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)

Acetazolamide is a useful prophylactic for acute mountain sickness causing marked reduction in headache, nausea, vomiting, weakness, etc. Improvements correlate with increased arterial oxygen concentrations, reduction in proteinuria and peripheral oedema and other objective measures of acute mountain sickness. Evidence that Acetazolamide is beneficial for pulmonary oedema or cerebral oedema is scanty because of the lower frequency of these severe forms of mountain sickness. Dexamethasone, used prophylactically, also reduces the symptoms of acute mountain sickness partly due to its euphoric effect. Use of Acetazolamide as a treatment for established acute mountain sickness has been investigated. Large doses of Acetazolamide increase arterial oxygen levels over a few hours and this leads to a reduction of symptoms but data is limited and faster acting carbonic anhydrides inhibitors such as Methazolamide may be preferable in an emergency situation. There is no comparison of the effectiveness of Acetazolamide with other drugs used for treating acute mountain sickness such as steroids and calcium channel blocking drugs. Also, there is no data on drug combinations which could have additive effects and thereby be more beneficial than individual drugs.
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PMID:Acetazolamide and high altitude diseases. 148 96

In order to assess the clinical and biological effects of glucocorticoids in the therapy of epidural spinal cord compression, the T8-10 epidural space of 50 rats was implanted with Walker 256 tumor. The rats were studied 10 to 20 days later when they became paraparetic. The regional blood-spinal cord transport constant (K, a function of the blood-spinal cord barrier) of 14Carbon-labeled aminoisobutyric acid was measured with quantitative autoradiography 6 hours after intravenous injection of low-dose (0.1 mg/kg), intermediate dose (1 mg/kg), and high-dose (10 mg/kg) dexamethasone. The effects of dexamethasone in these doses on the clinical signs and water content of the compressed cord were also evaluated 40 hours after treatment began. The K factor increased 730% in compressed compared with noncompressed spinal cords (p less than 0.001). Dexamethasone induced a dose-related reduction of both K (p = 0.007) and water content of the compressed cord (p less than 0.0001). Stabilization or, more rarely, improvement of weakness at 24 and 40 hours posttreatment correlated with the dose of dexamethasone (r = 0.88, p less than 0.001). This study demonstrates that dexamethasone has a dose-related beneficial clinical effect associated with an improvement of blood-spinal cord barrier breakdown and a reduction of the water content of the compressed cord. This study supports the use of highdose dexamethasone for the initial treatment of epidural spinal cord compression.
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PMID:A dose-response study of dexamethasone in a model of spinal cord compression caused by epidural tumor. 271 20

Dexamethasone treatment in the rat produced depolarization of extensor digitorum longus (EDL) muscle fibers but not soleus (SOL) fibers studied in vitro at 23 degrees C. The depolarization of EDL fibers was most prominent after 1 day of treatment (treated -77.5 +/- 1.1 mV, control -87.2 +/- 0.8 mV; mean +/- S.E.), and was associated with elevation of the action potential threshold and reduction of the action potential overshoot. In vivo, or in vitro in chloride-free solution, the resting potential and action potential threshold and overshoot of EDL fibers from glucocorticoid-treated and control rats were similar. Sodium currents were studied with a patch voltage clamp. Glucocorticoid treatment did not alter the voltage dependence of sodium channel activation or inactivation in fast twitch muscle fibers. Maximal inward currents occurred at about -29 mV and half-maximal inward currents at about -50 mV. Sodium channels were half inactivated at about -71 mV. Glucocorticoid treatment did not alter the sarcolemmal resistance or capacitance. We conclude that glucocorticoid treatment does not produce muscle weakness or atrophy by altering the excitability of muscle fibers.
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PMID:Effect of glucocorticoid treatment on the excitability of rat skeletal muscle. 629 91

The mean cross sectional area of synaptic vesicle profiles of the myoneural junction of rat diaphragm is increased significantly when rats are injected i.p. with single doses of 200 micrograms/kg dexamethasone 1/2 hr to 8 hr previously to a control injection of 0.9% NaCl. A maximum effect is observed at 8 hr after pretreatment with dexamethasone. The treatment of rats with hemicholinium-3 (300 micrograms/kg) induces a significant reduction of the vesicle size. Complete prevention of this decrease in vesicle size is already observed when the animals are pretreated with a single dose of 200 micrograms/kg dexamethasone 1/2 hr before treatment with 300 micrograms/kg hemicholinium-3. Dexamethasone in the same dose causes an optimum increase of the mean cross sectional area when it is given 1 hr before treatment of the animals with hemicholinium-3. It is concluded that glucocorticoids have direct actions in both "normal" motor nerve terminals and in motor nerve terminals with a deficient choline transport system, which may contribute to their proposed beneficial effects in certain cases of muscle weakness.
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PMID:Glucocorticoid-induced changes in synaptic vesicles of rat phrenic nerve terminals. 632 Jul 53

We explored the possibility that glucocorticoid-induced muscle weakness and atrophy resulted from impaired muscle membrane excitability. Male Sprague-Dawley rats received intramuscular injections of dexamethasone, cortisone acetate (equivalent anti-inflammatory doses), or saline for up to 28 days. Temporal patterns of change in muscle mass, twitch and tetanic tension, and membrane potential, cable parameters, and excitability were studied in vitro in the extensor digitorum longus (EDL), soleus (SOL), omohyoid (OMO), caudofemoralis (CF), and the sternomastoid muscles (membrane potential only). the membrane properties of EDL fibers were also studied in vivo (pentobarbital anesthesia). The relative severity of atrophy was OMO greater than CF greater than EDL greater than SOL. Reduction in twitch or tetanic tension never preceded atrophy. The twitch and tetanic tension (per g muscle) increased with glucocorticoid treatment. There were no significant changes in the time course of the twitch or tetanus. Dexamethasone produced more severe atrophy and force reduction than did cortisone acetate. Glucocorticoid treatment produced a depolarization of EDL muscle fibers measured in vitro at 23 degrees C, but this did not appear to be physiologically significant because EDL fibers studied in vivo were not depolarized and had normal action potential amplitudes and thresholds. Glucocorticoid treatment did not change the membrane resistance or capacitance. We conclude that glucocorticoid treatment did not produce muscle weakness by impairing sarcolemmal excitability or excitation-contraction coupling, but that the weakness resulted from muscle atrophy.
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PMID:Glucocorticoid-induced atrophy is not due to impaired excitability of rat muscle. 714 22

Acute mountain sickness (AMS) has long been recognised as a potentially life-threatening condition afflicting otherwise healthy normal individuals who ascend rapidly to high altitude where the partial pressure of oxygen (pO2) in the air is reduce. The symptoms of AMS (e.g. headache, poor appetite and nausea, fatigue and weakness, dizziness or light-headedness and poor sleep) are probably a consequence of disturbances in fluid balance brought about by severe tissue hypoxia. AMS can be prevented by an adequately slow ascent, which is the best method, but for those with limited time there are several drug therapies that provide a relatively good protection. Acetazolamide (250 mg twice daily or 500 mg slow release once daily), taken before and during, ascent is probably the treatment of choice; it improves gas exchange and exercise performance and reduces the symptoms of AMS in most individuals. Dexamethasone (4 mg, 4 times daily) is more of value for short term treatment or prevention, and should never be used for more than 2 to 3 days. Prophylactic use of progesterone looks promising, but more studies are required.
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PMID:Medicine and mechanisms in altitude sickness. Recommendations. 857 Sep 99

Neurological complications of immunisation are rare. We report the case of neuroallergic reaction 5 days after receiving the second course of DTP + Polio vaccine in a 4.5 month old girl. The pathological signs developed 48 hours after the vaccination. On admission the infant demonstrated a persistent fever (39 degrees C), resistant to Paracetamol, unusual crying, irritability, consciousness disorder, and opistotonus. Physical examination showed generalised mild, macular rash and redness and swelling at the injection site. The neurological assessment revealed weakness of upper and lower limbs, meningeal signs such as stiff neck, Kernigs and Brudzinski signs. There were no pathological changes in the CSF. The diagnosis was established as the neuro-allergic Adverse Event Following DPT + Polio Immunisation. After 10 day treatment with Dexamethasone and Phenobarbital the infant was discharged with no neurological changes. A psychomotorical development is good.
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PMID:[A severe adverse event after vaccine for diphtheria, tetanus, pertussis and poliomyelitis (DTP + polio) in a 4.5 month old infant]. 1110 23

Evidence for the effectiveness of corticosteroids in palliative care is anecdotal, and more information is required. From January to December 1999 a total of 376 consecutive patients admitted to a home palliative care program were longitudinally surveyed. Patients who started a corticosteroid treatment after admission on the basis of common indications prescribed by their home care physicians were selected. Fifty patients were enrolled in the study. Dexamethasone, in doses ranging from 4 to 16 mg, was the drug of choice. Corticosteroids were found to be effective in anorexia, weakness, headache, and nausea and vomiting. The reduction of symptom intensity was achieved in less than 3 days on average. However, no great advantages were found in terms of controlling drowsiness or confusional states associated with advanced illness because of cerebral involvement. It can be concluded from this study that: (a) corticosteroids may be effective in controlling anorexia, weakness, headache, and nausea and vomiting associated with cerebral involvement or bowel obstruction; (b) they should be stopped if no therapeutic effect has become evident within 3-5 days; (c) the treatment is not useful when given in the presence of severe neurological impairment resulting from the advanced stage of disease; (d) the range of adverse effects was acceptable for limited periods and in the circumstances in which the preparations were used in this study; and (e) corticosteroids may have an adjuvant role in potentiation of analgesic drugs. These findings will be very useful in the planning of future controlled studies designed to yield evidence-based data on the role of corticosteroids in the relief of specific symptoms.
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PMID:The use of corticosteroids in home palliative care. 1149 94

The present study reports a rare case of full-blown Cushing's disease several years after an episode of pituitary apoplexy. A 60 year-old woman complained of muscular weakness and generalized malaise. Ten years ago she had an episode of pituitary apoplexy. Diabetes mellitus was diagnosed at age 56, and thereafter she had been controlled her plasma glucose with diet therapy and oral hypoglycemic agents. She exhibited cushingoid feature of moon face and central obesity. Both plasma ACTH and serum cortisol levels were elevated to 170 pg/ml and 19.6 microg/dl, respectively. Dexamethasone suppression test showed that a large dose of 8 mg dexamethasone, but not a small dose of 2 mg, suppressed the pituitary-adrenocortical axis. CRH and methyrapone caused increases in plasma ACTH and serum cortisol levels. Brain T(1)-weighted magnetic resonance imaging depicted a low signal of pituitary tumor, which was not enhanced by gadolinium. The pituitary tumor was removed by transsphenoidal adenomectomy, and immunohistochemistry revealed an ACTH-producing adenoma. The evidence suggested the possibility that the two pituitary tumors with dormant period of several years were a recurrence of ACTH-producing tumors in the present patient.
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PMID:Full-blown Cushing's disease after an episode of pituitary apoplexy. 1461 5

We report the results of a phase 2 trial using lenalidomide plus dexamethasone (Rev/Dex) as initial therapy for myeloma. Thirty-four patients were enrolled. Lenalidomide was given orally 25 mg daily on days 1 to 21 of a 28-day cycle. Dexamethasone was given orally 40 mg daily on days 1 to 4, 9 to 12, and 17 to 20 of each cycle. Objective response was defined as a decrease in serum monoclonal protein level by 50% or greater and a decrease in urine M protein level by at least 90% or to a level less than 200 mg/24 hours, confirmed by 2 consecutive determinations at least 4 weeks apart. Thirty-one of 34 patients achieved an objective response, including 2 (6%) achieving complete response (CR) and 11 (32%) meeting criteria for both very good partial response and near complete response, resulting in an overall objective response rate of 91%. Of the 3 remaining patients not achieving an objective response, 2 had minor response (MR) and one had stable disease. Forty-seven percent of patients experienced grade III or higher nonhematologic toxicity, most commonly fatigue (15%), muscle weakness (6%), anxiety (6%), pneumonitis (6%), and rash (6%). Rev/Dex is a highly active regimen with manageable side effects in the treatment of newly diagnosed myeloma.
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PMID:Combination therapy with lenalidomide plus dexamethasone (Rev/Dex) for newly diagnosed myeloma. 1679 May 86


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