No abstract available.
Anticonvulsants* ; Carnitine* ; Liver*

No abstract available.
Carnitine* ; Renal Dialysis*

No abstract available.
Animals ; Carnitine* ; Heart* ; Myocardium* ; Rats*

No abstract available.
Adult ; Carnitine ; Hepatitis ; Humans ; Transferases

PURPOSE: Epileptic patients under prolonged treatment with anticonvulsants such as valproate tend to have low serum carnitine level. The object of this study is to observe the interrelationship between anticonvulsants and serum carnitine level and its related symptoms. METHODS: We measured the serum carnitine levels in 31 epileptic patients (18 males, 13 females) receiving diverse antiepileptic drugs and 32 healthy children (20 males, 12 females) using enzymatic cycling method. RESULTS: 1) Among the control group, total, free, and acyl-carnitine in serum were 50.04+/-11.44, 37.42+/-11.13, and 13.98+/-7.49micro mol/L (mean+/-S.D.), respectively, and no significant differences were observed between age and sex. 2) Among 31 patients with treatment, total serum carnitine level and free carnitine level below 2 standard deviation from the mean control value was not observed. 3) Among 31 patients with treatment, total serum carnitine level below 2 standard deviation from the age matched mean control value was not observed. 4) No significant relationship was observed between the serum carnitine level and the dosage, duration and the serum concentration of the antiepileptic drugs. 5) There were no abnormalities in serum AST, ALT levels among the patients treated. CONCLUSION: Although our study didn't reveal that serum carnitine level can be lowered in patients treated with anticonvulsants such as valproate, many others reported it. So periodic measurement of serum carnitine level before and after treatment with anticonvulsants should be considered.
Anticonvulsants* ; Carnitine* ; Child* ; Humans ; Male ; Valproic Acid

PURPOSE: The purpose of this study is to review the evidence comparing the efficacy and safety between L-carnitine and extracorporeal elimination therapy in the management of acute valproic acid L-carnitine vs Extracorporeal Elimination for Acute Valproic acid Intoxication METHODS: PubMed, Embase, Cochrane library, Web of Science, KoreaMed, KMbase, and KISS were searched, using the terms carnitine and valproic acid. All studies, regardless of design, reporting efficacy or safety endpoints were included. Reference citations from identified publications were reviewed. Both English and Korean languages were included. Two authors extracted primary data elements including poisoning severity, presenting features, clinical management, and outcomes. RESULTS: Thirty two articles including 33 cases were identified. Poisoning severity was classified as 3 mild, 11 moderate, and 19 severe cases. Nine cases were treated with L-carnitine while 24 cases received extracorporeal therapy without L-carnitine. All patients except one expired patient treated with hemodialysis recovered clinically and no adverse effects were noted. A case report comparing two patients who ingested the same amount of valproic acid showed increased ICU stay (3 vs 11 days) in case of delayed extracorporeal therapy. CONCLUSION: Published evidence comparing L-carnitine with extracorporeal therapy is limited. Based on the available evidence, it is reasonable to consider L-carnitine for patients with acute valproic acid overdose. In case of severe poisoning, extracorporeal therapy would also be considered in the early phase of treatment.
Carnitine* ; Humans ; Poisoning ; Renal Dialysis ; Valproic Acid*

No abstract available.
Cardiomyopathy, Dilated* ; Carnitine* ; Estrogens, Conjugated (USP)*

Carnitine is necessary for transport of long-chain fatty acids into mitochondria, to enter the beta-oxidation cycle. Four carnitine cycle defects have been described. The carnitine transporter mediates carnitine transport across the plasma membrane. Symptoms include hypoketotic hypoglycaemia and cardiomyopathy. Some affected subjects are asymptomatic. Newborn screening detects very low levels of free carnitine in some but not all. Carnitine palmitoyltransferase type IA (CPTI) transports long-chain fatty acyl-CoAs across the outer mitochondrial membrane. Affected infants have hypoketotic hypoglycaemia with catabolic stress, but otherwise remain well. Newborn screening tests reveal elevated free carnitine, (elevated C0/C16+C18). Sensitivity is unclear and confirmation needs leukocyte or fibroblast assays. Carnitine-acylcarnitine translocase transfers fatty acylcarnitines across the inner mitochondrial membrane. The most common presentation is sudden death in the first days. Carnitine palmitoyltransferase type II (CPTII) converts long-chain acylcarnitines to long-chain acylCoAs for beta-oxidation. Severe deficiency is lethal. Newborn screening for both disorders reveals elevated palmitoylcarnitine and enzymology or mutation analysis is needed for diagnosis. Late-onset CPTII is the most common disorder, presenting as muscle pain and rhabdomyolysis on severe exercise. All 4 disorders can be detected by newborn screening, with variable sensitivity. Late-onset CPTII probably cannot be detected. Carnitine transporter, CPTI and late-onset CPTII have proven treatment strategies.
Carnitine ; metabolism ; Carnitine O-Palmitoyltransferase ; deficiency ; Humans ; Infant, Newborn ; Metabolism, Inborn Errors ; diagnosis ; enzymology ; Neonatal Screening

Carnitine O-Palmitoyltransferase ; deficiency ; Female ; Humans ; Infant, Newborn

No abstract available.
Blood Platelets* ; Carnitine* ; Humans* ; Platelet Activating Factor* ; Spermatozoa*