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Biomedical subjects

L Bellodi

Publications and source records attributed to L Bellodi.

At least 19 recordsLinked to original sources
PubMed1999

Complex segregation analysis for obsessive compulsive disorder and related disorders.

Complex segregation analysis was applied to a sample of 107 Italian families with probands with obsessive compulsive disorder (OCD), using regressive logistic models to test for possible models of genetic transmission. We used two different phenotypic definitions of affection: 1) OCD; and 2) OCD plus Tourette's syndrome/chronic motor tics (CMT). Because of the potential relationship between OCD, Tourette's syndrome (TS), and other tic disorders, we considered these diagnoses to be determined by the same liability in subsequent steps of the analysis. For the 107 OCD families, the best fit was a dominant model of transmission (with a higher penetrance for females). When the phenotype boundaries were widened (OCD + CMT + TS), an unrestricted model of transmission became the best fit. We concluded that additional data are needed to support the hypothesis that Tourette's syndrome and OCD share a common etiology: on the basis of clinical and epidemiological considerations, the OCD phenotype probably presents a higher level of heterogeneity than the TS phenotype, and it could be regulated through different etiologic pathways.

Adolescent↗
PubMed1999

Effect of acute intravenous clomipramine and antiobsessional response to proserotonergic drugs: is gender a predictive variable?

BACKGROUND: Previous studies on serotonergic responsivity in obsessive-compulsive disorder (OCD) showed about 50% of patients experiencing an acute worsening of OC symptoms when administered meta-chlorophenylpiperazine or i.v. clomipramine. The aim of this study was to determine what variables influence the response to acute i.v. clomipramine. Could this response be predictive of the response to chronic treatment with two serotonergic drugs with differing selectivity profiles: clomipramine and fluvoxamine? METHODS: Fifty OC patients were consecutively recruited. All underwent a challenge with 25 mg i.v. clomipramine and placebo and were administered 10-week oral clomipramine or fluvoxamine according to a double-blind design. The efficacy of the antiobsessional treatment was evaluated by Yale-Brown Obsessive-Compulsive Scale and Clinical Global Impression scale scores. RESULTS: Obsessions worsened in 42% patients as rated by change values in 100-mm visual analogue scale scores for the clomipramine vs. placebo infusion. There was a significant difference in gender distribution between "worsened" and "unchanged" patients, since female subjects were more frequently "unchanged." Thirty-one patients completed the 10-week treatment. According to both qualitative and quantitative evaluations, female subjects showed a better antiobsessional response, and this difference was enhanced in the clomipramine-treated group. CONCLUSIONS: Results suggest a role for reproductive hormones in the pathophysiology or treatment of OC patients.

Administration, Oral↗
PubMed1999

A long-term prospective evaluation of first-degree relatives of panic patients who underwent the 35% CO2 challenge.

BACKGROUND: This follow-up study investigated the potential priming effect of the 35% CO2 challenge on the development of anxiety disorders and/or panic attacks in healthy first-degree relatives of panic patients across a period of 3-4 years subsequent to the challenge. METHODS: Thirty-one relatives who underwent the 35% CO2 challenge 3-4 years before and 14 relatives, free from psychiatric diagnoses in the same period, were directly reevaluated for the presence of anxiety disorders and panic attacks. RESULTS: None developed anxiety disorders and only 1, among relatives previously tested with the 35% CO2 challenge, reported sporadic panic attacks. CONCLUSIONS: The 35% CO2 challenge is a safe research paradigm in the investigation of healthy subjects with a familial vulnerability to panic, and CO2 hypersensitivity might be considered a trait marker of an underlying familial vulnerability to panic disorder.

Adult↗
PubMed1999

Excess of high activity monoamine oxidase A gene promoter alleles in female patients with panic disorder.

A genetic contribution to the pathogenesis of panic disorder has been demonstrated by clinical genetic studies. Molecular genetic studies have focused on candidate genes suggested by the molecular mechanisms implied in the action of drugs utilized for therapy or in challenge tests. One class of drugs effective in the treatment of panic disorder is represented by monoamine oxidase A inhibitors. Therefore, the monoamine oxidase A gene on chromosome X is a prime candidate gene. In the present study we investigated a novel repeat polymorphism in the promoter of the monoamine oxidase A gene for association with panic disorder in two independent samples (German sample, n = 80; Italian sample, n = 129). Two alleles (3 and 4 repeats) were most common and constituted >97% of the observed alleles. Functional characterization in a luciferase assay demonstrated that the longer alleles (3a, 4 and 5) were more active than allele 3. Among females of both the German and the Italian samples of panic disorder patients (combined, n = 209) the longer alleles (3a, 4 and 5) were significantly more frequent than among females of the corresponding control samples (combined, n = 190, chi2 = 10.27, df = 1, P = 0.001). Together with the observation that inhibition of monoamine oxidase A is clinically effective in the treatment of panic disorder these findings suggest that increased monoamine oxidase A activity is a risk factor for panic disorder in female patients.

Alleles↗
PubMed1998

Growth hormone response to growth hormone-releasing hormone stimulation in obsessive-compulsive disorder.

Two groups of 30 patients with obsessive-compulsive disorder and 30 age- and sex-matched healthy control subjects were given a growth hormone-releasing hormone (GHRH) stimulation test to determine: (1) whether the downstream function of the somatotropic axis (growth hormone = GH, somatomedin-C = SMD-C) was impaired; (2) what might be the central alteration responsible for such impairment; and (3) whether alterations might be linked to the etiopathogenesis of the disease. Basal values of GH and SMD-C were the same in patients and control subjects, but GH responses to GHRH stimulation were significantly lower in patients than in control subjects. The absence of a pathology of basal GH and SMD-C concentrations indicates that the blunted GH responses to GHRH stimulation are not due to a negative feedback mechanism and suggests that a central neurotransmitter-neuropeptide pathology might be involved in the phenomenon.

Adolescent↗
PubMed1998

The unipolar-bipolar dichotomy and the response to sleep deprivation.

Fifty-one inpatients affected by a major depressive episode were divided into four groups according to mood disorder diagnosis and previous clinical history (bipolar disorder type I; bipolar disorder type II; major depressive disorder with at least three previous depressive episodes; and single depressive episode patients) and administered three consecutive total sleep deprivation (TSD) cycles. Mood changes were rated with a reduced version of the Hamilton Depression Rating Scale and with self-administered visual analogue scales. TSD caused better clinical effects in bipolar and single-episode patients; in particular, unipolar patients lacked effects in perceived mood after the first TSD and showed worse Hamilton ratings in respect to the other groups after the three TSD treatments. Discriminant function analysis could correctly classify 80% of bipolar patients, post hoc, based on TSD response. Further researches on the clinical efficacy of TSD must take into account the heterogeneity of depression and of its biological substrate.

Adult↗
PubMed1998

Frontal lobe dysfunction in obsessive-compulsive disorder and major depression: a clinical-neuropsychological study.

Neuropsychological findings support a hypothesized relationship between obsessive-compulsive disorder (OCD) and the frontal lobe. The aim of the present study was to compare findings of neuropsychological tests of frontal lobe function in 28 OCD patients and 29 patients with major depressive disorder (MDD), all diagnosed according to DSM III-R criteria. The patient groups were homogeneous for educational level, handedness, duration of illness, and sex distribution. All 57 subjects received a battery of tests sensitive to frontal lobe dysfunction as well as the Wechsler Memory Scale (WMS). Clinical symptomatology in the MDD and OCD groups was assessed with the Hamilton Rating Scale for Depression and the Yale-Brown Obsessive-Compulsive Scale, respectively. The only significant difference between the two diagnostic groups for any of the neuropsychological indices, with age as a covariate, was in the Object Alternation Test, in which OCD patients had a significantly higher number of perseverative responses. Test performances were not correlated with clinical symptomatology or severity of illness. Our preliminary results confirm the hypothesis that there is a selective impairment of orbito-frontal cortex in OCD and seem to exclude the existence of specific frontal lobe dysfunction in MDD, even though the two disorders show clinical similarities.

Adult↗
PubMed1998

5HT2C CYS23/SER23 polymorphism is not associated with obsessive-compulsive disorder.

A great deal of evidence suggests that a genetic component underlies obsessive-compulsive disorder (OCD). The response to serotonergic medications and the worsening of obsessive symptoms after administration of serotonergic agonists indicate that serotonergic mechanisms are involved in OCD. We investigated the role of the Cys23Ser mutation of the 5HT2C receptor gene in the etiology of this disorder by performing an association study comparing a sample of 109 OCD patients with a sample of 107 healthy control subjects. No allelic or genotypic association of OCD with the 5HT2C receptor gene mutation was revealed in our data. We also extended the association analysis to a subsample of 39 OCD patients that had previously been submitted to a challenge test with clomipramine. In the subsample of OCD patients that received the challenge with clomipramine, no association between the 5HT2C receptor gene mutation and response to the challenge test was found. Our results exclude any specific role of the Cys23Ser mutation of 5HT2C receptor gene in the etiology of OCD: it seems probable that more complex genetic models are needed to explain the involvement of serotonergic elements in the etiology of this disorder.

Adult↗
PubMed1998

Plasma concentrations of interleukin-1 beta, interleukin-6 and tumor necrosis factor-alpha in anorexia and bulimia nervosa.

Plasma interleukin-1 beta (Il-1 beta) interleukin-6 (Il-6) and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured in 26 women with Anorexia Nervosa (AN), nine of the restricted type (AN-R) and 17 of the binge-eating/purging type (AN-BP), in 24 women with Bulimia Nervosa (BN) and in 26 healthy age- and sex-matched controls. Concentrations of the cytokines were measured at the beginning of the study before starting any treatment and then after 1 and 3 months of combined cognitive-behavioral and pharmacological therapy (fluoxetine for AN-R and AN-BP, amineptine for AN-BP and BN, and fluvoxamine for BN). Basal values of Il-1 beta, Il-6 and TNF-alpha, were the same in patients and controls and did not change during treatments, in spite of the improvement of the mental disorders. This seems to exclude the possibility that alterations of basal plasma cytokine secretion are involved in the etiopathogenesis of AN and BN.

Adolescent↗
PubMed1998

Effect of adjuvant pindolol on the antiobsessional response to fluvoxamine: a double-blind, placebo-controlled study.

On the basis of recent results indicating that adjuvant pindolol has the positive effect of shortening latency to antidepressant response to selective serotonin reuptake inhibitors, the primary aim of our study was to evaluate the effect of pindolol on latency to antiobsessional response to fluvoxamine. Fifteen non-depressed obsessive-compulsive inpatients (six men and nine women) were consecutively recruited and randomly assigned to an 8-week standardized double-blind treatment with fluvoxamine and pindolol (group A) or fluvoxamine and placebo (group B). Patients were assessed weekly using rating scales for obsessive-compulsive disorder [Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), National Institute of Mental Health Obsessive-Compulsive Scale], co-occurent depressive symptoms (Hamilton Depression Scale) and global function (Clinical Global Improvement), from baseline to the end of the study. In accordance with data from the literature, response to treatment was defined as a reduction in YBOCS total scores of > or = 35% and a score on the 'global improvement' item of the Clinical Global Improvement of < 3. Data were analysed using analyses of variance with repeated measures performed on YBOCS and Hamilton Depression Scale scores to evaluate the mean quantitative response within and between groups and, additionally, employing a survival analysis to compute the percentage of responders within each group. Neither quantitative nor qualitative analysis revealed any differences between the two treatment groups, and pindolol did not shorten the latency of antiobsessional response to fluvoxamine. The results of this preliminary study indicate that different biological mechanisms underly the antiobsessional and antidepressant responses to fluvoxamine.

Adult↗
PubMed1998

Anticipation of age at onset in panic disorder.

OBJECTIVE: Anticipation (i.e., the decrease in age at onset or the increase in severity of a disorder in successive generations) has recently been reappraised as a key to understanding the genetics of some familial illnesses. The purpose of this study was to search for possible anticipation in panic disorder. METHOD: Thirty-eight unilineal, multigenerational families with multiple directly interviewed members who had panic disorder were compared across two successive generations for 1) age at the first panic attack, 2) age at the onset of panic disorder, and 3) the highest degree of agoraphobia ever experienced, as a tentative index of severity of illness. Intergenerational pairwise comparisons were implemented according to four different sampling schemes: random pairs, random transmitting pairs, all possible pairs, and all possible transmitting pairs. RESULTS: Life table analyses showed a significant decrease in the time before the first episode of panic and onset of panic disorder from the older to the younger generation. Evidence for anticipation was found for both indexes of onset in all four sampling schemes. No evidence of a generational effect on the index of severity of agoraphobia was found. Corrections for possible biases suggested that these results are not likely to be simple artifacts. CONCLUSIONS: Anticipation is supported in this specific set of families and, if it is confirmed by other studies, a role for trinucleotide repeat sequences may be considered to account for the familial aggregation of panic disorder.

Adolescent↗
PubMed1998

CO2-induced panic attacks: a twin study.

OBJECTIVE: The authors investigated the role of genetic factors in 35% CO2-induced panic attacks. METHOD: Ninety twins recruited from the general population were challenged with one-vital-capacity inhalations of 35% CO2-65% O2. Probandwise concordance rates were calculated and rates compared for monozygotic and for dizygotic twins. RESULTS: A significantly higher concordance was found for 35% CO2-induced panic attacks among monozygotic than dizygotic twins (55.6% versus 12.5%). CONCLUSIONS: These results suggest a relevant role of genetic factors in 35% CO2-induced panic attacks.

Adult↗
PubMed1998

The cooccurrence of DSM-III-R personality disorders.

The distinction between personality disorder diagnoses is often unclear because of the frequent cooccurrence of one or more of the diagnoses. To date, studies using sample sizes large enough to evaluate the rates of cooccurrence in the less prevalent personality disorders have not been conducted. The Structured Interview for Diagnosis of Personality-Revised, a semistructured instrument designed to yield reliable personality disorder diagnoses, was used to evaluate 1116 subjects for the presence of DSM-III-R personality disorder diagnoses. Cooccurrence rates and odds ratios were calculated for each pair of diagnoses. There was a high degree of cooccurrence between the cluster A personality disorders, between the cluster C personality disorders, and between narcissistic, borderline, and histrionic disorders. In addition, there was also a high frequency of avoidant personality disorders within the cluster A personality disorder diagnoses. Possible explanations for the high degree of cooccurrence and the potential implications for the DSM-IV personality disorder diagnoses are discussed.

Adult↗
PubMed1997

Plasma interleukin-1 beta and tumor necrosis factor concentrations in obsessive-compulsive disorders.

Plasma interleukin-1 beta (Il-1 beta) and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured twice, at a 48-hour interval, in 27 drug-free obsessive-compulsive patients (12 women and 15 men) and in 27 sex-age-matched healthy controls. Il-1 beta and TNF-alpha concentrations were significantly lower in patients than in controls, whereas there were no differences in either group between men and women, between the samples of the two days, or, in the patients, between those who had and those who had not been previously treated with psychopharmacologic drugs.

Adolescent↗
PubMed1997

Dopamine function in obsessive-compulsive disorder: growth hormone response to apomorphine stimulation.

Indirect observations suggest that the dopaminergic system may be involved in the pathophysiology of obsessive-compulsive disorder (OCD). The dopaminergic function of 15 patients with OCD and 15 age/sex-matched controls was evaluated by measuring the growth hormone (GH) responses to stimulation with the dopaminergic agonist apomorphine (APO), which increases growth hormone-releasing hormone (GHRH), GH, and somatomedine C (SMD-C) secretions. Therefore, we measured basal plasma GH and SMD-C concentrations and GH responses to GHRH stimulation to exclude that a downstream pathology of the somatotropic axis could obscure the significance of the results of the APO test. The response of prolactin (PRL) to APO inhibition were also measured. Basal plasma levels of GH, SMD-C, and PRL, GH responses to GHRH stimulation, and PRL responses to APO inhibition did not differ in the two groups of subjects. GH responses to APO stimulation were blunted in obsessive-compulsive (OC) patients. The emetic response to the same stimulation was stronger in patients than in controls. These responses suggest that in our OC patients there is a dysregulation of the dopaminergic system, which is possibly expressed in different ways in the various areas of the central nervous system.

Adolescent↗
PubMed1997

Asthma and panic attacks.

Panic disorder (PD) and asthma share many common characteristics and have been found in epidemiological studies to be significantly comorbid. To investigate possible reasons for this overlapping, the authors evaluated 51 patients with asthma, assessing the prevalence of PD and sporadic panic attacks, the temporal relationship between these two disorders, and the familial risk for PD in the families of asthmatics. The results showed significantly higher prevalences of PD, sporadic panic attacks, and social phobia in asthmatics than those reported for the general population. In 9 (90%) of the asthmatics with PD, asthma appeared first. Finally, the morbidity risk for PD in families of asthmatics with PD (13.5%) was significantly higher than in families of asthmatics without evidence of panic (2%). Our results suggest that the high prevalence of PD in asthmatics might be related to a facilitating effect of asthma on the development of PD in subjects with familial predisposition to PD.

Adult↗