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)

Primary fibromyalgia (PF) has attracted much interest since the 80's. There are many controversies as to whether it is a true disease or not and many studies are carried on. In this study 32 patients which were accepted as PF were examined for some frequent symptoms and allergy and compared with controls. Migraine, irritable bowel syndrome, sleep disturbance and morning stiffness were investigated and found to be 40.6%, 12.5%, 71.9%, 68.8% respectively. Sleep disturbance and morning stiffness showed a positive correlation. Allergy background of PF patients was found frequently when compared with an age and sex matched control group. Though serum IgE levels were found elevated in PF group, they were not statistically significant. Allergic skin tests which could not be performed in the control group, were positive in 10 of 15 PF patients.
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PMID:Primary fibromyalgia and allergy. 913 33

The main mechanisms of the chronopathological forms of magnesium depletion associate a low Mg intake with various dysregulating biorhythms. The differentiation between forms with hyperfunction and forms with hypofunction of the biological clock is seminal and the main marker is the production of melatonin (MT). The clinical forms of the various patterns of the chronopathological forms of Mg depletion may be central or peripheral. The clinical forms with hyperfunction of the biological clock (marker: increase in MT) may associate diverse expressions of nervous hypoexcitability: depression (i.e. Seasonal affective disease); cephalalgias nocturnal, without photophobia (i.e. cluster headaches); dyssomnia LASPS (advanced sleep phase syndrome) particularly]; asthenia and myalgias (i.e. fibromyalgia, chronic fatigue syndrome). The main comorbidity is found with depressive states. The therapy relies on classical bright light phototherapy, sometimes associated with psychoanaleptics. The clinical forms with hypofunction of biological clock (marker: decrease in MT) may associate various signs of nervous hyperexcitability (HEN): anxiety (from generalized anxiety to panic attacks); cephalalgias diurnal with photophobia (mainly migraine); dyssomnia [DSPS (delayed sleep phase syndrome) particularly, jet lag, night work disorders, age related insomnia, sometimes with inappropriate behaviour; photogenic epilepsia, generalized or focal; some clinical forms of chronic fatigue syndrome and fibromyalgia. The main comorbidity is between migraine and epilepsia. The treatment relies on the diverse forms of darkness therapy, possibly with the help of some psycholeptics: anxiolytics and anticonvulsants. The indications of chromatotherapy remain to be validated.
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PMID:Chronopathological forms of magnesium depletion with hypofunction or with hyperfunction of the biological clock. 1263 82

Sleep disturbance is an important clinical complaint for individuals with nonmalignant pain conditions. This review is a broad introduction to the literature on sleep disturbance and chronic pain conditions. The article critically reviews studies of sleep disturbance in musculoskeletal pain, arthritis, headache, and fibromyalgia. Current neurobiological hypotheses regarding the pathogenesis of sleep disturbance and chronic pain, common comorbid disorders, and pharmacologic and non-pharmacologic treatments for sleep disturbance are reviewed.
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PMID:Sleep disturbance and nonmalignant chronic pain: a comprehensive review of the literature. 1510 4

Asthma is a chronic, inflammatory disorder of the airways leading to airflow limitation. Its worldwide rise, mainly in developed countries, is a matter of concern. Nocturnal asthma (NA) frequently occurs and concerns two thirds of asthmatics. But, it remains controversial whether NA is a distinct entity or is a manifestation of more severe asthma. Generally, it is considered as an exacerbation of the underlying pathology. The pathological mechanisms most likely involve endogenous circadian rhythms with pathological consequences on both respiratory inflammation and hyperresponsiveness. A decrease in blood and tissue magnesium levels is frequently reported in asthma and often testifies to a true magnesium depletion. The link with magnesium status and chronobiology are well established. The quality of magnesium status directly influences the Biological Clock (BC) function, represented by the suprachiasmatic nuclei and the pineal gland. Conversely, BC dysrythmias influence the magnesium status. Two types of magnesium deficits must be clearly distinguished: deficiency corresponding to an insufficient intake which can be corrected through mere nutritional Mg supplementation and depletion due to a dysregulation of the magnesium status which cannot be corrected through nutritional supplementation only, but requires the more or less specific correction of the dysregulation mechanisms. Both in clinical and in animal experiments, the dysregulation mechanisms of magnesium depletion associate a reduced magnesium intake with various types of stress including biological clock dysrhythmias. The differenciation between Mg depletion forms with hyperfunction of BC (HBC) and forms with hypofunction of BC (hBC) is seminal and the main biological marker is melatonin (MT) production alteration. We hypothesize that magnesium depletion with HBC or hBC may be involved in chronopathological forms of asthma. Nocturnal asthma would be linked to HBC, represented by an increase in MT levels. The corresponding clinical forms associate diverse expressions of nervous hypoexcitability such as depression, cluster headaches, dyssomnia, mainly advanced sleep phase syndrome, some clinical forms of chronic fatigue syndrome and of fibromyalgia. The main comorbidities are depression and/or asthenia. They take place during the night or the "bad" seasons (autumn and winter) when sunshine is at a minimum. The corresponding chronopathological therapy relies on bright light phototherapy sometimes with additional psychoanaleptics. Conversely, asthma forms linked to hBC are less frequently studied as a whole and present a decrease in MT levels. They associate various signs of nervous hyperexcitability such as anxiety, diurnal cephalalgia (mainly migraine), dyssomnia, mainly delayed sleep phase syndrome, and some clinical forms of chronic fatigue syndrome and of fibromyalgia. The treatment relies on diverse forms of "darkness therapy", possibly with the help of some psycholeptics. Finally, the treatment of asthma involves the maintenance of a standard dosing schedule of anti-asthma drugs, a balanced magnesium intake and the appropriate treatment of the chronopathological disorders.
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PMID:Magnesium depletion with hypo- or hyper- function of the biological clock may be involved in chronopathological forms of asthma. 1594 13

Sleep disturbance is prevalent in aging and painful rheumatologic populations, but it has largely been a neglected dimension of the routine clinical care of arthritis patients. Pain associated with osteoarthritis (OA) is a leading cause of disability worldwide, and factors that contribute to pain in OA are poorly understood. Sleep disturbance is not only a consequence of pain, it is also likely to play an integral role in pain expression. Emerging research suggests that many patients with OA demonstrate signs of generalized hyperalgesia and faulty central pain modulatory processing similar to other idiopathic pain disorders, such as fibromyalgia. Sleep disruption is increasingly recognized as a direct contributor to both hyperalgesia and impaired endogenous pain modulation. This article reviews the extant literature on sleep disturbance and hyperalgesia in patients with OA. We propose a conceptual working model describing pathways by which sleep disturbance interacts directly with central pain processing mechanisms and inflammatory processes, and indirectly with mood and physical functioning to augment clinical OA pain. The clinical and research implications of the model are discussed.
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PMID:Mechanisms by which sleep disturbance contributes to osteoarthritis pain: a conceptual model. 1988 86