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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of depression in the elderly was investigated in a random stratified sample of 100 subjects from the general population of Appignano (Macerata, Regione Marche, Italy). After sampling with the simple random method, each subject underwent a diagnostic work-up including: a) three psychodiagnostic tests (Short Scale for the Assessment of Mental Health--SSAMH, Geriatric Depression Scale--GDS, and Scale for the Self-evaluation of Depression from the Psychogeriatric Interview--PGI) and b) psychiatric evaluation (according to DSM-III-R diagnostic criteria). Results were as follows: a) all the 3 tests (SSAMH, GDS, PGI) were suitable for the goals of this research, with a sensibility of 95.4%, 90.9%, and 95.4%, and a specificity of 90.4%, 88.9%, and 90.5%, respectively; b) the prevalence of depression in the sample was 25.9% (26.1% in females and 25.6% in males); c) the most common disorder was dysthymia, with higher percentage in females than in males (75% and 50% of all the depressive syndromes, respectively); d) the prevalence of depression was higher in females 60-69 years old and in males 70-79 years old.
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PMID:[Clinical investigation on depression on a randomized and stratified sample in an elderly population]. 174 52

We addressed the hypothesis that platelets are not activated in association with effort-induced myocardial ischemia in stable coronary disease. Seventy-two patients undergoing a diagnostic bicycle exercise test were stratified according to the development of chest pain (yes/no, 33/39) and of exercise-induced ST-segment depression of at least 200 microV in the electrocardiogram (yes/no, 12/60). Noninvasive indexes of platelet activation and of platelet/vessel wall interaction (urinary excretion of the 2,3-dinor-metabolites of thromboxane A2 [Tx-M] and prostacyclin [PGI-M], respectively) were analyzed in samples collected in the basal state and after the test. Basal Tx-M and PGI-M did not differ in patients with (236 +/- 35 and 131 +/- 22 pg/mg creatinine, respectively) and without (185 +/- 16 and 101 +/- 13 pg/mg creatinine, respectively) chest pain, or in those with (178 +/- 45 and 162 +/- 41 pg/mg, respectively) and without (216 +/- 22 and 104 +/- 11 pg/mg, respectively) ST-segment depression during the test. Patients without chest pain or without ST-segment depression moderately increased (p less than 0.05) their urinary Tx-M (by 21% and 13%, respectively) and PGI-M (by 28% and 23%, respectively) after exercise. No significant increases were observed in those developing chest pain or ST depression during exercise. These data indicate that effort-induced myocardial ischemia is not associated with an increase in platelet activation or platelet/vessel wall interaction in patients with stable coronary disease.
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PMID:Excretion of thromboxane A2 and prostacyclin metabolites before and after exercise testing in patients with and without signs of ischemic heart disease. 222 75

The levels of TxB2 and 6-keto-PGI alpha in the coronary sinus and thoracic aorta blood were determined in 14 patients with angina pectoris and signs of coronary atherosclerosis. 12 patients were involved in a dynamic study: before, during and 10 minutes after ischaemia-inducing atrial pacing. In all the patients atrial pacing resulted in a typical episode of angina, in 7 of them ST-segment depression of not less than 2 mm was seen on the ECG. In one patient arachidonic acid metabolites were evaluated during the control period and during a spontaneous episode of angina accompanied by ST-segment elevations. In 8 of 9 patients TxB2 was produced by the myocardium during atrial pacing. During monitored evaluation of arachidonic acid metabolites one patient with spontaneous angina demonstrated a gradual lowering of the 6-keto-PGI alpha, it being minimal by the beginning of the episode; TxB2 level increased more rapidly.
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PMID:[Thromboxane and prostacyclin in patients with stenocardia in induced and spontaneous ischemia of the myocardium]. 375 53

Histories of childhood trauma have been reported previously in bulimic subjects but no study to date has assessed how these experiences may affect response to fluoxetine. Thirty outpatient subjects in a placebo-controlled trial of 60 mg of fluoxetine for the treatment of bulimia nervosa completed the Dissociative Experiences Scale and a self-report instrument assessing trauma. Response to treatment was measured with the Hamilton Depression Scale-17 (HAMD-17), the CGI, the PGI, and the change in number of binges per day. Subjects taking fluoxetine with histories of physical abuse showed a significantly greater drop in HAMD-17 scores than those without such histories. No relationship between a reported history of abuse and the response of binging to fluoxetine was found. A history of abuse does not appear to predict the response of binging to fluoxetine but may predict a greater response of nonspecific symptoms like depression.
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PMID:Dissociation, childhood trauma, and the response to fluoxetine in bulimic patients. 819 1

Results from placebo-controlled trials of antidepressants can be used to identify patients most likely to benefit from medication. Using data from a randomized clinical trial of fluoxetine versus placebo for 671 elderly outpatients with major depression, we evaluated characteristics of those who improved with and without active medication. We found that the choice of outcome measure made a difference when evaluating the effectiveness of fluoxetine relative to placebo and determining the accuracy of predictive variables in both treatment groups. Generally, less severe depression predicted favorable response (greater than 50% improvement on the 21-item Hamilton Rating Scale for Depression [HAM-D-21], less than 3 on the Clinical Global Impressions [CGI] and Patient Global Impressions [PGI] improvement scales) and remission (less than 9 on 6-week HAM-D-21) with both fluoxetine and placebo. Less anxiety/somatization was associated with favorable fluoxetine response, and lower levels of cognitive and sleep disturbance were associated with remission in the placebo group. By contrast, higher levels of psychomotor retardation in the placebo group were associated with clinician and patient ratings of much or very much improved. The similarities among responders in both groups may indicate that some in the fluoxetine group would have improved with placebo.
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PMID:Characteristics of fluoxetine versus placebo responders in a randomized trial of geriatric depression. 949 83

The phenomenon of self-immolation was studied in 22 young people, mostly students, who had indulged in this act to protest against the decision of the Government of India to enlarge the scope of reservations in jobs and educational institutions. Within a short span of time of arriving at one of the two treatment centres after attempting self-immolation, the subjects were interviewed and assessed on a semi-structured interview schedule to elicit sociodemographic and attitudinal data. The subjects were also rated on the Brief Psychiatric Rating Scale, Pierce's Suicide Intent Scale, the Superego Paranoia Depression Scale, the Hostility and Direction of Hostility Questionnaire, the PGI Locus of Control Scale and the Alienation Scale. All subjects except one were free of manifest psychopathology. The group as a whole had a high score on Pierce's Suicide Intent Scale and displayed internal locus of control orientation. Most were ambitious, aggressive, hostile and felt alienated. The absence of manifest psychopathology sets this group apart from cases of deliberate self-harm arising in the context of psychiatric morbidity. Thwarted ambitions, a sense of alienation and intropunitive hostility can lead to protest which at times becomes altruistic and results in self-immolation.
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PMID:A psychosocial study of 'self-immolation' in India. 950 7

Antithrombin (AT) is known as the most important natural inhibitor of thrombin activity and has been shown to improve distinct clinical parameters during the course of septic (endotoxin)-induced multiple organ dysfunction. We hypothesized that AT acts by inhibiting leukocyte activation and microvascular injury via the promotion of endothelial release of PGI(2), and therefore, we studied the effects of AT on leukocyte/endothelial cell interaction and microvascular perfusion during endotoxemia. In a skinfold preparation of Syrian hamsters, severe endotoxemia was induced by repeated administration of endotoxin intravenously [lipopolysaccharide (LPS), Escherichia coli, 2 mg/kg] at 0 and 48 h. AT (250 IU/kg) was administered intravenously at 0, 24, and 48 h (n = 6, AT group). In control animals (n = 5, control), LPS was given without AT supplementation. By intravital fluorescence microscopy, leukocyte-endothelial cell interaction and functional capillary density (FCD; measure of capillary perfusion) were analyzed during a 72-h period after the first LPS injection. AT significantly attenuated LPS-induced arteriolar and venular leukocyte adherence after both the first and the second LPS injection [P < 0.01, measures analysis of variance (MANOVA)]. In parallel, AT was effective in preventing LPS-induced depression of FCD after the first and the second LPS administration (P < 0.05, MANOVA). By pretreatment with the cyclooxygenase inhibitor indomethacin (n = 6), effects of AT on leukocyte adherence and FCD were found completely abolished. Thus our study indicates that AT exerts its beneficial effects in endotoxemia by reducing leukocyte-endothelial cell interaction and microvascular perfusion failure probably via liberation of prostacyclin from endothelial cells.
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PMID:Antithrombin reduces leukocyte adhesion during chronic endotoxemia by modulation of the cyclooxygenase pathway. 1089 21

Existing therapies for major depressive disorder (MDD) have either limited efficacy and/or poor tolerability. The present study examined the effects of duloxetine, a potent and balanced dual reuptake inhibitor of serotonin (5-HT) and norepinephrine (NE), in patients with MDD. Adult patients (N = 267) with MDD were randomly assigned to receive duloxetine (60 mg/day) or placebo in this 9-week, multi-center, double-blind, parallel-group clinical trial. Efficacy was evaluated using the 17-item Hamilton Depression Rating Scale (HAMD(17)), Visual Analog Scales (VAS) for pain, Clinical Global Impression of Severity (CGI-S), Patient's Global Impression of Improvement (PGI-I), and Quality of Life in Depression Scale (QLDS). Safety was evaluated by assessing discontinuation rates, adverse event rates, vital signs, and laboratory tests. Duloxetine (60 mg QD) significantly reduced the HAMD(17) total score compared with placebo at the end of 9-week therapy. Estimated probabilities of response and remission were 65 and 43%, respectively, for duloxetine compared with 42 and 28% for placebo. Duloxetine also reduced overall pain, back pain, shoulder pain and time in pain while awake significantly more than placebo. Global measures of improvement, including PGI-I and QLDS, were significantly improved by duloxetine compared with placebo. Discontinuations due to adverse events were more frequent for duloxetine-treated patients (12.5%) than for placebo-treated patients (4.3%). Nausea, dry mouth, dizziness, and constipation were more frequent for duloxetine than placebo. There was no significant incidence of hypertension, nor any other safety issues. Duloxetine 60 mg administered once daily appears to be a safe and effective treatment for MDD.
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PMID:Duloxetine 60 mg once daily dosing versus placebo in the acute treatment of major depression. 1239 7

This study evaluated and compared the performance of three self-report measures: (1) 30-item Inventory of Depressive Symptomatology-Self-Report (IDS-SR30); (2) 16-item Quick Inventory of Depressive Symptomatology-Self-Report (QIDS-SR16); and (3) Patient Global Impression-Improvement (PGI-I) in assessing clinical outcomes in depressed patients during a 12-week, acute phase, randomized, controlled trial comparing nefazodone, cognitive-behavioral analysis system of psychotherapy (CBASP), and the combination in the treatment of chronic depression. The IDS-SR30, QIDS-SR16, PGI-I, and the 24-item Hamilton Depression Rating Scale (HDRS24) ratings were collected at baseline and at weeks 1-4, 6, 8, 10, and 12. Response was defined a priori as a > or =50% reduction in baseline total score for the IDS-SR30 or for the QIDS-SR16 or as a PGI-I score of 1 or 2 at exit. Overall response rates (LOCF) to nefazodone were 41% (IDS-SR30), 45% (QIDS-SR16), 53% (PCI-I), and 47% (HDRS17). For CBASP, response rates were 41% (IDS-SR30), 45% (QIDS-SR16), 48% (PGI-I), and 46% (HDRS17). For the combination, response rates were 68% (IDS-SR30 and QIDS-SR16), 73% (PGI-I), and 76% (HDRS17). Similarly, remission rates were comparable for nefazodone (IDS-SR30=32%, QIDS-SR16=28%, PGI-I=22%, HDRS17=30%), for CBASP (IDS-SR30=32%, QIDS-SR16=30%, PGI-I=21%, HDRS17=32%), and for the combination (IDS-SR30=52%, QIDS-SR16=50%, PGI-I=25%, HDRS17=49%). Both the IDS-SR30 and QIDS-SR16 closely mirrored and confirmed findings based on the HDRS24. These findings raise the possibility that these two self-reports could provide cost- and time-efficient substitutes for clinician ratings in treatment trials of outpatients with nonpsychotic MDD without cognitive impairment. Global patient ratings such as the PGI-I, as opposed to specific item-based ratings, provide less valid findings.
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PMID:Self-reported depressive symptom measures: sensitivity to detecting change in a randomized, controlled trial of chronically depressed, nonpsychotic outpatients. 1557 8

Acute hypoxia increases ventilatory drive in conscious animals, resulting in tachycardia. Sustained hypoxia changes the initial chemoreflex ventilatory increase to secondary ventilatory depression, which then evokes a gradual secondary heart rate (HR) reduction. Prostacyclin (PGI(2)) release is known to potentiate alpha(2)-adrenoreceptor (alpha(2)-AR) mediated inhibition of sympathoactivation during ischaemia and hypoxia. We examined whether alpha(2)-AR mediated sympathoinhibition was responsible for limiting hypoxic heart rate increases during initial sympathoactivation, and subsequent secondary HR depression, and if PGI(2) is required for sympathoinhibition of HR. The responses of unrestrained PGI(2) synthase deficient (PGID) and wild type (WT) mice to acute hypoxia (10% O(2) for 30 min) were investigated by simultaneous telemetry, whole body plethysmography and open-flow respirometry. PGID mice exhibited potentiated .V(E) (p < 0.007) after intraperitoneal vehicle injection (n = 8), but not so HR responses compared to WT mice during sustained hypoxia. Idazoxan (alpha(2)-AR antagonist, i.p. bolus 3 mg/kg) pretreatment did not change hypoxic ventilatory response in either group, but significantly elevated hypoxic HR in WT mice only (p < 0.013). Sodium meclofenamate (cyclooxygenase inhibition, i.p. bolus 25 mg/kg) pretreatment eliminated the potentiated .V(E) of PGID and caused significant basal hypotension that led to a transient hypertensive response to hypoxia. From these results, we suggest that alpha(2)-AR activation is required for coupling HR to central inspiratory drive during acute hypoxia, and that PGI(2) is required to enhance the inhibition of sympathoactivation.
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PMID:Alpha2-adrenoreceptor mediated sympathoinhibition of heart rate during acute hypoxia is diminished in conscious prostacyclin synthase deficient mice. 1712 18


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