Increased Sensitivity to Glucocorticoids in Peripheral Blood Mononuclear Cells of Chronic Fatigue Syndrome Patients, without Evidence for Altered Density or Affinity of Glucocorticoid Receptors

Visser, J.H.M.; Lentjes, Eef G.W.M.; Haspels, Inge; Graffelman, W.; Blauw, Bep; Kloet, Ronald De; Nagelkerken, Lex

doi:10.2310/6650.2001.34047

Cited by 44 publications

(28 citation statements)

References 54 publications

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“…In a later study, employing a whole blood assay with LPS-stimulation, they further showed an increased GC sensitivity of IL-10, but not IL-12 production (Visser et al, 2001a). These results were replicated in a further study, in which they additionally reported that the differences in GC sensitivity were not attributable to variation of GR expression or binding affinity (Visser et al, 2001b). Accordingly, Gaab et al…”

Section: Gc Sensitivity In Psychiatric and Somatic Diseasesmentioning

confidence: 82%

Glucocorticoid Sensitivity in Humans-Interindividual Differences and Acute Stress Effects

Rohleder

Wolf

Kirschbaum

2003

Stress

102

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The hypothalamus pituitary adrenal (HPA)- axis is one of the major output systems of the neuroendocrine stress response. Its major end products, glucocorticoids (GCs), have a plethora of effects throughout the organism, most of which are believed to be protective against disturbances of homeostasis. However, negative effects have also been described under specific conditions of hyper- or hypo(re)activity of the HPA axis. Both beneficial and adverse effects of GCs ultimately depend on the target tissue sensitivity to these steroids. Recent findings suggest that GC sensitivity (a) may vary between different target tissues in the same organism, (b) shows large individual differences and (c) can be acutely changed in times of acute stress. In the present review, data are summarized which show differences in GC sensitivities in patients suffering from diverse somatic and psychiatric diseases, as well as chronically stressed individuals. Furthermore, studies are presented that show a rapid modulation of GC sensitivity in response to exercise or psychosocial stress in healthy adults. The response pattern of acute GC sensitivity modulation seems to be influenced by age and sex hormone status of the individual. While the GC signalling cascade may be subject to modulation at several levels, the pathway for acute modulation of GC sensitivity remains to be elucidated.

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Section: Gc Sensitivity In Psychiatric and Somatic Diseasesmentioning

confidence: 82%

Glucocorticoid Sensitivity in Humans-Interindividual Differences and Acute Stress Effects

Rohleder

Wolf

Kirschbaum

2003

Stress

102

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“…Further sup port for enhanced negative feedback and increased glucocorticoid sensitivity came from three in vitro studies. [44][45][46] Three new in vivo studies published in the past 8 years have lent further support to the presence of enhanced negative feedback and glucocorticoid receptor func tion. The first study 47 applied the lowdose DST to 34 female patients, 12 of whom had a history of childhood trauma.…”

Section: Suppression Studiesmentioning

confidence: 87%

Hypothalamic–pituitary–adrenal axis dysfunction in chronic fatigue syndrome

Papadopoulos¹,

Cleare²

2011

Nat Rev Endocrinol

228

153

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The weight of current evidence supports the presence of the following factors related to hypothalamic-pituitary-adrenal (HPA) axis dysfunction in patients with chronic fatigue syndrome (CFS): mild hypocortisolism; attenuated diurnal variation of cortisol; enhanced negative feedback to the HPA axis; and blunted HPA axis responsiveness. Furthermore, HPA axis changes seem clinically relevant, as they are associated with worse symptoms and/or disability and with poorer outcomes to standard treatments for CFS. Regarding etiology, women with CFS are more likely to have reduced cortisol levels. Studies published in the past 8 years provide further support for a multifactorial model in which several factors interact to moderate HPA axis changes. In particular, low activity levels, depression and early-life stress appear to reduce cortisol levels, whereas the use of psychotropic medication can increase cortisol. Addressing these factors-for example, with cognitive behavioral therapy-can increase cortisol levels and is probably the first-line approach for correcting HPA axis dysfunction at present, as steroid replacement is not recommended. Given what is now a fairly consistent pattern of findings for the type of HPA axis changes found in CFS, we recommend that future work focuses on improving our understanding of the cause and relevance of these observed changes.

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“…Visser and coworkers reported IL-10 to be increased (69) and normal (70), while another group reported it to be decreased (14).…”

Section: Inconsistent Levels Of Soluble Mediators Cytokines or Theimentioning

confidence: 99%

“…One group reported increases in IL-2 cytokine (58), while three groups found amounts of this cytokine to be at control levels (10,40,70).…”

Section: Inconsistent Levels Of Soluble Mediators Cytokines or Theimentioning

confidence: 99%

Evidence for the Presence of Immune Dysfunction in Chronic Fatigue Syndrome

Natelson¹,

Haghighi

Ponzio

2002

Clin Vaccine Immunol

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Chronic fatigue syndrome is a medically unexplained ailment characterized by new onset of fatigue accompanied by rheumatological, infectious, and neuropsychiatric symptoms. Because the ailment often begins suddenly with a flu-like presentation, early pathophysiological ideas as to cause included viral infection and immune activation. When early reports identified putative immunological abnormalities in this illness, it was given the name of chronic fatigue and immune dysfunction syndrome, or CFIDS.The purpose of this review is to evaluate the immunological literature to determine if strong evidence to support this notion exists. We collected and reviewed 239 published papers, of which only 72 fulfilled a set of criteria for use in this review. For this review, we developed the following criteria: papers had to be published in the peer review literature; patients had to be from a group with substantial fatigue lasting at least 6 months (the vast majority fulfilled either the 1988 [21] or the 1994 [13] case definition of chronic fatigue syndrome [CFS]); papers had to compare CFS patients to healthy controls; and actual data had to be shown with evidence of testing for statistical significance. So, for example, when a paper reported no difference between patients and controls for some immunological variables but actual data were not included, we did not include it. Also, if a report compared patient data to normative values rather than to the study's own control group, we did not include it.The numbers of immunologically active cells and immunologically active substances such as cytokines reported in the literature have mushroomed in the past decade. To keep this review manageable, we are reporting scientific papers only on those variables for which either consistent or inconsistent abnormalities were reported by more than one group. We did not review papers reporting immunological variables to be within normal limits but have listed those studies in which more than one group found such results in a table. We have chosen not to list those variables reported abnormal in only one study because those results have not yet been replicated. When inconsistent results among laboratories were found for any immunological variable, we reviewed the methods described in those papers in an effort to identify reasons for such discrepancies.Note: when a group published more than one paper and it was apparent that the two studies used many if not all of the patients whose data are in the second paper, we chose to include only the more recent paper or the one with the largest number of subjects. To provide several examples, Tirelli published two papers, the first with 205 subjects and the second with 265 patients (66, 67). When data from one variable appeared in both papers, we included data from only the latter. Our own group has published three papers using different statistical methods and making different comparisons when reviewing lymphocyte populations. Thus, we used the one paper that controlled for multiple comparisons (74)...

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Increased Sensitivity to Glucocorticoids in Peripheral Blood Mononuclear Cells of Chronic Fatigue Syndrome Patients, without Evidence for Altered Density or Affinity of Glucocorticoid Receptors

Abstract: In conclusion, PBMC of CFS patients display an increased sensitivity to glucocorticoids, which cannot be explained by number or affinity of the GR but should rather be attributed to molecular processes beyond the actual binding of the ligand to the GR.

Cited by 44 publications

References 54 publications

Glucocorticoid Sensitivity in Humans-Interindividual Differences and Acute Stress Effects

Glucocorticoid Sensitivity in Humans-Interindividual Differences and Acute Stress Effects

Hypothalamic–pituitary–adrenal axis dysfunction in chronic fatigue syndrome

Evidence for the Presence of Immune Dysfunction in Chronic Fatigue Syndrome

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