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

Two-hundred and eight patients with chronic fatigue syndrome (post-viral fatigue syndrome) completed a questionnaire which dealt both with their illness in general and with the extent to which they experienced specific symptoms. A factor analysis of the symptom data yielded four components: emotional distress; fatigue; somatic symptoms; and cognitive difficulty. Emotional disturbance is a common feature of the disorder and its role has been widely debated. When the symptom components were considered independently, fatigue, somatic symptoms and cognitive difficulty were associated with questionnaire items relating to general illness severity, but emotional distress was not. Thus negative emotions did not contribute directly to patients' perception of illness severity. They were, however, correlated with the other symptom components. It is argued that this correlation reflects a reciprocal influence, with negative emotions exacerbating fatigue and other key symptoms and the debilitating nature of these symptoms enhancing emotional vulnerability.
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PMID:Illness perception and symptom components in chronic fatigue syndrome. 156 77

Chronic fatigue syndrome is a chronic debilitating illness that is marked in the majority of cases by sudden onset of fatigue and flulike symptoms. Symptoms subsequently relapse and remit and may persist for years. Physical examination typically reveals relatively minor, nonspecific abnormalities in an apparently well patient. Although immunologic abnormalities are associated with chronic fatigue syndrome, tests for these features are expensive, nonspecific, and generally reserved for research purposes. The diagnosis is made on the basis of new onset of severe fatigue, a characteristic pattern of symptoms, and exclusion of other illnesses. Treatment is aimed at alleviating symptoms and helping patients adjust to the debilitating and chronic nature of the illness.
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PMID:Chronic fatigue syndrome. Recent advances in diagnosis and treatment. 157 31

During the past year many studies have been published on fibromyalgia and chronic fatigue syndromes. Randomized clinical trials using current operational diagnostic criteria were reported, but no single therapy has been highly effective in either condition. The working case definition of chronic fatigue syndrome has been criticized and suggestions for a new case definition have been made. Further understanding of the overlap of these three common disorders will also require that uniform diagnostic criteria be tested in chronic fatigue syndrome and myofascial pain syndrome.
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PMID:Fibromyalgia, chronic fatigue, and myofascial pain syndromes. 158 Nov 54

The chronic fatigue syndrome (CFS) is a poorly understood condition with nonspecific signs and symptoms, especially debilitating fatigue. Most patients can pinpoint the onset of their illness and usually describe a flu-like state. The search for an etiologic agent has focused on a number of viruses such as Epstein-Barr, enteroviruses, retroviruses, and human herpesvirus-6. Evidence supports persistent viral infection in a small percentage of CFS patients. Immunologic abnormalities do exist in CFS, which indicate the presence of immune activation in CFS patients. Although abnormal muscle biopsies have been found in some patients with CFS, strength and endurance appear normal, but perception of exertion may be abnormal. Patients with chronic fatigue have a high incidence of premorbid and concurrent psychiatric disorders, and on physical examination many often have reproducible tender points similar to fibromyalgic patients. Clinical evaluation should rule out other potential causes of fatigue, but elaborate diagnostic tests are seldom required. Presently, no specific treatment exists for CFS. A cognitive behavioral approach with or without the use of tricyclics has been advocated. Patients should be encouraged to maintain functional status and should not be discouraged from exercise. Several medications have been tried but with no definite clinical benefit.
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PMID:Chronic fatigue syndrome. 161 43

Chronic fatigue syndrome (CFS), which is characterized by devastating fatigue, mild fever, lymphadenopathy, headache, myalgia, insomnia and neuropsychiatric disorders, now has drawn much attentions from many physicians, researchers and even peoples in general society world wide. The pathogenesis of CFS is still remains to be clarified and clinico-pathological difference between CFS and mood disorder is controversial. In this paper, CFS would be reviewed in detail.
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PMID:[Chronic fatigue syndrome]. 161 75

Myalgic encephalomyelitis (ME) is a postviral syndrome whose dominant clinical features are exercise-induced muscle fatigue, disturbances in cognitive functioning and symptoms of overactivity of the autonomic nervous system. The syndrome tends to affect previously fit young adults between the ages of 20 and 40 but no age group is excluded. One recent epidemiological survey suggested a prevalence rate of 1.3 per 1000 adults, with females outnumbering males by 1.8:1. ME is currently the subject of intense medical (and media) debate, especially over its pathophysiology and management. It has also become known as the postviral/chronic fatigue syndrome (PVFS/CFS).
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PMID:ME: is it a genuine disease? 162 31

Chronic fatigue syndrome (CFS) is an idiopathic disorder in which the chief symptoms is profound fatigue. To explore the relationship between immune stimulation and fatigue, we developed a murine model for quantifying fatigue: reduction in voluntary running and delayed initiation of grooming after swimming. Inoculation of female BALB/c mice with Corynebacterium parvum antigen or the relatively avirulent Me49 strain of Toxoplasma gondii induced fatigue: baseline running reduced to less than 50 and 30% for 8 and 14 days, respectively, and delayed initiation of grooming after swimming in both immunologically stimulated groups. A threefold evaluation of serum transforming growth factor-beta levels, a cytokine increased in CFS patients, was found in fatigued C. parvum- and T. gondii-inoculated mice. This murine model appears promising for investigation of the pathogenesis of immunologically mediated fatigue.
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PMID:Immunologically mediated fatigue: a murine model. 164 46

To clarify the role of Epstein-Barr virus (EBV) infection and the value of EBV antibody testing in evaluating patients with chronic fatigue, we studied 200 consecutive patients with chronic fatigue (mean duration, 9 years). Complete EBV serologic panels were obtained for 154 patients, 35 (23%) of whom met serologic or clinical criteria for chronic or reactivated EBV infection. We compared these patients with chronic EBV infection (CEBV cases) to 35 age- and sex-matched patients who were selected from the same cohort of fatigued patients but who did not meet the criteria (CEBV control subjects). We found few differences between groups in demographic characteristics, clinical features, and symptoms; CEBV cases were more likely to meet criteria for the proposed chronic fatigue syndrome (14% vs 0%), and to report that they suffered from an influenza-like illness at the onset of their fatigue syndrome (34% vs 12%), that they lost their job because of their fatigue (37% vs 11%), and that their fatigue was improved by recreational activity (26% vs 3%). Physical examination and laboratory testing showed few abnormalities in either group. Psychiatric morbidity was common in both groups, including mood disorders (63% of CEBV cases vs 54% of CEBV controls), anxiety (11% vs 9%) and somatization disorder (9% in each group). We conclude that EBV serologic patterns have little clinical usefulness in evaluating patients with chronic fatigue.
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PMID:Antibodies to Epstein-Barr virus in patients with chronic fatigue. 164 95

We have endeavoured to find immunological indications of chronic virus infection in patients with chronic fatigue syndrome (myalgic encephalomyelitis) and to investigate immune responsiveness to viruses in such patients in comparison with normal subjects and patients with muscular dystrophy. Levels of circulating IgM immune complexes were elevated (above the 95% normal control range) in 10 (17%) of 58 patients with chronic fatigue syndrome, which was not significantly different from the normal controls or from dystrophy controls (by Mann Whitney U test). Levels of IgG complexes were only increased in 10% of patients. Lymphocyte proliferation in response to concanavalin A (Con A), assessed by increase in 3H-thymidine incorporation, did not differ between 14 patients and 18 normal subjects. The proliferative response to Coxsackie B virus antigen did not differ between chronic fatigue patients and normal subjects when expressed either as an increase in counts or as a stimulation index. Adjustment of the counts in relation to the proliferation response to Con A, as an indication of the overall proliferative response of the cell preparation, did not reveal any hidden difference. IgM antibodies to Coxsackie B viruses were not found in any of 20 patients and in 1 of 20 dystrophy controls. Significant levels of neutralizing antibodies to Coxsackie B viruses 1-5 were found in 6 out of 19 (32%) patients compared with 4 out of 17 (24%) dystrophy controls, which does not differ from currently expected normal incidence. Antibody titres to other respiratory viruses were also not notably different between the patient and control groups. In conclusion we can find no evidence for a definable viral aetiology for the chronic fatigue syndrome, neither in terms of a persistent infection nor an altered ability to respond to virus.
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PMID:Immune responsiveness in chronic fatigue syndrome. 156 Nov 98

Chronic fatigue syndrome is characterized by persistent or relapsing debilitating fatigue for at least 6 months in the absence of a medical diagnosis that would explain the clinical presentation. Because primary glucocorticoid deficiency states and affective disorders putatively associated with a deficiency of the arousal-producing neuropeptide CRH can be associated with similar symptoms, we report here a study of the functional integrity of the various components of the hypothalamic-pituitary-adrenal axis in patients meeting research case criteria for chronic fatigue syndrome. Thirty patients and 72 normal volunteers were studied. Basal activity of the hypothalamic-pituitary-adrenal axis was estimated by determinations of 24-h urinary free cortisol-excretion, evening basal plasma total and free cortisol concentrations, and the cortisol binding globulin-binding capacity. The adrenal cortex was evaluated indirectly by cortisol responses during ovine CRH (oCRH) stimulation testing and directly by cortisol responses to graded submaximal doses of ACTH. Plasma ACTH and cortisol responses to oCRH were employed as a direct measure of the functional integrity of the pituitary corticotroph cell. Central CRH secretion was assessed by measuring its level in cerebrospinal fluid. Compared to normal subjects, patients demonstrated significantly reduced basal evening glucocorticoid levels (89.0 +/- 8.7 vs. 148.4 +/- 20.3 nmol/L; P less than 0.01) and low 24-h urinary free cortisol excretion (122.7 +/- 8.9 vs. 203.1 +/- 10.7 nmol/24 h; P less than 0.0002), but elevated basal evening ACTH concentrations. There was increased adrenocortical sensitivity to ACTH, but a reduced maximal response [F(3.26, 65.16) = 5.50; P = 0.0015). Patients showed attenuated net integrated ACTH responses to oCRH (128.0 +/- 26.4 vs. 225.4 +/- 34.5 pmol/L.min, P less than 0.04). Cerebrospinal fluid CRH levels in patients were no different from control values (8.4 +/- 0.6 vs. 7.7 +/- 0.5 pmol/L; P = NS). Although we cannot definitively account for the etiology of the mild glucocorticoid deficiency seen in chronic fatigue syndrome patients, the enhanced adrenocortical sensitivity to exogenous ACTH and blunted ACTH responses to oCRH are incompatible with a primary adrenal insufficiency. A pituitary source is also unlikely, since basal evening plasma ACTH concentrations were elevated. Hence, the data are most compatible with a mild central adrenal insufficiency secondary to either a deficiency of CRH or some other central stimulus to the pituitary-adrenal axis. Whether a mild glucocorticoid deficiency or a putative deficiency of an arousal-producing neuropeptide such as CRH is related to the clinical symptomatology of the chronic fatigue syndrome remains to be determined.
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PMID:Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome. 165 82


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