Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 15 patients with rheumatoid arthritis (RA) and in 12 age- and sex-matched normal subjects, we evaluated inspiratory muscle strength and respiratory control system. Inspiratory muscle strength was assessed by measuring maximal inspiratory pressure (MIP). Respiratory drive was assessed by evaluating surface electromyographic activity of the diaphragm (EMGd) during both room-air breathing and hypercapnic rebreathing. Compared to the predicted value (mean +/- 1.65 SD), MIP was significantly reduced in nine patients (60%). All told, we noticed a significant inverse relationship in the patients between MIP and duration of steroid therapy (p less than 0.01). During room-air breathing, both EMGd and mouth occlusion pressure (P0.1), expressed both in actual values and as percentage of MIP, were significantly greater in patients than in the normal control group (p less than 0.001 for both). Both EMGd and P0.1 (%MIP) response slopes to CO2 were significantly greater in patients than in the normal control group (p less than 0.01 and p less than 0.001, respectively) and significantly related to the functional stage of disease. During quiet breathing and for a PETCO2 of 60 mm Hg, both EMGd (p less than 0.01 and p less than 0.05, respectively) and P0.1 (%MIP) (p less than 0.01 and p = 0.001, respectively) were inversely related to MIP. These results indicate that RA patients may exhibit inspiratory muscle weakness and increased respiratory drive. Steroid myopathy and rheumatoid myositis could explain the reduction in MIP, whereas neural afferents arising from respiratory muscle, lung, or joint receptors could be involved in the observed increase in neural drive.
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PMID:Inspiratory muscle strength and respiratory drive in patients with rheumatoid arthritis. 238 91

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

The functional and histologic picture of steroid-induced myopathy was systematically examined in eight patients with chronic obstructive pulmonary disease (COPD) and compared with control patients with COPD matched for age, sex, and degree of airflow obstruction. Steroid-induced myopathy was associated with severe peripheral muscle weakness, quadriceps force being 23 +/- 14 versus 71 +/- 23% in control patients with COPD (p < 0.001). In addition, clear ventilatory muscle weakness was present. PImax was 37 +/- 15 versus 67 +/- 24% in control patients (p < 0.001 ), and PEmax averaged 34 +/- 10 versus 74 +/- 23% (p < 0.001). Vital capacity tended to be slightly reduced compared with that in control patients (69 +/- 21 versus 80 +/- 16%, p = 0.11). The only biochemical abnormalities associated to steroid-induced myopathy were a moderately increased lactic dehydrogenase level (697 +/- 301 versus 421 +/- 128 IU/L, p < 0.001) and an increased creatine excretion in 24-h urine (990 +/- 609 versus 159 +/- 219 mg/24 h, p< 0.001). On quadriceps biopsy steroid-induced myopathy was characterized by increased variation in diameter of fibers, with several angular atrophic fibers and diffuse necrotic and basophilic fibers. In addition, increased amount of connective tissue in between fibers and increased number of subsarcolemmal and central nuclei were present. On ATPase stain diffuse fiber atrophy predominantly affecting fast fibers was present, but there was no indication that atrophy was confined to type IIb fibers in contrast to conventional thinking. On follow-up, survival of patients with steroid-induced myopathy was reduced in comparison with control patients with COPD with similar degree of airflow obstruction (p < 0.025).
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PMID:Functional and histologic picture of steroid-induced myopathy in chronic obstructive pulmonary disease. 866 61

We prospectively evaluated 15 adult cancer patients being treated with adrenocorticosteroids (steroids) to determine the frequency and time course of "steroid myopathy." Nine (60%) developed clinically detectable proximal muscle weakness that, in six, was severe enough to interfere with activities of daily living. Proximal muscle weakness developed within 15 days in eight of nine patients and was significantly related to the cumulative dose of steroid. Eight of nine patients with proximal muscle weakness, and two of six without such weakness, experienced a significant decline in respiratory function, leading to symptomatic dyspnea in four patients of the former group. In three patients who could be followed for more than 3 months off steroids, there was either improvement or resolution of the weakness and, when present, of the respiratory impairment. Steroid myopathy is a common complication among cancer patients receiving steroids. It can often affect respiratory function even when proximal limb muscles remain strong. Clinical recognition is important since steroid myopathy can lead to increased morbidity and may be reversible with reduction or discontinuation of steroids.
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PMID:Steroid myopathy in cancer patients. 974 67

An 8-year-old boy who had been diagnosed as systemic-onset juvenile rheumatoid arthritis were on treatment for 8 months with methotrexate and additional steroids during activation. At the end of the 8th month when the corticosteroid dose was 12.5 mg/day, he began to suffer from numbness and weakness in his hands. Physical examination, laboratory findings and electromyography results demonstrated myopathy. Steroid myopathy was considered. Corticosteroids were tapered and stopped. At follow-up clinical findings remitted and electromyography became normal at the 4th month. We present here this case to direct attention to drug-induced myopathy besides myopathy due to primary disease in connective tissue disorders whenever myopathy exists.
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PMID:Steroid myopathy in a child with juvenile rheumatoid arthritis. Case report. 1268 24

Steroid myopathy is a well-known adverse effect of glucocorticoids that causes muscle weakness and atrophy; however, its pathogenic mechanism is still unclear. Recently, oxidative stress was reported to contribute to steroid myopathy, but there is no report that actually attempts to measure hydroxyl radical. I developed an animal model of steroid myopathy in rat with dexamethasone (9-Fluoro-11beta,17, 21-trihydroxy-16alpha-methylpregna-1,4-diene-3,20-dione), and measured hydroxyl radical using the salicylate trapping method. There was significant dose-dependent relation between both 2,5- and 2,3-dihydroxybenzoic acids and dexamethasone in the treated group, compared to the control group. These results suggest that hydroxyl radical plays a role in the pathogenesis of steroid myopathy.
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PMID:Hydroxyl radical formation in skeletal muscle of rats with glucocorticoid-induced myopathy. 1617 71

Steroid myopathy is usually a slowly progressive disease, which causes weakness primarily to the proximal muscles of the upper and lower extremities. The monitoring of this problem is difficult in situations in which the primary disease itself produces muscle weakness. The distinguishing feature in steroid myopathy is the occurrence of creatinuria in the presence of normal muscle enzymes including creatine kinase and aldolase. To evaluate the usefulness of percent creatinuria {urinary excretion of creatine/(urinary excretion of creatine + urinary excretion of creatinine)} in the diagnosis of steroid myopathy, we measured percent creatinuria in 26 patients (14 male and 12 female) without muscle diseases before the initiation of steroid treatment We found that the median values of percent creatinuria of the male and female patients were 2.5% and 17.1%, and that the ratios of the male and female patients presenting with an elevated percent creatinuria (more than 10%) were 3 out of 14 patients (21.4%) and 8 out of 12 patients (66.7%), respectively. We also found one patient with mild renal dysfunction presenting with an elevated percent creatinuria but without muscle weakness or myalgia. These findings suggest that the measurement of percent creatinuria is of little value in the diagnosis of steroid myopathy with a cutoff value of 10%. Furthermore, it is important to measure percent creatinuria before the steroid treatment, while paying close attention to the measurement method, sex, renal function and protein level of the diet.
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PMID:[Reevaluation of validity of percent creatinuria for diagnosing steroid myopathy]. 1648 20

Steroid myopathy, characterized by muscle atrophy and weakness, is an adverse effect of high-dose steroid therapy. Weakness of proximal muscle that interferes with activities of daily living is a serious problem for patients with steroid myopathy. Here, we outline the pathogenic mechanism, diagnosis, and treatment of steroid myopathy. Recent studies have shown that steroid-mediated induction of ubiquitin ligases (atrogin-1, muscle RING finger-1) and suppression of mammalian/mechanistic target of rapamycin cause an imbalance between anabolism and catabolism of muscle proteins, resulting in muscle atrophy. Despite the progress in understanding the pathogenic mechanism, the diagnosis and treatment of steroid myopathy has not yet been established. Small changes in muscle enzymes, including CK, LDH, and aldolase, make it difficult to define diagnostic criteria. Furthermore, since there is no drug available for treating the disorder, the patients have no opinion except waiting for spontaneous recovery with steroid tapering and exercising. To address these issues, we introduce novel approaches involving branched-chain amino acids that aim at treatment and assessment of steroid myopathy.
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PMID:[Mechanism, diagnosis, and treatment of steroid myopathy]. 2420 Jun 15