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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four patients fulfilling the case definition for eosinophilia-myalgia syndrome are described, including one whose disease began in 1986. Each displayed a variety of symptoms: one suffered principally from myalgia and recovered spontaneously on discontinuation of L-tryptophan therapy; one exhibited progressive sclerodermiform skin changes, neuropathy, and myopathy; a third had prominent neuromuscular disease and sclerodermiform skin changes; and the fourth experienced profound weight loss, an axonal polyneuropathy, and perivascular lymphoid infiltrates simulating a lymphoma. Evidence of T-cell activation was present in peripheral blood and affected tissues during the clinically active progressive phase of disease. Among other manifestations pleural effusion, cutaneous vasculitis, joint contractures, and bloody diarrhea were observed. A history of L-tryptophan ingestion should be sought in patients with myalgia, fatigue, or the above outlined symptoms.
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PMID:Eosinophilia-myalgia syndrome associated with L-tryptophan ingestion. Analysis of four patients and implications for differential diagnosis and pathogenesis. 217 45

A 51-year-old female with systemic lupus erythematosus (SLE) was admitted in November 1987 because of general fatigue and muscular weakness. She was treated with prednisolone (PSL) 30 mg and azathioprine (AZP) 50 mg after failure in the management of thrombocytopenia by PSL 15 mg. She exhibited no splenomegaly. Muscular atrophy and weakness were seen in the proximal muscles. Her platelet count was 44,000/microliters. A bone marrow aspiration revealed an increase in megakaryocytes. The blood chemistry revealed a normal CPK level and an elevated LDH level, indicating a presence of steroid myopathy. A splenectomy was performed after an increase of platelet count by giving gamma-globulin 400 mg/kg for 5 days. The platelet count rose to 368,000/microliters on the 46th postoperative day. She was treated with PSL 5 mg and AZP 50 mg as postsplenectomy therapy. The splenectomy did not adversely affect other aspects of SLE, in particular, renal function. She had no major complications in the postoperative period. Her platelet count reached a plateau 4 months later and revealed 115,000/microliters 18 months postoperatively.
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PMID:[Effect of splenectomy for management of thrombocytopenia associated with systemic lupus erythematosus: a case report]. 231 6

Despite frequent therapeutic use, the potential of corticosteroids to produce respiratory muscle myopathy is unknown. We studied effects of chronic steroid treatment on diaphragm mass and function. Eleven Sprague-Dawley rats were treated with cortisone acetate (100 mg.kg-1.day-1 im) for 10 days. Controls (injected with vehicle) included 11 freely eating rats and 11 animals pair fed to match food intake of cortisone rats. Steroid treatment depressed body weight 30% compared with controls. Mass of diaphragm, gastrocnemius, and extensor digitorum longus showed significant atrophy (30%); heart and soleus were unaffected. Isometric contractile properties of costal diaphragm strips were studied in vitro using direct stimulation. The force-frequency relationship was markedly depressed by steroid treatment, both at low and high frequencies. However, force developed per unit cross-sectional area was similar among all three groups, as were twitch characteristics. When stimulated every minute, forces developed by control strips fell progressively, whereas the forces of cortisone-treated strips remained unchanged. When stimulated every 5 s, the fall in force was not different between groups. We conclude that cortisone weakened the diaphragm by decreasing muscle mass but made the diaphragm more resistant to one form of fatigue in vitro.
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PMID:Diaphragm atrophy and weakness in cortisone-treated rats. 260 49

Corticosteroids have been shown to produce a myopathy of peripheral skeletal muscle, characterized predominantly by Type II fiber atrophy. To determine if similar histologic and histochemical changes occur in the diaphragm and whether the in vitro contractile properties of this muscle are adversely affected by steroids, we studied two groups of hamsters. The experimental group received triamcinolone while a control group received saline, both given daily for 3 wk as i.m. injections. Soleus (Sol) and extensor digitorum longus (EDL) muscles and costal diaphragm muscle sections were stained for histologic (hematoxylin and eosin, modified Gomori trichrome) and histochemical (myosin ATPase, succinate dehydrogenase [SDH]) analysis. Muscle fiber proportions and cross-sectional areas (CSA) were measured from myosin ATPase sections. In vitro studies of isometric contractions were carried out on small strips of costal diaphragm, measuring maximal isometric twitch (Pt) and tetanus (Po) tensions, time to peak tension (TTP), half relaxation time (1/2 RT), force-frequency relationship, and fatigue characteristics (60 Hz tetani; duty cycle, 0.5). Triamcinolone treatment resulted in no change in muscle fiber proportions. There was no effect on Type I fiber CSA; however, there was Type IIa (Sol, EDL) and Type IIb (diaphragm, EDL) fiber atrophy in triamcinolone-treated animals. Pt and Po (normalized for weight) of diaphragm strips were not different. There was a prolongation in TTP and 1/2 RT, a left shift in the force-frequency curve, and a reduced fatiguability of triamcinolone-treated diaphragm (P less than 0.05). We conclude that a steroid myopathy could be explained by a loss of muscle mass (Type IIb fiber atrophy) rather than an intrinsic impairment in contractile function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathologic changes and contractile properties of the diaphragm in corticosteroid myopathy in hamsters: comparison to peripheral muscle. 262 59

Exertional muscle pain and fatigue are common complaints; some patients with these symptoms have a metabolic myopathy. We have performed graded exercise testing with analysis of expired ventilation on 13 individuals with various kinds of metabolic myopathies. Their results differed from normal and reflected the underlying biochemical abnormality. Patients with disorders of the mitochondrial electron transport chain demonstrated marked limitations in aerobic metabolism and a greatly reduced maximum oxygen consumption. During intense exertion, normal individuals increase carbon dioxide generation due to buffering of lactic acid. This did not occur in patients with McArdle disease, in whom the respiratory exchange ratio (carbon dioxide production/oxygen consumption) did not rise above 1.0 at maximum exercise. These results indicated a deficit in anaerobic metabolism. Pyruvate dehydrogenase complex allows pyruvate produced from carbohydrate metabolism to enter the citric acid cycle. Patients with this enzyme deficiency showed an initially normal pattern followed by an abrupt cessation in carbohydrate dependent aerobic metabolism at higher work loads. During high-intensity exercise, progressive anaerobic metabolism was not accompanied by additional oxygen consumption. Finally, results from a patient with carnitine palmitoyl transferase deficiency revealed an early dependence on carbohydrate metabolism. The ventilatory threshold occurred at a low percentage of maximal oxygen consumption, reflecting the limited availability of lipid substrates for aerobic metabolism. Detection of some muscle metabolic abnormalities can be made on small biopsy specimens. However, definitive diagnosis of the defect nearly always requires studies on fresh or frozen muscle tissue obtained by an open biopsy. The decision on how the tissue should be processed and which metabolic studies should be performed frequently needs to be made before the biopsy is obtained. Thus, a noninvasive method to initially characterize patients with potential metabolic disorders is useful. Exercise testing with expired gas analysis can indicate the presence of a metabolic myopathy and results can then be used to direct the appropriate biochemical evaluations.
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PMID:Metabolic myopathies: evaluation by graded exercise testing. 271 15

The presence of a peripheral myopathy in hypothyroidism has been well recognized. Involvement of the diaphragm has been suggested recently but the clinical spectrum never clearly defined. We studied three patients with hypothyroidism presenting with fatigue, dyspnea, exercise limitation, and in two, chronic alveolar hypoventilation (PaCO2 of 51 and 75 mm Hg) before and after thyroid hormone replacement. In all patients diaphragmatic strength as determined by the maximal transdiaphragmatic pressure was low (2, 13, and 64 cm H2O) and improved with therapy (86, 84, and 90 cm H2O). Similarly, all patients manifested a fatiguing breathing pattern, as determined by the diaphragmatic tension time index. These values (0.22, 0.55, and 0.36) decreased after hormone replacement (0.16, 0.20, and 0.15). These changes were associated with the correction of hypercarbia in the two patients with hypoventilation and an improvement in lung volumes and exercise endurance in all patients. This study confirms that in patients with hypothyroidism diaphragmatic dysfunction occurs more frequently than has been suspected and might be of varying severity. This dysfunction reverses with adequate hormone replacement.
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PMID:Hypothyroidism. A reversible cause of diaphragmatic dysfunction. 280 37

The atrophy produced by endocrine disorders is primarily due to alterations in protein and carbohydrate metabolism. Type II muscle fibers are more severely affected than are Type I fibers. Steroid myopathy and the myopathy associated with excess ACTH have a typical pattern of proximal weakness affecting the legs more than the arms. Steroid myopathy is usually not apparent until other signs of glucocorticoid excess are present. Treatments of steroid myopathy are as follows: Lower the dose of steroid, use a nonfluorinated glucocorticoid, and exercise or physical therapy. Adrenal insufficiency produces generalized weakness, muscle cramping, and fatigue in 50 per cent of patients. Some patients also develop hyperkalemic paralysis. The treatment is hormone replacement. Thyrotoxicosis produces myopathy caused by net protein catabolism, accelerated basal metabolic rate and impaired carbohydrate metabolism. Shortening of contraction time may result from accelerated myosin ATPase activity and enhanced calcium uptake by the sarcoplasmic reticulum. Depolarization of the muscle fiber and impaired Na-K activity in muscle may predispose to thyrotoxic periodic paralysis. Neuromuscular presynaptic impairment may account for the worsening of myasthenia gravis by thyrotoxicosis. In hypothyroidism, impaired energy metabolism may limit force generation. Slow contraction and relaxation reflect reduction in myosin ATPase activity and impaired calcium uptake by the sarcoplasmic reticulum. Treatment for thyroid-associated muscle disorders is restoration of a euthyroid state. Muscle weakness associated with hypopituitarism is due to loss of thyroid and adrenal cortical hormones. Children require growth hormone for muscle development. T3 and growth hormone synergize to maintain normal protein synthesis. Primary and secondary hyperparathyroidism and osteomalacia are often associated with proximal weakness and fatigability. The myopathy improves with restoration of normal PTH levels and vitamin D replacement. Hypoparathyroidism and pseudohypothyroidism are associated with tetany. Tetany is worsened by alkalosis and is treated by calcium and magnesium replacement.
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PMID:Endocrine myopathies. 306 2

Wasting of muscle and a negative nitrogen balance are obvious effects of malnutrition, and have led to the use of anthropometric measurements and nitrogen balance for its assessment. A positive nitrogen balance and an increase in limb muscle circumference are believed to be solid indices of the beneficial effects of nutritional support. In experiments with growing rats and in young children, nitrogen retention and growth are recognized to be the desirable effects of optimal nutritional intake. This concept has been applied to malnourished adult humans (nongrowing) who have been considered potentially able to "regrow" the lost tissue. Although it is true that patients receiving long-term (greater than 6 months) home total parenteral nutrition (TPN), gain body weight and nitrogen over many months and years of observation, these processes are not seen during shorter (less than 40 days) periods of nutritional intervention given in hospital. Despite adequate intakes of nitrogen and calories, little or no significant increase in total body nitrogen is seen in a variety of patients receiving TPN in hospital over several weeks, but nutritional support does appear to improve outcome in the form of reduced complications after a period of support so short that body composition is barely altered. For example, Young and Hill showed that although amino acids and amino acids plus calories both resulted in equivalent sparing of body nitrogen, the latter was associated with quicker wound healing and fewer complications. Thus, the outcome and body composition data suggest that reversal of the adverse effects of malnutrition is not based on improvement of the traditional parameters of nutrition, such as gain in body nitrogen, or a demonstrable increase in muscle mass, or in plasma proteins. On the basis of the foregoing evidence, there are grounds for suspecting that functional abnormalities in adult humans may not be the result of simple loss of lean tissue and therefore may recover before such lean tissue is regained. This hypothesis is supported by the observation of Klidjian et al who showed that muscle force is a good measure of outcome. One of the major organ systems of the human body is the musculoskeletal system, and therefore it would seem important to determine the effect of malnutrition on that system. Previous studies of muscle function have been largely related to the examination of fatigue, myopathy, and endocrine-metabolic abnormalities. Subsequently we undertook initial studies of muscle function in very malnourished patients as outlined below.
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PMID:Rhoads lecture--1988. Bulk or bounce--the object of nutritional support. 306 74

Four patients, each with a history of myocardial infarction and diffuse coronary artery disease, underwent application of left latissimus dorsi (LD) muscle with intact neurovascular bundle to the anterolateral wall of the left ventricle. The muscle was conditioned over a six-week period subsequent to operation in 3 patients and was conditioned preoperatively with a burst stimulus in the fourth. Biopsy specimens confirm the experimental data that human skeletal muscle can be electrically conditioned over a six- to ten-week period to contain mainly fatigue-resistant type I fibers. All patients survived the procedure, and 3 showed improvement secondary to aneurysmectomy. In Patient 1, a modified resection was performed, and at 28 months after operation, at the 75-W level of exercise, the ejection fraction was 54% paced versus 45% nonpaced. In Patient 2, at 12 months, the ejection fraction at rest was 44% paced versus 30% nonpaced. Doppler echo studies confirmed the presence of the flap and its function in the paced and nonpaced mode. The third patient died of a sudden ventricular arrhythmia 2 months following operation. An infected, nonfunctioning, degenerated flap was found at autopsy. Patient 4 did not have an aneurysm. She received a bypass graft to the right coronary artery and underwent cardiomyopexy in an attempt to relieve medically refractory incapacitating chronic congestive heart failure. Ten months postoperatively, ejection fraction at rest was 33% paced versus 25% nonpaced. Constrictive myopathy has not been encountered in any of these patients.
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PMID:Paced skeletal muscle for dynamic cardiomyoplasty. 325 62

Following treatment with amiodarone, a patient developed weight loss, fatigue and severe myopathy, without respiratory symptoms. A solitary lung infiltrate, impaired thyroid and liver function tests, and leukocytosis were evident. Biopsies from the lung lesion, liver, and bone marrow revealed foam cells. All these signs and symptoms subsided following cessation of amiodarone therapy. It is demonstrated that amiodarone may induce a localized lung lesion rather than diffuse pulmonary disease.
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PMID:Amiodarone pulmonary toxicity presenting as a solitary lung mass. 333 15


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