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Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The chronic fatigue syndrome (CFS) is a condition of unknown etiology, characterized by a persistent debilitating fatigue, the muscle-related symptoms and the neuropsychiatric symptoms. Recently, it has been reported that the patients with CFS might have impaired activation of the hypothalamic-pituitary-adrenal axis, and suggested that a part of the patho-genesis of CFS might be associated with abnormalities of the endocrine system. Herein, we show that the majority of Japanese patients with CFS had a serum dehydroepiandrosterone sulfate (DHEA-S) deficiency. Serum DHEA-S is one of the most abundantly produced hormones which is secreted from the adrenal glands, and its physiological function is thought to be a precursor of sex steroids. DHEA-S has recently been shown to have physiological properties, such as neurosteroids, which are associated with such psychophysiological phenomena as memory, stress, anxiety, sleep and depression. Therefore, the deficiency of DHEA-S might be related to the neuropsychiatric symptoms in patients with CFS.
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PMID:Dehydroepiandrosterone sulfate deficiency in chronic fatigue syndrome. 985 12

Dehydroepiandrosterone (DHEA) is a steroid hormone secreted primarily by the adrenal glands and to a lesser extent by the brain, skin, testes, and ovaries. It is the most abundant circulating steroid in humans and can be converted into other hormones, including estrogen and testosterone. It has been characterized as a pleiotropic "buffer hormone," with receptor sites in the liver, kidney, and testes, and has a key role in a wide range of physiological responses. Circulating levels of DHEA decline with age and a relationship has been suggested between lower DHEA levels and heart disease, cancer, diabetes, obesity, chronic fatigue syndrome, AIDS, and Alzheimer's disease. Other research suggests that autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis, and multiple sclerosis might be associated with declining DHEA levels.
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PMID:DHEA. Monograph. 1141 76

Chronic fatigue syndrome (CFS) is defined as constellation of the prolonged fatigue and several somatic symptoms, in the absence of organic or severe psychiatric disease. However, this is an operational definition and conclusive biomedical explanation remains elusive. Similarities between the signs and symptoms of CFS and adrenal insufficiency prompted the research of the hypothalamo-pituitary-adrenal axis (HPA) derangement in the pathogenesis of the CFS. Early studies showed mild glucocorticoid deficiency, probably of central origin that was compensated by enhanced adrenal sensitivity to ACTH. Further studies showed reduced ACTH response to vasopressin infusion. The response to CRH was either blunted or unchanged. Cortisol response to insulin induced hypoglycaemia was same as in the control subjects while ACTH response was reported to be same or enhanced. However, results of direct stimulation of the adrenal cortex using ACTH were conflicting. Cortisol and DHEA responses were found to be the same or reduced compared to control subjects. Scott et al found that maximal cortisol increment from baseline is significantly lower in CFS subjects. The same group also found small adrenal glands in some CFS subjects. These varied and inconsistent results could be explained by the heterogeneous study population due to multifactorial causes of the disease and by methodological differences. The aim of our study was to assess cortisol response to low dose (1 microgram) ACTH using previously validated methodology. We compared cortisol response in the CFS subjects with the response in control and in subjects with suppressed HPA axis due to prolonged corticosteroid use. Cortisol responses were analysed in three subject groups: control (C), secondary adrenal insufficiency (AI), and in CFS. The C group consisted of 39 subjects, AI group of 22, and CFS group of nine subjects. Subject data are presented in table 1. Low dose ACTH test was started at 0800 h with the i.v. injection of 1 microgram ACTH (Galenika, Belgrade, Serbia). Blood samples for cortisol determination were taken from the i.v. cannula at 0, 15, 30, and 60 min. Data are presented as mean +/- standard error (SE). Statistical analysis was done using ANOVA with the Games-Howell post-hoc test to determine group differences. ACTH dose per kg or per square meter of body surface was not different between the groups. Baseline cortisol was not different between the groups. However, cortisol concentrations after 15 and 30 minutes were significantly higher in the C group than in the AI group. Cortisol concentration in the CFS group was not significantly different from any other group (Graph 1). Cortisol increment at 15 and 30 minutes from basal value was significantly higher in C group than in other two groups. However, there was no significant difference in cortisol increment between the AI and CFS groups at any time of the test. On the contrary, maximal cortisol increment was not different between CFS and other two groups, although it was significantly higher in C group than in the AI group. Maximal cortisol response to the ACTH stimulation and area under the cortisol response curve was significantly larger in C group compared to AI group, but there was no difference between CFS and other two groups. Several previous studies assessed cortisol response to ACTH stimulation. Hudson and Cleare analysed cortisol response to 1 microgram ACTH in CFS and control subjects. They compared maximum cortisol attained during the test, maximum cortisol increment, and area under the cortisol response curve. There was no difference between the groups in any of the analysed parameters. However, authors commented that responses were generally low. On the contrary Scott et al found that cortisol increment at 30 min is significantly lower in the CFS than in the control group. Taking into account our data it seems that the differences found in previous studies papers are caused by the methodological differences. We have shown that cortisol increment at 15 and 30 min is significantly lower in CFS group than in C group. Nevertheless, maximum cortisol attained during the test, maximum cortisol increment, and area under the cortisol response curve were not different between the C and CFS groups. This is in agreement with our previous findings that cortisol increment at 15 minutes has the best diagnostic value of all parameters obtained during of low dose ACTH test. However, there was no difference between CFS and AI group in any of the parameters, although AI group had significantly lower cortisol concentrations at 15 and 30 minutes, maximal cortisol response, area under the cortisol curve, maximal cortisol increment, and maximal cortisol change velocity than C group. Consequently, reduced adrenal responsiveness to ACTH exists in CFS. In conclusion, we find that regarding the adrenal response to ACTH stimulation CFS subjects present heterogeneous group. In some subjects cortisol response is preserved, while in the others it is similar to one found in secondary adrenal insufficiency.
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PMID:[Disorder of adrenal gland function in chronic fatigue syndrome]. 1505 15

Since 1996 in our clinic, the regular practice of megadose vitamin C infusion with dehydroepiandrosterone-cortisol annex and the continuous intake of erythromycin and chloramphenicol have been found useful for the clinical control of the autoimmune disease interstitial pneumonia, also known as chronic fatigue syndrome. The long-term use of these two systems for the treatment of the autoimmune disease has led to the emergence of four problems of theoretical or practical importance, as described below: i) Should maintenance of the above core treatments be continued for prophylactic purposes in the absence of acute signs of pneumonia? Evidence indicated that their use was essential to arrest the dynamic activity of an intrapulmonary bacterial colony in the immunodeficient host, and that the 5-year survival rate of interstitial pneumonia patients would have been worse without the prophylactic practice of the 2 treatments. ii) Evidence was presented to suggest that the activity of the intrapulmonary bacterial colony was becoming less responsive because of the emergence of a drug-resistent mutant bacterium. The introduction of new antibiotics (kanamycin) was found to improve the acute signs of pneumonia. iii) The bone marrow function of one male patient with interstitial pneumonia was found to decline during the observation period of 9 years. It was speculated that his bone marrow, like his lungs, was in the course of fibrosis. iv) One female patient was diagnosed with breast cancer in the course of interstitial pneumonia treatment--an example indicating that the persistence of an autoimmune disease in an elderly subject might be associated with the emergence of malignancy. Dehydroepiandrosterone was shown to promote the recovery of hepatic function in the course of cancer chemotherapy with cyclophosphamide. The beneficial effect of the adrenal androgen was dose-dependent. The significance of this finding is discussed in the light of the steroid carcinogenesis concept. The reasoning behind the view that interstitial pneumonia and chronic fatigue syndrome are one disease is also discussed.
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PMID:Four problems with the clinical control of interstitial pneumonia, or chronic fatigue syndrome, using the megadose vitamin C infusion system with dehydroepiandrosterone-cortisol annex. 1663 32

Fatigue is a common debilitating complication of primary biliary cirrhosis (PBC), the pathophysiologic mechanism of which is poorly understood. Recently, the neuroactive steroid dehydroepinadrosterone sulfate (DHEAS) was reported to be implicated in Chronic Fatigue Syndrome in the absence of liver disease. The present study was undertaken to analyse fatigue scores and their relationship with disease severity and circulating levels of DHEAS as well as its precursors DHEA and pregnenolone in PBC patients with (n=15) or without fatigue (n=10) compared to control subjects (n=11). Fatigue was assessed using the fatigue impact scale (FIS) including cognitive, physical and psychosocial subclasses. Steroids were measured by radioimmunoassay or gas chromatography/mass spectrometry. Plasma concentrations of DHEAS were significantly reduced in PBC patients with fatigue as compared to controls, while those of its precursors DHEA and pregnenolone remained within the control range. Plasma levels of DHEAS in PBC patients were significantly correlated with fatigue severity as reflected by total FIS scores including total (rp=-0.42; p=0.018), as well as the cognitive (rp=-0.37; p=0.03), physical (rp=-0.48; p=0.006) and psychosocial (rp=-0.35; p=0.04) subclasses of fatigue scores. No correlation of fatigue scores was observed with indices of liver function. These findings suggest that reduced levels of the neurosteroid DHEAS may contribute to fatigue in patients with PBC; substitutive therapy using DHEAS or its precursor DHEA could be beneficial in the management of fatigue in patients with low levels of DHEAS.
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PMID:Reduced plasma dehydroepiandrosterone sulfate levels are significantly correlated with fatigue severity in patients with primary biliary cirrhosis. 1766 54

Patients with chronic fatigue syndrome (CFS) frequently associate the disease onset with a period of high physical and/or emotional stress. Alterations in hypothalamic-pituitary adrenal axis (HPA) function have been demonstrated. Although Cortisol production in patients with CFS has proven to be low, Dehydroepiandrosterone (DHEA) production has not been measured. DHEA output may be altered in this population. The purpose of this uncontrolled, prospective, 6 month study of 23 white women, ages 35-55 was to identify CFS patients with suboptimal serum levels of DHEA-sulphate (DHEA-S), defined as DHEA-S <2.0 microg/mL, and to treat those patients with oral DHEA. DHEA-S levels were re-measured after 4-6 weeks of oral DHEA therapy (25 mg). If DHEA-S remained <2.0 microg/ mL, or if no clinical response was achieved after 4-6 weeks of therapy, then an increased dose of DHEA was given. Physical and psychological impairment and disability status were measured by the MHAQII before DHEA intervention and at 3-month intervals. Of initially screened patients with CFS, 76% (116 of 153) were ages 35-55, and 89% (103 of 116) had suboptimal (<2.0 microg/mL) production of DHEA-S.Supplementation with DHEA to CFS patients lead to a significant reduction in the symptoms of CFS: pain (improved by 18%, p = 0.035), fatigue (decreased by 21%, p = 0.009)), activities of daily living (improved by 8.5%, p = 0.058), helplessness (decreased by 11%, p = 0.015), anxiety (decreased by 35%, p < 0.01), thinking (improved by 26%, p < 0.01), memory (improved by 17%, p < 0.05), and sexual problems (improved by 22%, p = 0.06) over the period of the trial. Further study is necessary to determine the safety and efficacy of supplementation of DHEA to this population in a controlled setting.
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PMID:A pilot study employing Dehydroepiandrosterone (DHEA) in the treatment of chronic fatigue syndrome. 1907 57

Fast scan cyclic voltammetry (FSV) with a nanostructured carbon fiber sensor (N-CFS) was developed for direct measurements of the purine metabolite 2,8-dihydroxyadenine (2,8-DHA; i.e. 6-amino-1H-purine-2,8-dione) in endothelial cell supernatants as a marker of cell stress. The 2,8-DHA was measured in the supernatant of aortic (AECs) and pulmonary artery endothelial cells (PAECs), which were maintained in Hank's Balanced Salt solution (HBSS) and exposed to physiological oxygen pressures as well as to oxidative stress, hypoxia (specifically 3% O(2) for AECs) and hyperoxia (20% O(2) for PAECs). Dilution of the supernatants with phosphate buffer in the ratio of 1 : 5 allowed the optimization of FSV measurements with the N-CFS in cell supernatants.The LOD for 2,8-DHA was 1 microM and the LDR was 2-15 microM with the sensitivity of (0.34 +/- 0.01) nA microM(-1) (R(2) = 0.99). The changes in 2,8-DHA concentration when the cells were exposed to stress confirm that PAECs can adapt to stress. However, the results also show that the tolerance of AECs to hypoxia is low. Cellular pathways involved in the response of PAECs and AECs to oxidative stress are outlined.
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PMID:Rapid measurements of 2,8-dihydroxyadenine (2,8-DHA) with a nanostructured electrochemical sensor in 5-fold diluted supernatants of endothelial cells exposed to oxidative stress. 2009 61

Fatigue syndromes exist on a continuum of severity from mild and transient to the disabling chronic fatigue syndrome, with oxidative stress linked to its pathogenesis. A thermolabile gliadin-combined plant superoxide dismutase (SOD) extract has shown potential in clinical trials as a therapeutic antioxidant. This study investigated the effects of 12 weeks of 500 mg/day of a SOD/gliadin supplement on fatigue. Thirty-eight women aged 50-65 years with self-perceived fatigue entered this randomized, double-blind, placebo-controlled trial. The primary outcome measure was general fatigue determined by the Multidimensional Fatigue Inventory (MFI). Secondary outcome measures included other measures of fatigue from the MFI and blood measures of oxidative stress, antioxidant status and hormones. There were no significant (P>0.05) differences between, or within groups, for decreases in general fatigue (active=1.6%, placebo=4.1%). There were no within or between group differences (P>0.05) in other measures of fatigue (physical fatigue, reduced activity, reduced motivation, mental fatigue and total fatigue score). In regard to the biochemical measures, there were non-significant (P>0.05) differences in increases in plasma SOD activity (active=7.1%, placebo=12.2%), plasma GPx activity (active=2.4%, placebo=0.7%), red blood cell GPx activity (active=9.8%, placebo=4.4%). Markers of oxidative stress were decreased but there were no differences (P>0.05) within or between groups; malondialdehyde (active=4.1%, placebo=1.6%), F-2 isoprostanes (active=14.7%, placebo=22.4%). There was a trend (P=0.08) for a decrease in cortisol in the active group (24.6%), however this was not significantly different from the decrease in the placebo participants (4.1%). DHEA differences were not significant (P<0.05) and declined 1.3% in the active group and 14.4% in the placebo group. In summary, the thermolabile SOD/gliadin supplement had no significant effect on self-perceived fatigue, antioxidants, oxidative stress or hormones in women aged 50-65 years.
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PMID:Effects of a gliadin-combined plant superoxide dismutase extract on self-perceived fatigue in women aged 50-65 years. 2104 31