Klinische Charakteristika von Patienten mit tardiven Dyskinesien

Held, Tilo; Weber, Th.; Krausz, H.; Ahle, Guido; Hager, Brant W.; Alfter, D.; Schulze, Thomas G.; Knapp, Michael; Maier, W.; Rietschel, Marcella

doi:10.1055/s-2000-11805

Cited by 8 publications

(4 citation statements)

References 2 publications

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“…Second, patients with TD had significantly higher scores on the general PANSS subscales, which suggests that somatic, anxiety, mood and other psychopathologic symptoms were higher in TD patients than in non-TD patients. This differs from the previous studies that found that only PANSS negative symptoms were associated with TD [32] and that the presence of TD was not correlated with higher PANSS scores [33] . Our study is subject to several limitations.…”

Section: Discussioncontrasting

confidence: 99%

No Association between Dopamine D4 Receptor Gene –521 C/T Polymorphism and Tardive Dyskinesia in Schizophrenia

Na¹,

Choi²,

Paik³

et al. 2007

Neuropsychobiology

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Tardive dyskinesia (TD) is a long-term adverse effect of antipsychotics. We evaluated whether a candidate functional polymorphism of the dopamine D4 receptor (DRD4) gene is associated with drug-induced TD in 209 Korean schizophrenic patients with TD (n = 83) and without TD (n = 126) who were matched for antipsychotic drug exposure and other relevant variables. There was no significant association of the genotype and allele frequencies determined by the –521 C/T SNP of DRD4 between TD and non-TD patients. In addition, there was no significant difference in terms of total Abnormal Involuntary Movement Scale scores among the 3 genotype groups. Within the limitations imposed by the size of the clinical sample, these findings suggest that the DRD4 –521 C/T SNP does not contribute significantly to the risk for TD.

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Section: Discussioncontrasting

confidence: 99%

No Association between Dopamine D4 Receptor Gene –521 C/T Polymorphism and Tardive Dyskinesia in Schizophrenia

Na¹,

Choi²,

Paik³

et al. 2007

Neuropsychobiology

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show abstract

“…All subjects underwent detailed interrogation of their drug history. Assessment of lifetime antipsychotic dose was done retrospectively based on medical records and patients' report in a standardized manner as described elsewhere [23]. To sum up the dosage level of different drugs, lifetime antipsychotic dose was converted into chlorpromazine equivalents (CPZ).…”

Section: Methodsmentioning

confidence: 99%

CYP2D6 Polymorphism and Tardive Dyskinesia in Schizophrenic Patients

et al. 2003

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Antipsychotic drug-induced tardive dyskinesia (TD) is a serious problem during psychopharmacologic treatment of schizophrenic patients. In search of genetic factors contributing to TD, there is a lack of consensus regarding the role of the polymorphic isozyme cytochrome P450 CYP2D6, which is involved in the oxidative metabolism of antipsychotic drugs. In the present case-control study, we tested the putative influence of the CYP2D6 genotype on the development of TD. Out of 157 patients, 109 were retrospectively selected meeting DSM IV criteria for schizophrenia or schizoaffective disorder, and 50 of them persistently presenting with TD. Genotyping detected the functional allele CYP2D6 *1, the known major defective alleles CYP2D6 *3, *4, *5, *6, and gene duplication. According to their number of functional CYP2D6 alleles, subjects were divided into carriers of none, one, or at least two functional CYP2D6 alleles. The proportions of these categories did not differ between patients and an ethnically homogenous control population (n = 195, p = 0.99) or between patients with and without TD (p = 0.818). Schizophrenic patients were carriers of gene duplication more often than healthy probands, without revealing statistical significance (p = 0.10). Out of seven patients with gene duplication, three developed persistent TD. Furthermore, patients with and without TD were comparable according to age, age of onset, gender, and duration of illness, but subjects with TD had taken more lifetime chlorpromazine equivalents (CPZ) than had patients without TD (chi 2-test, Student's t-test). Forward as well as backward logistic regression analyses confirmed that the presence of TD was influenced by lifetime CPZ but not by age, age of onset, gender, duration of illness, or CYP2D6 genotype. In contrast to the relevance of lifetime CPZ, the lifetime dose of antipsychotic drugs known to be metabolized by CYP2D6 did not significantly influence the presence of TD. In conclusion, our results provide no evidence for the contribution of CYP2D6 genotype to the development of TD in schizophrenic patients receiving long-term antipsychotic medication.

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“…Age, regardless of the duration of treatment, is an important risk factor for TD, as TD is five to six times more prevalent in the elder (445 years) than in younger patients. 3,4 Even though newer (or 'atypical') antipsychotics have a lower or perhaps negligible risk to induce TD, 5 classical (or typical) antipsychotics are, however, currently still prescribed for many reasons: Typical antipsychotics are less expensive than atypical antipsychotics, which may globally be one leading reason. Moreover, some patients do not respond or tolerate treatment with atypical antipsychotics that may cause side effects as weight gain or diabetes mellitus.…”

Section: Introductionmentioning

confidence: 99%