Human herpesvirus infection in drug-induced hypersensitivity syndrome, toxic epidermal necrolysis and Stevens-Johnson syndrome
Human herpesvirus infection in drug-induced hypersensitivity syndrome, toxic epidermal necrolysis and Stevens-Johnson syndrome
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人类疱疹病毒感染导致药物过敏综合征、中毒性表皮坏死松解症和史蒂文斯-约翰逊综合征
DOI:
10.1046/j.1440-1592.2003.00309.x
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发表时间:
2004
影响因子:
6.8
通讯作者:
Z. Ikezawa
中科院分区:
文献类型:
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作者:
M. Aihara;Naoko Mitani;Natsue Kakemizu;Y. Yamakawa;N. Inomata;Norihiko Ito;H. Komatsu;Y. Aihara;Z. Ikezawa
ABSTRACT Background Reactivation of human herpesvirus (HHV) infection, especially HHV-6, has been observed in patients with drug-induced hypersensitivity syndrome (DIHS). In toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS), the relevance of HHV infection to the symptoms is unclear. Methods Patients with a diagnosis of DIHS ( n = 7), TEN ( n = 5) and SJS ( n = 4) were included in the present study. These patients were evaluated for the presence of active HHV-6, HHV-7 and cytomegalovirus (CMV) infections by serological tests and polymerase chain reaction with blood. Results More than 3 weeks after the onset of DIHS, HHV-6 serological tests revealed a remarkable rise in IgG antibodies in six patients, including one treated without steroids. Human herpesvirus-6 DNA was detected in blood from three patients. In one patient with DIHS, reactivation of CMV was shown without reactivation of HHV-6, whereas in three patients anti-CMV IgG antibodies increased after the rise of anti-HHV-6 IgG antibodies. Anti-HHV-7 IgG antibodies did not show remarkable rises in any of these patients. As for patients with TEN and SJS, anti-HHV-6, anti-HHV-7 and anti-CMV IgG antibodies showed no significant increase, except for one patient in whom anti-HHV-6 and anti-HHV-7 IgG antibodies increased, but not more than 1: 160, after steroid therapy. Human herpesvirus-6 DNA was not detected in the blood of those patients. Conclusions Human herpesvirus-6 reactivation in patients with DIHS is not due to non-specific reactivation induced by steroid therapy, but to events specific to DIHS. We hypothesize that DIHS may occur as a result of reactivation of HHV, especially HHV-6, accompanied with an allergic reaction to drugs, followed by a substantial immune response to the virus that is probably responsible for visceral involvement.
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