Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024591 (malignant hyperthermia)
 2,353 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myoglobinuria or rhabdomyolysis occurs when myoglobin escapes into the blood and then into the urine after acute muscle necrosis. It can be a serious medical condition leading to renal failure and death. There are many causes including exertion, crush syndromes, ischaemia, metabolic disorders, exogenous toxins and drugs, heat stroke and hereditary disorders such as malignant hyperthermia. We report the case of a 17 year-old boy who developed myoglobinuria, renal failure and death 11 days after ingesting sodium monensin, possibly with the intention of developing muscles. Sodium monensin, the active principle of Rumensin(R), is a dietary additive used as a growth promoter for confined cattle. There are no previous reports of human intoxication. Accidental or experimental sodium monensin intoxication in animals produces similar findings to those seen in this case.
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PMID:Fatal rhabdomyolysis after acute sodium monensin (Rumensin) toxicity: case report. 1158 43

Rhabdomyolysis is a disorder characterized by acute damage of the sarcolemma of the skeletal muscle leading to release of potentially toxic muscle cell components into the circulation, most notably creatine phosphokinase (CK) and myoglobin, and is frequently accompanied by myoglobinuria. Therefore, the term myoglobinuria is often used interchangeably with the term rhabdomyolysis. This disorder may result in potential life-threatening complications such as acute myoglobinuric renal failure, hyperkalemia and cardiac arrest, disseminated intravascular coagulation, and compartment syndrome. The condition is etiologically heterogeneous and may result from a large variety of diseases affecting muscle membranes, membrane ion channels, and muscle energy supply including acquired causes (e.g., exertion, crush injury and trauma, alcoholism, drugs, and toxins) and hereditary causes (e.g., disorders of carbohydrate metabolism, disorders of lipid metabolism, or diseases of the muscle associated with malignant hyperthermia). In many patients with idiopathic recurrent rhabdomyolysis, specific inherited metabolic defects have not been recognized up to now.
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PMID:[Rhabdomyolysis and myoglobinuria]. 1279 89

The phenylalkylamine derivatives, 3,4-methylenedioxymethamphetamine (MDMA, ecstasy, XTC, Adam), 3,4-methylenedioxyethamphetamine (MDEA, MDE, Eve), and 3,4-methylenedioxyamphetamine (MDA), are psychostimulants with hallucinogenic properties. MDA is also a metabolite of both MDMA and MDEA. These drugs are ring-substituted amphetamine derivatives that produce hallucinogenic, entactogenic ('love drug'), and stimulating effects. MDMA was initially developed as an appetite suppressant, however, its use as a therapeutic drug has been very limited. Because of its effects as a hallucinogenic psychostimulant with relatively low toxicity, it has emerged over the last two decades as a common recreational psychostimulant or 'club drug' at 'raves'. MDMA, MDEA, and MDA are often referred to as 'rave' or 'designer' drugs. They are produced in clandestine laboratories and have an increasing presence on the illicit drug market worldwide. Significant adverse health effects have been reported that include: serotonin neurotoxicity, severe psychiatric disorders, renal failure, malignant hyperthermia, hepatitis, rhabdomyolysis, and disseminated intravascular coagulation. A number of fatal outcomes associated with severe MDMA intoxication have been reported.
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PMID:Measurement of 3,4-MDMA and related amines in diagnostic and forensic laboratories. 1591 45

A 65-year-old man underwent parathyroidectomy for hyperparathyroidism secondary to renal failure. Intra-operatively he received methylene blue infusion (7.5 mg.kg(-1), a total of 650 mg in 500 ml 0.9% sodium chloride) for visualisation of parathyroid glands. At the end of surgery, following extubation he developed agitation, intense shivering and hyperpyrexia, and his level of consciousness decreased to a Glasgow Coma score of 7. The differential diagnoses included methylene blue toxicity or malignant hyperpyrexia. His lungs were ventilated, and intravenous dantrolene was administered to control hyperpyrexia. Haemodialysis was started to remove the methylene blue dye. We review the literature on the pharmacological actions of methylene blue, and discuss the differential diagnosis and management of this patient.
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PMID:Hyperpyrexia and prolonged postoperative disorientation following methylene blue infusion during parathyroidectomy. 1715 45

A 57-year-old man with lung tumor was scheduled for right middle lobectomy under general anesthesia. The patient received glycerin enema 2 hours before anesthesia. Anesthesia was induced with propofol, fentanyl, ketamine and vecuronium. After the induction, urine of dark-red color was drained through the urinary catheter. Massive (3+) occult blood and few erythrocytes in the urine sediment were observed. Furthermore, blood analysis showed hemolysis with mild renal dysfunction (Cr 1.3 mg x dl(-1)). Although serum CPK and myoglobin increased, there was no apparent symptom that supported the onset of rhabdomyolysis induced by anesthetics, acute myocardial infarction or malignant hyperthermia. At this time, we noticed that blood sample taken before the induction had been hemolysed. With all the above information in mind, we suspected that the main cause of the hemoglobinuria could be the enema and the surgery was canceled. The patient made a good progress with laboratory data normalized on the 4th postanesthesia day. However, rectal ulcer developed as a possible late complication of the enema. Although it is well-known that glycerin enema could cause hemolysis, renal failure and rectal ulcer, the increase of CPK and myoglobin in serum made the diagnosis difficult from other conditions leading to rhabdomyolysis in this case.
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PMID:[Case of hemoglobinuria following glycerin enema]. 1757 10

Malignant hyperthermia (MH) is an uncommon and potentially life-threatening pharmacogenetic disorder. This abnormality in muscle metabolism can be triggered by a variety of agents (particularly general anesthetics and stress), resulting in a rapid heart rate increase, muscle rigidity, acidosis, temperature elevation, rhabdomyolysis, and renal failure. Immediate discontinuing of triggering agents, oxygenation, cooling, and dantrolene are necessary to treat an episode. MH-susceptible patients often indicate a positive family history of experiencing an adverse event during anesthesia. Few diagnostic tests are available to screen patients; the most accurate test is a skeletal muscle biopsy. MH-susceptible patients can undergo surgical procedures as necessary. Careful exploration of the medical history will allow the clinician to make the necessary modifications to treat and manage an episode expediently.
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PMID:Malignant hyperthermia and its implications in general dentistry. 1981 13

Human skeletal muscles contain the largest single pool of K+ in the body (2600 mmol, 46 times the total K+ content of the extracellular space). Intense exercise may double arterial plasma K+ in one min. This is because of excitation-induced release of K+ from the working muscle cells via K+ channels. This hyperkalemia is rapidly corrected by reaccumulation of K+ into the muscle cells via Na+,K+ pumps, often leading to hypokalemia. Hyperkalemia may also arise from muscle cell damage, excessive oral or intravenous administration of K+, acidosis, renal failure, depolarization of muscle cells with succinyl choline, activation of K+ channels by fluoride poisoning, hyperkalemic periodic paralysis, malignant hyperthermia, inhibition of the Na+,K+ pumps by digitalis glycosides or treatment with nonselective beta blockers. Hyperkalemia may cause arrhythmia and can be treated with beta2 agonists, insulin or hemodialysis. Hypokalemia may be induced by the stimulation of the Na+,K+ pumps in skeletal muscles seen postexercise, or by catecholamines, beta2 agonists, pheochromocytoma, theophylline, caffeine or insulin, by sepsis, myocardial infarction, trauma, burns and heart failure. Rare causes are hypokalemic periodic paralysis, inhibition of K+ channels by barium, chloroquine or barbiturates. Hypokalemia often reflects dietary K+ deficiency, alkalosis, renal or gastrointestinal loss of K+. Hypokalemia is more likely to cause arrhythmia than hyperkalemia and can be treated by oral or intravenous administration of K+ under frequent control of electrocardiogram and plasma K+. Because of their size and high contents of K+, Na+,K+ pumps and K+ channels, the skeletal muscles play a central role in the acute, from min-to-min ongoing regulation of plasma K+. This is decisive for the maintenance of muscle contractility and heart function.
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PMID:Hormonal and pharmacological modification of plasma potassium homeostasis. 2061 71

When assessing an acute coronary syndrome (ACS) by means of high serum levels of creatine kinase (CK) and its MB fraction (CK-MB), one must keep in mind that there are several other causes for an increase of these markers, such as myocarditis, pericarditis, heart failure, severe aortic stenosis, stroke, renal failure, malignant hyperthermia, Reye syndrome, polymyositis, and borreliosis (1). Also, there are cases when CK-MB is falsely increased due to certain abnormalities that occur in the CK isoenzymes. One such example is the formation of the so-called macro-creatine kinase complexes (macro-CK) that give a false increase of the CK-MB fraction. We report two clinical cases where macro-CK was the cause of apparent increase in serum CK and CK-MB: in a 79-year old male with a history of coronary disease and a 82-year old female with permanent atrial fibrillation.
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PMID:Macro-creatine kinase syndrome as an underdiagnosed cause of ck-mb increase in the absence of myocardial infarction: two case reports. 2370 Aug 84

Malignant hyperthermia syndrome is a family myopathy of pharmacogenetic nature, which appears as a skeletal muscle hypercatabolic syndrome linked to anesthesia. The incidence in pediatrics is 1 event per 10 000 surgeries. The clinical picture may have a rapid onset associated with succinylcholine, or a late onset related to inhalation agents. The clinical picture includes tachycardia, hyperthermia, hypercapnia, acidosis, muscle rigidity, hyperkalemia, renal failure and arrhythmia. Mortality without specific treatment is of 80% and drops to 7% with the use of dantrolene sodium. We report an 8-year-old patient admitted for phimosis surgery; having tachycardia, hypercapnia and muscle rigidity, he started treatment with dantrolene sodium in the operating room, which was maintained for 72 hours. He evolved the first 12 hours with low cardiac output and creatine phosphokinase maximum of 155,147 U/L. He remained with mechanical ventilation for 48 hours. Discharge was given on the sixth day without sequelae.
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PMID:[Malignant hyperthermia syndrome: case report]. 2572 36

Malignant hyperthermia is a hypermetabolic syndrome that appears in susceptible patients after exposure to certain anaesthetic drugs (succinylcholine, inhalation anaesthetics). Its incidence in Spain is 1 in 40,000 adults, with a 10% mortality rate. It is induced by an abnormal regulation of the ryanodine receptors, producing a massive release of calcium from the sarcoplasmic reticulum in the striate muscle. Clinical manifestations include: CO2 increase, tachycardia, haemodynamic instability, metabolic and respiratory acidosis, profuse sweating, hyperpyrexia, CPK increase, myoglobinuria, kidney failure, disseminated intravascular coagulation (DIC), and ending in cardiac arrest. Dantrolene sodium is a ryanodine receptor antagonist, and inhibits the release of intracellular calcium. Definitive diagnosis is achieved by the exposure of muscle fibres to caffeine and halothane. Protocols can help guarantee a reliable and secure management when this severe event occurs.
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PMID:Clinical protocol for the management of malignant hyperthermia. 2763 84


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