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)

Exertional rhabdomyolysis (ER) is a condition characterized by muscle pain, swelling, and weakness following some exertional stress, with or without concomitant heat stress. Athletes who experience ER often present to the emergency department, the training room, or the physician's office seeking guidance and care for this condition, often feeling it is simply normal delayed onset muscle soreness. The astute clinician must perform a thorough history and focused exam, in addition to ordering a serum creatine kinase (CK) and urinalysis. In this clinical setting, a CK equal to or greater than five times normal or a urine dipstick testing positive for blood with no demonstrable red blood cells upon microscopic assessment confirms the diagnosis. A urine or serum myoglobin is more definitive when expeditiously available. After treatment for ER, the provider must risk-stratify the athlete for risk of recurrence, consider further testing, and make the difficult decision on when, if, and under what conditions the athlete can safely return to play.
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PMID:Return to physical activity after exertional rhabdomyolysis. 1900 54

Polymyositis is an inflammation of muscle tissue of unknown etiology. It is characterized by symmetric, mainly proximal muscle weakness, muscle fiber damage proved on biopsy, increased enzymes and myoglobin, and has corresponding electromyography findings. Other systems such as joints, lungs, heart, and gastrointestinal system are involved. Lung involvement is rather common. The most frequent symptom represents shortness of breath caused by muscle weakness. We report a case of a 66 year old woman with primary idiopathic polymyositis. The clinical state of the patient was complicated by progressive muscle weakness, dysphagia, and respiratory failure. Due to the ineffectiveness of the treatment with corticsteroids and cyclophosphamide, treatment with high doses of immunoglobulins was started. A total of 100 g of i.v. immunoglobulin therapy was administered beginning on the 13th day after hospital admission. The state of the patient progressively improved and after 7 weeks of treatment in a significantly improved state the patient was transferred to a Rehabilitation Unit. We therefore conclude that IVIg therapy may be an effective therapeutic approach for the treatment of acute complications of polymyositis, especially in cases in whom other therapeutic strategies are ineffective or harmful (Ref. 10). Full Text (Free, PDF) www.bmj.sk.
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PMID:Successful therapy with intravenous immunoglobulin in the management of polymyositis. 1904 Jan 48

We report a case of rosuvastatin induced rhabdomyolysis in a low risk patient, who presented with five-day history of generalized muscle pain, weakness and easy fatigability associated with passing dark urine. Initial investigations showed creatinine 140micromol/L, creatine kinase (CK) 4566 U/L and serum myoglobin 2694 ng/ml with a significant increase in urine myoglobin. Although there were no obvious risk factors, the patient was diagnosed with rosuvastatin induced rhabdomyolysis. The drug was stopped on the first day of admission and the patient was initiated on intravenous fluid with cautious monitoring of serum electrolytes. On the following days the level of creatine kinase and serum myoglobin returned toward normal and consequently he was discharged without statins but on dietary therapy. On follow-up evaluation, the patient was symptom free his serum creatinine was 106micromol/L, whereas his LDL cholesterol was 2.1mmol/L. The rosuvastatin induced rhabdomyolysis is discussed and the danger of its use in low risk patients is emphasized.
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PMID:Rosuvastatin induced rhabdomyolysis in a low risk patient: a case report and review of the literature. 1914 97

A 16-year old girl presented with rapid onset of muscular weakness and a history of severe dysphagia, dysphonia and significant wasting. On examination, she was dystrophic (BMI 15.7) and had signs of myopathy. Laboratory findings confirmed myopathy (CPK 106.4 microkat/L (6384 IU/L), AST 2.86 microkat/L (171.6 IU/L), myoglobin 1582 microg/L). There was profound hypokalaemia (S-K 1.8 mmol/L) suggesting hypokalaemic paralysis. Diagnosis of distal renal tubular acidosis (dRTA) was based on combination of hyperchloremic metabolic acidosis, severe hypokalaemia, high urinary pH and positive value of urinary anion gap. There was evidence of other signs of renal tubular impairment (urinary beta-2-microglobulin 213 mg/L, glomerulotubular proteinuria 1.01g/24h). Autoimmune tests (rheumatoid factor, antinuclear antibodies, autoantibodies to Ro/SSA and La/SSB) together with symptoms of xerostomia with swallowing difficulties and atrophic glossitis suggested primary Sjogren's syndrome (SS) as the underlying cause of dRTA. The renal biopsy confirmed chronic tubulo-interstitial nephritis compatible with this diagnosis. Full recovery of muscle weakness and hypokalaemia and acidosis followed after potassium and alkali replacement therapy. Corticosteroids were administered with subsequent addition of cyclosporine A because of disease activity. In conclusion, primary SS is a rare diagnosis in childhood and adolescence and should be considered in patients presenting with hypokalaemic paralysis, as this might be due to dRTA, even in the absence of apparent sicca syndrome.
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PMID:Hypokalaemic Paralysis Revealing Sjogren's Syndrome in a 16-Year Old Girl. 1927 13

We present an adolescent with McArdle disease and recurrent acute kidney failure due to rhabdomyolysis. The patient was admitted with acute kidney failure for 3 times and due to a history of proximal weakness, fatigue, and muscular cramps after physical activities a glycogen-storage disease was suspected. Serum creatine phosphokinase and urine myoglobin were found to be elevated. McArdle disease was diagnosed based on pathologic examination of muscle tissue specimen. Patients presenting with rhabdomyolysis following strenuous exercise should be evaluated for McArdle disease.
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PMID:Recurrent acute kidney failure due to McArdle disease. 1937 43

Rhabdomyolysis is a common clinical syndrome and accounts for 7% of all cases of acute kidney injury (AKI) in the USA. It can result from a wide variety of disorders, such as trauma, exercise, medications and infection, but in the pediatric population, infection and inherited disorders are the most common causes of rhabdomyolysis. Approximately half of patients with rhabdomyolysis present with the triad of myalgias, weakness and dark urine. The clinical suspicion, especially in the setting of trauma or drugs, is supported by elevated creatinine kinase levels and confirmed by the measurement of myoglobin levels in serum or urine. Muscle biopsy and genetic testing should be performed if rhabdomyolysis is recurrent or metabolic myopathy is suspected. Early recognition is important to prevent AKI through the use of aggressive hydration. Prevention is important in patients with inherited forms, but novel therapies may be developed with the better understanding of the pathophysiology and genetics of rhabdomyolysis.
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PMID:Rhabdomyolysis: a review, with emphasis on the pediatric population. 1952 63

The new antivirals clevudine, telbivudine and emtricitabine may be potent agents for the treatment of hepatitis B virus (HBV). However, there have been no reports on serious adverse events associated with the use of clevudine. A son and his mother both had HBV infection (ages: 27 and 47 years, respectively), and they had received antivirus treatment with clevudine (30 mg daily). They developed progressive weakness of the lower extremities and difficulty arising from the ground. Both the patients had symptoms for the previous 3 approximately 4 months in process of 14 approximately 17 months of clevudine therapy. The physical examinations showed positive Gower's sign, a decreased gait velocity and symmetrical proximal weakness (MRC grade 4/5). Their blood tests at admission revealed elevated or positive HBs Ag, HBV DNA, AST, ALT, creatine kinase, LDH, myoglobin and CK-MB. For both patients, the electrodiagnostic studies indicated myopathy and the pathologic findings of biopsied muscles revealed myositis. Drug-induced polymyositis was suspected and the clevudine was finally withdrawn. The muscle weakness and laboratory findings were improved for both patients after conservative care. We report here on the first cases of polymyositis that may have been caused by administering the new nucleoside analog clevudine for treating HBV infection.
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PMID:Polymyositis in patients taking antiviral clevudine therapy: a report of two cases. 2020 82

Rhabdomyolysis, a term used to describe the rapid breakdown of striated muscle, is characterized by rupture and necrosis of muscle fibers. This process results in the release of cell breakdown products into the bloodstream and extracellular space. Although direct muscle injury remains the most common cause of muscle injury, additional causes include hereditary enzyme disorders, drugs, toxins, endocrinopathies, malignant hyperthermia, neuroleptic malignant syndrome, heatstroke, hypothermia, electrolyte alterations, diabetic ketoacidosis and non-ketotic hyperosmolar coma, severe hypo- or hyperthyroidism and bacterial or viral infections. The classic triad of symptoms includes muscle pain, weakness and dark urine, although more than 50% of the patients do not complain of muscle pain or weakness. Additional systemic symptoms include fever, general malaise, tachycardia, nausea and vomiting. The laboratory diagnosis is based essentially on the measurement of creatine kinase in serum or plasma. Plasma and urine myoglobin measurement might be useful in the early stages of the syndrome and for identifying a subset of patients with minor skeletal muscle injury. Patient monitoring is pivotal (the mortality rate is as high as 8%), and should be focused on preventing the detrimental consequences, that often include renal disease and coagulopathy. In the pre-hospital setting, forced hydration with 1.5-2 L of sterile saline solution should be started immediately, followed by 1.5-2 L/h. Following hospital admission, continuous hydration should be ensured, alternating the saline solution with a 5% glucose solution. In the presence of myoglobinuria, urine should be alkalinized by use of sodium bicarbonate solution. Clin Chem Lab Med 2010;48:749-56.
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PMID:Rhabdomyolysis: historical background, clinical, diagnostic and therapeutic features. 2044 60

Inflammatory myopathies are a heterogeneous group of conditions characterized by proximal muscle weakness, nonsuppurative inflammation of skeletal muscle, with elevated muscle enzyme levels and characteristic electromyography and muscle biopsy findings. The authors describe a clinical case of a young woman, admitted with a four day history of bilateral thigh myalgia. She was afebrile and without skin, mucosal or joint involvement. Thigh muscle palpation was painful. Complete blood count revealed leukopenia and thrombocytopenia. High levels of creatine kinase, serum aminotransferases and myoglobin were detected. Metabolic, toxic and drug-related causes were excluded as well as infectious diseases, malignant tumours and endocrine myopathies. Auto-antibodies for connective diseases were negative. Magnetic resonance imaging and electromyography of lower limbs were suggestive of inflammatory myopathy. Generalized muscle weakness and dysphagia were reported subsequently. Clinical and laboratorial improvement was seen after corticotherapy. Muscle biopsy revealed myopathy signs without inflammatory changes or vasculitis. After prednisolone reduction, presently without treatment, she remains asymptomatic with normal laboratorial findings. The authors emphasize in this case of inflammatory myopathy the unusual clinical and laboratory evolution and the importance of a cautious differential diagnosis.
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PMID:[Inflammatory myopathy with an unusual evolution]. 2071 Oct 99

Oral-ritodrine-hydrochloride-induced rhabdomyolysis is rare. We report a case of oral-ritodrine-hydrochloride-induced rhabdomyolysis in a pregnant woman with placenta previa without neuromuscular disorders. The patient was a 30-year-old, Japanese primigravida woman, who became pregnant spontaneously. At 23 gestational weeks, she was diagnosed as having placenta previa and prophylactic oral ritodrine hydrochloride (15 mg/day) was initiated. At 29 1/7 gestational weeks, she was referred to our hospital for perinatal management of placenta previa. Two days thereafter, vaginal bleeding accompanied by frequent uterine contractions occurred and she was admitted. On admission, laboratory tests revealed an abnormal increase of blood creatine kinase (CK) value of 7200 IU/L. CK-MB isoenzyme was 208 IU/L. Aspartate transaminase (163 IU/L), alanine transaminase (74 IU/L) and lactate dehydrogenase (536 IU/L) levels were also increased. The patient started to complain of extreme muscle pain in her upper and lower limbs and general weakness. The next day, laboratory tests revealed a tremendous increase of blood CK level of 87,300 IU/L, a blood myoglobin level of 11,200 ng/mL, and a urinary myoglobin level of 615 ng/mL. An emergency cesarean section was carried out. After delivery, the laboratory data improved gradually with the CK levels at 107 IU/L. If patients complain of muscular symptoms following oral ritodrine hydrochloride use, physicians should consider rhabdomyolysis.
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PMID:Rhabdomyolysis caused by tocolytic therapy with oral ritodrine hydrochloride in a pregnant woman with placenta previa. 2151 38


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