EMG changes in chronically dialyzed uraemic subjects undergoing d, 1-Carnitine treatment

Rossini, Paolo Maria; Marchionno, L.; Gambi, D.; Pirchio, M; Rosso, Goffredo Del; Albertazzi, A

doi:10.1007/bf02335405

Cited by 6 publications

(2 citation statements)

References 20 publications

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“…The D-isomer and the racemate (D,L-carnitine) are contraindicated. Historic use of racemic D,L-carnitine was associated with myasthenialike syndromes and cardiac dysrhythmias, which disappeared after L-carnitine administration [228]. D-Carnitine also competitively depletes cardiac and skeletal muscles and kidneys of L-carnitine [229].…”

Section: L-carnitinementioning

confidence: 99%

Drugs and pharmaceuticals: management of intoxication and antidotes

Smith

2010

Experientia Supplementum

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The treatment of patients poisoned with drugs and pharmaceuticals can be quite challenging. Diverse exposure circumstances, varied clinical presentations, unique patientspecific factors, and inconsistent diagnostic and therapeutic infrastructure support, coupled with relatively few definitive antidotes, may complicate evaluation and management. The historical approach to poisoned patients (patient arousal, toxin elimination, and toxin identification) has given way to rigorous attention to the fundamental aspects of basic life supportairway management, oxygenation and ventilation, circulatory competence, thermoregulation, and substrate availability. Selected patients may benefit from methods to alter toxin pharmacokinetics to minimize systemic, target organ, or tissue compartment exposure (either by decreasing absorption or increasing elimination). These may include syrup of ipecac, orogastric lavage, activated single-or multi-dose charcoal, whole bowel irrigation, endoscopy and surgery, urinary alkalinization, saline diuresis, or extracorporeal methods (hemodialysis, charcoal hemoperfusion, continuous venovenous hemofiltration, and exchange transfusion). Pharmaceutical adjuncts and antidotes may be useful in toxicant-induced hyperthermias. In the context of analgesic, anti-inflammatory, anticholinergic, anticonvulsant, antihyperglycemic, antimicrobial, antineoplastic, cardiovascular, opioid, or sedative-hypnotic agents overdose, N-acetylcysteine, physostigmine, L-carnitine, dextrose, octreotide, pyridoxine, dexrazoxane, leucovorin, glucarpidase, atropine, calcium, digoxin-specific antibody fragments, glucagon, high-dose insulin euglycemia therapy, lipid emulsion, magnesium, sodium bicarbonate, naloxone, and flumazenil are specifically reviewed. In summary, patients generally benefit from aggressive support of vital functions, careful history and physical examination, specific laboratory analyses, a thoughtful consideration of the risks and benefits of decontamination and enhanced elimination, and the use of specific antidotes where warranted. Data supporting antidotes effectiveness vary considerably. Clinicians are encouraged to utilize consultation with regional poison centers or those with toxicology training to assist with diagnosis, management, and administration of antidotes, particularly in unfamiliar cases.

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Section: L-carnitinementioning

confidence: 99%

Drugs and pharmaceuticals: management of intoxication and antidotes

Smith

2010

Experientia Supplementum

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“…Therefore, in this study, only 2 g 3 times weekly was given followed by 1 g 3 times weekly after 6 months. Since D.L-carnitine may provoke a myasthenic-like syn drome [12][13][14], only L-carnitine was used in this study. Because depletion of plasma and muscle carnitine is much greater with HD than with peritoneal dialysis, and because skeletal muscle carnitine deficiency is more se vere with long-term HD than with peritoneal dialysis [9], only patients receiving HD were selected.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the Effect of Intravenous <i>L</i>-Carnitine Therapy on Function, Structure and Fatty Acid Metabolism of Skeletal Muscle in Patients Receiving Chronic Hemodialysis

Siami

Clinton

Mrak

et al. 1991

Nephron

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Chronic hemodialysis (HD) leads to significant losses of carnitine from plasma and muscle. Because L-carnitine is important in the production of energy from fatty acid oxidation (FAO) in muscle, we examined the role of carnitine replacement by administering therapeutic doses of intravenous carnitine to 14 male patients receiving HD. Placebo or carnitine was given 2 g i.v. 3 times weekly for 6 months in a double-blind manner. To evaluate long-term toxicity of carnitine, all patients subsequently received 1 g i.v. carnitine for 10 months. Patients were rated for muscle strength each week. After 6 months, definite improvement in strength occurred in 4 of 7 carnitine-treated patients and in none of 7 controls. During the subsequent 10 months of carnitine administration, no adverse effects were noted and muscle strength improved in 9 of 14 patients. Muscle biopsy was performed in 13 patients before and after the first 6 months of treatment and in 6 healthy controls. FAO and carnitine were measured in each muscle biopsy. FAO was significantly lower in both carnitine- and placebo-treated HD patients compared to healthy controls. Although carnitine therapy increased the muscle concentration of carnitine 3-fold in muscle of HD patients, muscle FAO did not increase significantly and never reached the level of healthy controls. Muscle histopathology and ultrastructure were not specific for HD myopathy. Carnitine may be useful in treating some patients with muscle weakness related to HD.

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