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Interferon‐mediated fatigue
Author(s) -
Malik Ummekalsoom R.,
Makower Della F.,
Wadler Scott
Publication year - 2001
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(20010915)92:6+<1664::aid-cncr1494>3.0.co;2-9
Subject(s) - medicine , etiology , endocrine system , depression (economics) , chronic fatigue syndrome , autoimmunity , autoantibody , pathophysiology , alpha interferon , antidepressant , immunology , interferon , disease , hormone , antibody , hippocampus , economics , macroeconomics
Fatigue is a common side effect of interferon (IFN) therapy, reported in 70–100% of patients treated with IFN. The etiology of IFN‐mediated fatigue (IMF) is multifactorial, with endocrine failure, neuropsychiatric disturbance, autoimmunity, and cytokine dysregulation potentially being contributors. Thyroid dysfunction, associated with the development of autoantibodies, is seen in 8–20% of patients receiving IFN‐α. IFN‐α also suppresses the hypothalamic‐pituitary‐adrenal axis. In addition, IFN‐α therapy leads to depression and cognitive slowing, and depressed patients are predisposed to develop fatigue. Clinical management of IMF is challenging because the syndrome is variable in onset and severity and the pathophysiology is poorly understood. Current management typically centers on dose reduction, but ancillary nonpharmacologic measures may help improve symptoms. Other strategies include antidepressant or anxiolytic therapy and treatment of coexisting hypothyroidism. Future studies utilizing IFN should include quantitative guidelines for grading and managing IMF. Cancer 2001;92:1664–68. © 2001 American Cancer Society.