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

Symptoms of fatigue and activity impairment, atypical precordial pain, and cardiac arrhythmia frequently precede by years the development of congestive heart failure. Of 115 patients with these symptoms, 60 were diagnosed as having hypertensive cardiovascular disease, 27 mitral valve prolapse syndrome, and 28 chronic fatigue syndrome. These symptoms are common with diastolic dysfunction, and diastolic function is energy dependent. All patients had blood pressure, clinical status, coenzyme Q10 (CoQ10) blood levels and echocardiographic measurement of diastolic function, systolic function, and myocardial thickness recorded before and after CoQ10 replacement. At control, 63 patients were functional class III and 54 class II; all showed diastolic dysfunction; the mean CoQ10 blood level was 0.855 micrograms/ml; 65%, 15%, and 7% showed significant myocardial hypertrophy, and 87%, 30%, and 11% had elevated blood pressure readings in hypertensive disease, mitral valve prolapse and chronic fatigue syndrome respectively. Except for higher blood pressure levels and more myocardial thickening in the hypertensive patients, there was little difference between the three groups. CoQ10 administration resulted in improvement in all; reduction in high blood pressure in 80%, and improvement in diastolic function in all patients with follow-up echocardiograms to date; a reduction in myocardial thickness in 53% of hypertensives and 36% of the combined prolapse and fatigue syndrome groups; and a reduced fractional shortening in those high at control and an increase in those initially low.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Isolated diastolic dysfunction of the myocardium and its response to CoQ10 treatment. 824 99

A prospective randomized study was conducted to determine the optimal schedule of rhG-CSF (recombinant human granulocyte colony-stimulating factor). A group of 33 lung cancer patients treated with MVP therapy (mitomycin, vindesine, and cisplatin) were randomly assigned to three groups: an early prophylaxis group in which rhG-CSF was initiated on day 2 of the MVP cycle; a late prophylaxis group in which rhG-CSF was initiated on day 8; and a therapeutic group in which rhG-CFS was initiated after the onset of neutropenia. Ten patients who had received MVP therapy without rhG-CSF were also analyzed as a no-support group. The incidence of neutropenia was 80% (16/20 courses) in the early prophylaxis group, 44% (8/18) in the late prophylaxis group, 94% (17/18) in the therapeutic group, and 94% (16/17) in the no-support group. The incidence of neutropenia in the late prophylaxis group was less than in the early prophylaxis group (P<0.05), the therapeutic group (P<0.01), and the no-support group (P<0.01). The late prophylactic rhG-CSF schedule was therefore more effective in countering neutropenia than either the early prophylactic or therapeutic schedule.
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PMID:Optimal schedule for administering granulocyte colony-stimulating factor in chemotherapy-induced neutropenia in non-small-cell lung cancer. 860 58

Patients reporting sensitivity to multiple chemicals at levels usually tolerated by the healthy population were administered standardized questionnaires to evaluate their symptoms and the exposures that aggravated these symptoms. Many patients were referred for medical tests. It is thought that patients with chemical sensitivity have organ abnormalities involving the liver, nervous system (brain, including limbic, peripheral, autonomic), immune system, and porphyrin metabolism, probably reflecting chemical injury to these systems. Laboratory results are not consistent with a psychologic origin of chemical sensitivity. Substantial overlap between chemical sensitivity, fibromyalgia, and chronic fatigue syndrome exists: the latter two conditions often involve chemical sensitivity and may even be the same disorder. Other disorders commonly seen in chemical sensitivity patients include headache (often migraine), chronic fatigue, musculoskeletal aching, chronic respiratory inflammation (rhinitis, sinusitis, laryngitis, asthma), attention deficit, and hyperactivity (affected younger children). Less common disorders include tremor, seizures, and mitral valve prolapse. Patients with these overlapping disorders should be evaluated for chemical sensitivity and excluded from control groups in future research. Agents whose exposures are associated with symptoms and suspected of causing onset of chemical sensitivity with chronic illness include gasoline, kerosene, natural gas, pesticides (especially chlordane and chlorpyrifos), solvents, new carpet and other renovation materials, adhesives/glues, fiberglass, carbonless copy paper, fabric softener, formaldehyde and glutaraldehyde, carpet shampoos (lauryl sulfate) and other cleaning agents, isocyanates, combustion products (poorly vented gas heaters, overheated batteries), and medications (dinitrochlorobenzene for warts, intranasally packed neosynephrine, prolonged antibiotics, and general anesthesia with petrochemicals). Multiple mechanisms of chemical injury that magnify response to exposures in chemically sensitive patients can include neurogenic inflammation (respiratory, gastrointestinal, genitourinary), kindling and time-dependent sensitization (neurologic), impaired porphyrin metabolism (multiple organs), and immune activation.
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PMID:Profile of patients with chemical injury and sensitivity. 916 75

The nervous form of magnesium imbalance represents the best documented experimental and clinical aspects of magnesium disorders. The nervous form of primary magnesium deficit (MD) in the adult appears as the best descriptive model for analysis of the symptomatology, aetiology, physiopathology, diagnosis and therapy of the most frequent form of MD. Nervous hyperexcitability due to chronic MD in the adult results in a non-specific clinical pattern with associated central and peripheral neuromuscular symptoms, analogous to the symptomatology previously described in medical literature as latent tetany, hyperventilation syndrome, spasmophilia, chronic fatigue syndrome, neurocirculatory asthenia and idiopathic Barlow's disease. On encountering this non-specific pattern, the signs of neuromuscular hyperexcitability are of much greater importance. Trousseau's sign is less sensitive than Chvostek's sign, but their sensitivities are increased by hyperventilation (Von Bondsdorff's test). Examination of the precordial area will be conducted in order to search clinical stigmata of mitral valve prolapse (MVP) which is a frequent dyskinesia due to chronic MD (about a quarter to one-third of cases). The electromyogram (EMG) shows one (or several) trains of autorhythmic activities beating for more than 2 min of one of the three tetanic activities (uniplets, multiplets or 'complex tonicoclonic tracings') during one of the three facilitation procedures: tourniquet-induced ischaemia lasting 10 min. post-ischaemia lasting 10 min after the removal of the tourniquet and hyperventilation over 5 min. A repetitive EMG constitutes the principal mark of nervous hyperexcitability (NHE) due to MD. The echocardiogram (ECC) is the best tool for detecting MVP, the 2-dimensional ECC with pulsed Doppler being more accurate than time-motion ECC. The routine ionic investigations comprise five static tests: plasma and erythrocyte magnesium, plasma calcium and daily magnesiuria and calciuria. An evaluation of magnesium intake is desirable. Normal concentrations of magnesium in blood do not rule out the diagnosis of the nervous form of primary chronic MD. The histograms of MD group reveal Gaussian type magnesaemias with significantly lower means and the constituent elements can be individually hypo- (one-third of cases), normo- (about two-thirds of cases) and even, exceptionally, hyper-magnesaemic. The diagnosis of MD requires an oral magnesium load test. At physiological dose (5 mg of Mg/kg/day), oral magnesium is totally devoid of the pharmacological effects of parenteral magnesium. Corrections of symptomatology by this oral physiological magnesium load is the best proof that it was due to magnesium deficiency. In particular clinical forms, more sophisticated studies may be useful: standard and quantitative electroencephalograms, electropolygraphic studies of afternoon sleep, electronystagmography, optokinetic test, skin conductance reflex, psychometric inventories, standard or monitoring electrocardiogram, treadmill test, other static and dynamic investigations: e.g. ionized free Mg2+, lymphocyte Mg, brain Mg, cerebrospinal Mg, Mg balance, Mg parenteral load test, glucose load, and even radio-isotope study, the only one able to reveal intestinal magnesium hypersecretion. Nervous primary chronic MD progresses by phases of decompensation against a background of latency. Marginal magnesium deficiency, that is to say an insufficient magnesium intake which merely requires simple oral physiological supplementation, is fundamental in the aetiology of primary magnesium deficit. However a constitutional homeostatic lability of the nervous system or of magnesium metabolism such as belonging to the B35 type of HLA group must be involved. Part of the aetiology of this magnesium deficit is a magnesium depletion, where the disorder which induces magnesium deficit is related to a dysregulation of the control mechanisms of magnesium status which requires a more or less difficult
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PMID:Neurotic, neuromuscular and autonomic nervous form of magnesium imbalance. 936 38