The low dose ACTH test in chronic fatigue syndrome and in health

Scott, Lucinda V.; Medbak, S.; Dinan, Timothy G.

doi:10.1046/j.1365-2265.1998.00418.x

Cited by 64 publications

(38 citation statements)

References 35 publications

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“…Scott and colleagues [16] also reported reduced ACTH responses to CRH challenge, but noted reduced cortisol responses, whereas Cleare and colleagues [17] reported normal ACTH responses but attenuated cortisol responses. Tests utilizing ACTH administration demonstrate equally unclear results [15,18,19]. In light of this study, it is possible that genetic variations in POMC and NR3C1 may contribute to the pathophysiology of a subgroup of patients with chronic fatigue, and this heterogeneity may explain the previous inconsistencies in the literature.…”

Section: Discussionmentioning

confidence: 74%

Polymorphisms in Genes Regulating the HPA Axis Associated with Empirically Delineated Classes of Unexplained Chronic Fatigue

et al. 2006

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Chronic fatigue syndrome (CFS) is characterized by persistent or relapsing fatigue that is not alleviated by rest, causes substantial reduction in activities and is accompanied by a variety of symptoms. Its unknown etiology may reflect that CFS is heterogeneous. Latent class analyses of symptoms and physiological systems were used to delineate subgroups within a population-based sample of fatigued and nonfatigued subjects [1] . This study examined whether genetic differences underlie the individual subgroups of the latent class solution. Polymorphisms in 11 candidate genes related to both hypothalamic-pituitary-adrenal (HPA) axis function and mood-related neurotransmitter systems were evaluated by comparing each of the five ill classes (Class 1, n = 33; Class 3, n = 22; Class 4, n = 22; Class 5, n = 17; Class 6, n = 11) of fatigued subjects with subjects defined as well (Class 2, n = 35). Of the five classes of subjects with unexplained fatigue, three classes were distinguished by gene polymorphsims involved in either HPA axis function or neurotransmitter systems, including proopiomelanocortin (POMC), nuclear receptor subfamily 3, group C, member 1 (NR3C1), monoamine oxidase A (MAOA), monoamine oxidase B (MAOB), and tryptophan hydroxylase 2 (TPH2). These data support the hypothesis that medically unexplained chronic fatigue is heterogeneous and presents preliminary evidence of the genetic mechanisms underlying some of the putative conditions.

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Section: Discussionmentioning

confidence: 74%

Polymorphisms in Genes Regulating the HPA Axis Associated with Empirically Delineated Classes of Unexplained Chronic Fatigue

et al. 2006

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“…However, other studies found no difference in salivary cortisol concentrations between CFS and healthy controls [91,92]. Insight from pharmacological challenge studies testing specific levels of HPA axis regulation indicates enhanced feedback sensitivity [92][93][94][95], increased adrenocortical sensitivity to adrenocorticotropic hormone (ACTH), and a reduced maximal cortisol response compared to normal subjects [81,96], with nonsignificant findings being reported also [97,98]. Clearly, findings point toward relative hypocortisolism in CFS.…”

Section: Findings On Hpa Axis and Cfsmentioning

confidence: 84%

Stress as a Pathophysiological Factor in Functional Somatic Syndromes

Nater¹,

Fischer²,

Ehlert

2011

CPSR

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Functional somatic syndromes (FSS) are defined by a constellation of symptoms for which after thorough medical examination no structural pathology and no proportional tissue abnormalities can be identified. Pathophysiology of these syndromes has remained elusive and treatment options are limited. Current research efforts acknowledge the importance of stress as a potential risk factor in the manifestation and maintenance of FSS. A substantial body of research has focused on psychological stress factors as well as alterations of the endocrine stress system (the hypothalamicpituitary-adrenal, HPA axis, in particular), the immune system, and the autonomic nervous system (ANS). Dysregulation of these systems might explain some of the symptoms of FSS. In this review, we describe studies reporting stress-related findings in three of the most prevalent and well-described FSS, i.e. chronic fatigue syndrome (CFS), irritable bowel syndrome (IBS), and fibromyalgia syndrome (FMS). Psychobiological processes which seem to play a role in the translation of stress into functional symptoms and syndromes are discussed.

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“…[6][7][8][9][10] This downregulation of the hypothalamicpituitary-adrenal (HPA) axis in CFS stands in contrast to the upregulation seen in major depression. Serotonergic and noradrenergic hypothalamic pathways, [11][12][13] and growth hormone secretion 14 also are disrupted.…”

Section: Neuroendocrine Studiesmentioning

confidence: 88%

Role of Infection and Neurologic Dysfunction in Chronic Fatigue Syndrome

Komaroff

Cho²

2011

Semin Neurol

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Chronic fatiguing illnesses following well-documented infections and acute "infectious-like" illnesses of uncertain cause have been reported for many decades. Chronic fatigue syndrome (CFS) was first formally defined in 1988. There is considerable evidence that CFS is associated with abnormalities of the central and autonomic nervous systems. There also is evidence linking several infectious agents with CFS, although no agent has been proven to be a cause of the illness. Most of the infectious agents that have been linked to CFS are able to produce a persistent, often life-long, infection and thus are a constant incitement to the immune system. Most also have been shown to be neuropathogens. The evidence is consistent with the hypothesis that CFS, in some cases, can be triggered and perpetuated by several chronic infections that directly or indirectly affect the nervous system, and that symptoms are a reflection of the immune response to the infection.

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The low dose ACTH test in chronic fatigue syndrome and in health

Cited by 64 publications

References 35 publications

Polymorphisms in Genes Regulating the HPA Axis Associated with Empirically Delineated Classes of Unexplained Chronic Fatigue

Polymorphisms in Genes Regulating the HPA Axis Associated with Empirically Delineated Classes of Unexplained Chronic Fatigue

Stress as a Pathophysiological Factor in Functional Somatic Syndromes

Role of Infection and Neurologic Dysfunction in Chronic Fatigue Syndrome

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