Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Respiratory muscle strength (RMS) and endurance are often preserved in cystic fibrosis (CF) despite malnutrition, chronic airflow limitation, and hyperinflation. Inspiratory muscle function may be relatively preserved due to a selective "training stimulus" from chronic lung disease. Respiratory and peripheral muscle function were evaluated in 14 stable CF patients and 16 healthy control subjects. RMS was measured using static maximal pressures performed at FRC. Respiratory fatigue (RF) was assessed using 18 repeated static efforts (10 s on/5 s off) over 4.5 min. Peripheral function was evaluated by leg strength (LS) and leg fatigue (LF) measured during sprint efforts on an isokinetic cycle ergometer. Despite a lower weight (mean +/- SD, 94 +/- 9.6% ideal wt for CF patients versus 107 +/- 14.6% for controls) and elevated residual volume (RV)/TLC ratio (38 +/- 13.0 versus 22 +/- 5.3), the CF group maintained RMS (inspiratory 96 +/- 23.2 versus 114 +/- 33.2; expiratory 105 +/- 28.3 versus 123 +/- 40.9 cm H2O) but had decreased LS (590 +/- 201.7 versus 813 +/- 167.1 W). There were no differences between the groups with respect to RF or LF. For the control group, inspiratory and expiratory RMS correlated with LS (p < 0.01) and lean body mass (p < 0.01). For the CF group, while expiratory RMS (p < 0.05) and LS (p < 0.01) correlated with lean body mass and each other (p < 0.01), inspiratory RMS was independent of lean body mass and LS (p > 0.1). Female CF patients appeared to have a better preservation of inspiratory RMS than males with CF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Respiratory and peripheral muscle function in cystic fibrosis. 846 21

A 23 year old female presented with fatigue, Raynaud's syndrome, symmetric polyarthritis, lymphocytopenia, hypocomplementemia, IgG elevation, and antinuclear antibodies with anti-U1RNP specificity. A diagnosis of systemic lupus erythematosus (SLE) was made. Disseminated micronodular infiltration in the chest X-ray, a pattern of lymphocytic alveolitis by bronchoalveolar lavage, histologic demonstration of non-caseating epitheloid microgranulomas, and rapid reversal of lung disease upon low-dose methylprednisolone treatment led to a diagnosis of concomitant sarcoidosis. Clues to the diagnosis of sarcoidosis coexisting with SLE are discussed.
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PMID:Pulmonary sarcoidosis coexisting with systemic lupus erythematosus. 861 66

Reactive oxygen species, including free radicals, are produced through a number of biochemical reactions, often as a consequence of aerobic metabolism. A system of antioxidant enzymes and scavenger substrates provides protection of membrane lipids, proteins, and DNA. An imbalance between production of reactive oxygen species and antioxidant protection results in "oxidative stress." Oxidative stress is believed to contribute to numerous pathological conditions including atherosclerosis, obstructive lung disease, aging, and fatigue of skeletal muscles including the diaphragm. Strenuous exercise, inflammation, infection, obstructive lung diseases, etc. increase exposure of the diaphragm to reactive oxygen species. Emerging data indicate that reactive oxygen species alter diaphragm contractions primarily in response to low-frequency stimulation. The response of the diaphragm is profoundly influenced by the degree of oxidative stress, fatigue state, glutathione status, and age. Exercise training results in an upregulation of antioxidant enzyme activities in the diaphragm and thus could provide additional protection against oxidative stress.
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PMID:Oxidative stress, antioxidant status, and the contracting diaphragm. 949 38

It is now recognized that respiratory muscle fatigue contributes to the development of respiratory failure in some patients with lung disease. This observation has prompted an examination into the mechanisms of development of muscle fatigue, with the understanding that an elucidation of these processes may lead to new therapeutic approaches to the treatment of these patients. A series of recent studies examining this issue have, moreover, discovered that oxygen-derived free radicals generated during strenuous contraction may modulate respiratory muscle contractile function and contribute to the development of muscle fatigue. The data supporting this concept include: (a) direct (e.g. EPR, ESR studies) and indirect (evidence of lipid peroxidation, protein carbonyl formation, glutathione oxidation) evidence that there is heightened free radical production in contracting muscle, (b) evidence that pharmacologic depletion of muscle antioxidant stores increases degree of muscle fatigue present after a period of exercise, and (c) evidence that administration of agents that act as free radical scavengers retard the development muscle fatigue. Free radicals may produce these changes in muscle force generating capacity by interacting with and altering the function of a number of intracellular-biophysical processes (i.e. sarcolemmal action potential propagation, sarcoplasmic reticulum calcium handling, mitochondrial function, contractile protein interactions).
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PMID:Free radical induced respiratory muscle dysfunction. 954 53

Pulmonary mycotoxicosis (PM), also termed organic dust toxic syndrome or silo unloader's syndrome, is an acute illness resulting from massive inhalation of microbial toxins in organic dusts. It has not been well described histologically. Three cases of PM are presented in this report. Open lung biopsies were examined in each case. All of the patients were farmers with no prior lung disease. One had burning in his eyes, throat, and chest after exposure to moldy silage; chills, fever, dry cough, malaise, and weakness developed within 24 hours. Two patients presented with fever, progressive dyspnea, cough, and fatigue within 24 hours of emptying a corncrib, cleaning a chicken coop, and baling hay. Bilateral alveolar and interstitial infiltrates on chest roentgenograms and leukocytosis with neutrophilia were observed in all of the three patients. Two patients became hypoxemic and required mechanical ventilation. Histologic examination showed acute and organizing diffuse alveolar damage in two biopsy specimens and an acute bronchopneumonia in the third. One specimen had 1- to 10-microm ovoid organisms demonstrable with methenamine silver stains; cultures grew Fusarium and Penicillium species. The other two biopsy specimens had negative tissue cultures and special stains for organisms, although Penicillium species were grown from a preoperative bronchoalveolar lavage in one case. The two patients on mechanical ventilation recovered completely with high-dose steroids. The third patient recovered without steroids. No patient had residual functional deficits or chest radiographic abnormalities. PM can be distinguished from allergic and infectious diseases common in individuals exposed to large amounts of organic dust by its clinicopathologic features.
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PMID:Pulmonary mycotoxicosis: a clinicopathologic study of three cases. 961 95

Acute bronchiolitis is the commonest lower respiratory illness of infancy and early childhood, and it is usually associated with respiratory syncytial virus infection. In the majority of infants, the illness is self-limiting and hence management is directed at maintaining fluid intake, minimal handling and close observation. Children who develop apnoea, fatigue and/or feeding difficulties as well as progressive respiratory distress require hospital admission. Oxygen, intravenous fluids and minimal handling are the pillars of hospital management, and less than 1% of hospitalised infants require additional assisted ventilation. Pharmacological therapy of acute bronchiolitis is contentious. Sympathomimetics are the drugs most frequently used. Inhaled salbutamol (albuterol) has been associated with both positive and negative outcomes. Recent work suggests that nebulised racemic adrenaline (epinephrine) may be helpful in reducing respiratory distress, but further work is needed to confirm this finding. The use of the antiviral drug ribavirin (tribavirin) in acute bronchiolitis remains very contentious. The overwhelming majority of infants do not require the drug and debate remains as to its true effectiveness. The literature tends to support its use in patients with underlying heart or lung disease, but the drug may not be cost effective in this setting. However, the costs of ribavirin therapy could be reduced by the implementation of more rigid treatment guidelines. A reduction in the use of bronchodilators, antibiotics and corticosteroids would help to reduce the overall costs of management. To date, acute bronchiolitis has not lent itself to pharmacological treatment and prescribing should therefore be very strictly audited by clinicians.
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PMID:Rational prescribing for acute bronchiolitis. 1015 5

Dexamethasone is commonly administered to ventilator-dependent preterm infants with chronic lung disease. Infants receiving dexamethasone therapy frequently exhibit decreased rates of weight gain. The purpose of this investigation was to determine whether decreased growth in infants receiving dexamethasone therapy is caused by increased energy expenditure. Twelve infants were studied: 6 received dexamethasone treatment at 2 wk of age and crossed over to receive placebo treatment at 4 wk; the treatment order was reversed in the other 6 infants. The doubly labeled water method was used to determine energy expenditure for a 1-wk period during each treatment phase. The rate of weight gain during dexamethasone treatment was 6.5+/-10.6 and 20.0+/-5.7 g/kg/d during placebo treatment. Energy expenditure was 93.1+/-34.6 kcal/kg/d during dexamethasone treatment and 88.3+/-37.1 kcal/kg/d during placebo treatment. Energy intake was 119.2+/-29.0 kcal/kg/d during dexamethasone treatment and 113.8+/-23.7 kcal/kg/d during placebo treatment. The difference between intake and expenditure, or the energy available for growth, was 26.2+/-36.8 kcal/kg/d during dexamethasone treatment and 25.5+/-37.4 kcal/kg/d during placebo treatment. No significant differences were found in energy expenditure or energy intake between the treatment phases. The reduced growth seen in infants receiving dexamethasone treatment cannot be explained by increased energy expenditure or decreased energy intake, but may be due to differences in the composition of newly accreted tissue.
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PMID:Energy expenditure and energy intake during dexamethasone therapy for chronic lung disease. 1040 Jan 43

Patients with COPD have derangements in respiratory mechanics that may cause them to stop exercising before the exercising limb muscles reach their functional limits. However, because lung disease makes activity unpleasant, patients with chronic obstructive pulmonary disease (COPD) often adapt a sedentary lifestyle leading to progressive deconditioning. Deconditioning will lead to progressive deterioration in limb muscle function, which could adversely affect exercise capacity. The purpose of this study was to determine whether fatigue of the quadriceps muscle occurs after high intensity cycle exercise to the limits of tolerance in patients with moderate to severe COPD. Nineteen male patients with COPD (FEV(1) 1.54 +/- 0. 12 L; 42 +/- 3% predicted) exercised at 60 to 70% of their predetermined maximal work capacity until exhaustion. The femoral nerve was supramaximally stimulated with a figure-of-eight magnetic coil, and quadriceps twitch force (TwQ) was measured before and at 10, 30, and 60 min postexercise. Patients exercised at 53.7 +/- 4.1 watts for 10.4 +/- 1.4 min. Peak V O(2) was 1.24 +/- 0.08 L/min (51. 3 +/- 3.6% predicted). TwQ fell significantly postexercise; 79.2 +/- 5.4% of baseline value at 10 min postexercise (p < 0.005), 75.7 +/- 4.8% at 30 min postexercise (p < 0.001), and 84.0 +/- 5.0% at 60 min postexercise (p < 0.005). Acceptable M-waves from the quadriceps muscle (not obscured by stimulus artifact) were obtained in six subjects. M-wave amplitude was unchanged from baseline at all times postexercise indicating that the fall in TwQ was due to contractile fatigue and not to transmission failure. In conclusion, contractile fatigue of the quadriceps muscle occurs after high intensity cycle exercise to the limits of tolerance in patients with COPD.
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PMID:Quadriceps fatigue after cycle exercise in patients with chronic obstructive pulmonary disease. 1067 84

Complaints of poor sleep are very common in people with chronic respiratory disorders. In patients with chronic obstructive pulmonary disease (COPD), poor sleep may be due to many causes, including cough, excess mucous production, and frequent arousals from sleep caused by hypercapnia, as well as secondary to medications used to manage the lung disease. Patients with obstructive sleep apnea (OSA) also complain of excessive daytime sleepiness and fatigue due to poor-quality sleep, although the mechanism of sleep disruption is somewhat different from that in patients with COPD. Although benzodiazepines are often the drugs of choice for the management of insomnia, caution is suggested with the use of these agents in patients with chronic obstructive respiratory disease due to the reduction in upper airway muscle tone and blunting of the arousal response to hypercapnia. However, controlled trials with short-acting benzodiazepine receptor antagonists, including triazolam, zolpidem, and zaleplon, suggest that these agents may be safely used in selected patients who have mild to moderate COPD without daytime hypercapnia. Less data are available on the use of these agents for patients with OSA, but a preliminary trial using zaleplon suggests that respiratory function is not adversely affected in patients with mild to moderate OSA. Studies are needed to further define the benefit-risk ratio of the use of benzodiazepine receptor agonists for the management of insomnia in patients with chronic obstructive lung disease.
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PMID:Perspectives on the management of insomnia in patients with chronic respiratory disorders. 1075 6

Emphysema is a slowly progressive degenerative lung disease involving fragmentation and depletion of elastic fibers, loss of lung elastance, and architectural destruction with ectasia, tortuosity, and loss of bronchioles irrespective of localization or morphological type. Occurring under physiological conditions, predominantly in geriatrics, matrix laxity and destructive parenchymal lesions are indicative of a pathological loss of tissue tensile strength attributable to bioengineering or structural fatigue in repetitively stressed tissues. The occurrence of severe premature emphysema in inherited connective tissue diseases and under some experimental and iatrogenic conditions is supportive evidence. Experiments advocating unrestrained proteolysis as a cause or pathogenic factor are invalid, being based on a false premise and assumed causality.
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PMID:Proteinase imbalance versus biomechanical stress in pulmonary emphysema. 1089 Dec 92


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