M1627K mutation was previously identified in a sporadic case of PEPD from France, and we now report it in an English family. We confirm the initial characterization of mutant M1627K effect on fast-inactivation of Nav1.7 and extend the analysis to other gating properties of the channel. We also show that M1627K mutant channels render DRG neurons hyperexcitable. Our new data provide a link between altered channel biophysics and pain in PEPD patients.
Adverse drug reactions (ADR) are the cause of hospital admissions for millions of patients every year and are believed to be a major problem in terms of morbidity and hospital expenses. ADR are characterized by exceptional variety, both considering pathomechanism and clinical symptoms. During the time period between 2000-2004 at the Department of Dermatology a project was undertaken to monitor patients who were hospitalized as a result of ADR. Within five years 57 patients, including 30 men and 27 women were observed. The majority of the patients developed maculaopapular rash (16), urticaria medicamentosa and Quincke's edema (16) and erythema multiforme (15). The other cases included erythroderma (5), anaphylactic shock (2), lichenoid exanthem (1), bullous eruption (1) and Hoigne's syndrome (1). The most probable factors producing these changes were concluded to be non-steroid antiinflammation drugs (33%), antibiotics (7%) and other drugs from different pharmacological and chemical groups (carbamazepine, diltiazem, hydrocortisone, methotrexate and herbs). The frequency of occurrence of skin changes of particular type in age groups were also analyzed. The greatest number of skin changes in response to drug therapy was in the age group 41 - 60, while for the age group > 60 ADR revealed the greatest diversity in the clinical picture. The most probable explanation of these findings are the polypragmasy applied in the elderly patients and interdrug interaction as well as decreased efficiency of the organic clearances.
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IGE can exacerbate in the elderly, as different types of seizures including AS, subintrant myoclonia or repeated CGS. Our data suggest persistent IGE are quite frequent in an aged population and may be underestimated due to difficulties in diagnosis. Correctly diagnosed, adjustment of AED may offer substantial clinical improvements in IGE of the elderly.
We previously reported that foetal valproate exposure impairs intelligence quotient. In this follow-up investigation, we examined dose-related effects of foetal antiepileptic drug exposure on verbal and non-verbal cognitive measures. This investigation is an ongoing prospective observational multi-centre study in the USA and UK, which has enrolled pregnant females with epilepsy on monotherapy from 1999 to 2004. The study seeks to determine if differential long-term neurodevelopmental effects exist across four commonly used drugs (carbamazepine, lamotrigine, phenytoin and valproate). This report compares verbal versus non-verbal cognitive outcomes in 216 children who completed testing at the age of three years. Verbal and non-verbal index scores were calculated from the Differential Ability Scales, Preschool Language Scale, Peabody Picture Vocabulary Test and Developmental Test of Visual-Motor Integration. Verbal abilities were lower than non-verbal in children exposed in utero to each drug. Preconceptional folate use was associated with higher verbal outcomes. Valproate was associated with poorer cognitive outcomes. Performance was negatively associated with valproate dose for both verbal and non-verbal domains and negatively associated with carbamazepine dose for verbal performance. No dose effects were seen for lamotrigine and phenytoin. Since foetal antiepileptic drug exposure is associated with lower verbal than non-verbal abilities, language may be particularly susceptible to foetal exposure. We hypothesize that foetal drug exposure may alter normal cerebral lateralization. Further, a dose-dependent relationship is present for both lower verbal and non-verbal abilities with valproate and for lower verbal abilities with carbamazepine. Preconceptional folate may improve cognitive outcomes. Additional research is needed to confirm these findings, extend the study to other drugs, define the risks associated with drug treatment for seizures in the neonates, and understand the underlying mechanisms.
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Case-control study of SCDR with carbamazepine and HLA-B*1502. We recruited 32 cases, 5 with Steven Johnson Syndrome/Toxic Epidermolytic Necrolysis (SJS/TEN) (2 Chinese, 3 Malay), 6 with hypersensitivity syndrome (HSS) (5 Chinese, 1 Indian), 11 with minor drug reactions (9 Chinese, 2 Malay) and 10 controls (7 Chinese, 2 Malay, 1 Indian). HLA-B*1502 allelism was assayed. HLA-B*1502 status and the type of drug reaction were compared using univariate analysis. The time-span from treatment onset to reaction and the dose-time to reaction association in the 3 groups were analysed.
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Our results showed that cisplatin (5 mg/kg, IP) induced egregious pain (P < 0.01) on day 15. Acute administration of CBZ (5, 10, and 15 mg/kg, PO) caused significant (P < 0.05) increase in tail-flick time latency in a dose-dependent manner, in comparison with that observed in the control group. Furthermore, chronic administration of CBZ (5, 10, and 15 mg/kg, PO) increased (P < 0.05) the pain threshold on days 5 and 10. The analgesic effect of morphine (5 mg/kg, IP) was greater than that after acute CBZ administration (5, 10, and 15 mg/kg, PO).
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In the lithium phase, a low level of free T4 was associated with more affective episodes and greater severity of depression. Whether this mood instability is causally related to low free T4 levels and whether it can be attenuated with T4 replacement remain to be studied in a controlled setting.
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We identified 16 adults with Dravet syndrome, living in a tertiary care facility for people with epilepsy and an intellectual disability. We reviewed clinical history, genetic findings, the type and duration of sodium channels blockers that were used, seizure types and frequency, and the effect of a change in these medications.
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One type of pharmacokinetic/pharmacodynamic (PK/PD) relationship that is used to characterize the therapeutic action of a drug is the relationship between some univariate summary of the plasma-concentration-versus-time profile and the drug effect on a response outcome. Operationally, such a relationship may be observed in a large clinical trial where randomly sampled patients are randomized to different values of the concentration summary. If, under such conditions, the relationship between concentration and effect does not depend on the dose needed to attain the target concentration, such a relationship will be called a true PK/PD relationship. When the true PK/PD relationship is assessed as an object of estimation in a dose-controlled clinical trial (i.e. when dose is randomized), observed drug concentration is an outcome variable. The estimated PK/PD relationship between observed outcome and observed concentration, which we then refer to as the conventional PK/PD relationship, may be biased for the true PK/PD relationship. Because of this bias, the conventional relationship is called confounded for the true one. We show that diagnostics for confounding can be devised under reasonable assumptions. We then apply these diagnostics to PK/PD assessments of adults and children on oxcarbazepine adjunctive therapy. It was necessary to demonstrate the similarity of the true PK/PD relationships of adults and children on adjunctive therapy in order to support the approval of oxcarbazepine monotherapy in children by a bridging argument.
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To determine whether clinical neurologic diseases are associated with unique patterns of up- and down-regulated genes in whole blood and to explore the possibility of using peripheral blood as a surrogate tissue in these diseases.
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We aimed to investigate the frequency of seizure after acute carbamazepine poisoning and the important risk factors related to the outcomes of therapy.
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In a pragmatic, randomized clinical trial, 201 adults hospitalized with bipolar I manic or mixed episodes were randomized to divalproex or lithium, in addition to usual psychiatric care, and followed for 1 year. All subsequent treatment of bipolar disorder was managed by the patient's psychiatrist. Symptoms of mania and depression were evaluated at baseline and at hospital discharge. Assessments at the start of maintenance therapy and after 1, 3, 6, 9 and 12 months included manic and depressive symptoms, disability days and QOL. Medical resource use data were also collected monthly and costs were estimated using national sources.