Medication Description: Levodopa (Levodopum)

LEVODOPA (Levodopum). (-) - 3- (3, 4-Dioxyphenyl) -1-alanine, or 3-hydroxy-1-tyrosine.

Synonyms: Kaldopa, Levopa, Avodopa, Bendopa, Biodopa, Brocadopa, Caldopa, Cicandopa, Dalutrin, Deadopa, Dopacin, Dopaflex, Dopal, Dopar, Dopastin, Doprin, Eopopa, Doparin Medidopa, Oridopa, Pardopa, Parkidopa, Parmidin, Speciadopa, Tonodopa, Veldopa, etc.

White crystalline powder, slightly soluble in water, insoluble in alcohol.

Dioxyphenylalanine (abbreviated as dopa, or dopa) is a nutrient formed in the body from tyrosine and is a precursor of dopamine, which in turn is a precursor of norepinephrine (see Adrenaline).

Due to the fact that during parkinsonism, the content of dopamine in the basal ganglia of the brain is reduced, for the treatment of this disease it is advisable to use substances that increase the content of this amine in the central nervous system. Dopamine itself cannot be used for this purpose, as it does not penetrate the blood-brain barrier very well. It turned out that instead of dopamine, its precursor, dioxyphenylalanine (dopa), can be used, which, when administered orally, is absorbed, penetrates into the central nervous system, undergoes decarboxylation, turns into dopamine and, replenishing its reserves in the basal ganglia, stimulates dopamine receptors and provides a therapeutic treatment for parkinsonism .

A synthetic levorotatory isomer of dioxyphenylalanine - L-Dopa, which is much more active than the programal isomer, is used as a drug.

Levodopa is well absorbed when taken orally. The maximum concentration in the blood plasma is observed after 1 - 2 hours after administration. Excreted to a large extent (over 75%) by the kidneys, partly with feces.

Most of the levodopa is converted by decarboxylation in the tissues (liver, kidney, intestine) into dopamine, which does not penetrate the blood-brain barrier. To reduce the decarboxylation of levodopa is used with inhibitors of dof-decarboxylase (see Nakom, Madopar).

The use of L-DOPA in parkinsonism reduces primarily hypokinesia and rigidity, to a lesser extent and later, tremor, dysphagia, and drooling decrease. It is established that the therapeutic effect is achieved in 50 - 60% of patients. The rest of the effect is poorly expressed, the dose of the drug can not be increased due to side effects.

Prescribe the drug in Parkinson’s disease and symptomatic (postencephalitic, atherosclerotic, toxic) parkinsonism. There are indications of the efficacy of the drug in hereditary extrapyramidal diseases characterized by akinetorigidny syndrome. The effectiveness of L-Dopa in the treatment of deforming muscular dystonia has also been found. There is evidence of the treatment of L-DOPA reactive stuporous states (especially in patients with reduced dopamine excretion).

As a corrector in cases of parkinsonism caused by neuroleptics, L-Dov is not prescribed.