Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016053 (fibromyalgia)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Considerable knowledge has accumulated in recent decades concerning the significance of physical activity in the treatment of a number of diseases, including diseases that do not primarily manifest as disorders of the locomotive apparatus. In this review we present the evidence for prescribing exercise therapy in the treatment of metabolic syndrome-related disorders (insulin resistance, type 2 diabetes, dyslipidemia, hypertension, obesity), heart and pulmonary diseases (chronic obstructive pulmonary disease, coronary heart disease, chronic heart failure, intermittent claudication), muscle, bone and joint diseases (osteoarthritis, rheumatoid arthritis, osteoporosis, fibromyalgia, chronic fatigue syndrome) and cancer, depression, asthma and type 1 diabetes. For each disease, we review the effect of exercise therapy on disease pathogenesis, on symptoms specific to the diagnosis, on physical fitness or strength and on quality of life. The possible mechanisms of action are briefly examined and the principles for prescribing exercise therapy are discussed, focusing on the type and amount of exercise and possible contraindications.
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PMID:Evidence for prescribing exercise as therapy in chronic disease. 1664 91

Female sexual dysfunction (FSD) is a multifactorial set of conditions associated with multiple anatomical, physiological, biological, medical and psychological factors that can have major impact on self-esteem, quality of life, mood and relationships. Studies indicate that FSD is commonly seen in women who report a low level of satisfaction with partner relationship and in women with male partners who have erectile dysfunction. This complexity of FSD is augmented by the presence of chronic disease. Negative sexual effects are widely reported in studies of women with chronic diseases (such as metabolic syndrome, diabetes mellitus, chronic kidney disease, cancer, spinal cord injury, lupus, rheumatic diseases, Parkinson's disease, fibromyalgia and chronic pain) as compared to a general healthy female population. Physical problems, emotional problems and partnership difficulties arising from disease-related stress contribute to less active and less enjoyable sex life. Chronic pain, fatigue, low self-esteem as well as use of medications might reduce sexual function. These effects of chronic diseases on female sexual function still remain largely unstudied. The study by Manor and Zohar published in this issue of Harefuah draws our attention to the sexual dysfunction of women with breast cancer and examines their needs for information regarding their sexual function. In the absence of definite treatment evidence, psychological counseling, improved vaginal lubrication, low dose of hormonal therapy can be used to relieve FSD. Physicians must consider integrating diagnosis of their female patients' sexual needs and dysfunction, especially women with chronic diseases. Patients' education and counseling may contribute to a better quality of life in spite of their chronic disease.
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PMID:[Female sexual function and chronic disease]. 1650 15

Fibromyalgia is a prevalent syndrome characterized by chronic pain, fatigue, and insomnia. Patients with fibromyalgia commonly have an elevated body mass index and are physically inactive, 2 major risk factors for metabolic syndrome. Yet little is known about the relationship between chronic pain conditions and metabolic disturbances. Our study evaluated the risk for, and neuroendocrine correlates of, metabolic syndrome in this patient population. Women with fibromyalgia (n = 109) were compared with control healthy women (n = 46), all recruited from the community. Metabolic syndrome was identified by using criteria from the Adult Treatment Panel III with glycosylated hemoglobin concentrations substituted for serum glucose. Catecholamine and cortisol levels were determined from 12-hour overnight urine collections. Women with fibromyalgia were 5.56 times more likely than healthy controls to have metabolic syndrome (95% confidence interval, 1.25-24.74). Fibromyalgia was associated with larger waist circumference (P = .04), higher glycosylated hemoglobin (P = .01) and serum triglyceride (P < .001) levels, and higher systolic (P = .003) and diastolic (P = .002) blood pressure. Total and low-density lipoprotein cholesterol were also significantly higher in women with fibromyalgia (P = .001 and .02, respectively), although high-density lipoprotein cholesterol was in the reference range. These associations were not accounted for by age or body mass index. Meeting criteria for more metabolic syndrome components was related to higher urinary norepinephrine (NE)/epinephrine and NE/cortisol ratios (P < .001 and P = .009, respectively). Women with chronic pain from fibromyalgia are at an increased risk for metabolic syndrome, which may be associated with relatively elevated NE levels in conjunction with relatively reduced epinephrine and cortisol secretion.
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PMID:Metabolic syndrome in women with chronic pain. 1716 Dec 30

Recent research has implicated vitamin D deficiency (serum levels of 25-hydroxyvitamin D <50 nmol/L) with a number of chronic conditions, including autoimmune conditions such as multiple sclerosis, lupus, and psoriasis, and chronic conditions such as osteoporosis, osteoarthritis, metabolic syndrome, fibromyalgia and chronic fatigue syndrome. It has been assumed that low levels of 25-hydroxyvitamin D (25-D) accurately indicate vitamin D storage and vitamin D receptor (VDR)-mediated control of calcium metabolism and innate immunity. To evaluate this assumption, 25-D and 1,25-dihydroxyvitamin D3 (1,25-D) levels were measured in 100 Canadian patients with these conditions. Additionally, other inflammatory markers (CK, CRP) were measured. Results showed a strong positive association between these autoimmune conditions and levels of 1,25-D >110 pmol/L. However, there was little association with vitamin D deficiency or the other inflammatory markers, meaning that the results challenge the assumption that serum levels of 25-D are a sensitive measure of the autoimmune disease state. Rather, these findings support the use of 1,25-D as a clinical marker in autoimmune conditions. High levels of 1,25-D may result when dysregulation of the VDR by bacterial ligands prevents the receptor from expressing enzymes necessary to keep 1,25-D in a normal range.
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PMID:Vitamin D metabolites as clinical markers in autoimmune and chronic disease. 1975 77

Strength training (ST) has long been considered a promising intervention for reversing the loss of muscle function and the deterioration of muscle structure associated with advanced age but, until recently, the evidence was insufficient to support its role in the prevention or treatment of disease. In recent decades, there has been a long list of quality reviews examining the effects of ST on functional abilities and a few on risk factors for specific diseases, but none have provided a comprehensive assessment of ST as an intervention for a broad range of diseases. This review provides an overview of research addressing the effectiveness of ST as an intervention for the prevention or treatment of the adverse consequences of (i) aging muscle; (ii) the metabolic syndrome (MetS) and its components, i.e. insulin resistance, abdominal obesity, hyperlipidaemia and hypertension; (iii) fibromyalgia; (iv) rheumatoid arthritis; and (v) Alzheimer's disease. Collectively, these studies indicate that ST may serve as an effective countermeasure to some of the adverse consequences of the MetS, fibromyalgia and rheumatoid arthritis. Evidence in support of the hypothesis that ST reduces insulin resistance or improves insulin action comes both from indirect biomarkers, such as glycosylated haemoglobin (HbA(1c)), and insulin responses to oral glucose tolerance tests, as well as from more direct procedures such as hyperglycaemic and hyperinsulinaemic-euglycaemic clamp techniques. The evidence for the use of ST as a countermeasure of abdominal obesity is less convincing. Although some reports show statistically significant reductions in visceral fat, it is unclear if the magnitude of these changes are physiologically meaningful and if they are independent of dietary influences. The efficacy of ST as an intervention for reducing dyslipidaemia is at best inconsistent, particularly when compared with other pharmacological and non-pharmacological interventions, such as aerobic exercise training. However, there is more consistent evidence for the effectiveness of ST in reducing triglyceride levels. This finding could have clinical significance, given that elevated triglyceride is one of the five criterion measures for the diagnosis of the MetS. Small to moderate reductions in resting and exercise blood pressure have been reported with some indication that this effect may be genotype dependent. ST improves or reverses some of the adverse effects of fibromyalgia and rheumatoid arthritis, particularly pain, inflammation, muscle weakness and fatigue. Investigations are needed to determine how these effects compare with those elicited from aerobic exercise training and/or standard treatments. There is no evidence that ST can reverse any of the major biological or behavioural outcomes of Alzheimer's disease, but there is evidence that the prevalence of this disease is inversely associated with muscle mass and strength. Some indicators of cognitive function may also improve with ST. Thus, ST is an effective countermeasure for some of the adverse effects experienced by patients of many chronic diseases, as discussed in this review.
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PMID:Strength training as a countermeasure to aging muscle and chronic disease. 2142 88

Inflammation has been characterized as a double-edged sword, requiring a balance between health as maintained by regular exercise and activities that would exacerbate inflammatory diseases. The influence of exercise on inflammation is complex and has been widely studied in both healthy patient populations as well as populations of patients with many inflammatory and/or autoimmune rheumatic diseases. Inflammatory markers can be affected by the type of exercise and muscle contraction, as well as the intensity, duration, and consistency of the exercise sessions. Because of these potentially important effects, many members of the general public, as well as some clinicians, believe that exercise could exacerbate symptoms and accelerate the progression of such conditions. The effects of different types of exercise have been studied among patients with inflammatory conditions such as ankylosing spondylitis, systemic lupus erythematosus, rheumatoid arthritis, osteoarthritis, fibromyalgia, and idiopathic inflammatory myopathies, as well as congestive heart failure, type 2 diabetes mellitus, and metabolic syndrome, which are considered low-grade systemic inflammatory diseases. This review will help exercise professionals and clinicians understand the effects of exercise on inflammatory markers, as well as offer effective treatment options and recommendations for patients exercising with rheumatic or inflammatory conditions.
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PMID:Helpful or harmful? Potential effects of exercise on select inflammatory conditions. 2423 1

Vitamin B6 is an essential vitamin needed for many chemical reactions in the human body. It exists as several vitamins forms but pyridoxal 5'-phosphate (PLP) is the phosphorylated form needed for transamination, deamination, and decarboxylation. PLP is important in the production of neurotransmitters, acts as a Schiff base and is essential in the metabolism of homocysteine, a toxic amino acid involved in cardiovascular disease, stroke, thrombotic and Alzheimer's disease. This report announces the connection between a deficit of PLP with a genetically linked physical foot form known as the Morton's foot. Morton's foot has been associated with fibromyalgia/myofascial pain syndrome. Another gene mutation methylenetetrahydrofolate reductase (MTHFr) is now being recognized much commonly than previous with chronic fatigue, chronic Lyme diseases and as "the missing link" in other chronic diseases. PLP deficiency also plays a role in impaired glucose tolerance and may play a much bigger role in the obesity, diabetes, fatty liver and metabolic syndrome. Without the Schiff-base of PLP acting as an electron sink, storing electrons and dispensing them in the mitochondria, free radical damage occurs! The recognition that a phenotypical expression (Morton's foot) of a gene resulting in deficiency of an important cofactor enzyme pyridoxal 5'-phosphate will hopefully alert physicians and nutritionist to these phenomena. Supplementation with PLP, L5-MTHF, B12 and trimethylglycine should be used in those patients with hyperhomocysteinemia and/or MTHFR gene mutation.
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PMID:Morton's foot and pyridoxal 5'-phosphate deficiency: genetically linked traits. 2544 36

Impaired AMPK is associated with a wide spectrum of clinical and pathological conditions, ranging from obesity, altered responses to exercise or metabolic syndrome, to inflammation, disturbed mitochondrial biogenesis and defective response to energy stress. Fibromyalgia (FM) is a world-wide diffused musculoskeletal chronic pain condition that affects up to 5% of the general population and comprises all the above mentioned pathophysiological states. Here, we tested the involvement of AMPK activation in fibroblasts derived from FM patients. AMPK was not phosphorylated in fibroblasts from FM patients and was associated with decreased mitochondrial biogenesis, reduced oxygen consumption, decreased antioxidant enzymes expression levels and mitochondrial dysfunction. However, mtDNA sequencing analysis did not show any important alterations which could justify the mitochondrial defects. AMPK activation in FM fibroblast was impaired in response to moderate oxidative stress. In contrast, AMPK activation by metformin or incubation with serum from caloric restricted mice improved the response to moderate oxidative stress and mitochondrial metabolism in FM fibroblasts. These results suggest that AMPK plays an essential role in FM pathophysiology and could represent the basis for a valuable new therapeutic target/strategy. Furthermore, both metformin and caloric restriction could be an interesting therapeutic approach in FM.
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PMID:Metformin and caloric restriction induce an AMPK-dependent restoration of mitochondrial dysfunction in fibroblasts from Fibromyalgia patients. 2577 83

Fecal microbiota transplantation (FMT) is the infusion of liquid filtrate feces from a healthy donor into the gut of a recipient to cure a specific disease. A fecal suspension can be administered by nasogastric or nasoduodenal tube, colonoscope, enema, or capsule. The high success rate and safety in the short term reported for recurrent Clostridium difficile infection has elevated FMT as an emerging treatment for a wide range of disorders, including Parkinson's disease, fibromyalgia, chronic fatigue syndrome, myoclonus dystopia, multiple sclerosis, obesity, insulin resistance, metabolic syndrome, and autism. There are many unanswered questions regarding FMT, including donor selection and screening, standardized protocols, long-term safety, and regulatory issues. This article reviews the efficacy and safety of FMT used in treating a variety of diseases, methodology, criteria for donor selection and screening, and various concerns regarding FMT.
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PMID:Fecal Microbiota Transplantation: Current Applications, Effectiveness, and Future Perspectives. 2695 93

Epidemiological studies have shown that patients with psoriatic arthritis (PsA) are often affected by numerous comorbidities that carry significant morbidity and mortality. Reported comorbidities include diabetes mellitus, obesity, metabolic syndrome, cardiovascular diseases, osteoporosis, inflammatory bowel disease, autoimmune eye disease, non-alcoholic fatty liver disease, depression, and fibromyalgia. All health care providers for patients with PsA should recognize and monitor those comorbidities, as well as understand their effect on patient management to ensure an optimal clinical outcome.
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PMID:Comorbidities in Patients with Psoriatic Arthritis. 2817 40


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