Variability of response to neuroleptics in schizophrenia: Clinical, pharmacologic, and neuroendocrine correlates

Gelder, Michael; Kołakowska, T

doi:10.1016/0010-440x(79)90024-5

Cited by 17 publications

(6 citation statements)

References 61 publications

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“…Previous studies investigated whether PRL levels could be used as a reliable biomarker of antipsychotic response (Gelder and Kolakowska, 1979;Ohman and Axelsson, 1978;Siris et al, 1978), schizophrenia symptomatology (Cotes et al, 1978), or TD in schizophrenia subjects (Cohen et al, 1979;Csernansky et al, 1983Csernansky et al, , 1986Kirkpatrick et al, 1989;Pandey et al, 1977;Smith et al, 1977;Tamminga et al, 1977;Tenback et al, 2006b). Most of the findings support that antipsychotic drugs modulate PRL levels but PRL should not be used as indicator of treatment outcome or its side effects.…”

Section: Discussionmentioning

confidence: 92%

“…The idea to find the ''right'' antipsychotic for the each patient is not new (Tansella and Balestrieri, 1976) and a number of studies have tried to identify biomarkers to better monitor treatment response. In a study published in 1974, Clemens et al showed that antipsychotics alter prolactin (PRL) release (Clemens et al, 1974) leading to an interesting assumption that was studied few years later: PRL serum levels could reflect antipsychotic treatment response (Gelder and Kolakowska, 1979;Ohman and Axelsson, 1978;Siris et al, 1978) or specific clinical states in schizophrenia subjects (Cotes et al, 1978). Later studies do not corroborate this association and have shown that baseline levels of PRL are similar in healthy controls and schizophrenia patients (Goodnick et al, 2002).…”

Section: Introductionmentioning

confidence: 92%

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Prolactin as a biomarker for treatment response and tardive dyskinesia in schizophrenia subjects: old thoughts revisited from a genetic perspective

Souza

Meltzer

Lieberman

et al. 2011

Human Psychopharmacology

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Previous studies investigated whether prolactin (PRL) serum level was a biomarker of antipsychotic response, schizophrenia symptomatology, and tardive dyskinesia. Most of the findings support that antipsychotic drugs modulate PRL levels but PRL is not a steady indicator. Recent results suggest a genetic effect of PRL and PRL receptor (PRLR) polymorphisms in PRL levels indicating that independently of antipsychotic therapy subjects could have altered PRL levels due to their genetic background.We evaluated whether PRL and PRLR variants were associated with treatment outcome and tardive dyskinesia. We observed no association of PRL/PRLR polymorphism with treatment response (best genotypic results include PRL rs849885 and PRLR rs4703509 permuted p=0.326). Regarding tardive dyskinesia, the major allele of PRL rs37364 was nominally associated with risk for tardive dyskinesia in the European ancestry sub-sample (permuted p=0.183). Although we reported no significant associations, it is definitely worthy of investigation to see if together (genetic variants in the PRL system and PRL serum measures) could be a reliable biomarker for antipsychotic response and TD prevalence. Our results suggest that more studies in this context are required to shed light in the molecular mechanisms underlying antipsychotic response and tardive dyskinesia occurrence.

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Section: Discussionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 92%

Prolactin as a biomarker for treatment response and tardive dyskinesia in schizophrenia subjects: old thoughts revisited from a genetic perspective

Souza

Meltzer

Lieberman

et al. 2011

Human Psychopharmacology

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“…The theoretical limit of the kFD design is the aFD design where we would independently assign patients to doses randomly selected from the infinity of possible doses in the entire dose distribution. The derivations for the mFS design are identical to those for the 1FD design given in expressions The expected correlation between bioavailability and measures of clinical response is pBs which is, by definition, greater than pBs,D as indicated by equation (15).…”

Section: O B S K = Eibs1 -P E P S = E C B ( F L B S B + P M S M ) Imentioning

confidence: 99%

Mathematical models of complex dose‐response relationships: Implications for experimental design in psychopharmacologic research

Faraone¹,

Simpson²,

Brown³

1992

Statistics in Medicine

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We develop a mathematical model to account for the complex relationship between drug dose and clinical response in psychopharmacologic research. The model specifies relationships among drug dose, drug bioavailability, pharmacokinetic factors, course moderators, clinical response and the heterogeneity of the disorder, and allows for the derivation of results that have implications for experimental design in psychopharmacologic research. These results form the basis for computer simulations which indicate that random assignment to two fixed doses is more powerful and less sensitive to heterogeneity than assignment to clinically determined doses. Fixed dose designs, however, tend to overestimate the magnitude of drug bioavailability-clinical response relationships. Clinically determined dose designs are useful in some experimental situations; their effectiveness is enhanced by systematically reducing the clinically determined dose. Larger dose reductions improve the ability to detect bioavailability-clinical response relationships.

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“…A s clinical improvement may be caused both by drug response and by spontaneous remission, and as lack of clinical improvement may be caused both by insufficient pharmacological effect and a neuroleptic resistant condition, a division of the patients into 4 groups has been suggested: "responders", "remitters", "inadequately treated" and "neuroleptic resistant" (77). The most frequent cause of non-response has been thought to be inadequate dosage or noncompliance (78,79).…”

Section: Dosage Principlesmentioning

confidence: 99%

Chemotherapy With Neuroleptics

Knudsen

1985

Acta Psychiatr Scand

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Attempting to improve long-term neuroleptic treatment of schizophrenic patients several injectable depot neuroleptics have been developed. Moreover pharmacokinetic data increasingly have been clinically applied. On this background the purpose of the present paper has been to make an updated review of the clinical and pharmacokinetic knowledge of depot neuroleptic treatment.First, general aspects of antipsychotics have been summarized, and an outline of methodological questions relevant to clinical-pharmacological trials are given. Subsequently general aspects including pros & cons of depot administration are examined. Finally the available data of the various depot preparations have been scrutinized.It is concluded that our present pharmacokinetic knowledge of the particular depot preparations is incomplete. Thus more information of clinical relevant aspects are needed, e.g., the existence of a therapeutic range, maximumiminimum concentration ratio, and the significance of active metabolites.Comparing the various depot neuroleptics, no significant differences are seen regarding the clinical effects. However, the decanoate esters seem clinical superior to the corresponding enanthate esters explained by the more flat concentration curve of the decanoates.Apart from that, a comparison of the pharmacokinetic data is difficult because of the heterogenecy of the available data.Haloperidol, clopenthixol and perphenazine decanoates are among the best examined preparations in pharmacokinetic respects. A controlled double-blind comparative study of these preparations would be of interest.

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Variability of response to neuroleptics in schizophrenia: Clinical, pharmacologic, and neuroendocrine correlates

Cited by 17 publications

References 61 publications

Prolactin as a biomarker for treatment response and tardive dyskinesia in schizophrenia subjects: old thoughts revisited from a genetic perspective

Prolactin as a biomarker for treatment response and tardive dyskinesia in schizophrenia subjects: old thoughts revisited from a genetic perspective

Mathematical models of complex dose‐response relationships: Implications for experimental design in psychopharmacologic research

Chemotherapy With Neuroleptics

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