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Valproic Acid Toxicity

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162. Autism

signi?cant response c for repetitive behavior and stereotypy on risperidone Risperidone vs. haloperidol b Miral et al., 2008 126 behavior, social, sensory, language 0.01-0.08 mg/kg/d 30 children 8-18 y old EPS, weight gain, gynecomastia risperidone reported superior to haloperidol only on ABC total score, no subscales reported Mood stabilizers Valproic acid Hellings et al., 2005 127 irritability 20 mg/kg/d, average level 75-78 30 subjects 6-20 y old increased appetite, skin rash no signi?cant (...) .,homocystinuria), traumatic (e.g., head injury), toxic (e.g., fetal alcohol syndrome), 4 or genetic (e.g., chromosomal abnormality). Certain developmental disorders, most notably Landau-Kleffner syndrome, also should be ruled out. In this condition, a highly distinctive EEG abnormality is present and asso- ciated with development of a marked aphasia. 71 Genetic or neurologic consultation, neuroimaging, EEG, and additional laboratory tests should be obtained when relevant, based on examination or history(e.g

2014 American Academy of Child and Adolescent Psychiatry

163. DNA Polymerase Gamma (POLG)-related disorders

controlling eye movement), and progressive intellectual disability. In addition, hepatopathy (liver dysfunction) may occur in affected individuals. Importantly, the use of valproic acid (sodium valproate) in the treatment of seizures is known to precipitate liver failure (often rapidly and with fatal consequences) in those with POLG gene variants. Liver dysfunction may also occur in the absence of an exposure to valproic acid. With regard to the diagnosis of POLG-related disorders, affected individuals (...) POLG-positive patients, particularly in the early stages of the disease. In addition, each of these findings may be evident in individuals with other mitochondrial conditions. At the present time, the care for patients with POLG gene variants is symptom specific and primarily supportive in nature, with the goals of managing symptoms and preventing secondary complications (e.g., medication-induced liver toxicity). Final publication URL The report may be purchased from: Indexing Status Subject

2013 Health Technology Assessment (HTA) Database.

164. Osteoporosis: Prevention and Treatment

) • Thiazolidinediones (pioglitazone/Actos®, rosiglitazone/Avandia®) Miscellaneous • Anticonvulsants (phenytoin or phenobarbital > carbamazepine or valproic acid) b • Heparins (unfractionated > low molecular weight) Possible risk Miscellaneous • Lithium • Selective serotonin reuptake inhibitors • Antipsychotics (may cause hyperprolactinemia) • Excessive supplemental fluoride • Proton pump inhibitors • Topiramate >, greater than; >>, much greater than. a Inhaled beclomethasone (>1600 µg gaily) is associated with risk (...) acid, teriparatide, or denosumab; fractures occurring despite treatment; considering discontinuation of therapy; etc. b Lowest T-score from femoral neck, total hip, or combination of lumbar vertebra. Wards triangle is not predictive of fracture risk [D]. c If patient has had fracture without significant trauma, consider other causes of bone abnormality, e.g., malignancy. d Lifestyle = ensure appropriate intake of calcium and vitamin D, along with weight bearing exercise. 3 UMHS Osteoporosis

2013 University of Michigan Health System

165. Monitoring of Nonsteroidal Immunosuppressive Drugs in Patients With Lung Disease and Lung Transplant Recipients

for minimizing such risks include administering these drugs according to established, safe protocols; monitoring to detect manifestations of toxicity; and patient education. Hence, an evidence-based guideline for physicians can improve safety and optimize the likelihood of a successful outcome. To maximize the likelihood that these agents will be used safely, the American College of Chest Physicians established a committee to examine the clinical evidence for the administration and monitoring (...) of immunosuppressive drugs (with the exception of corticosteroids) to identify associated toxicities associated with each drug and appro- priate protocols for monitoring these agents. Methods: Committee members developed and re? ned a series of questions about toxicities of immunosuppressives and current approaches to administration and monitoring. A systematic review was carried out by the American College of Chest Physicians. Committee members were supplied with this information and created this evidence-based

2012 American College of Chest Physicians

166. Guidelines for the Evaluation and Management of Status Epilepticus

system infection: meningitis, encephalitis, abscess Stroke: ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, cerebral sinus thrombosis Head trauma with or without epidural or subdural hematoma Drug issues Drug toxicity Withdrawal from opioid, benzodiazepine, barbiturate, or alcohol Non-compliance with AEDs Hypoxia, cardiac arrest Hypertensive encephalopathy, posterior reversible encephalopathy syndrome Autoimmune encephalitis (i.e., anti-NMDA receptor antibodies, anti-VGKC complex (...) meningitis, inborn errors of metabolism, and ingestion are frequent causes of SE [34, 35] AED antiepileptic drug; CNS central nervous system; NMDA N-methyl-D-aspartic acid; SE status epilepticus; TBI traumatic brain injury; VGKC voltage-gated potassium channel Table 3 Suggested diagnostic work-up [21] The steps included in the diagnostic work-up should be completed as soon as possible and occur simultaneously and in parallel with treatment. All patients 1. Fingerstick glucose 2. Monitor vital signs. 3

2012 Neurocritical Care Society

167. Antiepileptic drug selection for people with hiv/aids

interaction between zidovudine and valproic acid in patients infected with human immunodeficiency virus . 24. Okulicz JF , Grandits GA , French JA , et al . Virologic outcomes of HAART with concurrent use of cytochrome P450 enzyme-inducing antiepileptics: a retrospective case control study . Bates DE , Herman RJ . Carbamazepine toxicity induced by lopinavir/ritonavir and nelfinavir . 26. Bonora S , Calcagno A , Fontana S , et al . Clinically significant drug interaction between tipranavir-ritonavir (...) and phenobarbital in an HIV-infected subject . 27. Burman W , Orr L . Carbamazepine toxicity after starting combination antiretroviral therapy including ritonavir and efavirenz . 28. Cazali N , Tran A , Treluyer JM , et al . Inhibitory effect of stiripentol on carbamazepine and saquinavir metabolism in human . 29. DiCenzo R , Peterson D , Cruttenden K , et al . Effects of valproic acid coadministration on plasma efavirenz and lopinavir concentrations in human immunodeficiency virus-infected adults . 30. Garcia

2012 American Academy of Neurology

168. Medical treatment of infantile spasms

drug ; BD = Breslow-Day ; CI = confidence interval ; ERG = electroretinogram ; FDA = Food and Drug Administration ; IVIg = IV immunoglobulin ; LEV = levetiracetam ; NZP = nitrazepam ; OR = odds ratio ; RCT = randomized controlled trial ; TPM = topiramate ; TRH = thyrotropin-releasing hormone ; TSC = tuberous sclerosis complex ; UKISS = United Kingdom Infantile Spasms Study ; VABS = Vineland Adaptive Behavioral Scale ; VGB = vigabatrin ; VPA = valproic acid ; ZNS = zonisamide Infantile spasms (...) (table e-4)? Previously reviewed and updated evidence. All previous and current studies were rated Class IV for treatment using valproic acid (VPA), , nitrazepam (NZP), , pyridoxine (vitamin B6), , zonisamide (ZNS), , IVIg, thyrotropin-releasing hormone (TRH), topiramate (TPM), ,e1 levetiracetam (LEV), e2 the ketogenic diet, e3,e4 and combination therapies using ACTH and VGB, e5 hydrocortisone, and VPA. e6 Sulthiame. One Class II randomized, double-blind, placebo-controlled study demonstrated a 30

2012 American Academy of Neurology

170. Study of the Safety, Pharmacokinetics and Efficacy of EDO-S101, in Patients With Advanced Solid Tumors

to prolong the QT/QTc interval. Patients who are being treated with Valproic Acid for any of its indication (epilepsy, mood disorder) must be excluded or must stop using the medication. Any serious medical condition that interferes with adherence to study procedures. Prior history of solid tumor malignancy diagnosed within the last three (3) years of study enrollment excluding adequately treated basal cell carcinoma of the skin, squamous cell carcinoma of the skin, or in situ cervical cancer, in situ (...) damage repair. This Phase 1/2 study will enroll patients with various advanced solid tumors. Condition or disease Intervention/treatment Phase Small-cell Lung Cancer Soft Tissue Sarcoma Triple-negative Breast Cancer Ovarian Cancer Endometrial Cancer Drug: Tinostamustine (EDO-S101) Phase 1 Phase 2 Detailed Description: The study consists of 2 phases: Phase 1: Dose Escalation until MAD Phase 2: Evaluation of Toxicity and Response Rate in Selected Solid Tumor Cohorts The study is designed as an open

2017 Clinical Trials

171. Toxicological Screening by GC-MS Among Children Admitted for a First Afebrile Seizure

will be performed on blood and urine samples to extensively screen for proconvulsive molecules (alcohols, polycyclic antidepressants, salicylates, anticonvulsive medications (carbamazepine, phenytoin, valproic acid), drugs (cocaine and its metabolites, amphetamines, methamphetamine (ecstasy), cannabis, buprenorphine, methadone, mephedrone, codeine, pholcodine, hydromorphone), benzodiazepines, caffeine, theophylline, lidocaine, isoniazid, mefenamic acid, tramadol, ephedrine). This analysis will be performed (...) of the patient and other associated symptoms or clinical signs. A seizure can be the first sign of acute intoxication and represents a severity criterion. Failure to detect the toxic cause of a seizure can lead to a delay in the access or administration of an antidote if applicable. This can lead to target organ toxicity due to the absence of specific treatment. In the current French guidelines for a first seizure, a toxicological analysis is recommended if there is a possibility of exposure to toxic

2017 Clinical Trials

172. Postnatal treatment using curcumin supplements to amend the damage in VPA-induced rodent models of autism. Full Text available with Trip Pro

Postnatal treatment using curcumin supplements to amend the damage in VPA-induced rodent models of autism. Valproic acid (VPA) is used as a first-line antiepileptic agent and is undergoing clinical trials for use as a treatment for many disorders. Mothers undergoing VPA treatment during early pregnancy reportedly show increased rates of autism among their offspring. The benefits of curcumin supplementation were investigated using an animal model of VPA-induced autism.The study was performed (...) using a rodent model of autism by exposing rat fetuses to valproic acid (VPA) on the 12.5th day of gestation. At 7 days from their birth, the animals were supplemented with a specific dose of curcumin. Forty neonatal male Western Albino rats were divided into four groups. Rats in group I received only phosphate-buffered saline, rats in group II were the prenatal VPA exposure newborns, rats in group III underwent prenatal VPA exposure supplemented with postnatal curcumin, and rats in group IV were

2017 BMC Complementary and Alternative Medicine

173. Dual Functional Mesoporous Silicon Nanoparticles Enhance the Radiosensitivity of VPA in Glioblastoma Full Text available with Trip Pro

attracted much attention because they selectively increase susceptibility of cancer cells to radiation and thus enhance biological effectiveness of radiotherapy. However, clinical translation of radiosensitizers has been severely limited by their potential toxicity to normal tissue. Recent advances in nanomedicine offer an opportunity to overcome this hindrance. In this study, a dual functional mesoporous silica nanoparticle (MSN) formulation of the valproic acid (VPA) radiosensitizer was developed (...) , which specifically recognized folic acid-overexpressing cancer cells and released VPA conditionally in acidic turmeric microenvironment. The efficacy of this targeted and pH-responsive VPA nanocarrier was evaluated as compared to VPA treatment approach in two cell lines: rat glioma cells C6 and human glioma U87. Compared to VPA treatment, targeted VPA-MSNs not only potentiated the toxic effects of radiation and led to a higher rate of cell death but also enhanced inhibition on clonogenic assay. More

2017 Translational oncology

174. Tolerated drugs in subjects with severe cutaneous adverse reactions (SCARs) induced by anticonvulsants and review of the literature Full Text available with Trip Pro

symptoms under therapy with phenytoin; 2 out of 6 presented with Stevens-Johnson syndrome under therapy with lamotrigine; and 2 out of 6 presented with a toxic epidermal necrolysis, one of them under therapy with valproic acid, and the other one under therapy with lamotrigine. Alternative anticonvulsants tolerated after the reaction were: clonazepam, levetiracetam, diazepam, delorazepam and lormetazepam.In our cases we observed that non aromatic anticonvulsants and benzodiazepines were well tolerated

2017 Clinical and molecular allergy : CMA

175. Valproate and sodium butyrate attenuate manganese-decreased locomotor activity and astrocytic glutamate transporters expression in mice Full Text available with Trip Pro

Valproate and sodium butyrate attenuate manganese-decreased locomotor activity and astrocytic glutamate transporters expression in mice Manganese (Mn) is an essential trace element, but chronic overexposure to this metal, either environmentally or occupationally may cause manganism, a disease analogous to Parkinson's disease. Inhibitors of histone deacetylases, such as valproic acid (VPA) and sodium butyrate (NaB) exert neuroprotective effects in various animal models of neurological disorders (...) in the cerebral cortical and cerebellar regions of mice. These results suggest that VPA and NaB exert protective effects against Mn toxicity seem in vitro are also shown in vivo. VPA and NaB pretreatment in mice enhancing astrocytic glutamate transporter GLT-1 expression as well as locomotor activities. Future research endeavors are warranted to determine if the therapeutic potential of VPA and NaB is via common molecular mechanism, namely, inhibition of histone deacetylases.Copyright © 2017. Published

2017 Neurotoxicology

176. Histone deacetylase inhibitors potentiate photodynamic therapy in colon cancer cells marked by chromatin-mediated epigenetic regulation of CDKN1A Full Text available with Trip Pro

fatty acids valproic acid and sodium phenylbutyrate (NaPB), as inhibitors of all-class versus nuclear HDACs, respectively. The selected HDACis manifest a favorable clinical toxicity profile and showed similar potencies and mechanisms in intragroup comparisons but different biological effects in intergroup analyses. HDACi combination with HY-PDT significantly attenuated cancer cell resistance to treatment and caused the two HDACi groups to become similarly potent. However, the short-chain fatty acids (...) treatments due to their non-genotoxic properties and epigenetic potential to sensitize cells to external stimuli. Therefore, this study attempts for the first time to investigate the therapeutic effects of HDACis in combination with visible light-mediated PDT against cancer. Specifically, the colorectal cancer cell model was used due to its known resistance to HY-PDT.Two chemical groups of HDACis were tested in combination with HY-PDT: the hydroxamic acids Saha and Trichostatin A, and the short-chain

2017 Clinical epigenetics

177. Epigenetic Reprogramming in Relapse/Refractory AML

period. -They have significant concurrent disease, illness, psychiatric disorder or social issue that would compromise patient safety or compliance, interfere with consent, study participation, follow up, or interpretation of study results. -They have a known allergy to any of the drugs used in the study. -Patients with Down syndrome are excluded. Patients with DNA fragility syndromes are excluded (e.g. Fanconi Anemia, Bloom Syndrome) They are receiving valproic acid (VPA) therapy. Patients (...) decitabine, vorinostat, fludarabine, high dose cytarabine, filgrastim (G-CSF) Drug: Decitabine Dose Level #0: 5 mg/m2 Dose Level #1: 7.5 mg/m2 Dose Level #2: 10 mg/m2 Dose Level #3: 15 mg/m2 Dose Level #4: 20 mg/m2 given IV over __ hour on days 1 through 5 Other Name: Dacogen Drug: Vorinostat Age <18: 180 mg/m2/day once daily PO. Age≥18: 200 mg twice daily PO. Other Name: Zolinza, SAHA, suberoylanilide acid Drug: Filgrastim (G-CSF) Given on days 5 until evidence of ANC recovery (>500/µL)5µg/kg/dose IV

2017 Clinical Trials

178. Study of MK-2118 Administered as Intratumoral Injection as Monotherapy and in Combination With Pembrolizumab (MK-3475) or by Subcutaneous Injection in Combination With Pembrolizumab in the Treatment of Adults With Advanced/Metastatic Solid Tumors or Lymph

: strong/moderate Cytochrome P450 2C9 (CYP2C9) inhibitors, such as: amiodarone, felbamate, fluconazole, miconazole, piperine, oxandrolone, fluorouracil and its derivatives (combination drug tegafur/gimeracil/oteracil [TS-1], Uftoral [UFT], tegafur, carmofur, doxifluridine, capecitabine), sulfaphenazole, cyclosporine, bucurol, tienilic acid; UGT1A3 inhibitors (including ritonavir, quinidine, probenecid, and valproic acid); or strong carbonyl reductase (CBR) inhibitors (including quercetin, menadione (...) : Dose-limiting Toxicities (DLTs) [ Time Frame: Arms 1, 2 & 3: Cycle 1 (Up to 21 days); Arm 4: Cycles 1 & 2 (Up to 35 days) ] A DLT is defined as the following toxicities, if related to study treatment: Grade 4 nonhematologic toxicity; Grade 4 hematologic toxicity lasting ≥7 days, except thrombocytopenia (Grade 4 thrombocytopenia of any duration, Grade 3 thrombocytopenia with clinically significant bleeding); Non-hematologic adverse event (AE) ≥Grade 3 (with exceptions); Grade 3 or Grade 4

2017 Clinical Trials

179. BV-CHEP Chemotherapy for Adult T-cell Leukemia or Lymphoma

, ketoconazole, itraconazole, ritonavir, macrolide antibiotics, erythromycin phenytoin, phenobarbital, carbamazepine, and valproic acid). Patients with a parenchymal brain lesion thought to be consistent with active lymphoma on screening CT/MRI. Of note, patients with cerebrospinal fluid (CSF) involvement alone are not excluded. Contacts and Locations Go to Information from the National Library of Medicine To learn more about this study, you or your doctor may contact the study research staff using (...) . After 6 cycles of BV + CHEP, responders (CR, PR or SD) who are not eligible for BMT and have CD30-positive ATLL will continue maintenance therapy with BV alone (1.8 mg/kg IV, every 21 days) until disease progression, withdrawal due to toxicity or death. Drug: Brentuximab Vedotin Brentuximab Vedotin will be given at 1.8 mg/kg IV over approximately 30 minutes on D1 every 21 days for 4-6 cycles. Responders (CR, PR or SD) who are not eligible for bone marrow transplant (BMT) and have CD30-positive ATLL

2017 Clinical Trials

180. Seizure Treatment in Glioma

Medical Center Information provided by (Responsible Party): j.a.f.koekkoek, Leiden University Medical Center Study Details Study Description Go to Brief Summary: Currently, treatment with a specific anti-epileptic drug mainly depends on the physicians' preference, as there are no studies supporting the use of one specific anticonvulsant in glioma patients. The overall aim of this randomized controlled trial is to directly compare the effectiveness of treatment with levetiracetam or valproic acid (...) in glioma patients with a first seizure. Condition or disease Intervention/treatment Phase Glioma Drug: Levetiracetam Drug: Valproic Acid Phase 4 Detailed Description: Currently, treatment of glioma patients with a specific anti-epileptic drug (AED) mainly depends on the physicians' preference, as there is no robust evidence from randomized controlled trials supporting the use of one specific anticonvulsant above the other in glioma patients. Levetiracetam and valproic acid are the most commonly used

2017 Clinical Trials

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