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Biomedical subjects

C Arancio

Publications and source records attributed to C Arancio.

15 recordsLinked to original sources
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

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↗
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

The 35% CO2 challenge test in patients with social phobia.

Panic disorder (PD) and social phobia (SP) share many clinical, demographic and biological characteristics. To investigate the relationships between the two disorders, the responses to inhalation of a 35% carbon-dioxide (CO2) and 65% oxygen (O2) gas mixture were assessed. Sixteen patients with PD, 16 patients with SP, 13 patients with both SP and PD, seven patients with SP who experienced sporadic unexpected panic attacks and 16 healthy control subjects inhaled one vital capacity of 35% CO2 or compressed air. A double-blind, randomized, crossover design was used. PD patients and SP patients showed similar anxiogenic reactions to 35% CO2, both stronger than seen in control subjects. Patients with both disorders and SP patients with sporadic unexpected panic attacks reacted similarly to subjects with PD or SP alone. These results suggest that PD and SP share a common hypersensitivity to CO2 and thus might belong to the same spectrum of vulnerability.

Adult↗
PubMed1997

Noradrenergic receptor sensitivity in obsessive compulsive disorder: II. Cortisol response to acute clonidine administration.

Sensitivity of pre-synaptic alpha-2- and post-synaptic alpha-1- and beta-adrenoceptors was investigated in 15 patients with obsessive-compulsive disorder (OCD) and in 15 age- and sex-matched healthy controls, by measuring cortisol responses to saline administration and to inhibition by clonidine (clon), a noradrenergic receptor agonist. Basal values of cortisol and responses to administration of saline and of clon were the same in patients and controls.

Adolescent↗
PubMed1997

Noradrenergic receptor sensitivity in obsessive-compulsive disorders: I. Growth hormone response to clonidine stimulation.

In 15 patients with obsessive-compulsive disorder (OCD) and in 15 healthy controls postsynaptic alpha-2-adrenoceptor sensitivity was examined by measuring the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) and to clonidine stimulation. Basal values of GH and somatomedin-C (SMD-C) and mean GH responses to GHRH were the same in patients and controls, thus suggesting that a peripheral pathology of the somatotropic axis should not be present. GH responses to clonidine stimulation were blunted in patients suggesting that post-synaptic alpha-2-adrenoceptors are subsensitive, possibly due to higher than normal noradrenergic secretion.

Adolescent↗
PubMed1997

Panic attacks: a twin study.

The role of genetic factors in panic disorder (PD) and sporadic panic attacks (SPAs) was investigated. A total of 120 twins recruited from the general population were interviewed for the presence of anxiety disorders and SPAs. A significantly higher concordance among MZ than DZ twins was found for PD (73% vs. 0%) but not for SPAs (57% vs. 43%). These results confirm a significant role of genetic factors in PD but suggest that genetic factors might not be crucial for the development of SPAs.

Adult↗
PubMed1995

Menstrual cycle-related sensitivity to 35% CO2 in panic patients.

In a double blind, random, cross-over design, 10 patients and seven controls inhaled one vital capacity of 35% CO2-65% O2 during their early-follicular and midluteal phases. Anxiety after CO2 intake was significantly stronger in the early-follicular phase than in the midluteal phase for patients. Controls had no anxiety reactions.

Administration, Inhalation↗
PubMed1995

Alpha 2-adrenergic receptor sensitivity in panic disorder: II. Cortisol response to clonidine stimulation in panic disorder.

The cortisol responses to acute administration of saline and of clonidine (Clon), 150 micrograms IV, were examined in 12 patients with panic disorder and agoraphobia, before and after 32 days of alprazolam therapy (2.5 mg/day), and in 12 normal controls. The responses in the Clon test corrected for the responses to saline differed in the two groups, and in patients were not changed by the therapy even though significant symptomatological improvement was achieved. The results suggest that presynaptic alpha 2- or postsynaptic alpha 1-beta-adrenoceptor sensitivity is impaired in panic disorder.

Adult↗
PubMed1995

Laboratory response of patients with panic and obsessive-compulsive disorders to 35% CO2 challenges.

OBJECTIVE: The DSM-III-R anxiety disorders section includes both panic disorder and obsessive-compulsive disorder. To evaluate the relationship between these two disorders, subject responses to inhalation of a 35% CO2 and 65% O2 mixture were assessed. METHODS: Twenty-three patients with panic disorder, 23 with obsessive-compulsive disorder, 12 with both obsessive-compulsive and panic disorder, and 23 healthy comparison subjects were given a single vital capacity inhalation of 35% CO2 and 65% O2 or a placebo mixture of compressed air. A double-blind, random, crossover design was used. RESULTS: Patients with panic disorder and patients with both panic disorder and obsessive-compulsive disorder showed similar strong anxiogenic reactions to 35% CO2; while patients with obsessive-compulsive disorder alone did not differ from comparison subjects. CONCLUSIONS: These results confirm that obsessive-compulsive disorder and panic disorder are two distinct syndromes and that patients with these disorders have different sensitivity to CO2 inhalation.

Administration, Inhalation↗
PubMed1995

Sensitivity to 35% CO2 in healthy first-degree relatives of patients with panic disorder.

OBJECTIVE: The authors tested the hypothesis that hyperreactivity to CO2 in healthy subjects represents an underlying familial vulnerability to panic disorder. METHOD: One vital-capacity inhalation of 35% CO2 and 65% O2 was administered to each of 84 patients with panic disorder, 23 healthy first-degree relatives of probands with panic disorder, and 44 healthy subjects with no family history of panic disorder. RESULTS: The first-degree relatives of the probands with panic disorder reacted significantly more than the healthy subjects and significantly less than the probands. CONCLUSIONS: These findings suggest an association between family history of panic disorder and hyperreactivity to 35% CO2 in healthy subjects.

Administration, Inhalation↗
PubMed1994

Carbon dioxide/oxygen challenge test in panic disorder.

The effects of a single inhalation of a 35% CO2/65% O2 gas mixture were examined in 71 patients with panic disorder with or without agoraphobia and 44 normal control subjects. Compared with the placebo condition, inhalation of air, the CO2/O2 mixture elicited a clear anxiety reaction only in panic disorder patients, who experienced a sudden rise of subjective anxiety as well as of several panic symptoms. Respiratory symptoms and the fear of dying best distinguished the patients from the control subjects. Baseline anxiety was not the key factor in explaining this differential reaction. The clinical features of panic disorder (namely, frequency of panic attacks, agoraphobia, anticipatory anxiety, and duration of illness) were not significantly related to the response to the challenge test, suggesting that CO2 reactivity might be a trait marker of panic disorder.

Administration, Inhalation↗
PubMed1994

Pharmacologic effect of toloxatone on reactivity to the 35% carbon dioxide challenge: a single-blind, random, placebo-controlled study.

The effect of a short treatment (7 days) with the reversible monoamine oxidase type A inhibitor toloxatone on the reactivity to the inhalation of 35% CO2 was evaluated in 18 panic patients who responded to 35% CO2 inhalation with panic before treatment. A single-blind, placebo-controlled design was applied. Panic patients were randomly assigned to the toloxatone (N = 10) or placebo (N = 8) groups and were given the 35% CO2 challenge on days 1 (before starting the treatment), 3, and 7. Patients on placebo did not report any significant changes in their reactivity to 35% CO2 during the three sessions, whereas patients on toloxatone reported a significant attenuation of the reactivity on day 7. These results indicate that (1) anxiety provoked by the inhalation of 35% CO2 is reproducible; (2) placebo has a negligible effect on 35% CO2 reactivity; and (3) reactivity to 35% CO2 is significantly attenuated by short treatment with toloxatone, possibly related to its antipanic activity.

Administration, Inhalation↗