Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

3H-Imipramine (3H-IMI) binding to platelet membranes was measured in 19 patients with agoraphobia with panic attacks, 9 patients with major depression, and 22 healthy subjects. In comparison to healthy subjects, the maximal number of binding sites (Bmax) was significantly decreased in depressed patients but not in panic disorder patients, and the apparent affinity of binding was slightly decreased in depressed patients but not in panic disorder patients. The Bmax and Kd of 3H-IMI platelet binding did not differ between panic disorder patients with and without a history of a major depressive episode. Thus, 3H-IMI platelet binding is clearly different in patients with panic disorder compared to those with an active depression. Because 3H-IMI binding is associated with the serotonin reuptake site in platelet and brain membranes, these findings give further support to abnormalities in serotonergic function in patients with major depression.
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PMID:Differential 3H-imipramine platelet binding in patients with panic disorder and depression. 303 80

Psychologic stressors are less potent stimuli of the HPA axis in humans than physical stressors, but they can cause mild changes in acute ACTH and cortisol production. These changes, however, are generally not of sufficient magnitude or duration to cause measurable changes in UFC excretion. Furthermore, chronic stress leads to an attenuation of the HPA axis response. This basic knowledge concerning psychologic stress helps explain the reason why patients with uncomplicated anxiety/panic disorder, a condition involving similar symptoms, do not demonstrate UFC abnormalities. Panic disorder, when accompanied by depression, however, is associated with an increase in UFC excretion which is probably more related to the depression than the panic state. Interestingly, panic disorder, when accompanied by agoraphobia, also shows an elevation in UFC levels which makes it endocrinologically distinct from uncomplicated panic disorder. The reason for this is unclear. Treatment of the panic disorder with benzodiazepines does not further lower the UFC levels in patients with uncomplicated panic disorder despite clinical improvement, but it does lower UFC levels into the normal range in those with concurrent depression and agoraphobia. Alteration in the UFC level with treatment is only partially related to clinical improvement.
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PMID:Similarities in hypothalamic-pituitary-adrenal axis activity between patients with panic disorder and those experiencing external stress. 304 3

Considerable research has been conducted to clarify relationships between panic disorder and major depression. From a number of perspectives, it now appears that panic disorder and major depression are not identical illnesses. While many patients with panic disorder are likely to experience an episode of major depression at some point during their lives, the timing of this occurrence is highly variable. While depression may be an expected and understandable result of having to live with chronic anxiety and phobic avoidance, the available evidence suggests that such a hypothesis is not particularly tenable. Depression can occur in individuals with or without severe agoraphobia and in individuals ill with panic for greater or lesser periods of time. Comorbidity in panic, particularly for social phobic or obsessive-compulsive symptomatology, does serve as a risk factor for the lifetime occurrence of depression and may denote a more severe illness. Biologic markers (Table 4), while of limited diagnostic utility in clinical practice, may reveal important pathophysiologic similarities and differences between panic disorder and major depression. Current evidence points to many areas of biologic overlap, with some important areas of independence (Fig. 7A). Although not extensively discussed in this chapter, several clinical parameters paint an analogous picture (Fig. 7B). There is a need for future studies of biologic markers in individuals over time, in various phases of illness. Furthermore, the study of multiple biologic markers in the same individuals would be a worthwhile pursuit, perhaps leading toward the delineation of underlying pathophysiologic mechanisms. In summary, then, we favor a conceptualization of panic disorder and major depression as nonidentical disorders with many shared characteristics. Future studies as suggested above, particularly when coupled with the power of genetic studies not described in this chapter, may eventually lead to a clearer demarcation of the boundaries between these two intriguing psychiatric syndromes.
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PMID:Panic disorder and major depression. A tale of two syndromes. 304 11

A double-blind comparative study of clomipramine and fluvoxamine was performed in 50 patients suffering from anxiety disorders (DSM-III). Patients were treated for 6 weeks with either 150 mg of clomipramine or 100 mg of fluvoxamine. The results show that both drugs at the dosages used are equipotent in reducing anxiety symptoms as assessed with the Hamilton Anxiety Scale and the Spielberger State-Trait Anxiety Inventory. Clomipramine differed from fluvoxamine in its efficacy with respect to associated depressive symptomatology in that it had a more pronounced effect on the Self Rating Depression Scale. The results support the hypothesis that brain serotonergic pathways are implicated in the pathophysiology of anxiety disorders, particularly in agoraphobia and panic disorders.
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PMID:Effect of serotonin uptake inhibitors in anxiety disorders; a double-blind comparison of clomipramine and fluvoxamine. 311 76

This study was designed to see whether the high vs low serum level of imipramine influenced the outcome of in vivo exposure therapy on patients with agoraphobia. Thirty-six subjects completed the Hopkins Symptom Checklist-90 one week before treatment and weekly throughout treatment. Both groups demonstrated equal improvement. It was noted that the rate of improvement differed for different symptom subscales: (1) Hostility, Paranoia and Psychotic symptom ratings improved over the first three weeks of treatment, (2) Interpersonal Sensitivity, Anxiety and Depression ratings improved throughout the first seven weeks of treatment and (3) Phobic Anxiety, Somatization and Obsessive Compulsure symptom ratings continued to improve throughout the entire 12 week course of treatment. Responsive vs nonresponsive subjects could be significantly differentiated after one week of treatment on the basis of their responses to the Psychoticism subscale.
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PMID:Different rates of improvement of different symptoms in combined pharmacological and behavioral treatment of agoraphobia. 320 96

The efficacy of clomipramine hydrochloride in the treatment of agoraphobia was investigated in an eight-week placebo-controlled double-blind study. One hundred eight women diagnosed as agoraphobic by DSM-III guidelines were randomly assigned to the clomipramine or placebo group; 70 women (mean age, 36.6 years) completed the eight-week trial. The study medication was prescribed on the basis of weekly increments to a maximum of 300 mg/d, with a mean dosage at week 8 in the clomipramine hydrochloride group of 82.8 mg/d. Assessments performed prior to the trial and at the four- and eight-week points included the completion of standardized questionnaires and daily diaries, as well as the administration of a Behavioral Approach Test. Clomipramine was significantly superior to the placebo on several indexes of phobic symptoms and on measures of depression and dysphoria. Results are discussed in terms of the hypothesized action of clomipramine and the pattern of significant findings.
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PMID:Clomipramine treatment of agoraphobic women. An eight-week controlled trial. 328 81

The use of the broad range of antidepressant drugs in depression, panic agoraphobia, and generalized anxiety is reviewed and the current ambiguous status of the benzodiazepines in anxiety disorders discussed. The place of newer antianxiety drugs (buspirone, propranolol) and antidepressant drugs (floxetine, bupropion, trazodone) in treatment is considered. Methods for adjusting dose and counteracting common drug side effects are presented.
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PMID:The drug treatment of anxiety and depression. 328 39

Thirty-seven patients participating in a controlled treatment study with imipramine were classified as high or low depressed simultaneously on two depression measures. Analysis of variance by 2 (high-low depressed) X 2 (high-low imipramine dosage) groupings revealed significant dose but no depression main effects. The greater dose effect observed in the low depressed group and the greater response rates found among high-dose patients with low initial depression strongly suggest that the beneficial effect of imipramine in agoraphobia was not primarily antidepressant in nature.
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PMID:Initial depression and response to imipramine in agoraphobia. 329 12

Eleven patients with panic disorder or agoraphobia with panic attacks completed an 8-week single-blind trial of trazodone (300 mg/day) without concurrent behavioral instructions. The measures of change included ratings of generalized and panic anxiety, phobias, and depression and a behavioral avoidance test, which were administered during a baseline period of placebo administration and at 4 and 8 weeks of the trial. There was significant improvement on all symptom dimensions, which suggests that trazodone may have specific antipanic and antiphobic actions and underscores the importance of serotonergic mechanisms in these anxiety disorders.
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PMID:Trazodone in the treatment of panic disorder and agoraphobia with panic attacks. 329 92

This naturalistic study examined the treatment response to imipramine of 60 patients who had panic disorder or agoraphobia with panic attacks. Only half of the patients could tolerate the drug, but of those who did, 88% obtained a markedly beneficial clinical effect. An amphetamine-like side effect accounted for most of the dropouts. More than one-half of the responders achieved clinical remission at doses (less than or equal to 100 mg/day) and plasma levels (less than or equal to 150 ng/ml) considered to be subtherapeutic for depression. There appears to be neither a clear threshold for response nor a therapeutic dose range for imipramine in the treatment of panic. Doses should be adjusted individually and increased conservatively.
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PMID:A naturalistic study of imipramine in panic disorder and agoraphobia. 330 Mar 74


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