ABSTRACT
El artículo tiene como objetivo describir las características de la psicoterapia psicoanalítica focalizada aplicada a niños sin cuidados parentales, atendidos en un Servicio de Psicología Clínica de Niños dependiente de la Universidad de Buenos Aires. Se presentan viñetas de un estudio de caso y se formulan observaciones sobre cuestiones teóricas y técnicas referidas a la determinación del foco terapéutico y los nudos conflictivos del paciente, al valor del encuadre del proceso psicoterapéutico y a la consideración de los vínculos transferenciales y contratransferenciales en el contenido de las intervenciones del psicoterapeuta
The objective of this article is to describe the characteristics of focused psychoanalytic psychotherapy applied to children who lack parental care, assisted in a Children Clinical Psychology Service of the University of Buenos Aires. Case study vignettes are presented and observations are made on theoretical and technical questions related to the determination of the therapeutic focus and the patient's conflicts, to the value of the framing of the psychotherapeutic process and the consideration of the transferential and countertransferential links in the content of the interventions of the psychotherapist
L'objectiu de l'article és descriure les característiques de la psicoteràpia psicoanalítica focalitzada aplicada a nens sense cures parentals, atesos en un Servei de Psicologia Clínica de Nens dependent de la Universitat de Buenos Aires. Es presenten vinyetes d'un estudi de cas i es formulen observacions sobre qüestions teóriques i técniques referides a la determinació del focus terapéutic i a la consideració dels vincles transferencials i contratransferencials en el contingut de les intervencions del psicoterapeuta
Subject(s)
Humans , Female , Child , Male , Psychotherapy/methods , Psychosocial Support Systems , Child Protective Services , Child, Orphaned/psychology , ArgentinaABSTRACT
Women with gestational diabetes (GDM) are a high risk group for early type 2 diabetes (T2D). Depression is a risk factor for T2D in the general population. We investigated in women after a recent pregnancy with GDM and without a clinical diagnosis of depression, whether mild to moderate depressive symptoms associate with pathologic glucose metabolism. In a cross-sectional analysis, we examined 173 women, 9 ± 3 months after delivery with several psychopathological assessments, 5-point oral glucose tolerance test with insulin, anthropometrics, and laboratory chemistry. In a subgroup of 101 women, abdominal visceral fat was quantified by magnetic resonance imaging (MRI). A total of 22 women (13%) showed mild to moderate depressive symptoms, and the proportion of women with pathologic glucose metabolism (impaired fasting glucose, impaired glucose tolerance, or T2D) was higher in this group than in the women without depressive symptoms (59.1% vs. 33.1%, p = 0.018). Women with depressive symptoms also had higher body mass index (BMI), systolic blood pressure, plasma leptin, plasma resistin, and abdominal visceral fat volume. Pathologic glucose metabolism (OR = 2.594, 95% CI: 1.021-6.592), systolic blood pressure (OR = 1.076, 95% CI: 1.027-1.128), and abdominal visceral fat volume (OR = 2.491, 95% CI: 1.142-5.433) remained, even after adjustment for BMI, associated with the presence of depressive symptoms. Taken together, we found depressive symptoms at a level not generally diagnosed in clinical practice in a subgroup of women with recent GDM. This subgroup also showed an unfavorable metabolic profile. Mild to moderate depressive symptoms may therefore help to identify this special subgroup.
Subject(s)
Blood Pressure/physiology , Depression/metabolism , Depression/physiopathology , Diabetes, Gestational/metabolism , Glucose Intolerance/metabolism , Intra-Abdominal Fat/metabolism , Adult , Biomarkers/metabolism , Cross-Sectional Studies , Depression/blood , Female , Glucose Intolerance/blood , Glucose Tolerance Test , Humans , Leptin/blood , Pregnancy , Resistin/bloodABSTRACT
AIMS/HYPOTHESIS: Low physical fitness (PF) is a risk factor for type 2 diabetes mellitus (T2D). Women with a history of gestational diabetes (GDM) are at risk for T2D at a young age, but the role of PF in this population is not clear. PF has also been found to correlate inversely with plasma leptin in previous studies. Here, we examine whether women who had GDM have lower PF than women after a normoglycemic pregnancy and, second, whether PF is associated with plasma leptin, independently of body fat mass. METHODS: Cross-sectional analysis of 236 participants in the PPSDiab Study (cohort study of women 3-16 months after delivery, 152 after gestational diabetes (pGDM), 84 after normoglycemic pregnancy (control subjects); consecutively recruited 2011-16); medical history, physical examination with bioelectrical impedance analysis (BIA), whole body magnetic resonance imaging (MRI) (n = 154), 5-point oral glucose tolerance test, cardiopulmonary exercise testing, clinical chemistry including fasting plasma leptin; statistical analysis with Mann-Whitney U and t -test, Spearman correlation coefficient, multiple linear regression. RESULTS: Women pGDM had lower maximally achieved oxygen uptake (VO2peak/kg: 25.7(21.3-29.9) vs. 30.0(26.6-34.1)ml/min/kg; total VO2peak: 1733(1552-2005) vs. 1970(1767-2238)ml/min; p<0.0001 for both), and maximum workload (122.5(105.5-136.5) vs. 141.0(128.5-159.5)W; p<0.0001). Fasting plasma leptin correlated inversely with PF (VO2peak/kg ρ = -0.72 p<0.0001; VO2peak ρ = -0.16 p = 0.015; max. load ρ = -0.35 p<0.0001). These associations remained significant with adjustment for body mass index, or for body fat mass (BIA and MRI). CONCLUSIONS/INTERPRETATION: Women with a recent history of GDM were less fit than control subjects. Low PF may therefore contribute to the risk for T2D after GDM. This should be tested in intervention studies. Low PF also associated with increased leptin levels-independently of body fat. PF may therefore influence leptin levels and signaling. This hypothesis requires further investigation.
Subject(s)
Diabetes, Gestational/blood , Diabetes, Gestational/physiopathology , Leptin/blood , Physical Fitness/physiology , Adult , Blood Glucose/metabolism , Body Mass Index , Cross-Sectional Studies , Diabetes Mellitus, Type 2/blood , Female , Glucose Tolerance Test , Humans , Linear Models , Oxygen Consumption , Pregnancy , Prospective Studies , Risk FactorsABSTRACT
We analyzed the association of sleep quality and glucose metabolism in women after gestational diabetes (pGDM) and in women after normoglycemic pregnancy (controls). Data during pregnancy and a visit within the first 15 months after delivery were collected from 61 pGDM and 30 controls in a prospective cohort study. This included a medical history, physical examination, questionnaires (Pittsburgh Sleep Quality Index (PSQI), and Perceived Stress Scale (PSS)), and 5-point oral glucose tolerance test with insulin measurements to determine indices of insulin sensitivity and insulin secretion. We used Spearman correlation coefficients and multivariate regression models for analysis.9.3 ± 3.2 months after delivery, pGDM had significantly higher fasting and 2 h glucose levels and lower insulin sensitivity than controls. There was no significant difference in age, BMI and sleep quality as assessed with the PSQI between the two groups. The PSQI score correlated with the ogtt-2 h plasma glucose in pGDM (δ = 0.41; p = 0.0012), but not in controls. This association was confirmed with a multivariate linear regression model with adjustment for age, BMI and months post-delivery. Perceived stress was an independent risk factor (OR 1.12; 95% CI 1.02-1.23) for impaired sleep. Our findings suggest that post-delivery sleep quality significantly influences glucose tolerance in women after GDM and that impaired sleep is associated with increased stress perception. Measures to improve of sleep quality and reduce perceived stress should therefore be tested as additional strategies to prevent progression to type 2 diabetes after GDM.
Subject(s)
Blood Glucose/metabolism , Diabetes Complications/complications , Diabetes, Gestational/physiopathology , Sleep Wake Disorders/etiology , Adult , Female , Glucose Tolerance Test , Humans , Pregnancy , Risk Factors , Surveys and QuestionnairesABSTRACT
BACKGROUND: Pubertal gynecomastia is a common problem occurring in up to 65% of adolescent boys. Gynecomastia comes at a time when self-image awareness is at its greatest and psychologically could be a psychologically disabling condition. Surgery is considered the mainstay of treatment for severe or persistent cases. A medical management aimed at altering the effective androgen/estrogen ratio has been suggested with inconstant results. Some promising results have been obtained by using anti-estrogens. Surprisingly there are no data on the estrogen receptor (ER) α and ß RNA expression in gynecomastia. AIM: We studied ER RNA subtypes in pubertal gynecomastia. METHODS: ERα and ß RNA were determined by real time RT-PCR in 50 mammary samples from pubertal boys with idiopathic gynecomastia subjected to reductive mammoplasty. To study ERα and ß pattern of expression, epithelial and stromal primary cell cultures were set up from fresh tissues. RESULTS: These analyses indicated that in all stromal cells ERß was expressed at higher level than ERα and in epithelial cells both ERα and ERß were barely detectable. CONCLUSIONS: Our data suggest that also stromal cells are involved in the pathophysiology of pubertal gynecomastia. The high level of expression of ERß seen in pubertal gynecomastia adds new insight on validation of ERß as a target for candidate diseases and exploration of ERß as a marker for clinical decision-making and treatment in pubertal gynecomastia. This could drive to search for new and selective anti-estrogen drugs for medical treatment of pubertal gynecomastia with a particular attention to the ERß-selective ligand.
Subject(s)
Estrogen Receptor alpha/genetics , Estrogen Receptor beta/genetics , Gynecomastia/genetics , Puberty , Adolescent , Cells, Cultured , Child , Estrogen Receptor alpha/metabolism , Estrogen Receptor beta/metabolism , Gene Expression Regulation , Gynecomastia/metabolism , Gynecomastia/pathology , Humans , Male , Primary Cell Culture , Puberty/genetics , Puberty/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolism , Stromal Cells/metabolism , Stromal Cells/pathology , Tissue DistributionSubject(s)
Adaptation, Psychological , Crime/legislation & jurisprudence , Adult , Aged , Canada , Humans , Middle AgedABSTRACT
BACKGROUND: The management of type I diabetes mellitus requires a careful balance between nutrient intake, energy expenditure and dose and timing of insulin. According to the recommendations of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) the calories should be prescribed according to energy needs to achieve and maintain a desirable body weight. Many studies have shown that diets in which carbohydrates provide 50-60% of total energy are associated with improved blood glucose control and lower levels of LDL cholesterol. Whenever acceptable to the patients, natural foods containing unrefined carbohydrate should be substituted for the highly refined carbohydrates that are low in fiber. The high risk of macrovascular disease in patients with diabetes dictates a need to restrict total fat (25-30% of total energy) and cholesterol intake (300 mg/day). ADA and EASD suggest that reduction of protein intake (0.8 g/kg/day) may reduce proteinuria and progression to renal failure during the earliest stages of diabetic nephropathy. METHODS: The goal of this study was to describe macronutrient intakes in type I diabetic patients of our Centre by a validated 3 day record. RESULTS: Mean energy intake was 2022+/-427 Kcal/die (vs 2596+/-501 recommended intake). Average protein intake was well above the level of 0.8 g/kg/day required to ensure an adequate protein intake in type I diabetes mellitus. Total fats contributed 29.8+/-7.4 of total energy (vs 27% recommended intake) and saturated fat provided significantly more than 10% of energy. Carbohydrates intake was above 50% of total energy but fiber intakes was substantially lower than the recommendation (12.7+/-5.5 vs 20.1+/-6.6 g/day). CONCLUSIONS: These data indicate current problems in the nutritional intake of type I diabetes mellitus; in fact the majority of our group of patients are not meeting the recommended dietary intakes for protein, total fat, saturated fat and fiber.
ABSTRACT
The use of GH treatment in subjects with a GH deficiency has led to contrasting results concerning its impact to develop thyroid hyperfunction, whereas many others have underlined the possible onset of hypothyroidism. A number of studies have been carried out over short periods in subjects with multiple tropin deficiencies, in healthy adults or adults with GH deficiencies, in healthy adults or adults with GH deficiencies. The aim of the present study was to assess the effect of prolonged treatment with biosynthetic GH on thyroid function in children with an isolated idiopathic GH deficiency. The study included 8 children (mean age 10.4 +/- 0.8 years) with GH deficiencies treated with biosynthetic GH and 8 children with familial retarded stature of a similar age (mean age 10.3 +/- 0.7 years) who represented the control group. Serum levels of T3, T4, FT3, FT4 and TSH were measured at the start of the study and after one year of continuous GH treatment in subjects with GH deficiency; the same tests were performed in the control group on recruitment and after one year's observation without therapy. T4 and FT4 levels diminished, but not significantly, whereas there was a significant increase in plasma levels of T3 and FT3 (p less than 0.01); TSH values were significantly reduced in the treated group (p = 0.025). No significant variations in thyroid parameters were found in the control group. These data support the hypothesis of an increased peripheral conversion of T4 into T3 due to GH therapy; in conclusion, however, no significant variation in thyroid function was observed following GH replacement therapy, even if prolonged, in subjects with an idiopathic isolated GH deficiency.