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)

Malnutrition, which is common in maintenance dialysis patients, is strongly associated with increased morbidity and mortality. An important contributing factor is anorexia, leading to reduced intake in relation to the recommended allowances, which for protein is higher than in healthy subjects. Uremic toxicity in underdialyzed patients may cause anorexia as a result of retention of toxic compounds in the middle molecular weight range, which are normally excreted in the urine. Various comorbidity factors and psychosocial and economic factors may also be associated with low nutritional intake. The hemodialysis procedure may reduce nutritional intake because of cardiovascular instability with nausea and vomiting and post-dialysis fatigue. Abdominal discomfort, absorption of glucose and amino acids, and peritonitis may reduce appetite in peritoneal dialysis patients. Underdialysis, if present, should be corrected and various catabolic factors such as acidosis, infections, and other comorbidity factors should be treated, dietary counseling should be given, and psychosocial and economic support should be provided when needed. Patients who remain malnourished despite such measures may be given parenteral or enteral nutritional supplementation. Peritoneal dialysis solutions with amino acids have been used successfully in CAPD patients who suffer from protein malnutrition. Recombinant human growth hormone and IGF-1 are new treatment alternatives that need further evaluation.
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PMID:Anorexia in dialysis patients. 873 65

Three cases are reported of hypoglycemia manifested by profound sinus bradycardia and fatigue, which responded to i.v. dextrose with prompt normalization of the cardiac rhythm. The cases involved 3 different patients and disease processes: a young female who had anorexia nervosa and profound malnutrition; an elderly, nondiabetic male who subsequently experienced a transient ischemic attack: and a patient who had diabetes mellitus managed with chronic, subcutaneous insulin administration. It is vitally important that the emergency physician recognize unusual clinical manifestations of hypoglycemia and fully evaluate such scenarios when hypoglycemia may occur. Untreated, hypoglycemia may result in significant chronic morbidity, and rarely, in death. Bradyarrhythmias--particularly sinus bradycardia--should be added to the list of potential clinical manifestations of hypoglycemia.
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PMID:Hypoglycemia manifested by sinus bradycardia: a report of three cases. 881 87

The purpose of this study was to examine the interactive effects of unilateral denervation (DN) and prolonged malnutrition (MN) on the structure and function of the diaphragm muscle (Dia). Four groups of rats were studied: control (Con), MN, DN, and DN-MN. MN began 2 wk after DN and lasted 4 wk. In both the DN and DN-MN groups, the relative loss in Dia weight exceeded the relative change in body weight. Compared with the Con group, Dia specific force was reduced by approximately 40% in both the DN and DN-MN groups but was unaffected in the MN group. Dia fatigue resistance improved in all experimental groups but to a greater extent in the DN and DN-MN groups. In both the DN and DN-MN groups, approximately 50% of Dia fibers were classified as type IIc, whereas fiber type proportions did not change in the MN group. In the DN group, only type IIb/x fibers atrophied, whereas all fiber types atrophied in the MN and DN-MN groups. We conclude that in the DN-MN group the reduction in specific force combined with the reduction in total cross-sectional area of the muscle significantly curtails Dia force-generating capacity.
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PMID:Interactive effects of denervation and malnutrition on diaphragm structure and function. 894 42

Impaired pulmonary gas exchange can result from lung parenchymal failure inducing oxygenation deficiency and fatigue of the respiratory muscles, which is characterized by hypercapnia or a combination of both mechanisms. Contractility of and coordination between the diaphragm and the thoracoabdominal respiratory muscles predominantly determine the efficiency of spontaneous breathing. Sepsis, cardiac failure, malnutrition or acute changes of the load conditions may induce fatigue of the respiratory muscles. Augmentation of spontaneous breathing is not only achieved by the application of different technical principles or devices; it also has to improve perfusion, metabolism, load conditions and contractility of the respiratory muscles. Intermittent mandatory ventilation (IMV) allows spontaneous breathing of the patient and augments alveolar ventilation by periodically applying positive airway pressure tidal volumes, which are generated by the respirator. Potential advantages include lower mean airway pressure (PAW), as compared with controlled mechanical ventilation, and improved haemodynamics. Suboptimal IMV systems may impose increased work and oxygen cost of breathing, fatigue of the respiratory muscles and CO2 retention. During pressure support ventilation (PSV), inspiratory alterations of PAW or gas flow (trigger) are detected by the respirator, which delivers a gas flow to maintain PAW at a fixed value (usually 5-20 cm H2O) during inspiration. PSV may be combined with other modalities of respiratory therapy such as IMV or CPAP. Claimed advantages of PSV include decreased effort of breathing, reduced systemic and respiratory muscle consumption of oxygen, prophylaxis of diaphragmatic fatigue and an improved extubation rate after prolonged periods of mechanical ventilation. Minimum alveolar ventilation is not guaranteed during PSV; thus, close observation of the patient is mandatory to avoid serious respiratory complications. Continuous positive airway pressure breathing (CPAP) maintains PAW above atmospheric pressure throughout the respiratory cycle, which may increase functional residual capacity and decrease the effort of breathing. CPAP has been conceptually designed for the augmentation of spontaneous breathing and requires the intact central and peripheral regulation of the respiratory system. Airway pressure release ventilation (APRV) improves alveolar ventilation by intermittent release of PAW, which is kept above atmospheric pressure by means of a high-flow CPAP system. The opening of an expiratory valve for 1-2 s induces a decreased PAW and lung volume, which increases rapidly to pre-exhalation values after closure of the valve due to the high gas flow within the circuit (90-100 1/min). APRV may improve haemodynamics and VA/Q distribution as compared with conventional mechanical ventilation. Biphasic positive airway pressure (BIPAP) is characterized by the combination of spontaneous breathing and time-regulated, pressure-controlled mechanical ventilation. During the respiratory cycle the ventilator generates two alternating CPAP levels, which can be modified with regard to time and pressure. As with APRV, alveolar ventilation is maintained even if the spontaneous breathing efforts of the patient cease, which improves the safety of both modes of respiratory therapy. The contribution of spontaneous breathing to total minute ventilation may be important, since a decreased shunt and improved VA/Q relationship have been observed in experimental non-cardiogenic lung oedema. These data give support to the concept that spontaneous breathing should be maintained and augmented in the setting of acute respiratory failure.
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PMID:[Augmented spontaneous breathing]. 896 3

As with many chronic diseases that express themselves late in life, osteoporosis is distinctly multifactorial both in etiology and in pathophysiology. Osteoporotic fractures occur because of a combination of injury and intrinsic bony fragility. The injury comes most often from a combination of falls, poor postural reflexes that fail to protect bony parts from impact, and reduced soft tissue padding over bony prominences. The bony fragility itself is a composite of geometry, low mass density, severance of microarchitectural connections in trabecular structures, and accumulated fatigue damage. Reduced bone mass, in turn, is caused by varying combinations of gonadal hormone deficiency, inadequate intakes of calcium and vitamin D, decreased physical activity, comorbidity, and the effects of drugs used to treat various unrelated medical conditions. Finally, the often poor outcome from hip fracture in the elderly is partly caused by associated protein-calorie malnutrition. An adequate preventive program for osteoporotic fracture must address as many of these factors as possible, ie, it must be as multifaceted as the disease is multifactorial.
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PMID:Pathophysiology of osteoporosis. 896 13

Deficiency of complex I (reduced nicotinamide adenine dinucleotide dehydrogenase-ubiquinone oxidoreductase) of the mitochondrial respiratory chain may be seen as a pure myopathy or as a neuromuscular disorder at presentation. Efficacy of long- term therapy for these disorders is yet to be established. We report the case of a female patient with complex I deficiency and skeletal myopathy, who has had a sustained clinical response to riboflavin during 3 years of therapy. Molecular studies found no mutations in the putative flavin mononucleotide binding site in the 51 kd subunit of complex I, but a T-to-C transition at nucleotide 3250 in the mitochondrial DNA tRNA(Leu(UUR)) gene was identified. This mutation has been reported in one other family in that five members had fatigue with or without muscle weakness. There were also five cases of unexplained infant deaths in that family and two cases in the family reported here. Riboflavin therapy should be attempted in all patients with complex I deficiency when the clinical presentation is one of isolated skeletal myopathy.
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PMID:Mitochondrial myopathy with tRNA(Leu(UUR)) mutation and complex I deficiency responsive to riboflavin. 900 64

Studies using nuclear magnetic resonance have shown that undernutrition affects muscle performance and energetics. It is unclear to what extent underfeeding and refeeding influence the availability of muscle glycogen, net glycogenolysis, skeletal muscle wasting, and recovery. We hypothesized that muscle performance is independent of muscle size and weight, is specific to muscle type, and is unrelated to muscle glycogen concentrations. Slow- and fast-twitch muscles were studied in three groups of adult male Wistar rats: well-fed controls, hypoenergetically fed (Hypo) rats, and rats refed for 4 d after the hypoenergetic diet. Glycogen concentrations and net glycogenolysis; serum glucose, insulin, and protein concentrations; and muscle weight, protein, and cross-sectional area were studied relative to the performance of both types of muscles. Our study controlled for muscle size, weight, and type and electrolyte-micronutrient deficiency. Undernutrition affected muscle performance in five ways. First, compared with controls, fatigue increased only in the soleus muscles of Hypo rats yet the maximal relaxation rate (MRR) decreased in both the soleus and extensor digitorum longus (EDL) muscles. Second, muscle glycogen concentrations did not significantly correlate with fatigue in either the soleus or the EDL although net glycogenolysis was significantly correlated with fatigue in the soleus (r = -0.64; P > 0.01 < 0.05). Third, lower glycogen concentrations did not hinder net glycogenolysis in the EDL of Hypo rats or the soleus of refed rats. Fourth, muscle weight, size, and protein were dissociated from function. Fifth, refeeding did not restore muscle endurance; however, the MRR of the soleus normalized. In conclusion, glycogen values and muscle performance did not correlate but net glycogenolysis correlated with fatigue in the soleus. Also, there was a dissociation between muscle weight, size, and protein and muscle function during hypoenergetic feeding and refeeding.
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PMID:Effect of hypoenergetic feeding and high-carbohydrate refeeding on muscle tetanic tension, relaxation rate, and fatigue in slow- and fast-twitch muscles in rats. 925 Jan 7

A 74-year-old man was admitted to our hospital because of edema of the lower legs, fever, and increasing fatigue. Laboratory evaluation revealed proteinuria, microhematuria, leukocytosis, thrombocytosis, anemia, a high level of C-reactive protein. A test for myeloperoxidase-antineutrophil cytoplasmic antibodies was highly positive. Microscopic polyarteritis nodosa was diagnosed and therapy with prednisolone was begun. Examination of a renal biopsy sample showed necrotizing crescentic glomerulonephritis. A chest roentgenogram and CT scan disclosed bilateral basilar interstitial changes. Six months later, the patient was admitted again because of disturbance of consciousness, malnutrition, and hyponatremia. After admission, alveolar infiltrates developed in the right lung and the patient died on the 5th hospital day as a result of respiratory failure. An autopsy revealed Candida pneumonia of the right lung and massive intra-alveolar hemorrhage, which was believed to have caused the respiratory failure. Other findings were usual interstitial pneumonia, cellular small-vessel angiitis in the lungs, and healed angiitis in the kidneys and liver. In this case of microscopic polyangiitis and chronic interstitial pneumonia, steroid therapy was effective against the angiitis, but the patient died of an opportunistic infection and alveolar hemorrhage.
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PMID:[Microscopic polyangiitis and pulmonary fibrosis in a patient who died of Candida pneumonia and intra-alveolar hemorrhage]. 936 70

We previously reported that patients with spinal muscular atrophy do not lose muscle strength over time as measured quantitatively. However, we noted that many patients with spinal muscular atrophy suffer from what they call fatigue. We wondered if we could measure fatigue during a single maximal voluntary contraction, whether fatigue might increase with time, independent of muscle strength, and whether increasing fatigue might correlate with loss of function in some patients. We measured fatigue during a single maximal voluntary contraction in a cohort of patients having spinal muscular atrophy using quantitative strength testing. We included only patients with spinal muscular atrophy aged 5 years or older, so they could follow instructions regarding muscle contraction, and who were followed for at least 2 years. Seventy-six children with spinal muscular atrophy and 24 untrained individuals, aged 5 to 57 years (mean, 16.8 years), were studied. There was no discernible abnormal fatigue in patients with spinal muscular atrophy compared to untrained controls using our methodology. Thus, spinal muscular atrophy may not be associated with fatiguability. Moreover, spinal muscular atrophy does not appear to cause progressive muscle fatigue with age or loss of function. It is possible that fatigue was undetectable by our methods. An alternative explanation is that what patients describe as fatigue may be caused by factors outside the neuromuscular system. Such factors may include chronic respiratory insufficiency with hypoventilation and carbon dioxide retention as well as chronic malnutrition and negative nitrogen balance.
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PMID:Muscle fatigue in spinal muscular atrophy. 937

Recent advances in our understanding of the pathogenesis of human immunodeficiency virus (HIV) disease and the important role that viral load plays in the initial selection of antiretroviral therapy significantly alters our management of this disease. Guidelines from the British HIV Association, International AIDS Society-USA, and United States Public Health Service panels regarding the selection of appropriate antiretroviral therapy, and from the Centers for Disease Control and Prevention on prophylaxis for opportunistic infections, have recently been published. Despite tremendous advances in treating the disease and its related complications, a comprehensive, long-term disease management plan that includes recognition of patient concerns about quality of life is lacking. New approaches to managing HIV disease must now include strategies that address patient concerns about fatigue, gastrointestinal distress, malnutrition, and weight loss. Patients must become more involved in decisions about selection of specific drugs and drug regimens and must be consulted about their expectations and needs. We have made significant strides in the treatment of HIV disease. We can readily reduce the viral burden to virtually undetectable levels, and we must continue to develop even more potent and tolerable treatment regimens. We can make patients live longer. Helping patients live better quality lives deserves further study.
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PMID:HIV infection and AIDS: new biology, therapeutic advances, and clinical implications. Introduction. 938 14


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