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BackgroundCoping with stress is defined as all activities undertaken by a human in a stressful situation. The effect of stress on depression, its role in triggering the subsequent phases of the disease, and the factors that mediate the stress-depression relationship become more and more often subjects of research in psychiatry and psychology. Factors important for the formation of depressive symptoms and disease progression are significantly associated with coping strategies used in the face of stress.The main aim of the study was to evaluate the most popular strategies of coping with stress in people with depression in comparison to healthy subjects.Material/MethodsInitial research was carried on 80 patients aged from 20 to 66 years with a diagnosis of depression. The control group consisted of 30 healthy subjects aged 22 to 57 years. Analysis of the most popular strategies of coping with stress was performed with the Multiphasic Inventory for Measuring Coping (COPE) by Carver, Scheier, and Weintraub.ResultsIn contrast with healthy people, patients with depression in stressful situations more often use strategies based on avoidance and denial and have more difficulties in finding positive aspects of stressful events.ConclusionsDepression may be an important factor in the negative assessment of one’s own ability to cope with difficult situations and can aggravate a tendency to perceive stressful events as overwhelming.

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The clinical implications of thyroid hormones in depression have been studied extensively and still remains disputable. Supplementation of thyroid hormones is considered to augment and accelerate antidepressant treatment. Studies on the role of thyroid hormones in depression deliver contradictory results. Here we assess theirs impact on depression severity and final clinical outcome in patients with major depression. Thyrotropin, free thyroxine (FT4), and free triiodothyronine (FT3) concentrations were measured with automated quantitative enzyme immunoassay. Depression severity and final clinical outcome were rated with 17-itemic Hamilton Rating Scale for Depression [HDRS(17)] and Clinical Global Impression Scales for severity and for improvement (CGIs, CGIi). FT3 and FT4 concentrations were significantly positively correlated with clinical improvement evaluated with CGIi (R = 0.38, P = 0.012; R = 0.33, P = 0.034, respectively). There was a significant correlation between FT4 concentrations and depression severity assessed in HDRS(17) (R = 0.31, P = 0.047). Male patients presented significantly higher FT3 serum levels (Z = 2.34, P = 0.018) and significantly greater clinical improvement (Z = 2.36, P = 0.018) when compared to female patients. We conclude that free thyroid hormones concentrations are associated with depression severity and have an impact on final clinical outcome. It can be more efficient to augment and accelerate the treatment of major depressive disorder with triiodothyronine instead of levothyroxine because of individual differences in thyroid hormones metabolism.

Background: The authors of this research study intended to verify whether there are any changes in gene expression in depressed patients without coexisting inflammatory diseases for selected immune-inflammatory factors that are particularly important in autoimmune disease pathogenesis (IL-17, IL-21, IL-23, IL-35, Foxp3). Methods: The study was carried out on a group of 190 patients with depression and 100 healthy volunteers. The severity of depressive symptoms was assessed using the Hamilton Depression Scale. RT-PCR was used to evaluate mRNA expression and ELISA was used to measure protein expression of these genes. Results: The level of gene expression for IL-17, IL-21, IL-23, and IL-35 was substantially higher in the group of patients with depression compared to the control group. The mean mRNA expression of Foxp3 was considerably reduced in patients suffering from depressive disorders. There was a statistically significant correlation between the number of hospitalizations and the expression of specific inflammatory factors. Conclusions: Expression of specific inflammatory genes may be a factor in the etiopathogenesis of depressive disorders. The duration of the disease seems to be more important for the expression of the genes in question than the severity of depression. These cytokines may affect the metabolism of neurotransmitters and neuroendocrine functions in the brain as well as be a marker and a new potential therapeutic target for recurrent depressive disorders.