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P.2.a. Mood disorders and treatment − Affective disorders (basic)
in sleeping and performing the daily routine. So it is not surprising that sometimes symptoms of depression are thought of by both the patient, and the doctor as being due to heart disease. Depression is the main driver of quality of life and requires prevention, detection, and management in its own right. Additional management strategies for depressed cardiac patients include cognitive behavioral therapy, antidepressant medication, and combined approaches [2]. The aim of this study is to demonstrate that diagnosing depression in a timely manner, and its appropriate treatment, resulted in increased quality of life of our patients and favorable outcome of their CVD. Method: We followed-up fifty CVD (50) patients, diagnosed with depression within the everyday work at the psychiatry department of the Health Center (primary healthcare) during six months. Diagnosis of depression was supported by the Hamilton Scale for Anxiety and Depression score at the baseline and after six-month treatment period. The patients were treated with combination of cognitive behavioral therapy, SSRI and Trozodon. In addition, the Olson–Barnes Quality of Life questionnaire was applied for measuring the quality of life both at the baseline and after six months of treatment. We also monitored if there was any alteration in cardiological treatment: either in number of medications administered simultaneously or in their dosage. We applied following statistic methods: descriptive statistics, Chisquare test, and Wilcoxon signed-rank test. Results: There was 34 (68%) female and 16 (32%) male patients. Mean age was 61.8 (sd= 3.34). As evaluated according to the Hamilton Anxiety and Depression Scale, 17 (34%) patients had score for mild depression, 22 (44%) moderate, and 12 (24%) had severe depression. All patients referred for psychiatric evaluation had one or combination of following cardiovascular conditions: hypertension (91%), arrhythmias (17%), myocardial infarction (27%), bundle branch block (32%). Patients were treated with standard combinations of cardiology medications. Re-evaluation at six months demonstrated significant difference (c2 = 8.703, p < 0.05) in Hamilton scores with more mildly depressed patients. Also, scores at Quality of Life scale demonstrated significant improvement (c2 = 27.771, p < 0.01) comparing with the baseline. Cardiological treatment was altered in 17.3% of patients, but the difference in either number of medications used concomitantly or their dosage was not significant. Conclusion: Timely diagnosis and adequate treatment of depression in CVD patients resulted in improvement of depression symptoms as well as quality of life. As for improvement of CVD outcome expressed as number of medications used concomitantly or their dosage, a prolong study is required to support our hypothesis. References [1] Lihtman J.H., Bigger J.T., Blumenthal J.A., 2008 Depression and Coronary Heart Disease Circulation118: 1768–1775 Published online before print September 29, 2008, doi: 10.1161/ CIRCULATIONAHA.108.190769. [2] Whooley M.A., de Jonge P., Vittinghoff E., Otte C., 2008 Depressive Symptoms, Health Behaviors, and Risk of Cardiovascular Events in Patients With Coronary Heart Disease JAMA 300(20): 2379–2388. doi: 10.1001/jama.2008.711.
P.2.a.003 Anxiety and depression symptoms among patients with type 2 diabetes mellitus and poor glycaemia control D. Bezykornoviene1 ° , V. Adomaitiene1 , V. Steibliene1 University of Health Sciences, Psychiatry, Kaunas, Lithuania
1 Lithuanian
The aim of this study was to investigate the prevalence of anxiety and depression symptoms among patients with T2DM, hospitalized due to poor glycaemia control; to examine the relationship between severity of psychiatric symptoms, socio-demographic factors and T2DM clinical characteristics. Methods: Sixty patients − 24 men (40%) and 36 women (60%), age 57.3±9.58 years (mean±SD), with diagnosis of T2DM, hospitalized in Endocrinology Clinic, Hospital of Lithuanian University of Health Sciences (LUHS) were evaluated for the presence of anxiety symptoms (using Beck Anxiety Inventory [BAI] scale) and depressive symptoms (using Beck’s Depression Inventory [BDI] scale). Both scales comprised of 21-question multiple-choice selfreport inventory each about how the subject has been feeling in the last week. The information about patients’ socio-demographic characteristics (age, gender, marital, education and social status), clinical characteristics and medical history (Body Mass Index [BMI], age of onset and duration of T2DMs, glycaemia control, complications and other somatic illnesses, use of medications and treatment adherence) were collected. The study was approved by Bioethics Committee of LUHS. Statistical data analysis was performed using SPSS 17.0. Means ± standard deviation (SD) and percentages for categorical variables were calculated. Associations between variables were assessed using chi squared test or Spearman correlation coefficient. Prognostic factors were analyzed using logistic regression analysis with adjustment with relevant confounders. Statistical significance level was set at 5% (P < 0.05). Results: Based on BAI scores anxiety symptoms reported 53 (88.3%) patients: 14 (23.3%) mild, 10 (16.7%) moderate and 29 (48.3%) severe anxiety symptoms. Mean anxiety score was significant higher between female than male patients (27.3±12.57 vs 17.9±11.90 respectively, p = 0.003). Based on BDI scores, depressive symptoms reported 33 (55%) patients: 23 (38.3%) mild and 10 (16.7%) moderate symptoms. Depressive symptoms score also was significant higher between females than males patients (12.6±6.75 vs 8.3±3.94, respectively; p = 0.005). Severity of anxiety score correlates positively with BMI (r = 0.300; p = 0.02) and with duration of T2DM, in years (r = 0.338; p = 0.008). There were correlation between anxiety symptoms and depressive symptoms severity (r = 0.452; p = 0.00). Only one risk factor − obesity (BMI >30) − was related to mild–moderate depressive symptoms at OR = 3.33 (95% CI [1.134–9.801], p = 0.026). Three risk factors − patient’s working disability at OR = 3.867 (95% CI [1.256−11–899], p = 0.016); concomitant arterial hypertension at 4.315 (95% CI [1.105–17.320], p = 0.028) and use of antihypertensive medications at 7.4 (95% CI [1.340–40.876]) were related to moderate–severe anxiety symptoms. Conclusions: – Nearly 90 percent of patients with T2DM and poor glycaemia control reported anxiety symptoms and more than half − depressive symptoms, with higher both symptoms severity among female patients. – More severe anxiety symptoms were related to higher BMI, longer duration of T2DM and more severe depressive symptoms. Obesity was the risk factor associated with more severe
P.2.a. Mood disorders and treatment − Affective disorders (basic) depression symptoms; patients’ disability, arterial hypertension and antihypertensive medication use − risk factors associated with more severe anxiety symptoms among patients with T2DM. – Due to small sample size data need to be treated as preliminary. References [1] Egede LE. Major depression in individuals with chronic medical disorders: prevalence, correlates and association with health resource utilization, lost productivity and functional disability. Gen Hosp Psychiatry. 2007 Sep-Oct; 29(5): 409−16. [2] Chen L I, Magliano DJ, Zimmet PZ. The worldwide epidemiology of type 2 diabetes mellitus − present and future perspectives. Nat Rev Endocrinol. 2011 Nov 8; 8(4): 228−36. [3] Collins MM1, Corcoran P, Perry IJ. Anxiety and depression symptoms in patients with diabetes. Diabet Med. 2009 Feb; 26(2):153−61.
P.2.a.004 The role of the catecholaminergic system in the antidepressant-like effect of the nociceptin antagonist BAN ORL 24 Twardowschy1 ° ,
Souza2 ,
Andreatini2 ,
Coimbra1
A. L.C. R. N.C. 1 School of Medicine of Ribeir˜ ao Preto, Pharmacology, Ribeir˜ao Preto, Brazil; 2 Federal University of Paran´a, Pharmacology, Curitiba, Brazil
The nociceptin/orphanin FQ (N/OFQ) peptide and N/OFQ peptide (NOP) receptor are widely distributed in the brain and regulates several central functions such as pain transmission, learning, memory, anxiety and depression [1]. BAN ORL 24 (BAN) is a new non-peptide ligand of NOP receptor having antagonistic actions in NOP receptors [2]. It has been reported that NOP receptor antagonists induce antidepressant-like effects, however its mechanism of action remains unknown. Previous work of our group already showed the antidepressant-like effect of the new antagonist of NOP receptors BAN. The aim of the present study was to investigate the catecholaminergic role on its mechanism of action as well as the hippocampal participation in the antidepressant-like effects of BAN. Swiss mice were subjected to tail suspension test (TST, n = 7 to 8 per group) and to open field test (OFT, n = 5 to 6 per group); and Wistar rats to forced swim test (FST, n = 7 per group). All tests were conducted like previously described in the literature. The drugs utilized (BAN, NOP antagonist; AMPT, a catecholamine synthesis inhibitor; and venlafaxine, serotonin and noradrenaline reuptake inhibitor) were dissolved in saline. One-way ANOVA showed that the immobility time in the TST was statistically different [F(5,37) = 12.0; p < 0.001] between the groups, and Tukey post-hoc test showed that the mice treated with BAN (5 mg/kg, i.p.) or venlafaxine (8 mg/kg, i.p.) reduced the immobility time when compared with saline group, p < 0.01 and p < 0.001 respectively. In addition, the animals pre-treated with AMPT (200 mg/kg, i.p.) plus BAN showed more immobility when compared with the animals treated only with BAN (p < 0.001). Similar outcomes were found between the AMPT plus venlafaxine group and venlafaxine alone group (p < 0.001). Furthermore, was verified if the hippocampus is involved in the antidepressant like effects of the BAN. Was found that microinjection of BAN (10 nmol/0.2ul) into the rats hippocampus reduced the immobility time [F(5,36) = 15.7; p < 0.001] and increased the climbing [F(5,36) = 7.7; p < 0.01], in the FST. The intraperitoneal pre-treatment of rats with catecholamine synthesis inhibitor (100 or 200 mg/kg), followed by microinjection of BAN, reverted the
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reduction of immobility caused by BAN alone (AMPT 100 mg/kg, p < 0.05; AMPT 200 mg/kg, p < 0.01) and also reverted the increase of climbing (AMPT 200 mg/kg, p < 0.01). Nevertheless, any treatment changed the swimming time in relation to the control group. To evaluate a possibly motor effect of BAN, was carried out the OFT. The one-way ANOVA do not showed any difference between the treatments in the number of crossings [F(3,18) = 0.71], time in the center of open field [F(3,18) = 0.71] and grooming time [F(3,18) = 0.71], showing that the BAN had no interaction with the physical stimulation. In summary, BAN ORL 24 exhibits pronounced antidepressantlike effects in different species and animal models, when injected peripherically or intrahippocampaly. These effects should be possibly by preventing the inhibitory effects of endogenous N/OFQ on brain monoaminergic (in particular cathecolaminergic) neurotransmission in the hippocampus. Participation of the NOP receptor system in mood modulation sets new potential targets for antidepressant drug development. References [1] Rizzi A, Molinari S, Marti M, Marzola G, Calo G, 2011. Nociceptin/orphanin FQ receptor knockout rats: in vitro and in vivo studies. Neuropharmacology 60, 572–579. [2] Liao YY, Trapella C, Chiou LC, 2009. 1-Benzyl-N-[3-[spiroisobenzofuran-1(3H),4 -piperidin-1-yl]propyl]pyrrolidine-2-carboxamide (Compound 24) antagonizes NOP receptor-mediated potassium channel activation in rat periaqueductal gray slices. Eur J Pharmacol 606, 84−89. Disclosure statement: This abstract is financially supported by an educational grant from FAPESP.
P.2.a.005 Blockade of D1 dopaminergic receptors corrects depression-like behaviour in gonadectomised rats treated with a low dose of testosterone J. Fedotova1 ° 1 Pavlov Institute of Physiology Russian Academy of Medical Sciences, Dept. of Neuroendocrinology, St. Petersburg, Russia Statement on the purpose of the study: Depressive disorders belong to the most frequent diseases worldwide showing a lifetime prevalence of up to 20%. The traditional focus on a prominent participation of the central serotonergic and noradrenergic systems in the mechanisms of depression is generally accepted. However, recent evidences suggest that the dysfunction of the central dopaminergic pathways may be a critical component of the neurobiological basis of depression [1]. On the other hand, both basic and clinical reports showing that gonadal hormones are involved in the modulation of depression [2]. Meanwhile, there is increasing evidence that androgens may alter neuronal excitability via interaction with different types of neurotransmitter membrane receptors [3]. The present work was devoted to the comparative analysis of the behavioral and hormonal status in the gonadectomized (GDX) male rat of middle age chronically treated with high-selective agonist of D1 dopaminergic receptors agonist − SKF-38393 or antagonist D1 -dopaminergic receptors − SCH-23390 alone or in a combination with low dose of testosterone propinate. Methods: Two weeks after surgery, GDX male rats of 3−4 months age began 14 days of treatment with the vehicle, a low dose of testosterone propionate (1.0 mg/kg, s.c.), D1 -like dopaminergic agonist, SKF-38393 (0.1 mg/kg, i.p.), D1 -dopaminergic antagonist, SCH-23390 (0.1 mg/kg, i.p.), SKF-38393 plus testosterone propionate or SCH-23390 plus testosterone propionate