EFE-CARN by Pisa farmaceutica, Mexico
Packing: 5×5 ml, 1 g of l-carnitine per ampoule
EFE-CARN is indicated for pathologies with its deficiency of primary origin: Genetic damage of normal biosynthesis or the use of levocarnitine from the diet.
In pathologies of secondary origin: Levocarnitine deficiencies that are accompanied by severe organic aciduria.
Levocarnitine deficiencies appear as: Elevation of triglycerides and increased concentration of free fatty acids, reduced ketogenesis, malnutrition in low birth weight and premature infants. Lipid infiltration of liver and muscle (Fatty liver, hepatic coma, liver cirrhosis, hepatomegaly, hepatic encephalopathy).
Severe chronic deficiency that can present as: Hypoglycemia (diabetes mellitus, diabetic ketoacidosis, endogenous obesity, hypothyroidism, Addison’s disease, Cushing’s syndrome); Progressive myasthenia, hypotonia, lethargy.
Catabolic states of levocarnitine (kidney failure treated with dialysis or hemodialysis, burns, sepsis, pregnancy, treatment with antineoplastics, treatments with valproic acid, surgeries and hyperthyroidism).
Neurological alterations, alterations in development and pediatric growth, as a nutritional supplement for athletes without previous pathologies, as a treatment for exogenous obesity.
PHARMACOKINETICS AND PHARMACODYNAMICS: L-Carnitine is a natural substance in the body of mammals, some plants and yeasts, being important in humans for the oxidation of fatty acids, facilitates the aerobic metabolism of carbohydrates, increases the rate of oxidative phosphorylation and favors the excretion of some organic acids.
Beta-oxidation of fatty acids at the mitochondrial level produces energy (in ATP) for which specific translocases in the mitochondrial and plasma membrane easily transport both free carnitine and its esters (acylcarnitines) from the cytosol to the interior of the mitochondria .
Fatty acid esters (of CoA) are formed almost exclusively in the cytosol and are not transported across the membrane; it also inhibits enzymes of the Krebs cycle; thus, fatty acid oxidation requires the formation of acylcarnitines and their translocation to the mitochondria, where CoA esters are reformed and metabolized to produce energy.
Catabolic states cause important metabolic changes with high energy consumption, in such a way that the demand for levocarnitine increases for the use of energy by oxidation of lipids and ketone bodies and amino acid chains.
Carnitine is synthesized from lysine residues in various proteins: The process begins with the formation of 6-N-trimethyl-lysine, through a series of reactions that include S-adenosyl-methionine, four micronutrients are required for the various enzymatic steps (ascorbic acid, niacin, pyridoxine and iron). Levocarnitine is known as part of the water-soluble vitamins and the B complex (BT).
Dietary levocarnitine is almost completely absorbed from the intestine (jejunum) largely by a saturation-sensitive transport mechanism; carnitine is transported into all cells by an active mechanism.
D-carnitine is also transported and can block the uptake of L-carnitine. Most carnitine is excreted in the urine and feces as acylcarnitine; 90% of unesterified carnitine is reabsorbed by the renal tubules.
DOSAGE AND ADMINISTRATION ROUTE: EFE-CARN is administered parenterally (intramuscularly or intravenously).
The usual dose is 50-100 mg/kg/day, both in adults and children two to three times a day.
Primary carnitine deficiency: Up to 4 g/day.
Nephropathy: In patients with prolonged hemodialysis of 40-80 mg/day, if the intravenous route is preferred, it is recommended to dilute it in the solutions (used after hemodialysis) and pass it slowly.
Cardiomyopathies and cardiovascular diseases of ischemic origin (coronary atherosclerosis, congestive heart failure, myocardial ischemia and intermittent claudication): An intravenous or intramuscular dose of 50 mg/kg/day is recommended.