Product Overview
Composition
1 tab. contains:
active substances:
levodopa - 250 mg,carbidopa - 25 mg;
Excipients:
pregelatinized starch - 45 mg;
corn starch - 6.5 mg;
blue dye (indigotine E132) - 0, -72 mg;
magnesium stearate - 4.2 mg;
MCC - up to 380 mg.
pharmachologic effect
The anti-Parkinsonian effect of levodopa is due to its conversion to dopamine directly in the central nervous system, which leads to the replacement of dopamine deficiency in the central nervous system (CNS). Dopamine formed in peripheral tissues does not participate in the implementation of the antiparkinsonian effect of levodopa (does not penetrate the central nervous system) and is responsible for most of the side effects of levodopa.
Carbidopa is an aromatic L-amino acid decarboxylase inhibitor that reduces the formation of dopamine in peripheral tissues, which indirectly leads to an increase in the amount of levodopa entering the central nervous system.
Nakom® provides an adequate reduction in symptoms of Parkinson's disease in a larger number of patients. The effect of the drug manifests itself during the first day from the start of administration, sometimes after taking the first dose. The maximum effect is achieved within 7 days.
Indications
Parkinson's disease treatment.
Contraindications
• hypersensitivity to the components of the drug;
• simultaneous administration of non-selective monoamine oxidase inhibitors (MAO);
• an interval of less than two weeks after the end of the intake of MAO inhibitors;
• angle-closure glaucoma;
• melanoma or suspicion of it;
• skin diseases of unknown etiology;
• age up to 18 years (the safety of the drug in children of younger and middle age has not been established);
• lactation period.
Carefully
• myocardial infarction with arrhythmias (history);
• chronic heart failure and other serious diseases of the cardiovascular system;
• severe lung diseases, including bronchial asthma;
• epileptic and other convulsive seizures (history);
• erosive and ulcerative lesions of the gastrointestinal tract (risk of bleeding from the upper gastrointestinal tract);
• diabetes mellitus and other decompensated endocrine diseases;
• severe renal and / or liver failure;
• open-angle glaucoma;
• extrapyramidal reactions caused by the use of the drug;
• pregnancy.
Side effects
The most common side effects are dyskinesias, including choreoid, dystonic, and other involuntary movements, as well as nausea. Muscle twitching and blepharospasm may be considered early signs on the basis of which a decision can be made to reduce the dose.
Benign, malignant and unspecified neoplasms, including cysts and polyps,
frequency unknown: malignant melanoma.
From the hemopoietic organs: rarely: leukopenia, anemia (including hemolytic), thrombocytopenia, agranulocytosis.
From the immune system: rarely: angioedema.
From the side of metabolism: often: anorexia; frequency unknown: loss or weight gain, edema.
From the psyche: often: sleep disturbance, including nightmares, hallucinations, depression (including with suicidal intentions), confusion; infrequently: agitation; rarely: psychotic reactions, including delusions, and paranoid thinking, increased libido.
Patients receiving dopamine antagonists exhibit pathological gambling addictions, hypersexuality, compulsive waste (craving for shopping), gluttony and overeating, increased libido. The reactions listed above basically disappeared after a dose reduction or cessation of treatment.
frequency unknown: anxiety, disorientation, euphoria, insomnia, bruxism.
From the nervous system:
very often: dyskinesias, including chorea, dystonia and other involuntary movements;
often: episodes of bradykinesia ("on-off" syndrome), dizziness, paresthesia, drowsiness, including less commonly drowsiness in the daytime and episodes of sudden falling asleep;
infrequently: syncope;
rarely: dementia, convulsions;
unknown frequency: ataxia, tremor of hands, extrapramidal disorders, malignant antipsychotic syndrome, muscle twitching, headache, decreased severity of intelligence, trismus, activation of the Bernard-Horner latent syndrome, insomnia, nervousness, euphoria, numbness, fainting, falling, impaired gait, feeling irritations, compulsions.
Convulsions have been reported, but a causal relationship with Nakom® has not been established.
From the sensory organs: frequency unknown: blepharospasm, diplopia, impaired vision, dilated pupils, oculogyric crises (tonic convulsions of the external muscles of the eyeball).
From the cardiovascular system: often: heart palpitations, orthostatic reactions, including episodes of lowering blood pressure; rarely: arrhythmias, phlebitis, increased blood pressure; frequency unknown: hot flashes, hyperemia.
From the respiratory system: often: shortness of breath; frequency unknown: hoarseness, abnormal breathing pattern.
From the gastrointestinal tract: often: vomiting, diarrhea; rarely: gastrointestinal bleeding, exacerbation of a duodenal ulcer, darkening of saliva; frequency unknown: dry oral mucosa, salivation, dysphagia, abdominal pain, constipation, bloating, dyspepsia, burning sensation of the tongue, a feeling of bitterness in the mouth, nausea, belching.
From the skin: infrequently: urticaria; rarely: itching, hemorrhagic vasculitis (Shenplein-Genoch purpura), alopecia, rash, sweat darkening; unknown frequency: increased sweating.
From the urinary system: rarely: dark urine; frequency unknown: urinary incontinence, urinary retention.
From the side of musculoskeletal and connective tissue: infrequently: muscle cramps; frequency unknown: muscle twitching.
From the reproductive system: frequency unknown: priapism.
General disorders and disorders at the injection site: often: chest pain; frequency unknown: asthenia, swelling, weakness, malaise, fatigue, malignant antipsychotic syndrome.
Laboratory indicators:
frequency unknown: increased activity of alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, increased bilirubin, urea nitrogen in blood plasma, urea in blood plasma, hypercreatininemia, hyperuricemia, a positive Coombs test.
It was reported a decrease in hemoglobin and hematocrit, hyperglycemia, leukocytosis, bacteriuria, hematuria.
Preparations containing carbidopa and levodopa can cause a false-positive reaction to ketone bodies in the urine if test strips are used to determine ketonuria. This reaction will not change after boiling urine samples. False negative results can be obtained using the glucose oxidase method for determining glucosuria.
Interaction
With simultaneous use with antihypertensive drugs, it is necessary to adjust the dose of the latter due to the risk of orthostatic hypotension.
With the simultaneous use of levodopa with monoamine oxidase inhibitors (MAOs) (with the exception of MAO-B inhibitors), circulatory disorders are possible (taking MAO inhibitors should be stopped at least 2 weeks before taking the drug).
This is due to the accumulation of dopamine and norepinephrine under the influence of levodopa, the inactivation of which is inhibited by MAO inhibitors, and a high likelihood of developing excitation, increased blood pressure (BP), tachycardia, facial redness, and dizziness.
Iron salts may decrease the bioavailability of levodopa and carbidopa; the clinical significance of this interaction is unknown.
With the simultaneous use of levodopa with β-adrenergic agonists, dithilin and drugs for inhalation anesthesia, an increased risk of developing heart rhythm disorders is possible.
D2 dopamine receptor antagonists (e.g. derivatives of butyrophenone, diphenylbutylpiperidine, thioxanthene, phenothiazine, risperidone), as well as isoniazid, reduce the therapeutic effect of levodopa.
There are reports of blocking the positive therapeutic effect of levodopa as a result of taking phenytoin and papaverine.
Lithium preparations increase the risk of dyskinesia and hallucinations.
Methyldopa enhances side effects.
The simultaneous use of tubocurarine increases the risk of arterial hypotension.
Levodopa absorption may be impaired in patients on a high protein diet because levodopa competes with certain amino acids.
Carbidopa inhibits the action of pyridoxine hydrochloride (vitamin B6), which accelerates the metabolism of levodopa to dopamine in peripheral tissues.
How to take, course of administration and dosage
The dose should be selected individually for each patient, which may require both correction of the individual dose and the frequency of administration of the drug. The shape of the tablet allows you to divide it into two parts with minimal effort.
The initial daily dose is 1/2 (half) of the tablet 1 or 2 times a day. However, this may not provide the optimal amount of carbidopa needed by many patients. If necessary, 1/2 tablet should be added every day or every other day until the optimum effect is achieved. The effect is observed already in the first day, sometimes after a single dose. The full effect of the drug is achieved in up to seven days.
The studies revealed that the saturation of peripheral decarboxylases of aromatic 1-amino acids is achieved by the introduction of 70-100 mg of carbidopa per day.
If the patient receives a lower dose of carbidopa, the likelihood of nausea and vomiting is higher.
When prescribing Nakom®, you can continue to take standard antiparkinsonian drugs (with the exception of levodopa as monotherapy), and dose adjustment is required.
Transition from levodopa preparations. Levodopa should be discontinued at least 12 hours before the start of treatment with Nakom® (24 hours in the case of prolonged action of levodopa drugs). The daily dose of Nakom® should provide approximately 20% of the previous daily dose of levodopa.
For patients taking more than 1500 mg of levodopa, the initial dose of Nakom® is 25/250 mg 3 or 4 times a day.
Maintenance therapy If necessary, the dose of Nakom® can be increased by 1 tablet every day or every other day until the maximum dose is reached - 8 tablets per day. Experience with a daily dose of carbidopa in excess of 200 mg is limited.
The maximum recommended dose is eight tablets of Nakom® per day (200 mg of carbidopa and 2000 mg of levodopa), which corresponds to approximately 3 mg / kg of carbidopa and 30 mg / kg of levodopa per kilogram of body weight with a patient weighing 70 kg.
Elderly patients: there is extensive experience in the use of levodopa and carbidopa in elderly patients.
Dose adjustment is not required.
Patients with renal / hepatic insufficiency: dose adjustment is not required.
Overdose
Treatment: gastric lavage, intake of activated carbon; careful monitoring and electrocardiographic monitoring should be provided in order to detect arrhythmias in a timely manner, and if necessary, adequate antiarrhythmic therapy should be carried out.
Measures for acute overdose of the drug Nakom® are basically the same as for acute overdose of levodopa. It should be noted that pyridoxine is not effective for removing the effect of the drug Nakom®.
It is also necessary to take into account concomitant therapy, which the patient receives along with the drug Nakom®.
Special instructions
Nakom® can be prescribed to patients who are already taking levodopa in monotherapy. However, the administration of levodopa in a single-component form must be stopped at least 12 hours before the appointment of the drug Nakom®.
In patients who previously took only levodopa, dyskinesias may occur, since carbidopa provides more efficient penetration of levodopa into the brain and, therefore, more dopamine is formed. If dyskinesia occurs, a dose reduction may be required.
Like levodopa, levodopa / carbidopa can cause involuntary movements and mental disorders. It is believed that these reactions are associated with an increase in dopamine levels in the brain after administration of levodopa, and the use of levodopa / carbidopa can cause relapse. Dose reduction may be required.
All patients should be closely monitored for the development of depression with concomitant suicidal tendencies.
In the treatment of patients who have previously been observed or are currently experiencing signs of psychosis, precautions should be observed.
Caution should be exercised with the concomitant administration of psychoactive drugs and levodopa / carbidopa). In some patients, blepharospasm may be an early sign of an overdose.
As with levodopa, when prescribing Nakom® to patients who have had myocardial infarction and have a history of atrial, nodular, or ventricular arrhythmias, a thorough preliminary examination is necessary.
Such patients are advised to regularly conduct cardiological examinations, especially when prescribing the first dose and during the selection of doses.
Levodopa / carbidopa should be used with caution in patients with severe cardiovascular or pulmonary diseases, bronchial asthma, kidney, liver, endocrine diseases or with indications of peptic ulcer (due to the possibility of gastrointestinal bleeding from the upper digestive tract) or history of cramps.
Patients with open-angle glaucoma while taking Nakom® should regularly monitor intraocular pressure.
MAO inhibitors should be discontinued at least two weeks before the start of treatment with Nacom®.
With the sudden cancellation of antiparkinsonian drugs, it is possible to develop a symptom complex resembling a malignant antipsychotic syndrome (muscle rigidity, fever, mental disorders and an increase in the concentration of serum creatinine phosphokinase). It is necessary to carefully examine patients during a period of a sharp decrease in the dose of Nakom® or its withdrawal, especially if the patient receives antipsychotic drugs.
Levodopa was accompanied by drowsiness and episodes of sudden falling asleep.
Extremely rarely reported cases of sudden falling asleep during daily activities, in some cases without awareness or warning signs.
If these symptoms appear, it is recommended that you consider reducing the dose.
It is necessary to periodically conduct a blood test, with prolonged therapy it is recommended to periodically monitor the functions of the cardiovascular system, liver and kidneys.
If general anesthesia is required, Nakom® can be taken as long as the patient is allowed to take the drug inside. If treatment is interrupted temporarily, then the usual dose may be prescribed again as soon as the patient is able to take the drug again orally.
Studies have shown that patients with Parkinson's disease have an increased risk of developing melanoma, therefore, patients taking Nakom® need to undergo regular examinations by a dermatologist.
It is not clear whether the increased risk is associated with Parkinson's disease or other factors, such as drugs used to treat Parkinson's disease.
Patients receiving dopamine antagonists exhibit pathological gambling addictions, hypersexuality, compulsive waste (craving for shopping), gluttony and overeating, increased libido. With the development of the above symptoms, a dose / treatment adjustment is recommended.
Nakom® is not recommended for the treatment of extrapyramidal disorders caused by drugs.
High protein foods may interfere with the absorption of the drug.
Influence on the ability to drive vehicles, mechanisms
In very rare cases, levodopa can cause drowsiness and cases of sudden onset of sleep. During treatment with Nakom®, patients should be informed of the possibility of sudden falling asleep. Patients with drowsiness and experiencing sudden falling asleep (cases of sudden falling asleep) should refrain from driving vehicles and engaging in potentially dangerous activities that require an increased concentration of attention and speed of psychomotor reactions.
Release form
Tablets.
