title: Cancer-related fatigue, inflammation and thyrotropin-releasing hormone.
abstract: Aging and aging related illnesses such as cancer have been associated with inflammatory changes. Cancer-related behavioral comorbidities such as fatigue, sleep disturbances, depression have also been associated with inflammation, hypothalamic-pituitary-adrenal (HPA) axis dysregulation and other neuroendocrine changes. From a clinical perspective, cancer-related fatigue demonstrates striking similarities with the cytokine-induced sickness phenomenon in animal models. Thyrotopin-releasing hormone (TRH) plays a homeostatic role in its interaction with several biological systems, including a critical role in its interactions with the immune system. Considerable evidence supports a pivotal role for TRH in the inflammatory processes with specific relevance to the "cytokine-induced sickness behavior" paradigm. Additionally, TRH exerts arousing and analeptic effects in instances of behavioral depression. In a small proof-of-concept study conducted by our group, we investigated TRH administration as a treatment fatigue in cancer survivors in comparison with saline administration using a double-blind, crossover design. We also evaluated impact of TRH/saline administration on the inflammatory markers in these patients. TRH administration was associated with significant improvement (p < 0.05) in fatigue levels as measured by the Visual Analog Scale-Energy (VAS-E), was associated with significant (p < 0.05) improvement in sleep disturbances and improved quality of life. Notably, TRH administration was associated with decrease in C-reactive protein (CRP) levels, a marker of inflammation. This decrease in CRP level with TRH administration was associated with improvement in energy levels as measured by the VAS-E. The present review supports potential utility of TRH-based therapeutics in medical and psychiatric disorders with underlying inflammatory processes.
authors: Department of Psychiatry, The Carol and Ray Neag Comprehensive Cancer Center University of Connecticut Health Center, USA. JKAMATH@uchc.edu
authors: Jayesh
authors: J
authors: Kamath
mesh_terms: D000367:Age Factors; D000375:Aging / Q000276:immunology / Q000378:metabolism; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage; D015897:Comorbidity; D018849:Controlled Clinical Trials as Topic; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005221:Fatigue / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000523:psychology; D006706:Homeostasis; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism / Q000523:psychology; D018836:Inflammation Mediators / Q000378:metabolism; D009369:Neoplasms / Q000150:complications* / Q000276:immunology / Q000378:metabolism / Q000523:psychology / Q000628:therapy; D011788:Quality of Life; D012893:Sleep Wake Disorders / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000523:psychology; D013973:Thyrotropin-Releasing Hormone / Q000008:administration & dosage / Q000378:metabolism*; D016896:Treatment Outcome
chemical_list: D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D013973:Thyrotropin-Releasing Hormone