Prevalence of respiratory diseases in patients with panic and obsessive compulsive disorders.
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Biomedical subjects
Publications and source records attributed to G Perna.
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Plasma interleukin-1 beta (IL-1 beta) concentrations were measured in 10 outpatients with panic disorder before and on days 30 and 32 of treatment with alprazolam (2-2.5 mg/day). IL-1 beta concentrations were found to be significantly higher in patients than in control subjects both before and during therapy. Thus, IL-1 beta levels may be a marker of panic disorder that is not related to the current level of symptomatology.
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.
Growth hormone (GH) and beta-endorphin (beta-EP) responses to clonidine stimulation were examined in 18 male heroin addicts, 9 with and 9 without previous histories of attention deficit disorder with hyperactivity (ADD-H) and conduct disorder (CD). Ten psychophysically healthy volunteers were used as controls. ADD-H/CD addicts had blunted GH and beta-EP responses as compared to controls while those of non-ADD-H/CD addicts were normal. This suggests that postsynaptic adrenoceptor sensitivity is decreased and, possibly, that presynaptic noradrenaline secretion is increased in ADD-H/CD patients with heroin addiction.
We studied the long-term antianginal and anti-ischemic effects of two dosage regimens designed to prevent tolerance to transdermal nitroglycerin (TNTG): (1) 10 mg TNTG applied for 16 h with a 'nitrate-free' interval of 8 h; (2) 10 mg TNTG applied for 16 h followed by a 'nitrate-low' interval of 5 mg applied for 8 h. 129 patients completing a 3-month study period were evaluated by repeated exercise tests. Both regimens significantly increased maximum exercise duration at 3 months, from 699.1 +/- 23.4 to 833 +/- 21.9 s and from 686.1 +/- 20 to 789.6 +/- 22.6 s, respectively, reduced the number of patients with 1 mm S-T segment depression and increased the time duration to 1 mm S-T segment depression. Marked reductions in anginal attacks was observed in both groups: from 6.5 to 0.15 attacks per week and from 6.0 to 0.15 attacks per week, respectively. No statistically significant differences were found between the groups, and both regimens were well tolerated. In conclusion, our results demonstrate sustained antianginal efficacy, without tolerance, of either 'nitrate-free' of 'nitrate-low' interval therapy with transdermal nitroglycerin.
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.
Since cholecystokinin (CCK) is known to be anxiogenic in experimental animals and to induce panic attacks in humans, lymphocyte CCK-8 concentrations were measured in 15 patients with panic disorder and 15 age- and sex-matched healthy subjects. The patients' levels were measured again after a 30-day course of alprazolam therapy, 1.5 mg/day. The CCK-8 concentrations were significantly lower in the patients than in the control subjects and did not change after alprazolam therapy. There was no correlation between the peptide values and levels of anxiety or frequency and severity of panic attacks.
Computerized EEG activity derived from the temporal lobes was investigated in normal subjects and panic disorder patients with and without depersonalization and/or derealization, in a resting condition and during an odor stimulation task. Panic patients without depersonalization or derealization showed an increase of fast and a decrease of slow activities independent of odor stimulation. Panic patients with depersonalization and/or derealization showed an increase of slow activity and bilateral lack of responsiveness in the fast alpha frequency band during odor stimulation. Findings suggest there are different EEG patterns in the temporal regions of the two different groups of panic patients during rest and activating conditions.
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Immunological, neuroendocrine and psychological parameters were examined in 14 psychophysically healthy subjects and in 17 panic disorder patients before and after a 30-day course of alprazolam therapy. T lymphocyte proliferation in response to the mitogen phytohemagglutinin, lymphocyte beta-endorphin (beta-EP) concentrations, plasma ACTH, cortisol and beta-EP levels were examined in basal conditions and after corticotropin-releasing hormone (CRH) stimulation. Cortisol inhibition by dexamethasone (DST) and basal growth hormone (GH) and prolactin levels were also examined. Depression, state or trait anxiety, anticipatory anxiety, agoraphobia, simple and social phobias, severity and frequency of panic attacks were monitored by rating scales. The immune study did not reveal any significant difference between patients and controls, or any effect of alprazolam therapy. The hormonal data for the two groups were similar, except for higher than normal basal ACTH and GH plasma levels, lower than normal ratios between the ACTH and cortisol responses to CRH, and blunted DST in some patients. All the impairments improved after alprazolam therapy, in parallel with decreases in anxiety and in severity and frequency of panic attacks.
This double-blind study of dihydroergocristine (DHEC, CAS 17479-19-5) versus placebo was performed in 240 elderly patients affected by chronic cerebrovascular disease or organic brain syndrome. The therapy was carried on for one year. Results pointed out a decrease of SCAG total score and a significant improvement of the target items "confusion, mental alertness and memory performance" after DHEC versus placebo. Furthermore the data show that DHEC maintained its activity throughout the 12-month trial period. Very few and mild side-effects were reported for both groups, thus confirming the well known good safety of the compound. Based on results of this 1-year investigation, it is concluded that DHEC treatment should not be abruptly interrupted, but continued for as long as possible.
We report on a 25-year-old man, referred for atypical chest pain and negative T waves in leads V5-V6. A cardiac tumor, localized in the posterolateral left ventricular wall was diagnosed in this patient by nuclear techniques and bidimensional echocardiography. A complex form of pluridistrectual dysmorphic disorder (hypertelorism, prognathism, frontal bossing, multiple cysts of the mandible, calcification in falx cerebri, etc) was also present, suggesting a limited form of Gorlin's syndrome (nevoid basal cell carcinoma syndrome).
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The time course of the plasma concentrations of isoniazid, rifampin, and pyrazinamide was assessed in a group of 13 patients with lung tuberculosis treated over a period of 2 months on a continuous daily basis with a fixed triple combination of the same drugs. The blood kinetics of the three antituberculosis drugs were determined on Days 1, 15, 30, and 60 of treatment. The triple combination employed in this study contained 50 mg isoniazid, 120 mg rifampin, and 300 mg pyrazinamide per tablet, the number of tablets ranging from four to seven per day according to the body weight of the patients. Almost superimposable plasma concentration curves for isoniazid were observed during the 4 days of the study. For rifampin, a fall in the plasma concentrations at the time intervals after the peak was observed comparing the data on Day 1 with those on Days 15, 30, and 60, which did not differ from each other. This finding is thought to be due to the well-known phenomenon of self-induction, which leads to an increased rate of disposal of the antibiotic from the blood compartment within the first and second weeks of continuous treatment. For pyrazinamide, an equilibrium in the opposite sense as that of rifampin seemed to take place within the 2 months of the study. Because of the relatively high plasma levels observed 24 h after each administration, an increase in plasma concentrations with respect to those observed on Day 1 was found on Days 15, 30, and 60, the levels on these days no differing from each other.(ABSTRACT TRUNCATED AT 250 WORDS)
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A pharmacokinetic study was carried out in 18 male patients in order to assess the blood concentrations of rifampicin after intravenous administration of 3 different doses (600, 900 and 1200 mg) over 3 different periods of infusion (1, 2 and 3 hours). The results show that, by increasing the dose and the rate of infusion higher and earlier peak concentrations are obtained. A kinetic analysis based on a one-compartment open model gives a good fitting of the data obtained experimentally. From these data one obtains for the volume of distribution a value of 48.1 +/- 17.2 liters and for the serum disappearance rate the value of 0.212 +/- 0.070 h-1 in adult subjects. It is possible to predict the time course of serum kinetics of the drug by using the equation (formula; see text).
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