The incidence of impaired carbohydrate metabolism in the examined group of subjects with risk factors

WSTĘP. Celem niniejszej pracy była ocena częstości zaburzeń gospodarki węglowodanowej w grupie osób z czynnikami ryzyka cukrzycy typu 2. MATERIAŁ I METODY. Badaniem objęto 330 osób, z których do dalszej analizy zakwalifikowano 201 osób [K - 62%, M - 38%, w wieku 58,5 &plusmn; 12,45 roku, ze wskaźnikiem masy ciała (BMI, body mass index) 35,5 &plusmn; 4,59 kg/m2], którzy czują się zdrowi, ale rozpoznano u nich czynniki ryzyka cukrzycy. Badania przeprowadzono w Klinice Endokrynologii i Diabetologii przy współudziale 4 poradni podstawowej opieki zdrowotnej (POZ). W 1. etapie badani wypełniali ankietę, umożliwiającą identyfikację czynników ryzyka cukrzycy oraz dokonywano pomiaru glikemii we krwi włośniczkowej na glukometrze. Wartość glikemii przygodnej wyższa lub równa 6,1 mmol/l była podstawą do dalszych badań - glukozy w osoczu krwi żylnej na czczo (FPG, fasting plasma glucose) lub testu z doustnym obciążeniem glukozy (OGTT, oral glucose tolerance test). WYNIKI. U 70 spośród 201 badanych (35%) wykryto: u 12 nieprawidłową glikemię na czczo (IFG, impaired fasting glucose), u 28 - upośledzoną tolerancję glukozy (IGT, impaired glucose tolerance,), u 30 - cukrzycę (DM, diabetes mellitus). Osoby z IFG, IGT, DM różniły się od osób bez tych zaburzeń (n = 131): wiekiem 64,8 &plusmn; 10,2 vs. 57,0 &plusmn; 12,7 roku (p < 0,001), BMI 30,1 &plusmn; 4,8 vs. 27,4 &plusmn; 4,2 kg/m2 (p < 0,001), liczbą czynników ryzyka 3,8 &plusmn; 1,1 vs. 3,2 &plusmn; 1,5 (p < 0,01), ciśnieniem tętniczym skurczowym 144,1 &plusmn; 22,3 vs. 135,5 &plusmn; 20,0 mm Hg (p < 0,01). W grupie osób z zaburzoną gospodarką węglowodanową stwierdzono częstsze występowanie następujących czynników ryzyka w porównaniu z grupą bez tych zaburzeń (wiek &#8805; 45 rż. - 98,6% vs. 86,2%, BMI > 25 kg/m2 - 84,2% vs. 68,7%, nadciśnienie tętnicze - 68,6% vs. 48%, dyslipidemia - 57,8% vs. 50%, IGT w wywiadzie - 8,9% vs. 7,1%, przebyty incydent sercowo-naczyniowy - 18,8% vs. 14,8). WNIOSKI. W grupie z zaburzoną gospodarką węglowodanową osoby badane były starsze, miały większą masę ciała oraz różniły się istotnie liczbą czynników ryzyka cukrzycy w porównaniu z grupą osób z prawidłową gospodarką węglowodanową. Najczęstszymi czynnikami ryzyka cukrzycy typu 2 u badanych osób, poza wiekiem, były nadwaga, nadciśnienie tętnicze i dyslipidemia.INTRODUCTION. The aim of this study was to evaluate of the incidence of impaired carbohydrate metabolism in the group of subjects with risk factors of type 2 diabetes mellitus (DM). MATERIAL AND METHODS. We studied 330 subjects and 201 of them were required to further investigations. This group consisted of 125 females (62%) and 76 males (38%) (mean age 58.5 &plusmn; 12.45 years, BMI 35.5 &plusmn; 4.59 kg/m2) who felt healthy but had risk factors of DM. The study was conducted in the Department of Endocrinology and Diabetology in cooperation with 4 general practitioners. In the first phase of the study subjects were asked to fill in a questionnaire in order to identify risk factors of DM. Capillary blood glucose was estimated by use of a glucometer. Subjects with incidental blood glucose above 6.1 mmol/l progressed to the second phase of the study - an estimation of FPG and, if required, OGTT. RESULTS. In 70 of 201 examined subjects (35%) we found: in 12 impaired fasting glucose (IFG), in 28 impaired glucose tolerance (IGT), in 30 DM. Subjects with IFG, IGT, DM were different from subjects without impaired carbohydrate metabolism in relation to: age (64.8 &plusmn; 10.2 vs. 57.0 &plusmn; 12.7 years - p < 0.001), BMI (30.1 &plusmn; 4.8 vs. 27.4 &plusmn; 4.2 kg/m2 -p < 0.001), number of risk factors (3.8 &plusmn; 1.1 vs. 3.2 &plusmn; 1.5 - p < 0.01), systolic blood pressure (144.1 &plusmn; 22.3 vs. 135.5 &plusmn; 20 mm Hg - p < 0.01). There was higher incidence of risk factors in the group with impaired carbohydrate metabolism in comparision to the group without abnormalities in carbohydrate metabolism: age &#8805; 45 years - 98.6% vs. 86.2%, BMI > 25 kg/m2 - 84.2% vs. 68.7%, arterial hypertension - 68.6% vs. 48%, dyslipidemia - 57.8% vs. 50%, the history of IGT 8.9% vs. 7.1%, the history of cardiovascular incident 18.8% vs. 14.8%. CONCLUSIONS. Subjects with impaired carbohydrate metabolism were older, had higher weight and more risk factors of DM in comparision to subjects without abnormalities in carbohydrate metabolism. The most frequent risk factors of DM in the examined group were, apart from age, excessive body mass, arterial hypertension and dyslipidemia

The N-terminal pro-brain natriuretic peptide as a marker of mitoxantrone-induced cardiotoxicity in multiple sclerosis patients

Background and purpose Mitoxantrone (MTX) has been shown to reduce progression of disability and number of clinical exacerbations in patients with progressive multiple sclerosis (MS). Prolonged administration of MTX, however, is limited by the risk of cardiotoxicity. Cardiac monitoring in MTX-treated patients includes usually measurement of left ventricular ejection fraction (LVEF) by means of echocardiography. The N-terminal pro-brain natriuretic peptide (NT-proBNP) represents a novel diagnostic tool in the assessment of heart failure. This study was aimed to evaluate the usefulness of NT-proBNP for early detection of MTX-induced cardiotoxicity in MS patients. Materials and methods We measured the NT-proBNP plasma levels in 45 MS patients who completed 24-month MTX therapy and in 37 MS patients of control group. Results The median NT-proBNP plasma value was 15.12pg/mL. In 12 MTX-treated patients (27%), NT-proBNP plasma values were elevated, though this subgroup of patients neither clinical showed evidence of myocardial damage nor had the LVEF value &lt;50%. In five patients with normal NT-proBNP, we observed LVEF decline &gt;10%. We did not observe correlations between the NT-proBNP levels and patient age, MS duration, relapses index, Extended Disability Status Scale (EDSS), MTX single dose and the total cumulative dose of MTX. In 8 patients (22%) from control group, NT-proBNP plasma levels were also elevated. Conclusions The results of our study confirm that MTX therapy is safe for carefully selected and closely monitored MS patients. We believe that serial evaluation of NT-proBNP levels (before, during and after MTX therapy) can identify MS patients at high risk for MTX-induced cardiotoxicity

Personality traits and risk of eating disorders among Polish women: the moderating role of self-esteem

ObjectivesPersonality traits should be taken into account when diagnosing individuals with disordered eating behaviors in the hope of better understanding their etiology and symptom progression and when planning treatment. The objective of this study was to attempt to determine the moderating role of self-esteem in the relationships between personality traits included in the Big Five model among Polish women and estimated risk of eating disorders.MethodsThe study was conducted among 556 Polish women from Zachodniopomorskie Voivodeship. The average age of the women under study was 34 years. A diagnostic survey was used as the research method, and the empirical data were collected using the following research tools: The NEO Five-Factor Inventory (NEO-FFI), Rosenberg Self-Esteem Scale (SES), ORTO – 15 Questionnaire, The Three-Factor Eating Questionnaire (TFEQ-13), and the authors’ original questionnaire. A multivariate linear regression analysis was conducted to examine the influence of selected independent variables. The assumptions for the linear regression model were satisfied, as indicated by the Ramsey Regression Equation Specification Error Test, White’s test, and the Jarque-Bera test.ResultsOnly the personality trait of neuroticism exhibits a statistically significant effect on the “Cognitive Restraint of Eating,” “Uncontrolled Eating,” and “Emotional Eating” scores (p &lt; 0.001). The moderation effect was demonstrated between self-esteem and the personality trait of conscientiousness on the “Cognitive Restraint of Eating” scale score. There is a moderation effect between self-esteem and the personality trait of extraversion on the “Uncontrolled Eating” subscale score. There is a moderation effect between self-esteem and the personality trait of conscientiousness on the “Uncontrolled Eating” scale score.ConclusionSelf-esteem was not a predictor of the occurrence of risk of eating disorders while playing a moderating role in the relationship between certain personality traits and estimated risk of eating disorders. A higher level of neuroticism was identified as an important predictor of higher results for orthorexia, Cognitive Restraint of Eating, Uncontrolled Eating, and Emotional Eating. It was also demonstrated that the orthorexia risk index decreased with increased extraversion and openness to experience. The results of this study suggest that eating behaviors and psychological factors should be included in psychological interventions in the treatment of eating disorders. The clinical goal can be considered to be an improvement in non-normative eating behaviors, such as a reduction in overeating episodes or eating less frequently in the absence of a hunger feeling. In order to assist these individuals in their attempts to achieve healthy behaviors, variables related to mental functioning can be then identified as important goals to support individuals in their efforts to change health behaviors by achieving better mental well-being

Pro Libris: Lubuskie Pismo Literacko-Kulturalne, nr 4 (2008)

172 s. : il

Polish statement on food allergy in children and adolescents

An adverse food reaction is defined as clinical symptoms occurring in children, adolescents or adults after ingestion of a food or chemical food additives. This reaction does not occur in healthy subjects. In certain individuals is a manifestation of the body hypersensitivity, i.e. qualitatively altered response to the consumed food. The disease symptoms observed after ingestion of the food can be triggered by two pathogenetic mechanisms; this allows adverse food reactions to be divided into allergic and non-allergic food hypersensitivity (food intolerance). Food allergy is defined as an abnormal immune response to ingested food (humoral, cellular or mixed). Non-immunological mechanisms (metabolic, pharmacological, microbiological or other) are responsible for clinical symptoms after food ingestion which occur in non-allergic hypersensitivity (food intolerance). Food allergy is considered a serious health problem in modern society. The prevalence of this disorder is varied and depends, among other factors, on the study population, its age, dietary habits, ethnic differences, and the degree of economic development of a given country. It is estimated that food allergy occurs most often among the youngest children (about 6-8% in infancy); the prevalence is lower among adolescents (approximately 3-4%) and adults (about 1-3%). The most common, age-dependent cause of hypersensitivity, expressed as sensitization or allergic disease (food allergy), are food allergens (trophoallergens). These are glycoproteins of animal or plant origine contained in: cow's milk, chicken egg, soybean, cereals, meat and fish, nuts, fruits, vegetables, molluscs, shellfish and other food products. Some of these allergens can cause cross-reactions, occurring as a result of concurrent hypersensitivity to food, inhaled or contact allergens. The development of an allergic process is a consequence of adverse health effects on the human body of different factors: genetic, environmental and supportive. In people predisposed (genetically) to atopy or allergy, the development of food allergy is determined by four allergic-immunological mechanisms, which were classified and described by Gell-Coombs. It is estimated that in approximately 48-50% of patients, allergic symptoms are caused only by type I reaction, the IgEmediated (immediate) mechanism. In the remaining patients, symptoms of food hypersensitivity are the result of other pathogenetic mechanisms, non-IgE mediated (delayed, late) or mixed (IgE mediated, non-IgE mediated). Clinical symptomatology of food allergy varies individually and depends on the type of food induced pathogenetic mechanism responsible for their occurrence. They relate to the organ or system in which the allergic reaction has occurred (the effector organ). Most commonly the symptoms involve many systems (gastrointestinal tract, skin, respiratory system, other organs), and approximately 10% of patients have isolated symptoms. The time of symptoms onset after eating the causative food is varied and determined by the pathogenetic mechanism of the allergic immune reaction (immediate, delayed or late symptoms). In the youngest patients, the main cause of food reactions is allergy to cow’s milk. In developmental age, the clinical picture of food allergy can change, as reflected in the so-called allergic march, which is the result of anatomical and functional maturation of the effector organs, affected by various harmful allergens (ingested, inhaled, contact allergens and allergic cross-reactions). The diagnosis of food allergy is a complex, long-term and time-consuming process, involving analysis of the allergic history (personal and in the family), a thorough evaluation of clinical signs, as well as correctly planned allergic and immune tests. The underlying cause of diagnostic difficulties in food allergy is the lack of a single universal laboratory test to identify both IgE-mediated and non-IgE mediated as well as mixed pathogenetic mechanisms of allergic reactions triggered by harmful food allergens. In food allergy diagnostics is only possible to identify an IgE-mediated allergic process (skin prick tests with food allergens, levels of specific IgE antibodies to food allergens). This allows one to confirm the diagnosis in patients whose symptoms are triggered in this pathogenetic mechanism (about 50% of patients). The method allowing one to conclude on the presence or absence of food hypersensitivity and its cause is a food challenge test (open, blinded, placebo-controlled). The occurrence of clinical symptoms after the administration of food allergen confirms the cause of food allergy (positive test) whereas the time elapsing between the triggering dose ingestion and the occurrence of clinical symptoms indicate the pathogenetic mechanisms of food allergy (immediate, delayed, late). The mainstay of causal treatment is temporary removal of harmful food from the patient’s diet, with the introduction of substitute ingredients with the nutritional value equivalent to the eliminated food. The duration of dietary treatment should be determined individually, and the measures of the effectiveness of the therapeutic elimination diet should include the absence or relief of allergic symptoms as well as normal physical and psychomotor development of the treated child. A variant alternative for dietary treatment of food allergy is specific induction of food tolerance by intended contact of the patient with the native or thermally processed harmful allergen (oral immunotherapy). This method has been used in the treatment of IgE-mediated allergy (to cow's milk protein, egg protein, peanut allergens). The obtained effect of tolerance is usually temporary. In order to avoid unnecessary prolongation of treatment in a child treated with an elimination diet, it is recommended to perform a food challenge test at least once a year. This test allows one to assess the body's current ability to acquire immune or clinical tolerance. A negative result of the test makes it possible to return to a normal diet, whereas a positive test is an indication for continued dietary treatment (persistent food allergy). Approximately 80% of children diagnosed with food allergy in infancy "grow out" of the disease before the age of 4-5 years. In children with non-IgE mediated food allergy the acquisition of food tolerance is faster and occurs in a higher percentage of treated patients compared to children with IgE-mediated food allergy. Pharmacological treatment is a necessary adjunct to dietary treatment in food allergy. It is used to control the rapidly increasing allergic symptoms (temporarily) or to achieve remission and to prevent relapses (long-term treatment). Preventive measures (primary prevention of allergies) are recommended for children born in a "high risk" group for the disease. These are comprehensive measures aimed at preventing sensitization of the body (an appropriate way of feeding the child, avoiding exposure to some allergens and adverse environmental factors). First of all, the infants should be breast-fed during the first 4-6 months of life, and solid foods (non milk products, including those containing gluten) should be introduced no earlier than 4 months of age, but no later than 6 months of age. An elimination diet is not recommended for pregnant women (prevention of intrauterine sensitization of the fetus and unborn child). The merits of introducing an elimination diet in mothers of exclusively breast-fed infants, when the child responds with allergic symptoms to the specific diet of the mother, are disputable. Secondary prevention focuses on preventing the recurrence of already diagnosed allergic disease; tertiary prevention is the fight against organ disability resulting from the chronicity and recurrences of an allergic disease process. Food allergy can adversely affect the physical development and the psycho-emotional condition of a sick child, and significantly interfere with his social contacts with peers. A long-term disease process, recurrence of clinical symptoms, and difficult course of elimination diet therapy are factors that impair the quality of life of a sick child and his family. The economic costs generated by food allergies affect both the patient's family budget (in the household), and the overall financial resources allocated to health care (at the state level). The adverse socio-economic effects of food allergy can be reduced by educational activities in the patient’s environment and dissemination of knowledge about the disease in the society

Argumentacja w edukacji: postulaty badań edukacyjnych w polskiej szkole argumentacji

Uwzględniając dotychczasową działalność Polskiej Szkoły Argumentacji, w szczególności jej działalność edukacyjną wyeksponowaną podczas XV konferencji ArgDiaP, sformułowaliśmy postulaty dotyczące dalszej działalności edukacyjnej Szkoły. Ich realizacja w ciągu najbliższych lat mogłaby stanowić grunt dla długoterminowych celów edukacyjnych, takich jak (1) opracowanie spójnego programu nauczania sztuki argumentowania i krytycznego myślenia w szkołach podstawowych i średnich oraz (2) zaprojektowanie ogólnopolskich standardów i ram nauczania przedmiotów powiązanych z argumentacją i krytycznym myśleniem na poziomie studiów uniwersyteckich