[From OPG to REMS: the role of a territorial health service in the implementation of security and non-custodial measures towards offenders with psychological problems]. / Dagli OPG alle REMS: il ruolo di un servizio sanitario territoriale nell'esecuzione delle misure di sicurezza detentive e non, nei confronti degli autori di reato con problemi psichici.

AIMS: Managing health care for people suffering from mental illness is undergoing deep changes in recent years in Italy. The purpose of this study is to describe the progressive process of overcoming the Forensic Hospitals in Italy (OPGs) and to identify the necessary care and rehabilitation pathways in this process, in the experience of the territorial health service in Salerno, Italy. METHODS: An analysis of the recent laws related to the ongoing process and an analysis of epidemiological and structural data referring to the time interval between 2010 and 2017 concerning the OPGs/Residential Services for the Execution of Security Measures (RSESM)/Mental Health System in Campania, Italy and in the territory of Salerno in particular. RESULTS: The acts governing the transition from OPG to RSESM include DPCM 1/4/2008 and subsequent "Conferenza Unificata" agreements, other laws and regional health organizational regulations. A thorough restructuring of the National Health Service is required. A substantial path in Campania has been completed, with the closure of OPGs, the realization of definitive RSESM, the Departments for Mental Health Care in prison, the Regional Technical Group for overcoming the OPGs, the territorial Services for overcoming the OPGs and for Mental Health in Prison. The result of these transformations is a deep change in the health care approach, as evidenced by the current changes in action in indicative parameters of care pathways and their outcomes. CONCLUSIONS: The new approach shows both improvement features and totally or partially unaddressed problematic features. As for the actual management issues, improvements in communication between Mental Health Care and the magistracy. The overall evaluation of the transformations in progress is positive. At this stage, it is crucial to identify and monitor indicators of the pathways of care and their outcomes and to implement synergies among the systems involved.

Investigation of the Endogenous Stress Response System in Patients with Chronic Schizophrenia.

OBJECTIVE: Cardiophysiological and neuroendocrine studies suggest that the two components of the endogenous stress response system, the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal (HPA) axis, are dysregulated in patients with schizophrenia. However, cardiophysiological measures are influenced by several confounding factors and the secretion of α-amylase in saliva is believed to represent a more reliable index of SNS activity. Therefore, to characterize the functional status of the SNS and HPA axis in schizophrenia we explored the concomitant salivary secretion of cortisol and α-amylase. METHODS: Saliva cortisol and α-amylase levels were measured after awakening in 30 patients with chronic schizophrenia and 22 healthy subjects. RESULTS: After awakening, saliva cortisol increased in a similar way in both patients and healthy controls, while saliva α-amylase concentrations showed a clear-cut decrease in healthy subjects but not in patients with schizophrenia. No significant correlation emerged between biochemical measures and patients' demographic or psychopathological characteristics. CONCLUSIONS: These findings demonstrate normal activity of the HPA axis with an enhanced SNS tone, which suggests a functional dissociation of the two components of the endogenous stress response system in patients with chronic schizophrenia. The pathophysiological significance of such dysregulation needs further studies to be clarified.

Flattened cortisol awakening response in chronic patients with schizophrenia onset after cannabis exposure.

Cannabis may play a causal role in the onset of some schizophrenia cases; however, the biological vulnerability that predisposes some individuals to develop schizophrenia after exposure to cannabis is not known. According to the diathesis-stress pathogenetic model, it is likely that the endogenous stress response system, including the hypothalamus-pituitary-adrenal (HPA) axis, could be involved. Therefore, we investigated the saliva cortisol awakening response (CAR) of 16 patients with schizophrenia onset after the exposure to cannabis (Can+) as compared to 12 patients with schizophrenia onset without cannabis exposure (Can-) and to 15 healthy controls. The CAR was assessed by collecting saliva samples at awakening and after 15, 30 and 60 min. As compared to healthy controls, Can+ schizophrenia patients exhibited significantly enhanced baseline saliva cortisol levels and a flattened CAR. No significant abnormality in both baseline cortisol levels and CAR was detected in Can- schizophrenia patients. These findings demonstrate a dysregulation of the HPA axis in chronic schizophrenic patients whose illness started after cannabis exposure but not in those with an illness onset without cannabis exposure. Further studies need to clarify whether this HPA dysregulation is a part of the biological background underlying the increased risk to schizophrenia after exposure to cannabis.

Investigation of factors associated to crossover from anorexia nervosa restricting type (ANR) and anorexia nervosa binge-purging type (ANBP) to bulimia nervosa and comparison of bulimia nervosa patients with or without previous ANR or ANBP.

OBJECTIVE: To characterize factors associated to diagnostic crossover from anorexia nervosa restricting type (ANR) and anorexia nervosa binge-purging type (ANBP) to bulimia nervosa (BN) and to compare BN individuals with initial ANR or ANBP to subjects with stable BN. METHOD: Two hundred thirty-eight patients with current and lifetime diagnosis of AN or BN underwent diagnostic, psychopathological, and historical examinations by means of ad hoc clinical interviews and rating scales. RESULTS: One hundred twenty-three individuals had a stable BN. Seventy patients had a diagnosis of ANR and 45 of ANBP at the time of disease onset; 24 ANR patients and 23 ANBP subjects developed BN, whereas 46 ANR patients and 22 ANBP subjects did not crossover. Although the rate of diagnostic crossover was higher in the ANBP group than in the ANR one, the difference was not statistically significant. Longer illness duration, higher maximum past body mass index (BMI), higher novelty seeking, and lower self-directedness resulted significantly associated to crossover from ANR to BN, whereas higher maximum past BMI, higher desired body weight, higher novelty seeking, and lower harm avoidance were significantly associated to crossover from ANBP to BN. As compared to stable BN subjects, BN patients with initial ANR exhibited lower minimum past BMI, lower desired body weight, higher drive for thinness, ascetism, and social insecurity scores; BN patients with initial ANBP exhibited lower minimum past BMI and decreased enteroceptive awareness scores. CONCLUSIONS: Different clinical and personality factors seem to be associated to crossover from ANR and ANBP to BN. Moreover, BN with initial ANR seems to differ clinically from stable BN. These findings may have therapeutic and prognostic implications.

Investigation of CNR1 and FAAH endocannabinoid gene polymorphisms in bipolar disorder and major depression.

Experimental data suggest that the endogenous cannabinoid system is involved in mood regulation, but no study has been performed so far to investigate the role of endocannabinoid genes in the susceptibility to major depression (MD) and/or bipolar disorder (BD). We assessed the CB1 receptor gene (CNR1) single nucleotide polymorphism (SNP) rs1049353 (1359 G/A) and the fatty acid amide hydrolase (FAAH) gene rs324420 SNP (cDNA 385C to A) for their associations with MD and/or BD in 83 Caucasian patients with recurrent MD, 134 Caucasian individuals with BD, and 117 Caucasian healthy subjects. The distribution of the CNR1 1359 G/A genotypes and alleles significantly differed among the groups (chi(2)=12.595; df=4, P=0.01 for genotypes; chi(2)=13.773; df=2, P=0.001 for alleles) with MD patients showing a higher frequency of both AG, GG genotypes and A allele as compared to healthy controls. The distribution of the FAAH cDNA 385C to A genotypes, according to the CC dominant model (AA+AC vs. CC), significantly differed among the groups (chi(2)=6.626; df=2, P=0.04), with both BD patients and MD patients showing a non-significant slightly higher frequency of the AC genotype. These findings, although preliminary, suggest that the CNR1 1359 G/A and the FAAH cDNA 385C to A gene variants may contribute to the susceptibility to mood disorders.

The cDNA 385C to A missense polymorphism of the endocannabinoid degrading enzyme fatty acid amide hydrolase (FAAH) is associated with overweight/obesity but not with binge eating disorder in overweight/obese women.

Endocannabinoids are involved in the modulation of eating behavior; hence, alterations of this system may play a role in obesity. Recently, a single nucleotide polymorphism (cDNA 385C to A) of the gene coding for fatty acid amide hydrolase (FAAH), the major degrading enzyme of endocannabinoids, has been found to be associated with obesity. However, the possibility that the FAAH gene cDNA 385C to A single nucleotide polymorphism (SNP) is associated to binge eating disorder (BED), a condition that frequently occurs in obese individuals, has not been investigated. In order to address this issue, we assessed the distribution of the cDNA 385C to A SNP in 115 overweight/obese subjects with BED, 74 non-BED patients with obesity and 110 normal weight healthy controls. As compared to healthy controls, the whole group of overweight/obese BED and non-BED patients had a significantly higher frequency of the CA genotype and the A allele of the FAAH gene cDNA 385C to A SNP. Moreover, the SNP resulted significantly correlated to the presence of overweight/obesity (F(2, 296)=3.58, P=0.02), but not to the occurrence of BED (F(2, 296)=0.98; P=0.3). The present study confirms previously published significant over-representations of the FAAH 385 A allele in overweight/obese subjects and presents new data in BED patients that the 385 mutation is not significantly associated with BED-related obesity.

Association between A218C polymorphism of the tryptophan-hydroxylase-1 gene, harm avoidance and binge eating behavior in bulimia nervosa.

Genes involved in serotonin transmission are likely involved in the biological predisposition to bulimia nervosa. We investigated whether the A218C polymorphism of the tryptophan-hydroxylase-1 gene was associated to bulimia nervosa and/or to some phenotypic aspects of the disorder. One hundred eighty Caucasian women (91 patients with bulimia nervosa and 89 healthy controls) were enrolled into the study. They underwent a blood sample collection for A218C polymorphism of the tryptophan-hydroxylase-1 genotyping and a clinical evaluation assessing comorbidity for Axis I and II psychiatric disorders, harm avoidance personality dimension and bulimic symptoms. The distribution of both tryptophan-hydroxylase-1 A218C genotypes and alleles did not significantly differ between patients and controls. Bulimic women with the AA genotype exhibited a more severe binge eating behavior and higher harm avoidance scores than those with CC genotype. These findings support the idea that tryptophan-hydroxylase-1 A218C polymorphism does not play a part in the genetic susceptibility to bulimia nervosa, but it seems to be involved in predisposing bulimic patients to a more disturbed eating behavior and higher harm avoidance.

The Leu72Met polymorphism of the ghrelin gene is significantly associated with binge eating disorder.

OBJECTIVES: The pathophysiological mechanisms underlying binge eating disorder are poorly understood. Evidence exists for the fact that abnormalities in peptides involved in the regulation of appetite, including ghrelin, may play a role in binge eating behavior. Genes involved in the ghrelin physiology may therefore contribute to the biological vulnerability to binge eating disorder. METHODS: We examined whether two polymorphisms of the ghrelin gene, the G152A (Arg51Gln) and C214A (Leu72Met), were associated with binge eating disorder. Ninety obese or nonobese women with binge eating disorder and 119 normal weight women were genotyped at the ghrelin gene. RESULTS: Statistical analyses showed that the Leu72Met ghrelin gene variant was significantly more frequent in binge eating disorder patients (chi2=5.940; d.f.=1, P=0.01) and was associated with a moderate, but significant risk to develop binge eating disorder (odds ratio=2.725, 95% confidence interval: 1.168-6.350). CONCLUSIONS: Although these data should be regarded as preliminary because of the small sample size, they suggest that the Leu72Met ghrelin gene variant may contribute to the genetic susceptibility to binge eating disorder.

No association of the Arg51Gln and Leu72Met polymorphisms of the ghrelin gene with anorexia nervosa or bulimia nervosa.

Genetic factors likely contribute to the biological vulnerability to anorexia nervosa (AN) and bulimia nervosa (BN). We investigated whether the Arg51Gln and/or the Leu72Met gene polymorphisms of the human ghrelin, a peptide involved in the regulation of eating behavior, were associated to AN and/or BN. Two-hundred-ninety-two Caucasian women (114 with BN, 59 with AN and 119 healthy controls) participated into the study. No significant differences were found in the frequencies of the Arg51Gln and the Leu72Met ghrelin gene variants among patients with AN or BN and healthy controls. Moreover, no significant differences emerged in eating-related phenotypic variables between patients carrying the Leu72Met genotype as compared to those with the Leu72Leu genotype. These results suggest that the Arg51Gln and the Leu72Met polymorphisms of the human ghrelin gene do not contribute to the genetic susceptibility to AN and BN.