NDLI: Flutamide-induced hepatic dysfunction in relation to steady-state plasma concentrations of flutamide and its metabolites

Content Provider	Springer Nature Link
Author	Aizawa, Yoshio Ikemoto, Isao Kishimoto, Koichi Wada, Tetsuro Yamazaki, Haruki Ohishi, Yukihiko Kiyota, Hiroshi Furuta, zomu Suzuki, Hideri Ueda, Masataka
Copyright Year	2003
Abstract	The frequency, severity, and outcome of flutamide-induced hepatic injury were prospectively evaluated in 55 patients with prostate cancer who received 125 mg of flutamide 3 times a day (daily dose: 375 mg) combined with an agonistic analogue of luteinizing hormone-releasing hormone. In addition, we examined plasma and urine concentrations of flutamide and its major metabolites 4 weeks after the beginning of flutamide therapy, and evaluated their significance in predicting flutamide-induced hepatic dysfunction. Hepatic function could be assessed in 50 patients and hepatic dysfunction during therapy was observed in 9 patients (18%); 3 patients (6%) were classified as having moderate liver dysfunction and 6 (12%) were classified as having mild liver dysfunction. The steady-state plasma levels of flutamide and its biologic active metabolite, hydroxyflutamide (OH-Flu), were not related to hepatic dysfunction. However, the concentration of another major metabolite, 4-nitro-3-(trifluoromethyl)phenylamine (FLU-1) was considerably higher in 2 patients who developed clinically significant hepatic dysfunction. These findings suggest that clinically significant hepatic dysfunction could be induced in patients with compromised flutamide metabolism, which leads to a high concentration of FLU-1. Based on results of this study, we propose that plasma FLU-1 levels are one of the predictive factors for flutamide-induced hepatic dysfunction. This hypothesis will be confirmed in a large-scale study.
Starting Page	149
Ending Page	156
Page Count	8
File Format	PDF
ISSN	03008177
Journal	Molecular and Cellular Biochemistry
Volume Number	252
Issue Number	1-2
e-ISSN	15734919
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2003-01-01
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cardiology Medical Biochemistry Oncology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Clinical Biochemistry Molecular Biology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Apolipoprotein C-III can specifically bind to hepatic plasma membranes

Tetrahydrobiopterin attenuates homocysteine induced endothelial dysfunction

Free radical induced respiratory muscle dysfunction

Mitochondrial dysfunction as a mediator of hippocampal apoptosis in a model of hepatic encephalopathy

Lymphosarcoma-induced alterations in hepatic adrenergic receptors: Implications to the hypoglycemia of cancer cachexia

Protective agent, erdosteine, against cisplatin-induced hepatic oxidant injury in rats

Plasma nitric oxide and iron concentrations in exercised rats are negatively correlated

Effect of chronic treatment with losartan on streptozotocin-induced renal dysfunction

Repiratory muscle dysfunction in sepsis

Flutamide-induced hepatic dysfunction in relation to steady-state plasma concentrations of flutamide and its metabolites

Similar Documents

Apolipoprotein C-III can specifically bind to hepatic plasma membranes

Tetrahydrobiopterin attenuates homocysteine induced endothelial dysfunction

Free radical induced respiratory muscle dysfunction

Mitochondrial dysfunction as a mediator of hippocampal apoptosis in a model of hepatic encephalopathy

Lymphosarcoma-induced alterations in hepatic adrenergic receptors: Implications to the hypoglycemia of cancer cachexia

Protective agent, erdosteine, against cisplatin-induced hepatic oxidant injury in rats

Plasma nitric oxide and iron concentrations in exercised rats are negatively correlated

Effect of chronic treatment with losartan on streptozotocin-induced renal dysfunction

Repiratory muscle dysfunction in sepsis

Flutamide-induced hepatic dysfunction in relation to steady-state plasma concentrations of flutamide and its metabolites