Duopa (carbidopa/levodopa)

No dosing information is available for this tab.

Levodopa and carbidopa are administered orally as fixed-combination or single-entity (carbidopa only) conventional tablets, orally disintegrating tablets, extended-release tablets, or extended-release capsules. Levodopa also is commercially available as a powder for oral inhalation. Carbidopa-levodopa enteral suspension is administered by direct intestinal infusion through a nasojejunal (NJ) tube or a percutaneous endoscopic gastrojejunostomy (PEG-J) tube.

In patients with moderate to severe motor fluctuations, better global improvement may be achieved in some patients when extended-release rather than conventional tablet preparations of carbidopa-levodopa are used. However, some studies have not found a substantial difference in ''off'' time between extended-release and immediate-release tablet preparations in such patients. In patients without motor fluctuations, the preparations were comparably effective but less frequent dosing was required with the extended-release preparation. Use of the extended-release capsule formulation of carbidopa-levodopa has been shown to improve ''off'' time compared with immediate-release preparations in patients with advanced parkinson disease. (See Absorption under Pharmacokinetics.)

Patients receiving other antiparkinsonian agents may continue taking these drugs while carbidopa-levodopa is administered; however, dosage adjustments of these drugs may be necessary.

Whenever a general anesthetic is required, levodopa may be continued as long as the patient is able to take fluids and medication orally. If therapy is interrupted, the patient should be observed for neuroleptic malignant syndrome and the usual daily dose may be given as soon as the patient can take oral medication.

No dosing information is available for this tab.

No dosing information is available for this tab.

There is no enhanced messaging for this drug.

Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

Agents Affecting Growth Hormone/Macimorelin

SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

MECHANISM OF ACTION: Agents affecting growth hormone may impact the accuracy of the macimorelin diagnostic test.(1)

CLINICAL EFFECTS: Concurrent use of agents affecting growth hormone may impact the accuracy of the macimorelin diagnostic test.(1)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: The US manufacturer of macimorelin states concurrent use with agents affecting growth hormone may impact the accuracy of the macimorelin diagnostic test. Discontinue growth hormone products at least 1 week before administering the macimorelin diagnostic test. Sufficient washout time of drugs affecting growth hormone release prior to administration of macimorelin is recommended.(1) Agents affecting growth hormone include: - Drugs that directly affect the pituitary secretion of growth hormone (e.g. somatostatin, insulin, glucocorticoids, cyclooxygenase inhibitors) - Drugs that may transiently elevate growth hormone concentrations (e.g. clonidine, levodopa, insulin) - Drugs that may blunt the growth hormone response (e.g. muscarinic antagonists, anti-thyroid medications, growth hormone products)

DISCUSSION: Concurrent use of agents affecting growth hormone may impact the accuracy of the macimorelin diagnostic test.(1)

Foslevodopa; Levodopa/Maois

SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.

MECHANISM OF ACTION: MAOIs inhibit the enzyme responsible for degradation of dopamine and norepinephrine which are formed by levodopa. Also, storage and release of dopamine and norepinephrine is increased. Foslevodopa is a prodrug of levodopa.

CLINICAL EFFECTS: Concurrent use of MAOIs may result in increased effects of levodopa, including tremor, hypertensive crisis, and postural hypotension.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: The US manufacturer of carbidopa/levodopa states that the concurrent use of nonselective MAO inhibitors is contraindicated. Carbidopa/Levodopa may be administered with recommended dosages of selective MAO-B inhibitors. The Canadian manufacturer of foslevodopa/foscarbidopa states that concurrent use of nonselective MAO inhibitors and selective MAO type A inhibitors is contraindicated. MAO inhibitors should be stopped at least 2 weeks prior to initiation of foslevodopa/foscarbidopa therapy. Foslevodopa/foscarbidopa may be administered with recommended dosages of selective MAO-B inhibitors. The addition of a decarboxylase inhibitor to the combination of a non-selective MAO inhibitor and levodopa may minimize risk of adverse effects. Phentolamine has been effective in treating hypertension caused by this interaction.

DISCUSSION: Hypertensive reactions, flushing, and palpitations have been reported as a result of this interaction. This interaction may be possible for several weeks after the discontinuation of a MAO inhibitor. At the recommended dosage of 10 mg/day, oral selegiline is presumed to be a selective MAO B inhibitor and would thus not be expected to interact with levodopa. Oral selegiline is indicated as an adjunct agent with levodopa in the management of Parkinsonian patients. However, selegiline administered transdermally for the treatment of depression is not selective for MAO-B. Methylene blue, when administered intravenously, has been shown to reach sufficient concentrations to be a potent inhibitor of MAO-A. Metaxalone is a weak inhibitor of MAO.

Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

Foslevodopa; Levodopa/Deutetrabenazine; Tetrabenazine

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Deutetrabenazine and tetrabenazine antagonize the action of levodopa by inhibiting monoamine reuptake in the presynaptic terminals, thereby depleting dopamine in the central nervous system.(1-4) Foslevodopa is a prodrug of levodopa.(5)

CLINICAL EFFECTS: Concurrent administration with deutetrabenazine or tetrabenazine may result in decreased effectiveness of levodopa.(1-4)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Recommendations for concurrent use of levodopa with tetrabenazine or deutetrabenazine vary in different regions. The Australian manufacturer of tetrabenazine states that concurrent use of levodopa is contraindicated. Levodopa should not be used concurrently with or within one day of discontinuing tetrabenazine.(1) The Australian and UK manufacturers of tetrabenazine state that tetrabenazine is contraindicated in patients with Parkinson's Disease.(1,2) Patients with levodopa-induced dyskinetic or choreiform movements should have their levodopa dose reduced rather than start concurrent therapy with tetrabenazine or deutetrabenazine.(3) If concurrent use is necessary, monitor patients for symptoms of parkinsonism. A dose reduction or discontinuation of tetrabenazine or deutetrabenazine may be required.(2-4)

DISCUSSION: Deutetrabenazine and tetrabenazine can antagonize the effect of levodopa.(1-4) Most manufacturers either recommend against concurrent use(2,3) or state that concurrent use is contraindicated.(4) The combination has been used in the treatment of levodopa-induced peak dose dyskinesias.(6)

Foslevodopa; Levodopa/Linezolid

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Linezolid is a weak, nonselective monoamine oxidase inhibitor (MAOI) that blocks the metabolism of dopamine and norepinephrine, which are formed by levodopa. Also, storage and release of dopamine and norepinephrine is increased.(1-2) Foslevodopa is a prodrug of levodopa.

CLINICAL EFFECTS: Concurrent use of linezolid may result in increased effects of levodopa, including tremor, hypertensive crisis, and postural hypotension.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: The US manufacturer of carbidopa/levodopa states that the concurrent use of nonselective MAO inhibitors is contraindicated.(1) The Canadian manufacturer of foslevodopa/foscarbidopa states that concurrent use of nonselective MAO inhibitors and selective MAO type A inhibitors is contraindicated. MAO inhibitors should be stopped at least 2 weeks prior to initiation of foslevodopa/foscarbidopa therapy.(2) The manufacturer of linezolid does not contraindicate the use of adrenergic agents but states that they should not be coadministered unless the patient is closely monitored for potential increases in blood pressure.(3) If concurrent therapy is warranted, patients should be monitored closely for hypertensive crisis. The addition of a decarboxylase inhibitor to the combination of a non-selective MAO inhibitor and levodopa may minimize risk of adverse effects. Phentolamine has been effective in treating hypertension caused by this interaction.

DISCUSSION: Hypertensive reactions, flushing, and palpitations have been reported as a result of the interaction between levodopa and other MAO inhibitors. In a case report, an 89-year-old female with COPD, sick sinus syndrome, atrial fibrillation, hypertension, history of CVA, ischemic colitis, and Parkinson's disease on many medications including carbidopa-levodopa for 6 years took linezolid for 8 days and developed seizure-like activity. The patient was afebrile and normotensive, but was tachycardic, lethargic, agitated, and exhibited clonus on examination 2 days after linezolid was discontinued.(4)

Levodopa/Iron Salts, Oral

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Iron salts appear to decrease the absorption of levodopa by chelate formation.

CLINICAL EFFECTS: The therapeutic effect of levodopa may be decreased.

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Separate the administration times of levodopa and iron by as much as possible. Observe the patient for a decrease in clinical response and adjust the dose of levodopa as necessary.

DISCUSSION: Ferrous sulfate administration produced decreases in the serum concentration of levodopa and area-under-curve (AUC). Patients receiving levodopa plus carbidopa also experienced a reduction in the serum concentration and AUC for carbidopa during concurrent administration of ferrous sulfate. In addition, a loss in therapeutic response was demonstrated.

Selected Dopamine Agonists/Selected Antiemetics

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Selected dopamine agonists are used to treat neurologic conditions such as Parkinson Disease (PD)or restless legs syndrome (RLS), and endocrine disorders such as hyperprolactinemia by directly or indirectly increasing dopamine concentrations at dopamine-2 (D2) receptors in the central nervous system (CNS). Antiemetic agents which block CNS D2 receptors may counteract this effect.(1-5)

CLINICAL EFFECTS: The efficacy of the dopamine agonist may be decreased, leading to exacerbation of the disease being treated. In patients with Parkinson disease motor symptoms may worsen, increasing the risk for falls, dysphagia or aspiration.(5) Patients with other conditions such as restless legs syndrome may also experience symptom exacerbation due to this combination.

PREDISPOSING FACTORS: Patients with Parkinson or Diffuse Lewy Body (DLB) disease are particularly susceptible to adverse effects of dopamine blockade.

PATIENT MANAGEMENT: Reassess antiemetic therapy and use an antiemetic without dopamine (D2) blocking effects if possible. If clinically appropriate and available, consider the use of a 5HT3 blocker (e.g. ondansetron) or domperidone (not available in the US).(4) If concomitant treatment is needed, monitor for loss of efficacy for the disease being treated by the dopamine agonist (e.g. Parkinson disease, restless legs syndrome) and adjust medication(s) or dosage if needed.(1-4) Counsel patients to report symptoms of disease exacerbation.

DISCUSSION: Patients with Parkinson or DLB disease are particularly susceptible to adverse effects of dopamine blockade. The European Academy of Neurology guideline for late Parkinson disease states that metoclopramide, cinnarizine and prochlorperazine must be avoided. Ondansetron or domperidone(not available in the US) may be used for nausea and vomiting.(5) Prescribing information for dopamine agonists warn of the risk for disease exacerbation when dopamine blocking agents are co-prescribed.(1-4)

Selected Dopamine Agonists/Selected Antipsychotics

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Selected dopamine agonists are used to treat neurologic conditions such as Parkinson Disease (PD)or restless legs syndrome, and endocrine disorders such as hyperprolactinemia by directly or indirectly increasing dopamine concentrations at D2 receptors in the central nervous system (CNS). Antipsychotic agents counteract this effect by blocking dopamine activity at CNS D2 receptors.(1-5)

CLINICAL EFFECTS: The efficacy of either agent may be decreased, leading to exacerbation of the disease being treated. In patients with Parkinson disease motor symptoms may worsen, increasing the risk for falls, dysphagia or aspiration.(4,7) Compared with Parkinson patients not receiving antipsychotic therapy, Parkinson patients receiving antipsychotics appear to have an increased mortality risk.(6) Patients with other conditions such as restless legs syndrome or a psychotic disorder may also experience symptom exacerbation due to this combination.

PREDISPOSING FACTORS: Patients with Parkinson or Diffuse Lewy Body (DLB) disease are particularly susceptible to adverse effects of dopamine blockade by antipsychotics.

PATIENT MANAGEMENT: Reassess the need for antipsychotic therapy. If psychosis or hallucinations are due to an antiparkinson agent, when possible consider reducing the dose or changing the antiparkinson agent before initiating antipsychotic therapy. In patients with PD and dementia, addition of a cholinesterase inhibitor (e.g. rivastigmine) may improve psychosis. If an antipsychotic is required, then an atypical antipsychotic should be used.(6,7) In patients with major psychotic disorders, consider reducing the dose, changing or stopping the dopamine agonist. The US manufacturer of ropinirole recommends treatment with dopamine agonists only if potential benefits outweigh risks.(1) The US manufacturer of entacapone states it should not ordinarily be used in patients with major psychotic disorders as entacapone may lead to an exacerbation of psychosis.(4)

DISCUSSION: An epidemiologic study evaluated 21,043 elderly patients with Parkinson disease to determine if recent initiation of a typical or atypical antipsychotic was associated with increased mortality. They found an adjusted odds ratio of 2.0 for death associated with atypical antipsychotics versus no antipsychotic They found an adjusted odds ratio of 2.4 for death associated with typical versus atypical antipsychotics. The authors noted the increased mortality found with typical antipsychotics supports current treatment recommendations to use atypical antipsychotic agents in patients with Parkinson disease.(6,7)

Selected Dopaminergic Agents/Slt Antipsychotics

SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.

MECHANISM OF ACTION: Selected dopaminergic agents are used to treat neurologic conditions such as Parkinson Disease (PD) or restless legs syndrome, and endocrine disorders such as hyperprolactinemia by directly or indirectly increasing dopamine concentrations at D2 receptors in the central nervous system (CNS). Antipsychotic agents counteract this effect by blocking dopamine activity at CNS D2 receptors.(1-5)

CLINICAL EFFECTS: The efficacy of either agent may be decreased, leading to exacerbation of the disease being treated. In patients with Parkinson disease motor symptoms may worsen, increasing the risk for falls, dysphagia or aspiration.(4,7) Compared with Parkinson patients not receiving antipsychotic therapy, Parkinson patients receiving antipsychotics appear to have an increased mortality risk.(6) Patients with other conditions such as restless legs syndrome or a psychotic disorder may also experience symptom exacerbation due to this combination.

PREDISPOSING FACTORS: Patients with Parkinson or Diffuse Lewy Body (DLB) disease are particularly susceptible to adverse effects of dopamine blockade by antipsychotics.

PATIENT MANAGEMENT: Reassess the need for antipsychotic therapy. If psychosis or hallucinations are due to an antiparkinson agent, when possible consider reducing the dose or changing the antiparkinson agent before initiating antipsychotic therapy. In patients with PD and dementia, addition of a cholinesterase inhibitor (e.g. rivastigmine) may improve psychosis. If an antipsychotic is required, then an atypical antipsychotic should be used.(6,7) In patients with major psychotic disorders, consider reducing the dose, changing or stopping the dopaminergic agent. The US manufacturer of ropinirole recommends treatment with dopaminergic agents only if potential benefits outweigh risks.(1) The US manufacturer of entacapone states it should not ordinarily be used in patients with major psychotic disorders as entacapone may lead to an exacerbation of psychosis.(4)

DISCUSSION: An epidemiologic study evaluated 21,043 elderly patients with Parkinson disease to determine if recent initiation of a typical or atypical antipsychotic was associated with increased mortality. They found an adjusted odds ratio of 2.0 for death associated with atypical antipsychotics versus no antipsychotic They found an adjusted odds ratio of 2.4 for death associated with typical versus atypical antipsychotics. The authors noted the increased mortality found with typical antipsychotics supports current treatment recommendations to use atypical antipsychotic agents in patients with Parkinson disease.(6,7)

Moderate Interaction: Assess the risk to the patient and take action as needed.

Amantadine; Foslevodopa; Levodopa/Bupropion

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Amantadine, levodopa, and bupropion have dopamine agonist effects. Toxicity may result from cumulative dopamine agonist effects.(1) Foslevodopa is a prodrug of levodopa.(2)

CLINICAL EFFECTS: Concurrent administration of amantadine/levodopa and bupropion may result in CNS toxicity, such as, restlessness, agitation, tremor, ataxia, gait disturbance, vertigo, and dizziness.(1)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Use caution when amantadine/levodopa and bupropion are used concurrently. Monitor for signs of CNS toxicity, which may include restlessness, agitation, tremor, ataxia, gait disturbance, vertigo, and dizziness.(1)

DISCUSSION: CNS toxicity has been reported with concurrent administration of amantadine and bupropion. Three out of six nursing home residents administered concurrent bupropion and amantadine developed confusion, restlessness, agitation, gross motor tremors, ataxia, gait disturbance, dizziness, and vertigo. Two patients had severe symptoms and were hospitalized.(3) In a case report, bupropion (75 mg twice daily) was added to amantadine, haloperidol, and benztropine. The patient became disoriented and agitated, developed visual and auditory hallucinations, impaired attention and memory, a fluctuating level of awareness, and unsteady gait.(4)

Foslevodopa; Levodopa/Isoniazid

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Isoniazid inhibits dopa decarboxylase, which is responsible for the decarboxylation of levodopa to dopamine.(1) Foslevodopa is a prodrug of levodopa.(2,3)

CLINICAL EFFECTS: Concurrent administration with isoniazid may result in decreased dopamine and decreased effectiveness of levodopa.(1-2,4-5)

PREDISPOSING FACTORS: None determined.

PATIENT MANAGEMENT: Monitor patients receiving concurrent therapy with isoniazid and levodopa or foslevodopa for worsening Parkinson's symptoms.(3) The dose of levodopa may need to be increased.(1)

DISCUSSION: In a case report, a 74-year-old woman with Lewy Body Dementia stable on levodopa started rifampin 450 mg, ethambutol 500 mg, and isoniazid 300 mg daily for tubercular pleurisy and subsequently developed dysphagia, which resolved after increasing her dose of levodopa.(1) In another case, a patient with idiopathic Parkinson's disease deteriorated after starting rifampin and isoniazid for pulmonary tuberculosis. Motor function test found that the patient's "on" period was 75% longer after stopping antitubercular therapy and levodopa area-under-curve (AUC) and maximum concentration (Cmax) were 37% and 33% higher, respectively, compared to values obtained during TB therapy.(4) In a study of 20 patients, isoniazid 290 mg given to Parkinson's patients on levodopa resulted in reduced levodopa-induced choreic dyskinesias but intolerable worsening of Parkinson's symptoms.(5)

Selected Dopamine Agonists/Select Atypical Antipsychotics

SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.

MECHANISM OF ACTION: Selected dopamine agonists are used to treat neurologic conditions such as Parkinson Disease (PD) or restless legs syndrome, and endocrine disorders such as hyperprolactinemia by directly or indirectly increasing dopamine concentrations at D2 receptors in the central nervous system (CNS). Antipsychotic agents counteract this effect by blocking dopamine activity at CNS D2 receptors.(1-5)

CLINICAL EFFECTS: The efficacy of either agent may be decreased, leading to exacerbation of the disease being treated, e.g. Parkinson disease or a psychotic disorder. Dopamine agonists linked to this monograph are: bromocriptine, entacapone, levodopa, pergolide, pramipexole, ropinirole and rotigotine. Atypical antipsychotics linked to this monograph are: aripiprazole, asenapine, iloperidone, lumateperone, lurasidone, paliperidone, quetiapine, risperidone, ziprasidone and zotepine.

PREDISPOSING FACTORS: Patients with Parkinson or Diffuse Lewy Body (DLB) disease are particularly susceptible to adverse effects of dopamine blockade by antipsychotics.

PATIENT MANAGEMENT: Reassess the need for antipsychotic therapy. If psychosis or hallucinations are due to an antiparkinson agent, when possible consider reducing the dose or changing the antiparkinson agent before initiating antipsychotic therapy. In patients with PD and dementia, addition of a cholinesterase inhibitor (e.g. rivastigmine) may improve psychosis. If an antipsychotic is required, then an atypical antipsychotic should be used.(6,7) In patients with major psychotic disorders, consider reducing the dose, changing, or stopping the dopamine agonist. The US manufacturer of ropinirole recommends treatment with dopamine agonists only if potential benefits outweigh risks.(1) The US manufacturer of entacapone states it should not ordinarily be used in patients with major psychotic disorders as entacapone may lead to an exacerbation of psychosis.(4)

DISCUSSION: An epidemiologic study evaluated 21,043 elderly patients with Parkinson disease to determine if recent initiation of a typical or atypical antipsychotic was associated with increased mortality. They found an adjusted odds ratio of 2.0 for death associated with atypical antipsychotics versus no antipsychotic. They found an adjusted odds ratio of 2.4 for death associated with typical versus atypical antipsychotics. The authors noted the increased mortality found with typical antipsychotics supports current treatment recommendations to use atypical antipsychotic agents in patients with Parkinson disease.(6,7) Two clozapine trials showed significant improvement in psychosis without worsening of motor symptoms. In contrast, two olanzapine trials were associated with unacceptable worsening of motor symptoms. Risperidone has also been associated with motor worsening in case reports. Quetiapine evaluations have been conflicting with several small studies showing improvement in psychotic symptoms while a more rigorous trial showed no improvement.(6)

There is no enhanced messaging for this drug.

• Angle-closure glaucoma

• Acute myocardial infarction
• Bronchospastic pulmonary disease
• Cardiac arrhythmia
• Depression
• Dyskinesia
• Gastrointestinal ulcer
• Impulse control disorder
• Peptic ulcer
• Psychotic disorder
• Pyridoxine deficiency
• Suicidal ideation

• Disease of liver
• Malignant melanoma
• No disease contraindications
• Open angle glaucoma
• Peripheral neuropathy

There is no enhanced messaging for this drug.

More Frequent

• Akathisia
• Orthostatic hypotension

Less Frequent

• Blepharospasm

Rare or Very Rare

• Abnormal hepatic function tests
• Accidental fall
• Acute myocardial infarction
• Agranulocytosis
• Anemia
• Bullous dermatitis
• Cardiac arrhythmia
• Drug-induced psychosis
• Duodenal ulcer
• Extrapyramidal disease
• Hemolytic anemia
• Hyperbilirubinemia
• Hypertension
• Hyperventilation
• IgA vasculitis
• Impulse control disorder
• Increased alanine transaminase
• Increased aspartate transaminase
• Leukopenia
• Ocular hypertension
• Oculogyric crisis
• Priapism
• Pyridoxine-dependent seizure
• Suicidal
• Suicidal ideation
• Thrombocytopenic disorder

More Frequent

• Altered mental status
• Ataxia
• Constipation
• Dyskinesia
• Headache disorder
• Insomnia
• Nausea
• Symptoms of anxiety
• Vomiting

Less Frequent

• Acquired dystonia
• Acute cognitive impairment
• Anorexia
• Blurred vision
• Depression
• Diarrhea
• Dizziness
• Dream disorder
• Dyspepsia
• Fatigue
• Flushing
• General weakness
• Muscle fasciculation
• Peripheral edema
• Peripheral neuropathy
• Urine discoloration
• Xerostomia

Rare or Very Rare

• Acquired horner syndrome
• Acute abdominal pain
• Alopecia
• Bruxism
• Cough
• Diplopia
• Drowsy
• Drug-induced hot flash
• Dysgeusia
• Dysphagia
• Edema
• Euphoria
• Flatulence
• Gastrointestinal irritation
• Hallucinations
• Hiccups
• Hoarseness
• Hyperhidrosis
• Hypoesthesia
• Increased libido
• Leg pain
• Malaise
• Memory impairment
• Nervousness
• Phlebitis
• Pyridoxine deficiency
• Sialorrhea
• Sore throat
• Sudden onset of sleep
• Syncope
• Trismus
• Urinary incontinence
• Urinary retention
• Weight gain
• Weight loss

No enhanced messaging available.

No enhanced messaging available.

There are no adequate and well-controlled studies of levodopa and carbidopa in pregnant women. Reproduction studies in rodents using levodopa and carbidopa at dosages approximately 5 and 2 times greater than the maximum human dosage, respectively, have shown adverse effects on fetal and postnatal growth and viability, and studies in rabbits using the drug alone or in conjunction with carbidopa have shown visceral and skeletal malformations. Levodopa and carbidopa should be administered to pregnant women or women who might become pregnant only when the benefits to the mother outweigh the possible risks to the mother and fetus.

Levodopa is distributed into human milk. Carbidopa is distributed into milk in rats; it is not known whether carbidopa is distributed into human milk. Levodopa-carbidopa should be used with caution in nursing women. The known benefits of breast-feeding should be considered along with the mother's clinical need for the drug and any potential adverse effects on the infant from the drug or underlying maternal condition.

No enhanced messaging available.

No enhanced messaging available.