A comparison between delusional and non-delusional depressives

Bellini, L.; Gatti, Franco; Gasperini, M.; Smeraldi, Enrico

doi:10.1016/0165-0327(92)90075-h

Cited by 41 publications

(21 citation statements)

References 21 publications

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“…It also seems to be a common clinical assumption that psychosis is simply an indicator of the degree of severity in depression and that psychosis will eventually develop if a depression becomes sufficiently severe. This ‘severity-psychosis’ hypothesis is supported by some studies of PD [35,36] and also underlies the current classification of PD in both the DSM-IV and the ICD-10, where the disorder only figures as a subtype of severe depression. However, recent findings call into question this theory.…”

Section: Introductionmentioning

confidence: 55%

Considerations on the ICD-11 Classification of Psychotic Depression

Østergaard

Rothschild

Uggerby

et al. 2012

Psychother Psychosom

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Section: Introductionmentioning

confidence: 55%

Considerations on the ICD-11 Classification of Psychotic Depression

Østergaard

Rothschild

Uggerby

et al. 2012

Psychother Psychosom

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“…Concomitant psychotropic drugs were not allowed, except flurazepam at bedtime (upto 45 mg) or lithium maintenance (n ¼ 27). A decrease in HAMD scores to 8 or less, with Delusion factor equal to 0 (items 2, 15, 20) [Bellini et al, 1992;Bech et al, 1993;Sobin and Sackeim, 1997], was considered the response criterion. After the procedure had been fully explained to all subjects, informed consent was obtained.…”

Section: Samplementioning

confidence: 99%

Further evidence of a combined effect of SERTPR and TPH on SSRIs response in mood disorders

Serretti

Cusin

Rossini

et al. 2004

American J of Med Genetics Pt B

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We reported an independent association of the short variant of the serotonin transporter gene-linked polymorphic region (SERTPR) and tryptophan hydroxylase (TPH) genes with antidepressant response to selective serotonin reuptake inhibitors (SSRIs). The aim of the present study was to confirm the effect of the SERTPR and TPH gene variants on the SSRIs antidepressant activity in a new sample of major and bipolar depressives. Two hundred and twenty one inpatients (major depressives = 128, bipolar disorder = 93) were treated with SSRIs (fluvoxamine or paroxetine) for 6 weeks; the severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression (HAMD). SERTPR and TPH variants were determined using PCR-based techniques, 220 subjects genotyped for SERTPR and 221 for TPH that were never included in previous studies. SERTPR*s/s variant association with a poor response to SSRI treatment was confirmed, even if with less significant P values (P = 0.034), independently from clinical variables; pooling the present sample with previous ones we observed a highly significant effect (P < 0.000001). TPH*A/A variants showed higher HAMD scores throughout the trial but with only a trend in the same direction of our previous study in terms of a worse response of A/A genotypes. Thus, the previous positive association was not fully replicated for TPH. The present independent replication confirms SERTPR variants as a liability factor for antidepressant efficacy while the TPH effect is not unequivocal.

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“…HAMD items were pooled into the following factors: Core (items 1, 2, 7, 8, 10, 13), Sleep (items 4, 5, 6), Activity (items 7, 8), Psychic anxiety (items 9, 10), Somatic anxiety (items 11, 12, 13), Delusion (items 2, 15, 20). [32][33][34][35][36][37] The power of our sample for detecting differences amongst 5-HTTLPR variants was calculated considering an alpha value of 5% two-tailed. With these parameters in our sample we had a high power (0.80) to detect a medium-small effect size (0.35) that corresponded to a difference of approximately 2.1 points between the two alleles on the total HAMD.…”

Section: Discussionmentioning

confidence: 99%

Serotonin transporter gene (5-HTTLPR) is not associated with depressive symptomatology in mood disorders

et al. 1999

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Disturbances of the serotoninergic neutrotransmitter system have been implicated in the pathogenesis of mood disorders. A functional polymorphism in the upstream regulatory region of the serotonin transporter gene (5-HTTLPR) has been recently reported to be associated with both unipolar and bipolar disorder. In this study, we investigated the possibility that the 5-HTTLPR might be associated with depressive symptomatology in a sample of mood disorder subjects. One hundred and thirty-two psychiatric inpatients affected by major depressive (n = 67) and bipolar (n = 65) disorder (DSM-IV) were assessed at admission by the Hamilton Depression Rating Scale (HAMD-21, divided into Core, Sleep, Activity, Psychic anxiety, Somatic anxiety and Delusion clusters) and were typed using PCR techniques. The only prior treatment permitted was low dose benzodiazepines (Ͻ5 mg diazepam or equivalent); no prior (Ͻ2 weeks) antidepressant or neuroleptic treatment was allowed. 5-HTTLPR variants were not associated with total depressive symptomatology as measured by HAMD. The short 5-HTTLPR variant was marginally associated with higher psychic anxiety scores (F = 7.11, d.f. = 1,262, P = 0.008). The association was stronger among bipolars and early onset subjects. 5-HTTLPR variants were not associated with the remaining symptom clusters. The upstream regulatory region of the serotonin transporter gene has not, therefore, a major influence on the depressive symptomatology in mood disorder subjects.

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A comparison between delusional and non-delusional depressives

Cited by 41 publications

References 21 publications

Considerations on the ICD-11 Classification of Psychotic Depression

Considerations on the ICD-11 Classification of Psychotic Depression

Further evidence of a combined effect of SERTPR and TPH on SSRIs response in mood disorders

Serotonin transporter gene (5-HTTLPR) is not associated with depressive symptomatology in mood disorders

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