Gene/Protein Disease Symptom Drug Enzyme Compound
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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 use of sustained release tri-iodothyronine (SR-T3) in clinical practice, has gained popularity in the complementary and alternative medical community in the treatment of chronic fatigue with a protocol (WT3) pioneered by Dr. Denis Wilson. The WT3 protocol involves the use of SR-T3 taken orally by the patient every 12 hours according to a cyclic dose schedule determined by patient response. The patient is then weaned once a body temperature of 98.6 degrees F has been maintained for 3 consecutive weeks. The symptoms associated with this protocol have been given the name Wilson's Temperature Syndrome (WTS). There have been clinical studies using T3 in patients who are euthyroid based on normal TSH values. However, this treatment has created a controversy in the conventional medical community, especially with the American Thyroid Association, because it is not based on a measured deficiency of thyroid hormone. However, just as estrogen and progesterone are prescribed to regulate menstrual cycles in patients who have normal serum hormone levels, the WT3 therapy can be used to regulate metabolism despite normal serum thyroid hormone levels. SR-T3 prescription is based exclusively on low body temperature and presentation of symptoms. Decreased T3 function exerts widespread effects throughout the body. It can decrease serotonin and growth hormone levels and increase the number of adrenal hormone receptor sites. These effects may explain some of the symptoms observed in WTS. The dysregulation of neuroendocrine function may begin to explain such symptoms as alpha intrusion into slow wave sleep, decrease in blood flow to the brain, alterations in carbohydrate metabolism, fatigue, myalgia and arthralgia, depression and cognitive dysfunction. Despite all thermoregulatory control mechanisms of the body and the complex metabolic processes involved, WT3 therapy seems a valuable tool to re-establish normal body functions. We report the results of 11 patients who underwent the WT3 protocol for the treatment of CFS. All the patients improved in the five symptoms measured. All patients increased their basal temperature. The recovery time varied from 3 weeks to 12 months.
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PMID:Supraphysiological cyclic dosing of sustained release T3 in order to reset low basal body temperature. 1688 75

Fibromyalgia (FM) and chronic fatigue syndrome (CFS) patients often have memory and cognitive complaints. Objective cognitive testing demonstrates long-term and working memory impairments. In addition, CFS patients have slow information-processing, and FM patients have impaired control of attention, perhaps due to chronic pain. Neuroimaging studies demonstrate cerebral abnormalities and a pattern of increased neural recruitment during cognitive tasks. Future work should focus on the specific neurocognitive systems involved in cognitive dysfunction in each syndrome.
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PMID:Cognitive dysfunction in fibromyalgia and chronic fatigue syndrome: new trends and future directions. 1709 41

Chronic fatigue occurring in previously healthy children and adolescents is a vexing problem encountered by pediatric practitioners and the impact of fatigue in youngsters should not be underestimated. In its severe form, it is often associated with mood disorders. Findings in children and adolescent cases suggest that severe unexplained fatigue might precede the development of fatigue-related illness, such as childhood chronic fatigue syndrome (CCFS). This is a disabling condition characterized by severe disabling fatigue and a combination of symptoms, the prominent features being self-reported impairments in concentration and short-term memory, sleep disturbances and autonomic symptoms that cannot be explained by medical or psychiatric illness. We have encountered such patients with these complaints; their major symptoms include: general fatigue, fever, headache (not migraine), and memory disturbance. From our clinical experience, we have inferred that patients with CCFS might experience changes in brain function levels, which induce an autonomic imbalance and engender symptoms such as general fatigue, higher-order level cognitive dysfunction, and memory disturbance.
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PMID:[School phobia and childhood chronic fatigue syndrome (CCFS)]. 1756 7

Syndromes characterized by pain, fatigue, mood disorder, cognitive dysfunction, and sleep disturbance have been referred to as stress-related somatic disorders by virtue of the observation that onset and exacerbation of symptoms occur with stress. These syndromes include but are not limited to fibromyalgia, chronic fatigue syndrome, temporomandibular disorder, and irritable bowel syndrome. As with most chronic illnesses, genetic susceptibility and lifetime environmental exposures play a role in creating vulnerability to disease. Cumulative lifetime stress has been associated with a number of physiologic changes in the brain and body that reflect dysregulated hormonal and autonomic activity. Exposure to the stressor of violence is likely to create a state of vulnerability for the stress-related somatic syndromes and also to contribute to symptom expression and severity. Understanding the relationship between violence, stress, and somatic syndromes will help in clarifying the consequences of violence exposure to long-term health and health-related quality of life.
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PMID:Violence, stress, and somatic syndromes. 1759 47

Chronic fatigue syndrome (CFS) is a specific clinical condition that characterises unexplained disabling fatigue and a combination of non-specific accompanying symptoms for at least 6 months, in the absence of a medical diagnosis that would otherwise explain the clinical presentation. Other common symptoms include headaches, myalgia, arthralgia, and post-exertional malaise; cognitive difficulties, with impaired memory and concentration; unrefreshing sleep; and mood changes. Similar disorders have been described for at least two centuries and have been differently named neurasthenia, post-viral fatigue, myalgic encephalomyelitis and chronic mononucleosis. Recent longitudinal studies suggest that some people affected by chronic fatigue syndrome improve with time but that most remain functionally impaired for several years. The estimated worldwide prevalence of CFS is 0.4-1% and it affects over 800,000 people in the United States and approximately 240,000 patients in the UK. No physical examination signs are specific to CFS and no diagnostic tests identify this syndrome. The pathophysiological mechanism of CFS is unclear. The main hypotheses include altered central nervous system functioning resulting from an abnormal immune response against a common antigen; a neuroendocrine disturbance; cognitive impairment caused by response to infection or other stimuli in sentient people. The current concept is that CFS pathogenesis is a multifactorial condition. Various studies have sought evidence for a disturbance in immunity in people with CFS. An alteration in cytokine profile, a decreased function of natural killer (NK) cells, a presence of autoantibodies and a reduced responses of T cells to mitogens and other specific antigens have been reported. The observed high level of pro-inflammatory cytokines may explain some of the manifestations such as fatigue and flu-like symptoms and influence NK activity. Abnormal activation of the T lymphocyte subsets and a decrease in antibody-dependent cell-mediated cytotoxicity have been described. An increased number of CD8+ cytotoxic T lymphocytes and CD38 and HLA-DR activation markers have been reported, and a decrease in CD11b expression associated with an increased expression of CD28+ T subsets has been observed. This review discusses the immunological aspects of CFS and offers an immunological hypothesis for the disease processes.
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PMID:Immunological aspects of chronic fatigue syndrome. 1880 65

A subset of patients who present for neuropsychological testing report dysfunction in daily life activities secondary to cognitive deficits, but are found on formal testing to have no objective abnormalities, raising the possibility of "neurocognitive hypochondriasis." Such a case is presented, and the factors that appear to give rise to this presentation are explored. Cases of hypochondriacal overconcern regarding cognitive function are likely not rare, particularly given research showing there is little correlation between objective report of cognitive dysfunction and actual test scores in such conditions as mild traumatic brain injury, chronic fatigue syndrome, fibromyalgia, toxic mold exposure, and post-polio syndrome.
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PMID:Fixed belief in cognitive dysfunction despite normal neuropsychological scores: neurocognitive hypochondriasis? 1892 66

This study assessed the relationship between illness intrusiveness, symptoms, disability and depression in patients with myalgic encephalomyelitis (ME). Participants were 16 patients with ME and eight patients with ME plus co-morbid disorders. The patients with co-morbid disorders reported greater illness intrusiveness than the patients with ME alone, but there were no differences between the groups on the other variables. Significant correlations were found between illness intrusiveness on the one hand, and fatigue, cognitive dysfunction, disability and depression, on the other. We conclude that ME is a disabling illness, which has a major impact on various life domains.
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PMID:Illness intrusiveness in myalgic encephalomyelitis: an exploratory study. 1923 88

This study addresses, among other things, the debate as to whether cognitive deficits do occur with a diagnosis of Chronic Fatigue Syndrome (CFS). Previous studies have indicated a potential mismatch between subjective patient ratings of impairment and clinical assessment. In an attempt to tackle some of the methodological problems faced by previous research in this field, this study recruited a large sample of CFS patients where adequate diagnosis had been made and administered an extensive battery of measures. In doing so this study was able to replicate previous published evidence of clear cognitive impairment in this group and demonstrate also that these deficits occurred independent of psychopathology. The conclusion drawn is that cognitive impairments can be identified if appropriate measures are used. Furthermore, the authors have shown that performance changes in these measures have been used to assess both efficacy of a treatment regime and rates of recovery.
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PMID:An investigation into the cognitive deficits associated with chronic fatigue syndrome. 1945 31

Patients with chronic fatigue syndrome (CFS) are affected by symptoms of cognitive dysfunction and neurological impairment, the cause of which has yet to be elucidated. However, these symptoms are strikingly similar to those of patients presented with D-lactic acidosis. A significant increase of Gram positive facultative anaerobic faecal microorganisms in 108 CFS patients as compared to 177 control subjects (p<0.01) is presented in this report. The viable count of D-lactic acid producing Enterococcus and Streptococcus spp. in the faecal samples from the CFS group (3.5 x 10(7) cfu/L and 9.8 x 10(7) cfu/L respectively) were significantly higher than those for the control group (5.0 x 10(6) cfu/L and 8.9 x 10(4) cfu/L respectively). Analysis of exometabolic profiles of Enterococcus faecalis and Streptococcus sanguinis, representatives of Enterococcus and Streptococcus spp. respectively, by NMR and HPLC showed that these organisms produced significantly more lactic acid (p<0.01) from (13)C-labeled glucose, than the Gram negative Escherichia coli. Further, both E. faecalis and S. sanguinis secrete more D-lactic acid than E. coli. This study suggests a probable link between intestinal colonization of Gram positive facultative anaerobic D-lactic acid bacteria and symptom expressions in a subgroup of patients with CFS. Given the fact that this might explain not only neurocognitive dysfunction in CFS patients but also mitochondrial dysfunction, these findings may have important clinical implications.
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PMID:Increased d-lactic Acid intestinal bacteria in patients with chronic fatigue syndrome. 1956 98

Fibromyalgia is a chronic functional illness that presents with widespread musculoskeletal pain as well as a constellation of symptoms including fatigue, cognitive dysfunction, sleep difficulties, stiffness, anxiety, and depressed mood. The diagnosis of fibromyalgia, similar to other functional disorders, requires that organic diseases are not causing the symptoms. Systemic and rheumatic diseases can be ruled out by a patient history, physical examination, and laboratory investigations. Because there are no specific laboratory tests for fibromyalgia, the 1990 American College of Rheumatology (ACR) classification criteria have been used in clinical settings; however, they are not ideal for individual patient diagnosis. Clinicians should be aware of limitations inherent in using tender points in the diagnosis of fibromyalgia. The multiple symptoms of fibromyalgia often overlap with those of related disorders and may further complicate the diagnosis. One of the most challenging diagnostic dilemmas that clinicians face is distinguishing fibromyalgia from other central pain disorders (e.g., irritable bowel syndrome, chronic fatigue syndrome, migraine). Screening questions based on published criteria can be used as a first approach in diagnosing functional illnesses. Numerous studies report a higher prevalence of psychiatric disorders in patients with fibromyalgia. Therefore, a careful history and evaluation should be taken for the presence of primary mood disturbances. To date, there is no "gold standard" for diagnosing fibromyalgia. Until a better clinical case definition of fibromyalgia exists, all diagnostic criteria should be interpreted with caution, considered rudimentary, and subject to modification.
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PMID:Diagnosis and differential diagnosis of fibromyalgia. 1996 92


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