[Renal transplantation, anxiety and depressive disorders and quality of life]. / Transplantation rénale, troubles anxiodépressifs et qualité de vie.

Until now there are few data in the literature describing psychiatric comorbidity in patients waiting for renal transplantation. We have conducted a cross sectional study estimating the prevalence of anxiety and depressive disorders in three groups of renal transplant patients, before transplantation, six months and one year after. The MINI was used to estimate the prevalence of anxiety and depressive disorders. Anxiety and depressive symptoms were assessed using the HAD. Patients' quality of life was also assessed using the SF-36. This study did not find any major impact of renal transplantation on the prevalence of structured psychiatric disorders. Indeed, the prevalence of depressive and anxiety disorders did not differ significantly between the three groups. The mean scores of anxiety did not differ significantly between the three groups in contrast to the mean scores of depression, which differed significantly between the group "before transplantation" and the group "one year after transplantation". We did not find any significant difference concerning the scores of patient's quality of life between the three groups, except for the item "health perceived by the patients themselves". Health perceived by the patients was greater in the group "after transplantation". The quality of life of dialysed or transplant patients was strongly correlated with anxiety and depressive symptoms scores, emphasizing the major interest of a multidisciplinary approach for these patients.

Concordance of deficit and non-deficit subtypes in siblings affected with schizophrenia.

Deficit and non-deficit subtypes were examined for their concordance in 83 sibling pairs of 109 schizophrenic patients belonging to 46 multiply affected families. Using a sib-pair method, we have found that the distribution of deficit and non-deficit syndromes in sibling pairs of schizophrenic patients differed significantly from chance expectation. This familial aggregation suggests that the syndrome may be used to define phenotypes for genetic studies.

The Emotional Stroop task: a comparison between schizophrenic subjects and controls.

The colour-word Emotional Stroop task (ES task) has been proposed to assess the interferences between emotion and attention. Using this task, first, we examined how attention (using reaction times) can be modified by emotionally relevant words in schizophrenics as compared with controls as a function of the emotional significance of the word; second, we tested the assumption that schizophrenics with the most negative symptoms will show higher impairment in relationship to negative emotional words. In general, schizophrenics were slower to react. In both groups, mean reaction times were slower for emotional as compared with neutral words. No significant differences were observed between negative and positive words either in schizophrenics (n=21) or in controls (n=20). Even in the most negative schizophrenic patients, there were no differences between negative and positive words. There were no significant interactions between type of stimulus and any clinical variables (PANSS negative or non negative categorization, etc.). Also, there were no statistically significant correlations between reaction times and neuroleptic dosage or anhedonia scores. In conclusion, schizophrenia patients showed the same degree of interference from emotional words as compared with controls. Moreover, patients with a higher level of negative symptoms did not differently experience positive and negative words.

Hyperprolinemia is a risk factor for schizoaffective disorder.

DNA sequence variations within the 22q11 DiGeorge chromosomal region are likely to confer susceptibility to psychotic disorders. In a previous report, we identified several heterozygous alterations, including a complete deletion, of the proline dehydrogenase (PRODH) gene, which were associated with moderate hyperprolinemia in a subset of DSM III schizophrenic patients. Our objective was (i) to determine whether hyperprolinemia is associated with increased susceptibility for any of three psychiatric conditions (schizophrenia, schizoaffective disorder and bipolar disorder) and (ii) to establish a correlation between hyperprolinemia and PRODH genotypes. We have conducted a case-control study including 114 control subjects, 188 patients with schizophrenia, 63 with schizoaffective disorder and 69 with bipolar disorder. We report that, taking into account a confounding effect due to valproate treatment, hyperprolinemia is a risk factor for DSM IIIR schizoaffective disorder (P=0.02, Odds ratio=4.6, 95% confidence interval 1.3-16.3). We did not detect 22q11 interstitial deletions associated with the DiGeorge syndrome among the 320 patients of our sample and we found no association between common PRODH polymorphisms and any of the psychotic disorders. In contrast, we found that five rare PRODH alterations (including a complete PRODH deletion and four missense substitutions) were associated with hyperprolinemia. In several cases, two variations were present simultaneously, either in cis or trans in the same subject. A total of 11 from 30 hyperprolinemic subjects bore at least one genetic variation associated with hyperprolinemia. This study demonstrates that moderate hyperprolinemia is an intermediate phenotype associated with certain forms of psychosis.

The promoter -194 C polymorphism of the nicotinic alpha 7 receptor gene has a protective effect against the P50 sensory gating deficit.

As suggested by several studies, abnormal sensory gating measured by the P50 paradigm could be an endophenotype predisposing to schizophrenia. In a previous work, we have shown a significant association between the presence of at least one -2 bp deletion located within exon 6 of the CHRNA7-like gene and the P50 abnormality in the general population. A recent study involved polymorphisms located in the core promoter region of the CHRNA7 gene as risk factors for the P50 inhibitory deficit. Screening for promoter variants in a large population of schizophrenic patients (n=111) and control subjects (85), for whom auditory-evoked potentials had been recorded did not allow us to replicate these results. By contrast, we showed a significant association between the -194 C allele and a T/C ratio <0.45, thus demonstrating a protective effect of this variant for the sensory gating deficit. Such conflicting results can be reconciled if we consider that the -194 C polymorphism has no causative effect, but is in linkage disequilibrium with other causal variations for the P50 sensory gating deficit, and that different alleles are in disequilibrium in different populations.