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Levetiracetam is being looked at in psychiatric and neurologic conditions such as Tourette syndrome, and anxiety disorder. However, its most serious adverse effects are behavioral, and its benefit-risk ratio in these conditions is not well understood.
The volume of distribution of levetiracetam is similar to entire body water. Levetiracetam modestly binds to plasma proteins (less than 10%).
Levetiracetam does not undergo extensive metabolism, and the metabolites formed are not athletic and do not exert pharmacological activity.
Metabolism of levetiracetam is not by liver cytochrome P enzymes, but through other metabolic pathways such as hydrolysis and hydroxylation.
In persons with normal kidney function, levetiracetam is eliminated from the body primarily by the kidneys with about 66 percent of the original drug passed unchanged into urine. The plasma half-life of levetiracetam in adults is about 6 to 8 hours.
The absorption of levetiracetam tablets and oral solution is rapid and essentially finish. The bioavailability of levetiracetam is shut to percent, and the effect of food on absorption is minor.
Brivaracetam, a chemical analogue to levetiracetam, is a racetam derivative with similar properties.
The most common adverse effects of levetiracetam treatment include CNS effects such as somnolence, decreased energy, headache, dizziness, mood swings and coordination difficulties. These adverse effects are most pronounced in the first month of therapy. About 4% of patients dropped out of pre-approval clinical trials due to these side effects.
About 13% of people taking levetiracetam experience adverse neuropsychiatric symptoms, which are generally mild. These include agitation, hostility, apathy, anxiety, emotional lability, and depression. Serious psychiatric adverse side effects that are reversed by drug discontinuation happen in about 1%.
These include hallucinations, suicidal thoughts, or psychosis. These occurred mostly within the first month of therapy, but they could develop at any time during treatment.
Although rare, Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), which appears as a painful spreading rash with redness and blistering and/or peeling skin, own been reported in patients treated with levetiracetam. The incidence of SJS following exposure to anti-epileptics such as levetiracetam is about 1 in 3,
Levetiracetam should not be used in people who own previously shown hypersensitivity to levetiracetam or any of the inactive ingredients in the tablet or oral solution.
Such hypersensitivity reactions include, but are not limited to, unexplained rash with redness or blistered skin, difficulty breathing, and tightness in the chest or airways.
In a study, the incidence of decreased bone mineral density of patients on levetiracetam was significantly higher than those for other epileptic medications.
Levetiracetam, along with other anti-epileptic drugs, can increase the risk of suicidal behavior or thoughts. People taking levetiracetam should be monitored closely for signs of worsening depression, suicidal thoughts or tendencies, or any altered emotional or behavioral states.
Kidney and liver
Kidney impairment decreases the rate of elimination of levetiracetam from the body.
Individuals with reduced kidney function may require dose adjustments. Kidney function can be estimated from the rate of creatinine clearance.
Dose adjustment of levetiracetam is not necessary in liver impairment.
No significant pharmacokinetic interactions were observed between levetiracetam or its major metabolite and concomitant medications. The pharmacokinetic profile of levetiracetam is not influenced by phenytoin, phenobarbital, primidone, carbamazepine, valproic acid, lamotrigine, gabapentin, digoxin, ethinylestradiol, or warfarin.
Society and culture
Levetiracetam is available as regular and extended release oral formulations and as intravenous formulations.
The immediate release tablet has been available as a generic in the United States since , and in the UK since  The patent for the extended release tablet will expire in 
The branded version Keppra is manufactured by UCB Pharmaceuticals Inc.
In Aprecia’s 3d-printedorally disintegrating tablet form of the drug was approved by the FDA, under the trade name Spritam.
Levetiracetam is effective for treatment of generalized tonic-clonic epilepsy. It has been approved in the United States as add-on treatment for myoclonic, and tonic-clonic seizures. Levetiracetam has been approved in the European Union as a monotherapy treatment for epilepsy in the case of partial seizures or as an adjunctive therapy for partial, myoclonic, and tonic-clonic seizures.
Levetiracetam is sometimes used off label to treat status epilepticus
Levetiracetam is effective as add-on treatment for partial (focal) epilepsy.
Levetiracetam has not been found to be useful for treatment of neuropathic pain, nor for treatment of essential tremors. Levetiracetam has not been found to be useful for treating autism, but is an effective treatment for partial, myoclonic, or tonic-clonic seizures associated with autism spectrum disorder.
Levetiracetam is effective as single-drug treatment for newly diagnosed focal epilepsy in adults. It reduces focal seizures by 50% or more as an add-on medication.
Prevention of seizures
Based on low-quality evidence, levetiracetam is about as effective as phenytoin for prevention of early seizures after traumatic brain injury. It may be effective for prevention of seizures associated with subarachnoid hemorrhages.
Levetiracetam is a pregnancy category C drug.
Studies in female pregnant rats own shown minor fetal skeletal abnormalities when given maximum recommended human doses of levetiracetam orally throughout pregnancy and lactation.
Studies were conducted to glance for increased adverse effects in the elderly population as compared to younger patients. One such study published in Epilepsy Research showed no significant increase in incidence of adverse symptoms experienced by young or elderly patients with central nervous system (CNS) disorders.
Levetiracetam may be safely used with caution in children over the age of 4. However, it has not been sure whether it can be safely given to children under the age of 4.
Mechanism of action
The exact mechanism by which levetiracetam acts to treat epilepsy is unknown.
Levetiracetam does not exhibit pharmacologic actions similar to that of classical anticonvulsants. It does not inhibit voltage-dependent Na+ channels, does not affect GABAergic transmission, and does not bind to GABAergic or glutamatergic receptors. However, the drug binds to SV2A, a synaptic vesicleglycoprotein, and inhibits presynapticcalcium channels, reducing neurotransmitter release and acting as a neuromodulator.
This is believed to impede impulse conduction across synapses.