)-infected T-cells, anti-HTLV-I cytotoxic T cells and macrophages into the patients' cerebrospinal fluid and by intrathecally formed anti-HTLV-I antibod