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Title: | Enhanced generation of reactive oxygen species by interferon-γ may have contributed to successful treatment of invasive pulmonary aspergillosis in a patient with chronic granulomatous disease. |
Authors: | Yamashita, Kouhei Miyoshi, Takashi Arai, Yasuyuki ![]() ![]() ![]() Mizugishi, Kiyomi Takaori-Kondo, Akifumi Ueyama, Takehiko |
Author's alias: | 山下, 浩平 |
Keywords: | Chronic granulomatous disease Invasive pulmonary aspergillosis Interferon-γ Reactive oxygen species Voriconazole |
Issue Date: | 24-Mar-2013 |
Publisher: | Springer Japan |
Journal title: | International journal of hematology |
Volume: | 97 |
Issue: | 4 |
Start page: | 505 |
End page: | 510 |
Abstract: | Invasive pulmonary aspergillosis (IPA) is a life-threatening complication of chronic granulomatous disease (CGD), a rare inherited disorder of phagocytes that is characterized by a defect in the production of reactive oxygen species (ROS) caused by mutations in NADPH oxidase 2. Here, we report a case of successful treatment of IPA complicated with CGD by the administration of interferon-γ (IFN-γ) in combination with voriconazole. The patient carried a splice site mutation in the CYBB gene, and the neutrophils could produce a certain amount of ROS. In this case, augmentation of ROS generation in the patient's neutrophils was observed after in vivo IFN-γ treatment, which may be attributable to the induction of a normal CYBB gene in the myeloid progenitor cells. This treatment, in combination with voriconazole, may have contributed to the reversal of IPA in this patient. These results suggest that the in vivo use of IFN-γ may augment ROS generation in CGD neutrophils, thus leading to the successful treatment of severe IPA. |
Rights: | The final publication is available at Springer via http://dx.doi.org/10.1007/s12185-013-1315-y この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。This is not the published version. Please cite only the published version. |
URI: | http://hdl.handle.net/2433/196751 |
DOI(Published Version): | 10.1007/s12185-013-1315-y |
PubMed ID: | 23526099 |
Appears in Collections: | Journal Articles |

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