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Glucocorticoid receptor polymorphisms and haplotypes associated with chronic fatigue syndrome
Rajeevan MS, Smith AK, Dimulescu I, Unger ER, Vernon SD, Heim C, Reeves WC
Genes , Brain and Behavior 2006; doi:10.1111/j.1601-183X.2006.00244.x.
Summary
There is increasing evidence that the pathophysiology of CFS involves dysregulation of immune functions and hypothalamic-pituitary-adrenal (HPA) axis activity. The HPA axis is an important brain modulator of stress and has a variety of effects, cortisol activity being one. This study looked at differences in one gene that involves cortisol receptors on cells and has a major role in HPA axis function. We measured 9 different variants of the gene among people with CFS, unexplained fatigue not CFS (which we term ISF), and non fatigued controls who volunteered for the Wichita in-hospital study. We found that several variants of the gene (NR3C1) were more common in persons with CFS and were also associated with severity of functional impairment and severity of fatigue.
Abstract
Chronic fatigue syndrome (CFS) is a significant public health problem of unknown etiology, the pathophysiology has not been elucidated, and there are no characteristic physical signs or laboratory abnormalities. Some studies have indicated an association of CFS with deregulation of immune functions and hypothalamic– pituitary–adrenal (HPA) axis activity. In this study, we examined the association of sequence variations in the glucocorticoid receptor gene (NR3C1) with CFS because NR3C1 is a major effector of the HPA axis. There were 137 study participants (40 with CFS, 55 with insufficient symptoms or fatigue, termed as ISF, and 42 nonfatigued controls) who were clinically evaluated and identified from the general population of Wichita, KS. Nine single nucleotide polymorphisms (SNPs) in NR3C1 were tested for association of polymorphisms and haplotypes with CFS. We observed an association of multiple SNPs with chronic fatigue compared to non-fatigued (NF) subjects ( P < 0.05) and found similar associations with quantitative assessments of functional impairment (by the SF-36), with fatigue (by the Multidimensional Fatigue Inventory) and with symptoms (assessed by the Centers for Disease Control Symptom Inventory). Subjects homozygous for the major allele of all associated SNPs were at increased risk for CFS with odds ratios ranging from 2.61 (CI 1.05–6.45) to 3.00 (CI 1.12–8.05). Five SNPs, covering a region of approximately 80 kb, demonstrated high linkage disequilibrium (LD) in CFS, but LD gradually declined in ISF to NF subjects. Furthermore, haplotype analysis of the region in LD identified two associated haplotypes with opposite alleles: one protective and the other conferring risk of CFS. These results demonstrate NR3C1 as a potential mediator of chronic fatigue, and implicate variations in the 5’ region of NR3C1 as a possible mechanism through which the alterations in HPA axis regulation and behavioral characteristics of CFS may manifest.
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