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J. Gaab, D. Huster, R. Peisen, V. Engert, V. Heitz, T. Schad, T. H. Schurmeyer, and U. Ehlert, “Hypothalamic-Pituitary-Adrenal Axis Reactivity in Chronic Fatigue Syndrome and Health under Psychological, Physiological, and Pharmacological Stimulation,” Psychosomatic Medicine, Vol. 64, No. 6, 2001, pp. 951-962.

has been cited by the following article:

• TITLE: Possible Genetic Dysregulation in Pediatric CFS

  AUTHORS: Leonard A. Jason, Matthew Sorenson, Nicole Porter, Molly Brown, Athena Lerch, Constance Van der Eb, Judy Mikovits

  KEYWORDS: Pediatric, Chronic Fatigue Syndrome, Hypocortisolism, Glucocorticoid Receptor Expression

  JOURNAL NAME: Psychology, Vol.1 No.4, November 18, 2010

  ABSTRACT: Hypocortisolism is a frequent finding in individuals with chronic fatigue syndrome (CFS) and could play an explanatory role in the development of illness symptomatology. The etiologic mechanism behind this finding could be genetic variance in glucocorticoid receptor expression (GR) or increased resistance to the effects of glucocorticoids. Several investigators believe that allelic variance in a GR (NR3C1) mediates the expression of chronic fatigue possibly through influence on hypothalamic-pituitary-adrenal (HPA) axis function [1]. In addition, several immunologic variables are associated with CFS. The nuclear factor kappa beta (NFkB) pathway is heavily involved in cellular transcription and regulation and has been shown to be associated with the development of CFS. The NFkB pathway is directly regulated by and influences the presence of GR [2]. Our study focused on assessing whether such inflammatory transcription is occurring during adolescent years. Findings indicated decreased expression of NFKB1, NFKB2, and NR3C1. A decrease in the expression of these genes may have effects on immune cell function and cytokine production that could explain immunologic findings seen in individuals with CFS.