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Biomedical subjects

G Perna

Publications and source records attributed to G Perna.

At least 19 recordsLinked to original sources
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↗
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

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

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

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↗
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↗
PubMed1997

Modification of 35% carbon dioxide hypersensitivity across one week of treatment with clomipramine and fluvoxamine: a double-blind, randomized, placebo-controlled study.

The effects of short treatments (7 days) with clomipramine and fluvoxamine on the reactivity to inhalations of 35% CO2/65% O2 were compared in 39 panic patients who had positive responses to 35% CO2 inhalations. A double-blind, randomized, placebo-controlled design was applied. Each patient was given the 35% CO2 challenge on days 0 (before starting treatment), 3, and 7. Patients on placebo did not report any significant changes in their reactivity to 35% CO2 across the three sessions, whereas patients on clomipramine and fluvoxamine reported a significant attenuation of the reactivity on day 7. These results indicate that treatments with clomipramine and fluvoxamine decrease hypersensitivity to 35% CO2 after a few days, suggesting a relevant role of the modulation of CO2 sensitivity by the serotonergic system in antipanic properties of these compounds.

Adult↗
PubMed1996

Family history of panic disorder and hypersensitivity to CO2 in patients with panic disorder.

OBJECTIVE: The authors investigated the relationships between hypersensitivity to CO2 and familial-genetic risk for panic disorder in patients with panic disorder. METHOD: Morbidity risks for panic disorder were calculated for families of 203 patients with panic disorder, each of whom was challenged with 35% CO2. RESULTS: Patients who reacted with a positive response to the 35% CO2 challenge showed a genetic risk for panic disorder (morbidity risk = 14.4%) that was significantly higher than that for patients who did not react (morbidity risk = 3.9%). CONCLUSIONS: These findings support the idea that hypersensitivity to CO2 might be associated with a subtype of panic disorder specifically related to a greater familial loading.

Adult↗
PubMed1995

T-lymphocyte cholecystokinin-8 and beta-endorphin concentrations in eating disorders: I. Anorexia nervosa.

Baseline concentrations of cholecystokinin-8 (CCK-8) and beta-endorphin (beta-EP) were measured in T-lymphocytes from 33 restricting patients with anorexia nervosa (AN-R), 23 binging/purging patients with anorexia nervosa (AN-BP), and 24 healthy volunteers. CCK-8 basal values were significantly lower and beta-EP values significantly higher in AN-R and AN-BP patients than in normal volunteers. Levels of the peptides were measured three more times during a 4-month combined cognitive-behavioral/psychopharmacological treatment (nortriptyline or fluoxetine in AN-R, fluoxetine or amineptine in AN-BP). CCK-8 values fluctuated (nonsignificantly) during each treatment, while beta-EP values decreased (to a significant degree only in fluoxetine-treated AN-R patients).

Adolescent↗
PubMed1995

T-lymphocyte concentrations of cholecystokinin-8 and beta-endorphin in eating disorders: II. Bulimia nervosa.

Concentrations of cholecystokinin-8 (CCK-8) and beta-endorphin (beta-EP) in T-lymphocytes of 26 women with bulimia nervosa (BN) and in 26 age- and sex-matched healthy comparison subjects were measured. Ten patients were then treated with 300 mg/day of fluvoxamine, p.o., and five patients were treated with 300 mg/day of amineptine, p.o., for 4 months. Concentrations of the two peptides were measured again after 1, 2, and 4 months of therapy. Basal CCK-8 values were significantly lower in patients than in healthy subjects. During fluvoxamine therapy, CCK-8 values increased, reaching normal levels by month 4 of treatment. No such increase occurred during amineptine therapy. Baseline beta-EP values were normal in the bulimic patients but had declined by month 4 of fluvoxamine therapy.

Adolescent↗
PubMed1995

Hypersensitivity to inhalation of carbon dioxide and panic attacks.

Thirteen healthy subjects with infrequent panic attacks and without agoraphobia who did not meet DSM-III-R criteria for panic disorder, 43 patients with panic disorder, and 43 healthy control subjects who never experienced panic attacks underwent one vital capacity inhalation of 35% CO2. Healthy subjects with infrequent panic attacks reacted similarly to patients with panic disorder and more strongly than healthy subjects who never experienced panic attacks. The results suggest that (a) subjects with sporadic unexpected panic attacks and patients with panic disorder belong to the same spectrum of vulnerability and (b) CO2 hypersensitivity might be a trait marker of panic attacks rather than of a clinical diagnosis of panic disorder.

Administration, Inhalation↗