Neuropsychiatric adverse effects of interferon-α: Recognition and management
Recombinant preparations of the cytokine interferon (IFN)-alpha are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFN alpha induces a variety of neuropsychiatric adverse effects, including an acut...
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| Published in | CNS drugs Vol. 19; no. 2; pp. 105 - 123 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hong Kong
Adis International
01.01.2005
Auckland Wolters Kluwer Health, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1172-7047 |
| DOI | 10.2165/00023210-200519020-00002 |
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| Abstract | Recombinant preparations of the cytokine interferon (IFN)-alpha are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFN alpha induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high-dose IFN alpha, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFN alpha-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 21-58% of patients receiving IFN alpha, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFN alpha dosage and treatment duration. The available data support two approaches to the pharmacological management of IFN alpha-induced depression: antidepressant pretreatment or symptomatic treatment once IFN alpha has been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFN alpha-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFN alpha-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression-specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may be more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin-noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally, IFN alpha appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFN alpha and antidepressants should be stopped, an emergency psychiatric consultation should be obtained, and treatment with a mood stabilizer should be initiated. |
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| AbstractList | Recombinant preparations of the cytokine interferon (IFN)-alpha are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFN alpha induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high-dose IFN alpha, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFN alpha-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 21-58% of patients receiving IFN alpha, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFN alpha dosage and treatment duration. The available data support two approaches to the pharmacological management of IFN alpha-induced depression: antidepressant pretreatment or symptomatic treatment once IFN alpha has been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFN alpha-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFN alpha-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression-specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may be more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin-noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally, IFN alpha appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFN alpha and antidepressants should be stopped, an emergency psychiatric consultation should be obtained, and treatment with a mood stabilizer should be initiated. Recombinant preparations of the cytokine interferon (IFN)- alpha are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFNalpha induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high- dose IFNalpha, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFNalpha-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 21-58% of patients receiving IFNalpha, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFNalpha dosage and treatment duration. The available data support two approaches to the pharmacological management of IFNalpha-induced depression: antidepressant pretreatment or symptomatic treatment once IFNalpha has been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFNalpha-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFNalpha-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression- specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may be more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin- noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally, IFNalpha appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFNalpha and antidepressants should be stopped, an emergency psychiatric consultation should be obtained, and treatment with a mood stabiliser should be initiated. Recombinant preparations of the cytokine interferon (IFN)- α are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFNα induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high-dose IFNα?, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFNα-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 2158% of patients receiving IFNα, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFNα dosage and treatment duration. The available data support two approaches to the pharmacological management of IFNα-induced depression: antidepressant pretreatment or symptomatic treatment once IFNαhas been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFNα-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFNα-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression-specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may be more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin-noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally, IFNα appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFNαand antidepressants should be stopped, an emergency psychiatric consultation should be obtained, and treatment with a mood stabiliser should be initiated. Recombinant preparations of the cytokine interferon (IFN)-alpha are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFN alpha induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high-dose IFN alpha, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFN alpha-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 21-58% of patients receiving IFN alpha, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFN alpha dosage and treatment duration. The available data support two approaches to the pharmacological management of IFN alpha-induced depression: antidepressant pretreatment or symptomatic treatment once IFN alpha has been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFN alpha-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFN alpha-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression-specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may be more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin-noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally, IFN alpha appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFN alpha and antidepressants should be stopped, an emergency psychiatric consultation should be obtained, and treatment with a mood stabilizer should be initiated.Recombinant preparations of the cytokine interferon (IFN)-alpha are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFN alpha induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high-dose IFN alpha, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFN alpha-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 21-58% of patients receiving IFN alpha, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFN alpha dosage and treatment duration. The available data support two approaches to the pharmacological management of IFN alpha-induced depression: antidepressant pretreatment or symptomatic treatment once IFN alpha has been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFN alpha-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFN alpha-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression-specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may be more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin-noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally, IFN alpha appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFN alpha and antidepressants should be stopped, an emergency psychiatric consultation should be obtained, and treatment with a mood stabilizer should be initiated. Recombinant preparations of the cytokine interferon (IFN)-α are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFNα induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high-dose IFNα, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFNα-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 21–58% of patients receiving IFNα, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFNα dosage and treatment duration. The available data support two approaches to the pharmacological management of IFNα-induced depression: antidepressant pretreatment or symptomatic treatment once IFNα has been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFNα-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFNα-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression-specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may he more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin-noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally. IFNα appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFNα and antidepressants should be stopped, an emergency psychiatric consultation should he obtained, and treatment with a mood stabiliser should be initiated. |
| Audience | Academic |
| Author | DEMETRASHVILI, Marina CAPURON, Lucile MILLER, Andrew H RAISON, Charles L |
| AuthorAffiliation | Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, USA |
| AuthorAffiliation_xml | – name: Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, USA |
| Author_xml | – sequence: 1 givenname: Charles L surname: RAISON fullname: RAISON, Charles L organization: Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, United States – sequence: 2 givenname: Marina surname: DEMETRASHVILI fullname: DEMETRASHVILI, Marina organization: Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, United States – sequence: 3 givenname: Lucile surname: CAPURON fullname: CAPURON, Lucile organization: Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, United States – sequence: 4 givenname: Andrew H surname: MILLER fullname: MILLER, Andrew H organization: Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia, United States |
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| Keywords | Human Confusion psychosis Alpha interferon Toxicity Mental disorder Mania Depression Review |
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| References | 10086482 - J Clin Psychiatry. 1999;60 Suppl 4:40-55; discussion 56 3399889 - Science. 1988 Jul 29;241(4865):540-5 9482535 - Semin Oncol. 1998 Feb;25(1 Suppl 1):9-13 11799348 - J Clin Psychopharmacol. 2002 Feb;22(1):86-90 7583704 - Cancer Invest. 1995;13(6):561-6 8855176 - Hepatology. 1996 Oct;24(4):778-89 8561204 - Am J Psychiatry. 1996 Feb;153(2):231-7 12544378 - J Clin Psychopharmacol. 2003 Feb;23(1):78-86 12715261 - Arch Womens Ment Health. 2003 Feb;6(1):15-22 9482538 - Semin Oncol. 1998 Feb;25(1 Suppl 1):30-8 2049759 - Cancer. 1991 Jul 1;68(1):88-92 14719046 - J Psychiatry Neurosci. 2004 Jan;29(1):11-7 12823087 - J Clin Psychiatry. 2003 Jun;64(6):708-14 12399946 - Mol Psychiatry. 2002;7(9):942-7 1560801 - N Engl J Med. 1992 May 7;326(19):1250-6 10408496 - Lancet. 1999 Jul 10;354(9173):131-2 9146076 - Rinsho Shinkeigaku. 1997 Jan;37(1):54-6 11583749 - Lancet. 2001 Sep 22;358(9286):958-65 6402063 - Br Med J (Clin Res Ed). 1983 Jan 22;286(6361):262-4 12699949 - Lancet. 2003 Apr 12;361(9365):1240 12583926 - Gen Hosp Psychiatry. 2003 Jan-Feb;25(1):34-8 11121525 - Brain Res. 2000 Dec 1;885(1):14-24 2115748 - Am J Psychiatry. 1990 Aug;147(8):1091 1450297 - Biol Psychiatry. 1992 Nov 1;32(9):834-8 1775506 - Pharmacol Rev. 1991 Dec;43(4):425-73 11093071 - Neuropsychobiology. 2000;42 Suppl 1:43-5 14709760 - Psychosomatics. 2004 Jan-Feb;45(1):49-57 2027482 - Neurology. 1991 May;41(5):672-6 12047006 - Palliat Med. 2002 May;16(3):261-3 8029260 - Pharmacol Biochem Behav. 1994 Apr;47(4):901-5 3307672 - Arch Intern Med. 1987 Sep;147(9):1577-80 9819446 - N Engl J Med. 1998 Nov 19;339(21):1485-92 11406895 - Am J Hosp Palliat Care. 2001 May-Jun;18(3):187-92 8835651 - J Affect Disord. 1996 Jun 20;39(1):31-8 12944327 - Am J Psychiatry. 2003 Sep;160(9):1554-65 9819961 - Psychosomatics. 1998 Nov-Dec;39(6):562-4 1542935 - Trends Pharmacol Sci. 1992 Jan;13(1):24-8 8561218 - Am J Psychiatry. 1996 Feb;153(2):294 15050647 - Brain Behav Immun. 2004 May;18(3):205-13 2890808 - Lancet. 1987 Nov 21;2(8569):1175-8 12577943 - Dig Dis. 2002;20(3-4):284-8 7989716 - J Hepatol. 1994 Aug;21(2):241-3 11274622 - N Engl J Med. 2001 Mar 29;344(13):961-6 12188106 - Prog Neuropsychopharmacol Biol Psychiatry. 2002 May;26(4):731-46 12872204 - World J Biol Psychiatry. 2003 Jul;4(3):115-8 12618532 - Psychosomatics. 2003 Mar-Apr;44(2):104-12 12954918 - Psychosomatics. 2003 Sep-Oct;44(5):417-20 9435767 - Arch Gen Psychiatry. 1998 Jan;55(1):88-9 10458496 - Tohoku J Exp Med. 1999 Jan;187(1):79-82 10500295 - Immunol Today. 1999 Oct;20(10):469-73 12030950 - Aliment Pharmacol Ther. 2002 Jun;16(6):1091-9 12082564 - Mol Psychiatry. 2002;7(5):468-73 6830692 - Br J Cancer. 1983 Mar;47(3):419-22 14728113 - J Clin Psychiatry. 2003 Dec;64(12):1502-10 6206681 - Acta Neurol Scand. 1984 Jul;70(1):42-6 12297606 - Psychosomatics. 2002 Sep-Oct;43(5):378-85 11927189 - Neuropsychopharmacology. 2002 May;26(5):643-52 9144108 - J Neuropsychiatry Clin Neurosci. 1997 Spring;9(2):273-6 10829053 - J Clin Oncol. 2000 Jun;18(11):2316-26 9638401 - Hepatogastroenterology. 1998 Mar-Apr;45(20):328-30 9818630 - J Clin Psychiatry. 1998 Oct;59(10):502-8 11062791 - Med J Aust. 2000 Oct 2;173(7):359-61 9819447 - N Engl J Med. 1998 Nov 19;339(21):1493-9 2509916 - N Engl J Med. 1989 Nov 30;321(22):1501-6 3232542 - Acta Psychiatr Scand. 1988 Nov;78(5):622-6 9536584 - Int J Clin Pract. 1997 Oct;51(7):447-50 10849263 - J Viral Hepat. 2000 May;7(3):211-7 10401474 - Am J Psychiatry. 1999 Jul;156(7):1120 12540795 - Hepatology. 2003 Feb;37(2):443-51 12544372 - J Clin Psychopharmacol. 2003 Feb;23(1):27-30 8480744 - Am J Gastroenterol. 1993 May;88(5):760-1 7739681 - N Engl J Med. 1995 Jun 1;332(22):1457-62 12724470 - J Neuropsychiatry Clin Neurosci. 2003 Spring;15(2):242-3 14677080 - Pharmacopsychiatry. 2003 Nov;36 Suppl 3:S203-6 14992966 - Am J Psychiatry. 2004 Mar;161(3):429-35 9566274 - Neuropsychobiology. 1998;37(2):93-7 12324553 - N Engl J Med. 2002 Sep 26;347(13):975-82 12832253 - Am J Psychiatry. 2003 Jul;160(7):1342-5 14709758 - Psychosomatics. 2004 Jan-Feb;45(1):29-33 7625459 - Am J Psychiatry. 1995 Aug;152(8):1130-8 10223879 - N Engl J Med. 1999 Apr 29;340(17):1370 12075031 - Psychosomatics. 2002 May-Jun;43(3):171-4 12598790 - AIDS. 2003 Mar 7;17(4):638-40 12450640 - J Affect Disord. 2002 Dec;72(3):237-41 12518079 - Ann Med Interne (Paris). 2002 Nov;153(7 Suppl):2S22-30 2464673 - J Neurooncol. 1988 Dec;6(4):355-9 11926717 - J Clin Psychiatry. 2002 Mar;63(3):194-8 12195441 - J Neurol. 2002 Aug;249(8):983-7 14573318 - Biol Psychiatry. 2003 Nov 1;54(9):906-14 6171272 - Biochem Biophys Res Commun. 1981 Jul 30;101(2):472-8 10682234 - Clin Neuropharmacol. 2000 Jan-Feb;23(1):59-61 12183762 - Oncol Nurs Forum. 2002 Aug;29(7):E85-90 11965836 - Hawaii Med J. 2002 Mar;61(3):48, 57 11607923 - Semin Clin Neuropsychiatry. 2001 Oct;6(4):277-94 10831463 - Am J Psychiatry. 2000 Jun;157(6):867-76 1387028 - Brain Res. 1992 Feb 28;573(2):318-20 8903371 - Hepatology. 1996 Nov;24(5):1034-40 9597349 - Depress Anxiety. 1998;7 Suppl 1:24-32 6194882 - Cancer Treat Rep. 1983 Oct;67(10):958-61 4082913 - Acta Neurol Scand. 1985 Nov;72(5):475-80 11447988 - Gen Hosp Psychiatry. 2001 May-Jun;23(3):168-70 2009031 - Arch Gen Psychiatry. 1991 Apr;48(4):303-7 11874221 - J Clin Psychiatry. 2002 Feb;63(2):166-7 10581980 - Psychosomatics. 1999 Nov-Dec;40(6):510-2 10960166 - Biol Psychiatry. 2000 Aug 15;48(4):327-9 8895006 - J Hepatol. 1996 Sep;25(3):283-91 9068931 - Clin Pharmacokinet. 1997;32 Suppl 1:1-21 |
| References_xml | – reference: 12047006 - Palliat Med. 2002 May;16(3):261-3 – reference: 11406895 - Am J Hosp Palliat Care. 2001 May-Jun;18(3):187-92 – reference: 11927189 - Neuropsychopharmacology. 2002 May;26(5):643-52 – reference: 14709760 - Psychosomatics. 2004 Jan-Feb;45(1):49-57 – reference: 9144108 - J Neuropsychiatry Clin Neurosci. 1997 Spring;9(2):273-6 – reference: 9482535 - Semin Oncol. 1998 Feb;25(1 Suppl 1):9-13 – reference: 12699949 - Lancet. 2003 Apr 12;361(9365):1240 – reference: 12544378 - J Clin Psychopharmacol. 2003 Feb;23(1):78-86 – reference: 7739681 - N Engl J Med. 1995 Jun 1;332(22):1457-62 – reference: 12944327 - Am J Psychiatry. 2003 Sep;160(9):1554-65 – reference: 11607923 - Semin Clin Neuropsychiatry. 2001 Oct;6(4):277-94 – reference: 8561218 - Am J Psychiatry. 1996 Feb;153(2):294 – reference: 10408496 - Lancet. 1999 Jul 10;354(9173):131-2 – reference: 10458496 - Tohoku J Exp Med. 1999 Jan;187(1):79-82 – reference: 11926717 - J Clin Psychiatry. 2002 Mar;63(3):194-8 – reference: 9819446 - N Engl J Med. 1998 Nov 19;339(21):1485-92 – reference: 12832253 - Am J Psychiatry. 2003 Jul;160(7):1342-5 – reference: 2509916 - N Engl J Med. 1989 Nov 30;321(22):1501-6 – reference: 10500295 - Immunol Today. 1999 Oct;20(10):469-73 – reference: 10831463 - Am J Psychiatry. 2000 Jun;157(6):867-76 – reference: 9566274 - Neuropsychobiology. 1998;37(2):93-7 – reference: 6402063 - Br Med J (Clin Res Ed). 1983 Jan 22;286(6361):262-4 – reference: 8480744 - Am J Gastroenterol. 1993 May;88(5):760-1 – reference: 11965836 - Hawaii Med J. 2002 Mar;61(3):48, 57 – reference: 10849263 - J Viral Hepat. 2000 May;7(3):211-7 – reference: 7989716 - J Hepatol. 1994 Aug;21(2):241-3 – reference: 1775506 - Pharmacol Rev. 1991 Dec;43(4):425-73 – reference: 8029260 - Pharmacol Biochem Behav. 1994 Apr;47(4):901-5 – reference: 2115748 - Am J Psychiatry. 1990 Aug;147(8):1091 – reference: 12324553 - N Engl J Med. 2002 Sep 26;347(13):975-82 – reference: 1450297 - Biol Psychiatry. 1992 Nov 1;32(9):834-8 – reference: 9597349 - Depress Anxiety. 1998;7 Suppl 1:24-32 – reference: 14677080 - Pharmacopsychiatry. 2003 Nov;36 Suppl 3:S203-6 – reference: 8561204 - Am J Psychiatry. 1996 Feb;153(2):231-7 – reference: 12399946 - Mol Psychiatry. 2002;7(9):942-7 – reference: 6171272 - Biochem Biophys Res Commun. 1981 Jul 30;101(2):472-8 – reference: 11874221 - J Clin Psychiatry. 2002 Feb;63(2):166-7 – reference: 12583926 - Gen Hosp Psychiatry. 2003 Jan-Feb;25(1):34-8 – reference: 6830692 - Br J Cancer. 1983 Mar;47(3):419-22 – reference: 14728113 - J Clin Psychiatry. 2003 Dec;64(12):1502-10 – reference: 11062791 - Med J Aust. 2000 Oct 2;173(7):359-61 – reference: 11447988 - Gen Hosp Psychiatry. 2001 May-Jun;23(3):168-70 – reference: 10086482 - J Clin Psychiatry. 1999;60 Suppl 4:40-55; discussion 56 – reference: 11121525 - Brain Res. 2000 Dec 1;885(1):14-24 – reference: 12823087 - J Clin Psychiatry. 2003 Jun;64(6):708-14 – reference: 14573318 - Biol Psychiatry. 2003 Nov 1;54(9):906-14 – reference: 14709758 - Psychosomatics. 2004 Jan-Feb;45(1):29-33 – reference: 1387028 - Brain Res. 1992 Feb 28;573(2):318-20 – reference: 12195441 - J Neurol. 2002 Aug;249(8):983-7 – reference: 6206681 - Acta Neurol Scand. 1984 Jul;70(1):42-6 – reference: 10829053 - J Clin Oncol. 2000 Jun;18(11):2316-26 – reference: 12297606 - Psychosomatics. 2002 Sep-Oct;43(5):378-85 – reference: 11093071 - Neuropsychobiology. 2000;42 Suppl 1:43-5 – reference: 15050647 - Brain Behav Immun. 2004 May;18(3):205-13 – reference: 2027482 - Neurology. 1991 May;41(5):672-6 – reference: 12188106 - Prog Neuropsychopharmacol Biol Psychiatry. 2002 May;26(4):731-46 – reference: 8855176 - Hepatology. 1996 Oct;24(4):778-89 – reference: 8895006 - J Hepatol. 1996 Sep;25(3):283-91 – reference: 12598790 - AIDS. 2003 Mar 7;17(4):638-40 – reference: 12082564 - Mol Psychiatry. 2002;7(5):468-73 – reference: 7625459 - Am J Psychiatry. 1995 Aug;152(8):1130-8 – reference: 4082913 - Acta Neurol Scand. 1985 Nov;72(5):475-80 – reference: 3232542 - Acta Psychiatr Scand. 1988 Nov;78(5):622-6 – reference: 14992966 - Am J Psychiatry. 2004 Mar;161(3):429-35 – reference: 11274622 - N Engl J Med. 2001 Mar 29;344(13):961-6 – reference: 10581980 - Psychosomatics. 1999 Nov-Dec;40(6):510-2 – reference: 3307672 - Arch Intern Med. 1987 Sep;147(9):1577-80 – reference: 12724470 - J Neuropsychiatry Clin Neurosci. 2003 Spring;15(2):242-3 – reference: 12030950 - Aliment Pharmacol Ther. 2002 Jun;16(6):1091-9 – reference: 10960166 - Biol Psychiatry. 2000 Aug 15;48(4):327-9 – reference: 14719046 - J Psychiatry Neurosci. 2004 Jan;29(1):11-7 – reference: 1542935 - Trends Pharmacol Sci. 1992 Jan;13(1):24-8 – reference: 9638401 - Hepatogastroenterology. 1998 Mar-Apr;45(20):328-30 – reference: 12577943 - Dig Dis. 2002;20(3-4):284-8 – reference: 8835651 - J Affect Disord. 1996 Jun 20;39(1):31-8 – reference: 2049759 - Cancer. 1991 Jul 1;68(1):88-92 – reference: 9819961 - Psychosomatics. 1998 Nov-Dec;39(6):562-4 – reference: 10682234 - Clin Neuropharmacol. 2000 Jan-Feb;23(1):59-61 – reference: 12715261 - Arch Womens Ment Health. 2003 Feb;6(1):15-22 – reference: 12540795 - Hepatology. 2003 Feb;37(2):443-51 – reference: 1560801 - N Engl J Med. 1992 May 7;326(19):1250-6 – reference: 8903371 - Hepatology. 1996 Nov;24(5):1034-40 – reference: 6194882 - Cancer Treat Rep. 1983 Oct;67(10):958-61 – reference: 9146076 - Rinsho Shinkeigaku. 1997 Jan;37(1):54-6 – reference: 9536584 - Int J Clin Pract. 1997 Oct;51(7):447-50 – reference: 9435767 - Arch Gen Psychiatry. 1998 Jan;55(1):88-9 – reference: 12544372 - J Clin Psychopharmacol. 2003 Feb;23(1):27-30 – reference: 3399889 - Science. 1988 Jul 29;241(4865):540-5 – reference: 12954918 - Psychosomatics. 2003 Sep-Oct;44(5):417-20 – reference: 12183762 - Oncol Nurs Forum. 2002 Aug;29(7):E85-90 – reference: 9818630 - J Clin Psychiatry. 1998 Oct;59(10):502-8 – reference: 2890808 - Lancet. 1987 Nov 21;2(8569):1175-8 – reference: 10223879 - N Engl J Med. 1999 Apr 29;340(17):1370 – reference: 9482538 - Semin Oncol. 1998 Feb;25(1 Suppl 1):30-8 – reference: 12618532 - Psychosomatics. 2003 Mar-Apr;44(2):104-12 – reference: 7583704 - Cancer Invest. 1995;13(6):561-6 – reference: 12872204 - World J Biol Psychiatry. 2003 Jul;4(3):115-8 – reference: 9068931 - Clin Pharmacokinet. 1997;32 Suppl 1:1-21 – reference: 11799348 - J Clin Psychopharmacol. 2002 Feb;22(1):86-90 – reference: 10401474 - Am J Psychiatry. 1999 Jul;156(7):1120 – reference: 11583749 - Lancet. 2001 Sep 22;358(9286):958-65 – reference: 12450640 - J Affect Disord. 2002 Dec;72(3):237-41 – reference: 9819447 - N Engl J Med. 1998 Nov 19;339(21):1493-9 – reference: 12518079 - Ann Med Interne (Paris). 2002 Nov;153(7 Suppl):2S22-30 – reference: 12075031 - Psychosomatics. 2002 May-Jun;43(3):171-4 – reference: 2464673 - J Neurooncol. 1988 Dec;6(4):355-9 – reference: 2009031 - Arch Gen Psychiatry. 1991 Apr;48(4):303-7 |
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| Snippet | Recombinant preparations of the cytokine interferon (IFN)-alpha are increasingly used to treat a number of medical conditions, including chronic viral... Recombinant preparations of the cytokine interferon (IFN)- α are increasingly used to treat a number of medical conditions, including chronic viral hepatitis... Recombinant preparations of the cytokine interferon (IFN)- alpha are increasingly used to treat a number of medical conditions, including chronic viral... Recombinant preparations of the cytokine interferon (IFN)-α are increasingly used to treat a number of medical conditions, including chronic viral hepatitis... |
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| SubjectTerms | Antiviral Agents - adverse effects Behavioral Symptoms - chemically induced Behavioral Symptoms - epidemiology Behavioral Symptoms - prevention & control Biological and medical sciences Drug toxicity and drugs side effects treatment Hepatitis C, Chronic - drug therapy Humans Interferon-alpha - adverse effects Medical sciences Mood Disorders - chemically induced Mood Disorders - physiopathology Neoplasms - drug therapy Pharmacology. Drug treatments Prevalence Psychiatric Status Rating Scales Recognition (Psychology) Risk Factors Toxicity: nervous system and muscle |
| Title | Neuropsychiatric adverse effects of interferon-α: Recognition and management |
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