A fatty acid with anticonvulsant properties used in the treatment of epilepsy. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of voltage dependent sodium channels.
Drugs used to prevent SEIZURES or reduce their severity.
Compounds that inhibit HISTONE DEACETYLASES. This class of drugs may influence gene expression by increasing the level of acetylated HISTONES in specific CHROMATIN domains.
Agents that are used to treat bipolar disorders or mania associated with other affective disorders.
An anticonvulsant used to control grand mal and psychomotor or focal seizures. Its mode of action is not fully understood, but some of its actions resemble those of PHENYTOIN; although there is little chemical resemblance between the two compounds, their three-dimensional structure is similar.
An agent that causes the production of physical defects in the developing embryo.
An anticonvulsant especially useful in the treatment of absence seizures unaccompanied by other types of seizures.
A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)
An anticonvulsant that is used to treat a wide variety of seizures. It is also an anti-arrhythmic and a muscle relaxant. The mechanism of therapeutic action is not clear, although several cellular actions have been described including effects on ion channels, active transport, and general membrane stabilization. The mechanism of its muscle relaxant effect appears to involve a reduction in the sensitivity of muscle spindles to stretch. Phenytoin has been proposed for several other therapeutic uses, but its use has been limited by its many adverse effects and interactions with other drugs.
Deacetylases that remove N-acetyl groups from amino side chains of the amino acids of HISTONES. The enzyme family can be divided into at least three structurally-defined subclasses. Class I and class II deacetylases utilize a zinc-dependent mechanism. The sirtuin histone deacetylases belong to class III and are NAD-dependent enzymes.
Congenital abnormalities caused by medicinal substances or drugs of abuse given to or taken by the mother, or to which she is inadvertently exposed during the manufacture of such substances. The concept excludes abnormalities resulting from exposure to non-medicinal chemicals in the environment.
A class of weak acids with the general formula R-CONHOH.
Formation of an acetyl derivative. (Stedman, 25th ed)
Substances used for their pharmacological actions on GABAergic systems. GABAergic agents include agonists, antagonists, degradation or uptake inhibitors, depleters, precursors, and modulators of receptor function.
Heterocyclic rings containing three nitrogen atoms, commonly in 1,2,4 or 1,3,5 or 2,4,6 formats. Some are used as HERBICIDES.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A compound suggested to be both a nootropic and a neuroprotective agent.
A childhood seizure disorder characterized by rhythmic electrical brain discharges of generalized onset. Clinical features include a sudden cessation of ongoing activity usually without loss of postural tone. Rhythmic blinking of the eyelids or lip smacking frequently accompanies the SEIZURES. The usual duration is 5-10 seconds, and multiple episodes may occur daily. Juvenile absence epilepsy is characterized by the juvenile onset of absence seizures and an increased incidence of myoclonus and tonic-clonic seizures. (Menkes, Textbook of Child Neurology, 5th ed, p736)
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
Elevated level of AMMONIA in the blood. It is a sign of defective CATABOLISM of AMINO ACIDS or ammonia to UREA.
Removal of toxins or metabolites from the circulation by the passing of blood, within a suitable extracorporeal circuit, over semipermeable microcapsules containing adsorbents (e.g., activated charcoal) or enzymes, other enzyme preparations (e.g., gel-entrapped microsomes, membrane-free enzymes bound to artificial carriers), or other adsorbents (e.g., various resins, albumin-conjugated agarose).
Small chromosomal proteins (approx 12-20 kD) possessing an open, unfolded structure and attached to the DNA in cell nuclei by ionic linkages. Classification into the various types (designated histone I, histone II, etc.) is based on the relative amounts of arginine and lysine in each.
Congenital malformations of the central nervous system and adjacent structures related to defective neural tube closure during the first trimester of pregnancy generally occurring between days 18-29 of gestation. Ectodermal and mesodermal malformations (mainly involving the skull and vertebrae) may occur as a result of defects of neural tube closure. (From Joynt, Clinical Neurology, 1992, Ch55, pp31-41)
Choleretic used to allay dry mouth and constipation due to tranquilizers.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A disorder characterized by the onset of myoclonus in adolescence, a marked increase in the incidence of absence seizures (see EPILEPSY, ABSENCE), and generalized major motor seizures (see EPILEPSY, TONIC-CLONIC). The myoclonic episodes tend to occur shortly after awakening. Seizures tend to be aggravated by sleep deprivation and alcohol consumption. Hereditary and sporadic forms have been identified. (From Adams et al., Principles of Neurology, 6th ed, p323)

Differential display PCR reveals novel targets for the mood-stabilizing drug valproate including the molecular chaperone GRP78. (1/1188)

Differential display polymerase chain reaction was used to identify genes regulated by the mood-stabilizing drug valproate (VPA). Four differentially displayed valproate-regulated gene fragments were isolated in rat cerebral cortex after i.p. injection of sodium VPA (300 mg/kg) for 3 weeks, and their expression was confirmed by Northern and slot blot analysis in rat cerebral cortex and C6 glioma cells. Sequencing analysis revealed three previously unidentified cDNA fragments in addition to a sequence with 100% homology with a molecular chaperone, 78-kDa glucose-regulated protein (GRP78). VPA treatment did not increase mRNA expression of 70-kDa heat shock protein, which is a related stress-induced molecular chaperone protein. All four candidate genes, including GRP78, showed similar VPA concentration-dependent increases in mRNA abundance. Another commonly prescribed mood-stabilizing anticonvulsant, carbamazepine, also increased GRP78 mRNA expression in C6 glioma cells, whereas lithium had no effect at doses up to 2 mM. Immunoblotting revealed that GRP78 protein levels were also increased in C6 glioma cells treated with VPA under the same conditions. Nuclear runoff analysis showed that VPA increased GRP78 gene transcription. Because GRP78 possesses molecular chaperone activity, binds Ca2+ in the endoplasmic reticulum, and protects cells from the deleterious effects of damaged proteins, the present findings suggest that VPA (and possibly carbamazepine) treatment may target one or more of these processes.  (+info)

Does withdrawal of different antiepileptic drugs have different effects on seizure recurrence? Further results from the MRC Antiepileptic Drug Withdrawal Study. (2/1188)

One thousand and thirteen patients, in remission of epilepsy for at least 2 years, were randomized to continued therapy or slow withdrawal over 6 months and were followed up for a median period of 5 years. At the time of randomization 83% of patients were receiving monotherapy with carbamazepine (237 patients), phenobarbitone/primidone (72 patients), phenytoin (184 patients) or valproate (228 patients) in low doses, and plasma levels were below the usual optimal range. The most important factor determining seizure recurrence was continued therapy, which was the case for barbiturates, phenytoin and valproate. There was no significant difference for patients taking carbamazepine at randomization, because of a low rate of recurrence in those withdrawing treatment. The difference between carbamazepine and other drugs was not explained by differences in covariate prognostic factors. There was no evidence that withdrawal of phenobarbitone was associated with withdrawal seizures. These data provide unique evidence for the effectiveness of standard antiepileptic drugs as monotherapy. The results for carbamazepine may be open to a number of interpretations.  (+info)

Perphenazine distribution in a postmortem case. (3/1188)

The case of a 34-year-old, mentally challenged, Caucasian female found dead in a group home is presented. Empty containers of perphenazine and valproic acid were found next to her bed. The perphenazine had been prescribed to another patient. No anatomic cause of death was determined at autopsy. Comprehensive testing of the heart blood for ethanol and drugs identified perphenazine at a concentration of 4.4 mg/L and valproic acid at a concentration of 950 mg/L. The distribution of perphenazine in other specimens was consistent with previously reported phenothiazine cases. The medical examiner ruled that the cause of death in this case was multiple drug intoxication and the manner of death was suicide.  (+info)

Effects of valproate and other antiepileptic drugs on brain glutamate, glutamine, and GABA in patients with refractory complex partial seizures. (4/1188)

Preclinical studies suggested valproate increased brain gamma-aminobutyric acid (GABA) with no major effects on brain glutamate or glutamine. Valproate increased human cerebrospinal fluid GABA and glutamine in some studies; others reported no effect. In vivo measurements of glutamate, glutamine, and GABA were made of a 14 cm3volume in the occipital cortex using a1H spectroscopy with a 2.1 Tesla magnetic resonance spectrometer and an 8 cm surface coil. Ten control subjects and 14 patients with refractory complex partial seizures were examined. Brain glutamine concentrations were above normal in three of five patients taking valproate and two of nine taking carbamazepine or phenytoin. Mean glutamine levels of patients taking valproate were higher than control subjects and patients taking carbamazepine or phenytoin. Brain glutamate concentrations were above normal in four of nine patients taking phenytoin or carbamazepine and two of five taking valproate. Brain GABA levels were below normal in four of nine patients taking carbamazepine or phenytoin and one of five taking valproate. Above normal glutamate or below normal GABA was present in nine of 14 patients and may contribute to their refractory epilepsy. Increased brain glutamine associated with valproate therapy may reflect mild hyperammonemia.  (+info)

Pharmacoeconomic and health outcome comparison of lithium and divalproex in a VA geriatric nursing home population: influence of drug-related morbidity on total cost of treatment. (5/1188)

OBJECTIVE: Clinicians use mood stabilizers for treating agitation in older patients, but limited information is available regarding side effects and costs in clinical practice. Total costs of treatment were assessed for a subset of geriatric patients receiving either lithium carbonate or divalproex sodium for agitation. STUDY DESIGN: Retrospective cohort examination of the medical records of 72 patients, 55 years of age or older, in a Veterans Administration long-term, skilled nursing care facility, with a diagnosis of dementia or bipolar affective disorder or both. PATIENTS AND METHODS: Patients treated with lithium or divalproex during the previous 4 years (1994-1997) were evaluated. Quantitative information was collected and compared regarding routine care, including cost of treatment and laboratory monitoring; and occurrence of adverse events and associated diagnostic and treatment measurements. RESULTS: Routine care costs for the 2 groups were similar. The lower annual acquisition cost per patient-year for lithium ($15 vs $339 for divalproex) was offset by higher laboratory monitoring costs associated with its administration ($278 vs $53 for divalproex). Examining the adverse events showed that the lithium group had more medication-related adverse events (32 total) than the divalproex group (10 total) and more severe occurrences, including 6 cases requiring medical intensive care unit (MICU) hospitalization. The total mean cost of treating drug-related mild-to-moderate morbidity was $3472 for lithium and $672 for divalproex. An additional cost per admission of $12,910 ($77,462 for all 6 cases) increased total morbidity-related expenditures in the lithium group to $80,934. CONCLUSIONS: Treating geriatric patients with lithium requires careful monitoring because of side effects. Staffing and resource limitations of a skilled nursing care facility may compromise optimal lithium monitoring in elderly patients. The collected data indicated that divalproex does not result in as many as or as severe adverse events and is, therefore, a safer treatment. The use of lithium was not only more expensive (on average $2875 more per patient) than treatment with divalproex but, more importantly, it was associated with poorer patient outcomes.  (+info)

Panipenem, a carbapenem antibiotic, enhances the glucuronidation of intravenously administered valproic acid in rats. (6/1188)

Previously, a significant decrease in the trough plasma-concentration of valproic acid (VPA) owing to the concomitant administration of panipenem (PAPM)/betamipron, a carbapenem antibiotic, in epileptic patients was reported. To determine the site and mechanism of the drug interaction between VPA and PAPM, we performed in vivo and in vitro experiments using rats. A 30 mg/kg bolus dose of VPA was given i.v. to normal Sprague-Dawley rats, nephrectomized rats, and hepatectomized rats, with and without prior treatment of PAPM. PAPM treatment resulted in a significant reduction of biological half-life and a significant increase of total body clearance in normal rats. The effects of PAPM on the disposition kinetics of VPA were also observed in nephrectomized rats, whereas hepatectomy abolished the interaction completely. Thus, the site of interaction was identified as the liver. At steady state, PAPM treatment significantly increased total body clearance, the biliary excretion rate of VPA glucuronide, and the apparent metabolic clearance of VPA by glucuronidation, but did not affect the biliary excretion clearance of VPA glucuronide. Initial uptake velocity of VPA into rat hepatocytes proportionally increased as a function of VPA concentration added and was not affected by PAPM. The plasma-unbound fraction of VPA in vitro was not altered by PAPM. These data demonstrate that PAPM does not affect the uptake of VPA into the liver, the plasma-unbound fraction, and the excretion process of VPA glucuronide. Consequently, PAPM appears to enhance the rate of metabolism of VPA to VPA glucuronide in the liver.  (+info)

Bipolar disorder in old age. (7/1188)

OBJECTIVE: To review the classification, clinical characteristics, and epidemiology of bipolar disorders in old age with a special focus on neurologic comorbidity, high mortality, and management. QUALITY OF EVIDENCE: Most available data is gleaned from retrospective chart reviews and cohort studies. Treatment recommendations are based on evidence from younger populations and a few anecdotal case reports and series involving elderly people. MAIN MESSAGE: While relatively rare in the community setting, mania in old age frequently leads to hospitalization. It is associated with late-onset neurologic disorders (especially cerebrovascular disease) involving the right hemisphere and orbitofrontal cortex. Prognosis is relatively poor; morbidity and mortality rates are high. Management of bipolarity includes cautious use of mood stabilizers, especially lithium and divalproex. CONCLUSIONS: Mania in old age should trigger a careful assessment of underlying neurologic disease, especially cerebrovascular disease. Close clinical follow up is essential.  (+info)

A case of fever following antiepileptic treatment. (8/1188)

A 23-year-old female patient treated with 900 mg oxcarbazepine for complex partial seizures is presented. Good seizure control and slight fever were noted a few weeks after drug administration. Reduction of oxcarbazepine and replacement with valproate resulted in a transient normothermia. Because of fever reappearance, vigabatrin was added and valproate was gradually reduced. Seizures reappeared, but the body temperature fell below 37 degrees C. Substitution of valproate for lamotrigine resulted in seizure control but abnormal body temperature (37- 37.6 degrees C) was noted again. Repeated hospital admission for clinical and laboratory investigation before any change of treatment revealed no other abnormal findings. The patient's abnormal temperature possibly reflects a derangement of high-level temperature control.  (+info)

Valproic acid is a medication that is primarily used as an anticonvulsant, which means it is used to treat seizure disorders. It works by increasing the amount of gamma-aminobutyric acid (GABA) in the brain, a neurotransmitter that helps to reduce abnormal electrical activity in the brain. In addition to its use as an anticonvulsant, valproic acid may also be used to treat migraines and bipolar disorder. It is available in various forms, including tablets, capsules, and liquid solutions, and is usually taken by mouth. As with any medication, valproic acid can have side effects, and it is important for patients to be aware of these and to discuss them with their healthcare provider.

Anticonvulsants are a class of drugs used primarily to treat seizure disorders, also known as epilepsy. These medications work by reducing the abnormal electrical activity in the brain that leads to seizures. In addition to their use in treating epilepsy, anticonvulsants are sometimes also prescribed for other conditions, such as neuropathic pain, bipolar disorder, and migraine headaches.

Anticonvulsants can work in different ways to reduce seizure activity. Some medications, such as phenytoin and carbamazepine, work by blocking sodium channels in the brain, which helps to stabilize nerve cell membranes and prevent excessive electrical activity. Other medications, such as valproic acid and gabapentin, increase the levels of a neurotransmitter called gamma-aminobutyric acid (GABA) in the brain, which has a calming effect on nerve cells and helps to reduce seizure activity.

While anticonvulsants are generally effective at reducing seizure frequency and severity, they can also have side effects, such as dizziness, drowsiness, and gastrointestinal symptoms. In some cases, these side effects may be managed by adjusting the dosage or switching to a different medication. It is important for individuals taking anticonvulsants to work closely with their healthcare provider to monitor their response to the medication and make any necessary adjustments.

Histone Deacetylase Inhibitors (HDACIs) are a class of pharmaceutical compounds that inhibit the function of histone deacetylases (HDACs), enzymes that remove acetyl groups from histone proteins. Histones are alkaline proteins around which DNA is wound to form chromatin, the structure of which can be modified by the addition or removal of acetyl groups.

Histone acetylation generally results in a more "open" chromatin structure, making genes more accessible for transcription and leading to increased gene expression. Conversely, histone deacetylation typically results in a more "closed" chromatin structure, which can suppress gene expression. HDACIs block the activity of HDACs, resulting in an accumulation of acetylated histones and other proteins, and ultimately leading to changes in gene expression profiles.

HDACIs have been shown to exhibit anticancer properties by modulating the expression of genes involved in cell cycle regulation, apoptosis, and angiogenesis. As a result, HDACIs are being investigated as potential therapeutic agents for various types of cancer, including hematological malignancies and solid tumors. Some HDACIs have already been approved by regulatory authorities for the treatment of specific cancers, while others are still in clinical trials or preclinical development.

Antimanic agents are a class of medications primarily used to treat mania, a symptom of bipolar disorder. These agents help to control and reduce the severity of manic episodes, which can include symptoms such as elevated or irritable mood, increased energy, decreased need for sleep, racing thoughts, and impulsive or risky behavior.

The most commonly used antimanic agents are mood stabilizers, such as lithium and valproate (Depakote), and atypical antipsychotics, such as olanzapine (Zyprexa), risperidone (Risperdal), quetiapine (Seroquel), and aripiprazole (Abilify). These medications work by altering the levels or activity of certain neurotransmitters in the brain, such as dopamine, serotonin, and norepinephrine.

Electroconvulsive therapy (ECT) is also considered an effective antimanic treatment for severe mania that has not responded to medication. ECT involves applying electrical currents to the brain while the patient is under anesthesia, which induces a seizure and can help to reduce symptoms of mania.

It's important to note that antimanic agents should only be used under the supervision of a qualified healthcare provider, as they can have significant side effects and interactions with other medications. Additionally, a comprehensive treatment plan for bipolar disorder typically includes psychotherapy, education, and support to help manage the condition and prevent future episodes.

Carbamazepine is an anticonvulsant medication that is primarily used to treat seizure disorders (epilepsy) and neuropathic pain. It works by decreasing the abnormal electrical activity in the brain, which helps to reduce the frequency and severity of seizures. Carbamazepine may also be used off-label for other conditions such as bipolar disorder and trigeminal neuralgia.

The medication is available in various forms, including tablets, extended-release tablets, chewable tablets, and suspension. It is usually taken two to four times a day with food to reduce stomach upset. Common side effects of carbamazepine include dizziness, drowsiness, headache, nausea, vomiting, and unsteady gait.

It is important to note that carbamazepine can interact with other medications, including some antidepressants, antipsychotics, and birth control pills, so it is essential to inform your healthcare provider of all the medications you are taking before starting carbamazepine. Additionally, carbamazepine levels in the blood may need to be monitored regularly to ensure that the medication is working effectively and not causing toxicity.

Teratogens are substances, such as certain medications, chemicals, or infectious agents, that can cause birth defects or abnormalities in the developing fetus when a woman is exposed to them during pregnancy. They can interfere with the normal development of the fetus and lead to a range of problems, including physical deformities, intellectual disabilities, and sensory impairments. Examples of teratogens include alcohol, tobacco smoke, some prescription medications, and infections like rubella (German measles). It is important for women who are pregnant or planning to become pregnant to avoid exposure to known teratogens as much as possible.

Ethosuximide is a medication that belongs to a class of drugs called anticonvulsants or anti-seizure medications. It is primarily used to treat absence seizures, also known as petit mal seizures, which are a type of seizure characterized by brief, sudden lapses in consciousness.

Ethosuximide works by reducing the abnormal electrical activity in the brain that leads to seizures. It does this by inhibiting the formation of sodium channels in the brain, which helps to stabilize the electrical impulses and reduce the likelihood of seizure activity.

Like all medications, ethosuximide can have side effects, including stomach upset, dizziness, headache, and sleepiness. It is important for patients to follow their doctor's instructions carefully when taking this medication and to report any bothersome or persistent side effects promptly. Ethosuximide may also interact with other medications, so it is important to inform your healthcare provider of all medications you are taking before starting ethosuximide therapy.

Epilepsy is a chronic neurological disorder characterized by recurrent, unprovoked seizures. These seizures are caused by abnormal electrical activity in the brain, which can result in a wide range of symptoms, including convulsions, loss of consciousness, and altered sensations or behaviors. Epilepsy can have many different causes, including genetic factors, brain injury, infection, or stroke. In some cases, the cause may be unknown.

There are many different types of seizures that can occur in people with epilepsy, and the specific type of seizure will depend on the location and extent of the abnormal electrical activity in the brain. Some people may experience only one type of seizure, while others may have several different types. Seizures can vary in frequency, from a few per year to dozens or even hundreds per day.

Epilepsy is typically diagnosed based on the patient's history of recurrent seizures and the results of an electroencephalogram (EEG), which measures the electrical activity in the brain. Imaging tests such as MRI or CT scans may also be used to help identify any structural abnormalities in the brain that may be contributing to the seizures.

While there is no cure for epilepsy, it can often be effectively managed with medication. In some cases, surgery may be recommended to remove the area of the brain responsible for the seizures. With proper treatment and management, many people with epilepsy are able to lead normal, productive lives.

Phenytoin is an anticonvulsant drug, primarily used in the treatment of seizures and prevention of seizure recurrence. It works by reducing the spread of seizure activity in the brain and stabilizing the electrical activity of neurons. Phenytoin is also known to have anti-arrhythmic properties and is occasionally used in the management of certain cardiac arrhythmias.

The drug is available in various forms, including immediate-release tablets, extended-release capsules, and a liquid formulation. Common side effects of phenytoin include dizziness, drowsiness, headache, nausea, vomiting, and unsteady gait. Regular monitoring of blood levels is necessary to ensure that the drug remains within the therapeutic range, as both low and high levels can lead to adverse effects.

It's important to note that phenytoin has several potential drug-drug interactions, particularly with other anticonvulsant medications, certain antibiotics, and oral contraceptives. Therefore, it is crucial to inform healthcare providers about all the medications being taken to minimize the risk of interactions and optimize treatment outcomes.

Histone deacetylases (HDACs) are a group of enzymes that play a crucial role in the regulation of gene expression. They work by removing acetyl groups from histone proteins, which are the structural components around which DNA is wound to form chromatin, the material that makes up chromosomes.

Histone acetylation is a modification that generally results in an "open" chromatin structure, allowing for the transcription of genes into proteins. When HDACs remove these acetyl groups, the chromatin becomes more compact and gene expression is reduced or silenced.

HDACs are involved in various cellular processes, including development, differentiation, and survival. Dysregulation of HDAC activity has been implicated in several diseases, such as cancer, neurodegenerative disorders, and cardiovascular diseases. As a result, HDAC inhibitors have emerged as promising therapeutic agents for these conditions.

"Drug-induced abnormalities" refer to physical or physiological changes that occur as a result of taking medication or drugs. These abnormalities can affect various organs and systems in the body and can range from minor symptoms, such as nausea or dizziness, to more serious conditions, such as liver damage or heart rhythm disturbances.

Drug-induced abnormalities can occur for several reasons, including:

1. Direct toxicity: Some drugs can directly damage cells and tissues in the body, leading to abnormalities.
2. Altered metabolism: Drugs can interfere with normal metabolic processes in the body, leading to the accumulation of harmful substances or the depletion of essential nutrients.
3. Hormonal imbalances: Some drugs can affect hormone levels in the body, leading to abnormalities.
4. Allergic reactions: Some people may have allergic reactions to certain drugs, which can cause a range of symptoms, including rashes, swelling, and difficulty breathing.
5. Interactions with other drugs: Taking multiple medications or drugs at the same time can increase the risk of drug-induced abnormalities.

It is important for healthcare providers to monitor patients closely for signs of drug-induced abnormalities and to adjust medication dosages or switch to alternative treatments as necessary. Patients should also inform their healthcare providers of any symptoms they experience while taking medication, as these may be related to drug-induced abnormalities.

Hydroxamic acids are organic compounds containing the functional group -CONHOH. They are derivatives of hydroxylamine, where the hydroxyl group is bound to a carbonyl (C=O) carbon atom. Hydroxamic acids can be found in various natural and synthetic sources and play significant roles in different biological processes.

In medicine and biochemistry, hydroxamic acids are often used as metal-chelating agents or siderophore mimics to treat iron overload disorders like hemochromatosis. They form stable complexes with iron ions, preventing them from participating in harmful reactions that can damage cells and tissues.

Furthermore, hydroxamic acids are also known for their ability to inhibit histone deacetylases (HDACs), enzymes involved in the regulation of gene expression. This property has been exploited in the development of anti-cancer drugs, as HDAC inhibition can lead to cell cycle arrest and apoptosis in cancer cells.

Some examples of hydroxamic acid-based drugs include:

1. Deferasirox (Exjade, Jadenu) - an iron chelator used to treat chronic iron overload in patients with blood disorders like thalassemia and sickle cell disease.
2. Panobinostat (Farydak) - an HDAC inhibitor approved for the treatment of multiple myeloma, a type of blood cancer.
3. Vorinostat (Zolinza) - another HDAC inhibitor used in the treatment of cutaneous T-cell lymphoma, a rare form of skin cancer.

Acetylation is a chemical process that involves the addition of an acetyl group (-COCH3) to a molecule. In the context of medical biochemistry, acetylation often refers to the post-translational modification of proteins, where an acetyl group is added to the amino group of a lysine residue in a protein by an enzyme called acetyltransferase. This modification can alter the function or stability of the protein and plays a crucial role in regulating various cellular processes such as gene expression, DNA repair, and cell signaling. Acetylation can also occur on other types of molecules, including lipids and carbohydrates, and has important implications for drug metabolism and toxicity.

GABA (gamma-aminobutyric acid) agents are pharmaceutical drugs that act as agonists at the GABA receptors in the brain. GABA is the primary inhibitory neurotransmitter in the central nervous system, and it plays a crucial role in regulating neuronal excitability.

GABA agents can enhance the activity of GABA by increasing the frequency or duration of GABA-mediated chloride currents at the GABA receptors. These drugs are often used as anticonvulsants, anxiolytics, muscle relaxants, and sedatives due to their ability to reduce neuronal excitability and promote relaxation.

Examples of GABA agents include benzodiazepines, barbiturates, non-benzodiazepine hypnotics, and certain anticonvulsant drugs such as gabapentin and pregabalin. It is important to note that while these drugs can be effective in treating various medical conditions, they also carry the risk of dependence, tolerance, and adverse effects, particularly when used at high doses or for prolonged periods.

Triazines are not a medical term, but a class of chemical compounds. They have a six-membered ring containing three nitrogen atoms and three carbon atoms. Some triazine derivatives are used in medicine as herbicides, antimicrobials, and antitumor agents.

Enzyme inhibitors are substances that bind to an enzyme and decrease its activity, preventing it from catalyzing a chemical reaction in the body. They can work by several mechanisms, including blocking the active site where the substrate binds, or binding to another site on the enzyme to change its shape and prevent substrate binding. Enzyme inhibitors are often used as drugs to treat various medical conditions, such as high blood pressure, abnormal heart rhythms, and bacterial infections. They can also be found naturally in some foods and plants, and can be used in research to understand enzyme function and regulation.

Piracetam is a nootropic drug, which is primarily used in the treatment of cognitive disorders. It is a cyclic derivative of the neurotransmitter GABA (gamma-aminobutyric acid). Piracetam is believed to work by reducing the permeability of cell membranes in the brain, which may enhance communication between neurons and improve memory and learning.

Medically, piracetam is used off-label for a variety of conditions related to cognitive decline or impairment, such as Alzheimer's disease, dementia, and age-related cognitive decline. It has also been studied in the treatment of myoclonus (involuntary muscle jerks), dyslexia, and other neurological disorders.

It is important to note that while piracetam has shown some promise in improving cognitive function in certain populations, its effectiveness is still a subject of ongoing research and debate. Additionally, piracetam is not approved by the U.S. Food and Drug Administration (FDA) for any medical use, although it is available as a dietary supplement in the United States.

As with any medication or supplement, it's important to consult with a healthcare provider before taking piracetam to ensure that it is safe and appropriate for your individual needs.

Absence epilepsy is a type of epilepsy characterized by recurrent brief episodes of "absences," or staring spells, that can last from a few seconds to several minutes. These episodes are often accompanied by subtle body movements such as lip smacking or eyelid flutters. Absence epilepsy is most commonly diagnosed in children and adolescents, and it is more common in girls than boys.

The seizures in absence epilepsy are caused by abnormal electrical activity in the brain, specifically in a part of the brain called the cortex. These abnormal electrical discharges occur in a pattern that involves both sides of the brain simultaneously. This differs from other types of epilepsy, which may involve only one side of the brain or specific areas within a single hemisphere.

Absence seizures are typically brief and do not cause confusion or disorientation after they end. However, if they occur frequently, they can interfere with learning and social development. In some cases, absence epilepsy may be associated with other types of seizures, such as generalized tonic-clonic (grand mal) seizures or myoclonic jerks.

The diagnosis of absence epilepsy is usually made based on the characteristic symptoms and the results of an electroencephalogram (EEG), which can detect the abnormal electrical activity in the brain during a seizure. Treatment typically involves medication to control the seizures, such as ethosuximide or valproic acid. In some cases, a ketogenic diet may also be recommended as an alternative treatment option.

A drug interaction is the effect of combining two or more drugs, or a drug and another substance (such as food or alcohol), which can alter the effectiveness or side effects of one or both of the substances. These interactions can be categorized as follows:

1. Pharmacodynamic interactions: These occur when two or more drugs act on the same target organ or receptor, leading to an additive, synergistic, or antagonistic effect. For example, taking a sedative and an antihistamine together can result in increased drowsiness due to their combined depressant effects on the central nervous system.
2. Pharmacokinetic interactions: These occur when one drug affects the absorption, distribution, metabolism, or excretion of another drug. For example, taking certain antibiotics with grapefruit juice can increase the concentration of the antibiotic in the bloodstream, leading to potential toxicity.
3. Food-drug interactions: Some drugs may interact with specific foods, affecting their absorption, metabolism, or excretion. An example is the interaction between warfarin (a blood thinner) and green leafy vegetables, which can increase the risk of bleeding due to enhanced vitamin K absorption from the vegetables.
4. Drug-herb interactions: Some herbal supplements may interact with medications, leading to altered drug levels or increased side effects. For instance, St. John's Wort can decrease the effectiveness of certain antidepressants and oral contraceptives by inducing their metabolism.
5. Drug-alcohol interactions: Alcohol can interact with various medications, causing additive sedative effects, impaired judgment, or increased risk of liver damage. For example, combining alcohol with benzodiazepines or opioids can lead to dangerous levels of sedation and respiratory depression.

It is essential for healthcare providers and patients to be aware of potential drug interactions to minimize adverse effects and optimize treatment outcomes.

Hyperammonemia is a medical condition characterized by an excessively high level of ammonia (a toxic byproduct of protein metabolism) in the blood. This can lead to serious neurological symptoms and complications, as ammonia is highly toxic to the brain. Hyperammonemia can be caused by various underlying conditions, including liver disease, genetic disorders that affect ammonia metabolism, certain medications, and infections. It is important to diagnose and treat hyperammonemia promptly to prevent long-term neurological damage or even death. Treatment typically involves addressing the underlying cause of the condition, as well as providing supportive care such as administering medications that help remove ammonia from the blood.

Hemoperfusion is a medical procedure that involves passing a patient's blood through an external device to remove toxic substances or excess therapeutic drugs. In this process, the patient's blood is circulated outside the body, where it passes through a cartridge containing adsorbent material (such as activated charcoal or synthetic resins). These materials bind to and eliminate harmful molecules from the blood, which are then discarded.

Hemoperfusion can be used in various clinical situations, such as:

1. Drug overdoses: To remove toxic levels of drugs that cannot be effectively eliminated by conventional methods like dialysis.
2. Poisoning: To eliminate harmful toxins from the bloodstream in cases of acute poisoning or envenomation.
3. Liver failure: In patients with liver dysfunction, hemoperfusion can help remove waste products and toxins that the damaged liver cannot process effectively.
4. Septicemia: To eliminate bacterial toxins from the bloodstream in severe cases of sepsis or septic shock.

It is important to note that hemoperfusion is not a common procedure and is typically reserved for specific, life-threatening situations where other treatment options have been exhausted. The use of this technique requires specialized equipment, trained medical personnel, and close monitoring of the patient's clinical status during and after the procedure.

Histones are highly alkaline proteins found in the chromatin of eukaryotic cells. They are rich in basic amino acid residues, such as arginine and lysine, which give them their positive charge. Histones play a crucial role in packaging DNA into a more compact structure within the nucleus by forming a complex with it called a nucleosome. Each nucleosome contains about 146 base pairs of DNA wrapped around an octamer of eight histone proteins (two each of H2A, H2B, H3, and H4). The N-terminal tails of these histones are subject to various post-translational modifications, such as methylation, acetylation, and phosphorylation, which can influence chromatin structure and gene expression. Histone variants also exist, which can contribute to the regulation of specific genes and other nuclear processes.

Neural Tube Defects (NTDs) are a group of birth defects that affect the brain, spine, or spinal cord. They occur when the neural tube, which forms the early brain and spinal cord of the embryo, does not close properly during fetal development. This can result in various conditions such as:

1. Anencephaly: a severe defect where most of the brain and skull are missing. Infants with anencephaly are usually stillborn or die shortly after birth.
2. Spina bifida: a condition where the spine does not close properly, leaving a portion of the spinal cord and nerves exposed. This can result in various neurological problems, including paralysis, bladder and bowel dysfunction, and hydrocephalus (fluid buildup in the brain).
3. Encephalocele: a condition where the skull does not close properly, allowing the brain to protrude through an opening in the skull. This can result in various neurological problems, including developmental delays, vision and hearing impairments, and seizures.

NTDs are thought to be caused by a combination of genetic and environmental factors, such as folic acid deficiency, obesity, diabetes, and exposure to certain medications during pregnancy. Folic acid supplementation before and during early pregnancy has been shown to reduce the risk of NTDs.

Anethole trithione is not a medical term, but a chemical compound. It's a synthetic compound that has been used in the past as a medication to treat certain types of cancer, specifically germ cell tumors and ovarian cancer. However, its use in medicine is no longer common due to the development of other more effective and less toxic treatments.

Anethole trithione works by damaging the DNA of cancer cells, which can lead to their death. It was often used in combination with other chemotherapy drugs to increase its effectiveness.

It's important to note that anethole trithione is not approved for use in many countries and should only be administered under the supervision of a qualified healthcare professional.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Juvenile Myoclonic Epilepsy (JME) is a genetic condition that is characterized by the occurrence of myoclonic seizures, which are sudden, brief, shock-like jerks of muscles typically occurring in the arms and legs. These seizures usually begin in adolescence or early adulthood, between 12 to 18 years of age.

JME is a type of generalized epilepsy, meaning that it involves abnormal electrical activity throughout the brain rather than just one area. In addition to myoclonic seizures, individuals with JME may also experience absence seizures (brief periods of staring and unresponsiveness) and/or tonic-clonic seizures (generalized convulsions).

The condition is often inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the gene mutation from a parent with JME. However, not all cases are familial, and some may result from new genetic changes (mutations) that occur spontaneously.

JME is typically treated with anticonvulsant medications such as valproate or lamotrigine to control seizures. Lifestyle modifications, including avoiding sleep deprivation, stress, and excessive alcohol consumption, may also help reduce the frequency of seizures. With appropriate treatment, most individuals with JME can lead normal or near-normal lives.

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The glucuronidation of valproic acid was typified by high K(m) values with microsomes and expressed UGTs (2.3-5.2mM). The ... Valproic acid glucuronidation kinetics were carried our with three human UGT isoforms: UGT1A6, UGT1A9, and UGT2B7 as well as ... No significant inhibition of UGT1A1 or UGT1A6 by valproic acid was observed. These data indicate that valproic acid inhibition ... UGT1A1 and UGT2B15 which do not glucuronidate valproic acid. Valproic acid inhibited UGT1A9 catalyzed propofol glucuronidation ...
Side Effect Profile of Enteric-Coated Divalproex Sodium Versus Valproic Acid. Joseph Levine, K. N. Roy Chengappa, and Haranath ... Sir: Valproic acid and its derivatives are important agents in the treatment of patients with bipolar illness. This drug has ... We present here a case report of a naturalistic A-B-A design, which included the replacement of divalproex by valproic acid ... Two representative derivatives are valproic acid and divalproex sodium (the enteric-coated derivative), the latter being more ...
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... , Yudhisman Imran ... Valproic Acid Dosage and Toxicity. The starting daily dose of valproic acid is generally 15 mg/ kg. At a weekly interval this ... Valproic Acid in Epilepsy. Valproic acid has been proven to be an effective therapy for generalized epilepsy, and is considered ... Effects of valproic acid in pregnancy. There are only few prospective studies on the effects of valproic acid during pregnancy ...
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Conjugation of glutathione with a toxic metabolite of valproic acid, (E)-2-propyl-2,4-pentadienoic acid, catalyzed by rat ... The hepatotoxic metabolite of the anticonvulsant drug valproic acid (VPA), namely (E)-2-propyl-2,4-pentadienoic acid (E)-2,4- ... Conjugation of glutathione with a toxic metabolite of valproic acid, (E)-2-propyl-2,4-pentadienoic acid, catalyzed by rat ... Conjugation of glutathione with a toxic metabolite of valproic acid, (E)-2-propyl-2,4-pentadienoic acid, catalyzed by rat ...
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Tesoro, E. P., Brophy, G. M., & Cohen, H. (2015). Valproic acid. In H. Cohen (Ed.), Casebook in clinical pharmacokinetics and ...
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