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

Depressive psychosis with anxiety or without it is the most spread disorder among the patients with diabetes mellitus. According to our investigations the depression was found in 36.6% of cases of patients with the I type diabetes mellitus which affects negatively their mental working ability. Based on the mentioned above we aimed to study a sensory and psychoemotional productivity of patients with the type I diabetes mellitus for their further purposeful treatment. Thirty patients with the type I diabetes mellitus were observed and divided into two groups -- 19 -- without and 11 with a depression. Sensor and motor reaction was studied by means of Landolt's rings in computerized mode. A deterioration of the patients' mental working ability while resolving the simple sensor and motor task is expressed as the increased quantity of missed reactions on the light stimulus and chaotic character of the reaction time histograms that is stipulated by the diminished ability to concentrate attention be carrying out a monotonous work. Psychoemotional test has proved our conclusion drawn by means of sensor-motor task, but the analysis of the reaction time histograms allows suggesting that given contingent of patients fulfill the task of the various conditions of resolving easier then the monotonous one.
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PMID:[Sensory and psychoemotional productivity in the type I diabetes mellitus]. 1630 53

Considerable knowledge has accumulated in recent decades concerning the significance of physical activity in the treatment of a number of diseases, including diseases that do not primarily manifest as disorders of the locomotive apparatus. In this review we present the evidence for prescribing exercise therapy in the treatment of metabolic syndrome-related disorders (insulin resistance, type 2 diabetes, dyslipidemia, hypertension, obesity), heart and pulmonary diseases (chronic obstructive pulmonary disease, coronary heart disease, chronic heart failure, intermittent claudication), muscle, bone and joint diseases (osteoarthritis, rheumatoid arthritis, osteoporosis, fibromyalgia, chronic fatigue syndrome) and cancer, depression, asthma and type 1 diabetes. For each disease, we review the effect of exercise therapy on disease pathogenesis, on symptoms specific to the diagnosis, on physical fitness or strength and on quality of life. The possible mechanisms of action are briefly examined and the principles for prescribing exercise therapy are discussed, focusing on the type and amount of exercise and possible contraindications.
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PMID:Evidence for prescribing exercise as therapy in chronic disease. 1664 91

Cerebral dysfunctions, including a high incidence of depression, are common findings in human type 1 diabetes mellitus. An association between depression and defective hippocampal neurogenesis has been proposed and, in rodents, antidepressant therapy restores neuronal proliferation in the dentate gyrus. Hippocampal neurogenesis is also deficient in diabetic mice, which led us to study whether the selective serotonin reuptake inhibitor fluoxetine influences cell proliferation in streptozotocin-diabetic animals. Diabetic and control C57BL/6 mice received fluoxetine (10 mg/kg/day, i.p., 10 days) and dentate gyrus cell proliferation was measured after a single injection of 5-bromo-2'-deoxyuridine (BrdU). Diabetic mice showed reduced cell proliferation. Fluoxetine treatment, although having no effect in controls, corrected this parameter in diabetic mice. The phenotype of newly generated cells was analysed by confocal microscopy after seven daily BrdU injections, using Tuj-1/beta-III tubulin as a marker for immature neurones and glial fibrillary acidic protein for astrocytes. In controls, the proportion of Tuj-1-BrdU-positive cells over total BrdU cells was approximately 70%. In vehicle-treated diabetic mice, immature neurones decreased to 56% and fluoxetine brought this proportion back to control values without affecting astrocytes. Therefore, fluoxetine preferentially increased the proliferation of cells with a neuronal phenotype. In addition, neurones were counted in the hilus of the dentate gyrus; a 30% decrease was found in diabetic mice compared with controls, whereas this neuronal loss was prevented by fluoxetine. In conclusion, fluoxetine treatment restored neuroplasticity-related hippocampal alterations of diabetic mice. These findings may be potentially important to counteract diabetes-associated depression in humans.
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PMID:Reduced hippocampal neurogenesis and number of hilar neurones in streptozotocin-induced diabetic mice: reversion by antidepressant treatment. 1655 17

A 69-year-old male patient with type 1 diabetes mellitus had been under treatment at our outpatient clinic since the age of 65. He had previously undergone surgery for esophageal cancer at the age of 55; the excised portion of the esophagus was replaced by a retrosternal gastric tube. He was admitted to our hospital for suspected pneumonia on April 8, 2004. An electrocardiogram (ECG) on admission showed marked ST depression in leads V1 and V2, and prominent negative T waves in leads I and aVL; however, the T waves unexpectedly flattened after 2 minutes and the ST depression resolved after about 4 hours. On January 7, 2005, we performed a deep breathing test to analyze the effects of movements of the thoracic wall and intrathoracic structures on the ECG. In this test, deep inspiration induced ST depression reaching 0.5 mV in leads V1 to V3; this resolved on switching to deep expiration. ECG changes together with chest computed tomography images supported the concept that the ST-T abnormalities were induced by cardiac compression caused by expansion of the gastric tube between the sternum and heart. We have reviewed 7 other similar reported cases.
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PMID:Marked reversible ST-T abnormalities induced by cardiac compression from a retrosternal gastric tube used to reconstruct the esophagus after tumor resection. A case of a diabetic patient and mini-review of 7 reported patients. 1682 54

We report about a 41-year old male patient who presented to the emergency room with acute chest pain, exertion dyspnoea, muscle stiffness, myalgia and adynamia. There was no history of coronary artery disease but known arterial hypertension and insulin dependent diabetes mellitus. Four weeks before submission the patient had been thyroidectomized after he had been diagnosed with papillary thyroid carcinoma and was now awaiting further radioiodine therapy. The thyroid-stimulating hormone level was markedly elevated to 67 mU/l (normal range 0.27-4.20 mU/l) and fT4 significantly reduced to 0.19 ng/ml (normal range 0.9-1.9 ng/ml). CK was elevated to 328 U/l, cardiac Troponin I (Stratus CS) above the threshold with 0.13 microg/l and Elecsys third generation troponin T above the threshold with 0.04 microg/l. The electrocardiogram showed a normal sinus rhythm and did not reveal any signs of ST-elevation or -depression. During follow-up a cardiac MRI was performed, showing normal dimensions and function but a very small area of diffuse myocardial damage, atypical of ischemic injury. In coronary angiography normal coronary arteries were found. We conclude that cardiac troponins I and T may be elevated in severe hypothyroidism without coronary artery disease due to diffuse myocardial injury which can be imaged by MRI.
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PMID:Positive cardiac troponin I and T and chest pain in a patient with iatrogenic hypothyroidism and no coronary artery disease. 1708 20

The objective of this article was to establish the characteristics of depressiveness among adolescents with diabetes. Adolescents aged 14 and 16 years suffering from diabetes, healthy ones, and their parents were enrolled in the study. A total of 260 adolescents (100 adolescents with type 1 diabetes mellitus and 160 healthy ones) were interviewed. To measure adolescents' depressiveness, a new scale was constructed using different questionnaires (Maastricht, Hamilton, Beck). Parents' depressiveness was measured with Beck depression scale. This study showed that 16-year-old girls with diabetes were more depressed than the healthy ones. Mothers of 14-year-old adolescents and 16-year-old girls with diabetes are more depressed than the healthy adolescents' mothers. Results of the study confirmed that depressiveness of 14- and 16-year-old girls with diabetes and that of their mothers were related. The relationship between the depressiveness of mothers of 14-year-old boys with diabetes mellitus and bad glycemic control of their sons was determined. The following peculiarities of depressiveness among adolescents with diabetes were found: 14-year-old girls had more negative attitude toward themselves; 16-year-old girls were very sensitive and had depressed mood; 16-year-old boys complained about lowered daily activity.
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PMID:[Characteristics of depressiveness among adolescents with diabetes mellitus]. 1729 86

We have previously shown that type 2 diabetes (T2D) in the mouse is associated with increased responsivity to innate immune challenge. Here we demonstrate that in a mouse model of type 1 diabetes (T1D) LPS-dependent suppression of social exploration (SE) is augmented and dependent on hyperglycemia. T1D was induced in mice with intraperitoneal (i.p.) streptozotocin (STZ). After 4d, STZ treated mice had blood glucose levels of 417+/-34mg/dl compared to 160+/-11mg/dl in non-STZ treated mice. When these diabetic mice were challenged with i.p. lipopolysaccharide (LPS), LPS-induced depression of SE was nearly 2.7-fold greater in diabetic mice at 2h than in non-diabetic mice. Examination of peritoneal proinflammatory cytokine levels 2h after LPS administration showed that diabetic mice had 4-, 2.5- and 3.6-fold greater concentrations of IL-1beta, IL-6 and TNF-alpha, respectively, when compared to non-diabetic mice. Control of blood glucose levels with injected insulin in diabetic mice improved 2h post LPS-induced loss of SE by 3.9-fold. Interestingly, insulin given intracerebroventricularly to diabetic mice did not impact LPS-induced loss of SE but did increase basal SE 8, 12 and 24h later. Finally, administration of STZ to hyperglycemic/hyperinsulinemic db/db mice did not alter LPS-induced loss of SE. Taken together these findings indicate that mice with T1D have augmented loss of SE in response to LPS and this is due to hyperglycemia and not to insulin.
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PMID:LPS-dependent suppression of social exploration is augmented in type 1 diabetic mice. 1732 Nov 7

Present analyses used data from the Pittsburgh Epidemiology of Diabetes Complications Study, a prospective study of subjects with childhood type 1 diabetes (T1D), diagnosed between 1950 and 1980. Baseline exams took place 1986-1988 with biennial exams since. The Framingham risk equation was applied to generate the probability of risk for coronary heart disease (CHD) (MI, CHD death, or Q-waves) in 552 CHD free subjects who experienced 42 events over the 10-year follow-up period. Probabilities were split in to deciles. Expected and observed events were compared and demonstrated poor prediction. Risk factors previously found to be associated with CHD in T1D other than those in the Framingham risk function (age, smoking, cholesterol/HDLc, systolic blood pressure) were compared within the highest risk deciles. In men, elevated fibrinogen (p=0.007), white blood cell count (WBC) (p=0.037), albumin excretion rate (AER) (p=0.0001), and lower HDLc (p=0.048) were predictive. In females, higher Beck Depression Inventory (p=0.008), HbA1 (p=0.008), AER (p=0.01), LDLc (p=0.007), fibrinogen (p=0.006), WBC (p=0.005), non-HDLc (p=0.0005), WHR (p=0.003), and estimated glucose disposal rate (p=0.002) were associated. Risk factors not considered by the Framingham risk equation may account for the lack of fit and should be examined further.
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PMID:Cardiovascular disease risk prediction in type 1 diabetes: accounting for the differences. 1746 46

Diabetes mellitus as well as psychiatric disorders are common. These may occur with one another and/or one may worsen the other. Psychological stress may follow screening for diabetes, as well as when diabetes is first identified. Acting through the hypothalamo-pituitary-adrenal axis, stress may initiate or worsen hyperglycaemia. Depression may be a risk factor for the development of diabetes; it also commonly occurs in subjects with diabetes. Identification and management are both important in preventing the disability. A variety of antipsychotic medications, especially the newer agents can induce weight gain, dyslipidaemia, insulin resistance and diabetes. Therefore in choosing a drug, one must consider the risk factors and screen for metabolic syndrome. Subjects with type 1 diabetes can have cognitive dysfunction, eating disorders and developmental disturbances. Physicians caring for people with diabetes must be trained to recognize and manage co-morbid psychiatric conditions that commonly occur. A biopsychosocial disease model for both conditions can leverage the social strengths and medical knowledge in developing countries.
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PMID:Psychiatric co-morbidity & diabetes. 1749 58

This study investigated the prevalence of mothers' anxiety, depression, and posttraumatic stress disorder (PTSD) symptoms triggered by their child's type 1 diabetes and identified individual diabetes-related traumatic stressors. Sixty mothers of children who had been diagnosed with diabetes within the past 5 years were interviewed using the Structured Clinical Interview (SCID) DSM-IV-PTSD module, and completed the Posttraumatic Stress Diagnostic Scale (PDS) and the Hospital Anxiety and Depression Scale (HADS). Fifteen percent of participants met criteria for partial and 10% for full PTSD. Fifty-five percent of participants identified hearing about their child's diagnosis as the traumatic stressor. Forty percent of participants reported moderate to severe symptoms of state-anxiety and 17% moderate to severe symptoms of depression. This study highlights the significant emotional impact this diagnosis in children can have on mothers, and identifies a population with clinical needs.
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PMID:Anxiety, depressive, and posttraumatic stress symptoms in mothers of children with type 1 diabetes. 1795 36


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