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 evidence has accrued in the last two decades to support the hypothesis that alterations in serotonergic neuronal function in the central nervous system occur in patients with major depression. These findings include the following: (a) reduced cerebrospinal fluid (CSF) concentrations of 5-hydroxyindoleacetic acid (5-HIAA), the major metabolite of serotonin (5-HT) in drug-free depressed patients; (b) reduced concentrations of 5-HT and 5-HIAA in postmortem brain tissue of depressed and (or) suicidal patients; (c) decreased plasma tryptophan concentrations in depressed patients and a profound relapse in remitted depressed patients who have responded to a serotonergic antidepressant when brain tryptophan availability is reduced; (d) in general, all clinically efficacious antidepressants augment 5-HT neurotransmission following chronic treatment; (e) clinically efficacious antidepressant action by all inhibitors of 5-HT uptake; (f) increases in the density of 5-HT2 binding sites in postmortem brain tissue of depressed patients and suicide victims, as well as in platelets of drug-free depressed patients; (g) decreased number of 5-HT transporter (determined with [3H]imipramine or [3H]paroxetine) binding sites in postmortem brain tissue of suicide victims and depressed patients and in platelets of drug-free depressed patients. In our studies, this reduction in platelet 5-HT transporter binding is not due to prior antidepressant treatment of hypercortisolemia and is not observed in mania, Alzheimer disease, schizophrenia, panic disorder, fibromyalgia, or atypical depression. In a pilot study, this deficit predicted treatment response to an experimental antidepressant. These findings support the hypothesis that alterations in 5-HT neurons play a role in the pathophysiology of depression.
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PMID:Role of serotonin in the pathophysiology of depression: focus on the serotonin transporter. 1949 50

Erythrocyte transketolase activity coefficient (ETK-AC) and affinity for coenzyme (Km TPP) were assessed in 50 patients with transketolase abnormalities such as fibromyalgia or senile dementia of Alzheimer's type, before and after magnesium (Mg), thiamin+pyridoxine (B1,B6), high energy phosphates (HEP) (phosphocreatinine of adenosine triphosphate), and piracetam. Compared to 12 untreated patients, ETK-AC was significantly decreased with B1,B6 (P < 0.05, n = 10); Km-TPP was significantly decreased with HEP (P < 0.05, n = 20) and piracetam (P < 0.01, n = 5). In nine other patients treated with HEP + B1,B6 + magnesium, ETK-AC and Km TPP were both significantly decreased.
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PMID:Effects of magnesium, high energy phosphates, piracetam and thiamin on erythrocyte transketolase. 805 63

Studies have found that people with HIV have significant reductions in S-adenosylmethionine (SAMe). SAMe is an important ingredient in reactions used to make a substance that holds myelin, the coating on nerve fibers, together. SAMe also has been shown to have value in treating fibromyalgia and Alzheimer's disease. The drug may have potential use in fighting liver disease as well by increasing glutathione production and reducing the symptoms of cholestasis. Methionine, a substance made into SAMe by the body, might help improve HIV-related myelopathy. A study is currently enrolling patients with HIV to evaluate methionine's effectiveness in treating myelopathy. Side effects of methionine include nausea, vomiting, drowsiness, and irritability. Contact information is provided.
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PMID:SAMe as it ever was? 1136 83

Substance P (SP) is a neuropeptide which is widely distributed in the periphery and the central nervous system (CNS), where it is co-localised with other neurotransmitters such as serotonin or dopamine and where it acts as a neuromodulator. SP has been proposed to play a role in the aetiopathology of asthma, inflammatory bowel disease, emesis, psoriasis, as well as neuropsychiatric disorders including pain syndromes (e.g. migraine and fibromyalgia) and affective disorders, anxiety disorders, schizophrenia and Alzheimer's disease. This review focuses on the role of SP in the pathogenesis of affective disorders. It summarises the current knowledge on measurements of SP in the CSF and serum in patients with depressive disorders or fibromyalgia, effects of SP-application in humans, SP-receptor expression in postmortem brains and the modulation of SP levels in the course of antidepressant treatment. It also discusses the promise of substance P-receptor antagonists (SPA) for the treatment of affective disorders and their proposed mechanism of action. In summary, much more research is needed to elucidate the role of SP in the pathogenesis of depression. SPA are promising as future drugs for the treatment of affective disorders, but current clinical trials have yet to be completed to draw a firm conclusion. Key words: substance P, neurokinin1-receptor, affective disorders, depression, review.
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PMID:Substance P and Substance P receptor antagonists in the pathogenesis and treatment of affective disorders. 1269 75

Quality of life is an important indicator in assessing the burden of disease, especially for chronic conditions. The Health Utilities Index (HUI) is a recently developed system for measuring the overall health status and health-related quality of life (HRQL) of individuals, clinical groups, and general populations. Using the HUI (constructed based on eight attributes: vision, hearing, speech, mobility, dexterity, cognition, emotion, and pain/discomfort) to measure the HRQL for chronic disease patients and to detect possible associations between HUI system and various chronic conditions, this study provides information to improve the management of chronic diseases. This study is of interest to data analysts, policy makers, and public health practitioners involved in descriptive clinical studies, clinical trials, program evaluation, population health planning, and assessments. Based on the Canadian Community Health Survey (CCHS) for 2000-01, the HUI was used to measure the quality of life for individuals living with various chronic conditions (Alzheimer/other dementia, effects of stroke, urinary incontinence, arthritis/rheumatism, bowel disorder, cataracts, back problems, stomach/intestinal ulcers, emphysema/COPD, chronic bronchitis, epilepsy, heart disease, diabetes, migraine headaches, glaucoma, asthma, fibromyalgia, cancers, high blood pressure, multiple sclerosis, thyroid condition, and other remaining chronic diseases). Logistic Regression Model was employed to estimate the associations between the overall HUI scores and various chronic conditions. The HUI scores ranged from 0.00 (corresponding to a state close to death) to 1.00 (corresponding to perfect health); negative scores reflect health states considered worse than death. The mean HUI score by sex and age group indicated the typical quality of life for persons with various chronic conditions. Logistic Regression results showed a strong relationship between low HUI scores (< or = 0.5 and 0.06-1.0) and certain chronic conditions. Age- and sex-adjusted Odds Ratio (OR) and p values showed an effect among individuals diagnosed with each chronic disease on the overall HUI score. Results of this study showed that arthritis/rheumatism, heart disease, high blood pressure, cataracts, and diabetes had a severe impact on HRQL. Urinary incontinence, Alzheimer/other dementia, effects of stroke, cancers, thyroid condition, and back problems have a moderate impact. Food allergy, allergy other than food, asthma, migraine headaches, and other remaining chronic diseases have a relatively mild effect. It is concluded that major chronic diseases with significant health burden were associated with poor HRQL. The HUI scores facilitate the measurement and interpretation of results of health burden and the HRQL for individuals with chronic diseases and can be useful for development of strategies for the prevention and control of chronic diseases.
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PMID:Using Health Utility Index (HUI) for measuring the impact on health-related quality of Life (HRQL) among individuals with chronic diseases. 1534 14

Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health, disease, and aging. A wide range of seemingly unrelated disorders, such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis, have underlying pathophysiological mechanisms in common, namely reactive oxygen species (ROS) production, the accumulation of mitochondrial DNA (mtDNA) damage, resulting in mitochondrial dysfunction. Antioxidant therapies hold promise for improving mitochondrial performance. Physicians seeking systematic treatments for their patients might consider testing urinary organic acids to determine how best to treat them. If in the next 50 years advances in mitochondrial treatments match the immense increase in knowledge about mitochondrial function that has occurred in the last 50 years, mitochondrial diseases and dysfunction will largely be a medical triumph.
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PMID:Mitochondrial dysfunction and molecular pathways of disease. 1723 70

Deficits in cognitive function may impact one's ability to attend to stimuli, think clearly, reason, and remember. Impaired cognitive function is a common complaint among older women presenting for treatment in both mental health and medical care settings, and differential diagnosis of type and extent of cognitive impairment is important for appropriate treatment planning and prognosis. Although overall gender differences in prevalence of cognitive dysfunction are minimal, it is important when treating older women to take into account unique challenges they face in the aging process that impact the cause, type and extent of cognitive complaints with which they present in clinical settings. The current paper provides an overview to guide accurate diagnosis, particularly in women, of different types of cognitive impairment under the broad category of dementias, including Alzheimer's, Lewy Body Disease, Vascular Dementia, and due to general medical conditions such as coronary artery bypass surgery, head injury, menopause, hypothyroidism, breast cancer treatment, Fibromyalgia, and chronic fatigue. In addition, emotional factors such as depression in older female patients complicate differential diagnosis of cognitive impairment and must be addressed. Given the multiplicity of causes of cognitive difficulties for women across the life span, careful assessment is crucial; the current paper reviews assessment strategies to prepare an integrated, biopsychosocial strategy for identifying particular cognitive deficits and related psychological and medical problems. In addition, prognostic indicators and treatment planning are discussed to help the practitioner organize an empathic, reasoned and multifaceted treatment approach to maximize recovery, minimize deterioration, and manage symptoms for older women in the context of their social support system and living environment.
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PMID:Cognitive functioning and aging in women. 1758 77

Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health and disease. Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis. Medications have now emerged as a major cause of mitochondrial damage, which may explain many adverse effects. All classes of psychotropic drugs have been documented to damage mitochondria, as have stain medications, analgesics such as acetaminophen, and many others. While targeted nutrient therapies using antioxidants or their precursors (e. g., N-acetylcysteine) hold promise for improving mitochondrial function, there are large gaps in our knowledge. The most rational approach is to understand the mechanisms underlying mitochondrial damage for specific medications and attempt to counteract their deleterious effects with nutritional therapies. This article reviews our basic understanding of how mitochondria function and how medications damage mitochondria to create their occasionally fatal adverse effects.
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PMID:Medication-induced mitochondrial damage and disease. 1862 87

Although evidence shows that several dopamine neurotransmission pathway genes are associated with specific clinical pain syndromes, such as fibromyalgia, chronic headache, and postoperative pain, the exact role of dopamine in pain processing is not fully understood. The aim of this study was to explore the relationship between functional polymorphisms in dopaminergic candidate genes and sensitivity to pain in healthy subjects. Healthy subjects (n=192; 105 F, 87 M) were exposed to experimental tonic cold pain (1 degrees C) and phasic heat pain (47 degrees C) stimuli. DNA samples were obtained from both participants and their parents. The relationships between pain response (intensity in response to heat and cold; threshold and tolerance in response to cold only) and the functional Variable Number of Tandem Repeat (VNTR) polymorphisms of three dopamine-related genes were investigated using a Transmission Disequilibrium Test (TDT). Specifically, 30-bp repeat in the promoter region of the monoamine oxidase-A gene (MAO-A), 40-bp repeat in the 3'-untranslated region of the dopamine transporter gene (DAT-1), and 48-bp repeat in the exon 3 of the dopamine receptor 4 gene (DRD4) were examined. Significant associations between cold pain tolerance and DAT-1 (p=0.008) and MAO-A (p=0.024) polymorphisms were found. Specifically, tolerance was shorter for carriers of allele 10 and the rarer allele 11, as compared to homozygous for allele 9, and for carriers of allele 4 as compared to homozygous for allele 3, respectively. These results, together with the known function of the investigated candidate gene polymorphisms, suggest that low dopaminergic activity can be associated with high pain sensitivity and vice versa.
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PMID:Associations between polymorphisms in dopamine neurotransmitter pathway genes and pain response in healthy humans. 1979 78

During the last 20 years, numerous clinical trials have examined the therapeutic usefulness of melatonin in different fields of medicine. The objective of this article is to review, in depth, the science regarding clinical trials performed to date. The efficacy of melatonin has been assessed as a treatment of ocular diseases, blood diseases, gastrointestinal tract diseases, cardiovascular diseases, diabetes, rheumatoid arthritis, fibromyalgia, chronic fatigue syndrome, infectious diseases, neurological diseases, sleep disturbances, aging and depression. Melatonin has been also used as a complementary treatment in anaesthesia, hemodialysis, in vitro fertilization and neonatal care. The conclusion of the current review is that the use of melatonin as an adjuvant therapy seems to be well funded for macular degeneration, glaucoma, protection of the gastric mucosa, irritable bowel syndrome, arterial hypertension, diabetes, side effects of chemotherapy and radiation in cancer patients or hemodialysis in patients with renal insufficiency and, especially, for sleep disorders of circadian etiology (jet lag, delayed sleep phase syndrome, sleep deterioration associated with aging, etc.) as well as in those related with neurological degenerative diseases (Alzheimer, etc.,) or Smith-Magenis syndrome. The utility of melatonin in anesthetic procedures has been also confirmed. More clinical studies are required to clarify whether, as the preliminary data suggest, melatonin is useful for treatment of fibromyalgia, chronic fatigue syndrome, infectious diseases, neoplasias or neonatal care. Preliminary data regarding the utility of melatonin in the treatment of ulcerative colitis, Crohn's disease, rheumatoid arthritis are either ambiguous or negative. Although in a few cases melatonin seems to aggravate some conditions, the vast majority of studies document the very low toxicity of melatonin over a wide range of doses.
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PMID:Clinical uses of melatonin: evaluation of human trials. 2042 9


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