A presença de depressão no paciente com diabetes mellitus (DM) parece relacionar-se a alterações no curso clínico da doença. O objetivo deste trabalho é realizar uma revisão sistemática sobre a associação entre o DM e depressão. Foi realizada uma pesquisa bibliográfica utilizando as bases de dados MEDLINE e LILACS para identificar artigos relevantes, publicados entre 1990 e 2001, que avaliassem esta associação. Foram analisadas informações referentes à prevalência, ao impacto e ao tratamento da depressão no DM. A prevalência de depressão no DM variou de 0 a 60,5%. Sintomas depressivos relacionaram-se a um pior controle glicêmico, a um aumento e a uma maior gravidade das complicações clínicas, a uma piora da qualidade de vida e ao comprometimento de aspectos sociais, econômicos e educacionais ligados ao DM. O tratamento da depressão está relacionado à melhora dos níveis glicêmicos, podendo contribuir para um melhor controle de diversos aspectos relacionados ao DM. The presence of depression in a patient with diabetes mellitus (DM) seems to be related to changes in the clinical course of the disease. The purpose of this study is to perform a systematic review on the association of DM and depression. A bibliographic search was performed using the MEDLINE and LILACS databases to identify relevant articles, published from 1990 to 2001, which evaluate this relationship. Information concerning prevalence, impact and treatment of depression in DM were analyzed. The prevalence of depression varied from 0 to 60.5%. The presence of depressive symptoms were associated with a poor glycemic control, an increase in the number and severity of clinical complications, a worse quality of life and impairment of social, educational and economic aspects related to DM. The treatment of depression is associated with an improvement in glycemic levels, which may contribute to a better control of several aspects related to DM. (Arq Bras Endocrinol Metab 2003;47/1:19-29)
AIMTo evaluate the impact of genetic polymorphisms in uridine 5′-glucuronosylytansferases UGT1A1 and UGT1A3 and iodothyronine-deiodinases types 1 and 2 on levothyroxine (T4; 3,5,3′,5′-triiodo-L-thyronine) dose requirement for suppression of thyrotropin (TSH) secretion in patients with differentiated thyroid cancer (DTC). METHODSPatients (n = 268) submitted to total thyroidectomy and ablation by 131 I, under T4 therapy for at least 6 months were recruited in three public institutions in Brazil. Multivariate regression modelling was applied to assess the association of T4 dosing with polymorphisms in UGT1A1 (rs8175347), UGT1A3 (rs3806596 and rs1983023), DIO1 (rs11206244 and rs2235544) and DIO2 (rs225014 and rs12885300), demographic and clinical variables. RESULTSA regression model including UGT1A haplotypes, age, gender, body weight and serum TSH concentration accounted for 39% of the inter-individual variation in the T4 dosage. The association of T4 dose with UGT1A haplotype is attributed to reduced UGT1A1 expression and T4 glucuronidation in liver of carriers of low expression UGT1A1 rs8175347 alleles. The DIO1 and DIO2 genotypes had no influence of T4 dosage. CONCLUSIONUGT1A haplotypes associate with T4 dosage in DTC patients, but the effect accounts for only 2% of the total variability and recommendation of pre-emptive UGT1A genotyping is not warranted. WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT• Inter-individual variation in L-thyroxine (T4) doses required for suppression of thyrotropin (TSH) in patients with differentiated thyroid cancer (DTC) is considerable and multifactorial. Age, gender and body weight explain part of this variability.• To exert its inhibitory control of TSH secretion, T4 must be deiodinated to T3 (3,5,3′-triiodo-L-thyronine) by iodothyronine-deiodinases types 1 (D1) and 2 (D2). Genetic polymorphisms in D1 and D2 have been associated with circulating levels of T3 and T4 and/or TSH, with controversial results. • T4 is metabolized in human liver by UDP-glucuronyltransferases, especially UGT1A1 and UGT1A3 and readily excreted into bile as thyroxine glucuronide. A common polymorphism in UGT1A1 (-53(TA)n, rs8175347) has been associated with the T4 dose required for TSH suppression in DTC patients. WHAT THIS STUDY ADDS• Multivariate regression modelling was applied to assess the association of T4 dosing in 268 Brazilian DTC patients with polymorphisms in DIO1 (rs11206244 and rs2235544), DIO2 (rs225014 and rs12885300), UGT1A1 (rs8175347) and UGT1A3 (rs3806596 and rs1983023), in addition to demographic and clinical variables. • A regression model including UGT1A haplotypes, age, gender, body weight and serum TSH concentration accounted for 39% of the inter-individual variation in the T4 dosage. The association of T4 dose with UGT1A haplotype is attributed to reduced UGT1A1 expression and T4 glucuronidation in liver of carriers of low expression UGT1A1 rs8175347 alleles. The DIO1 and DIO2 genotypes had no influence of T4 dosage.• UGT1A haplotypes associate with T4 dosage in DTC patients, but the ef...
Para avaliar a utilidade dos fitoestrogênios (FE) na terapia de reposição hormonal da menopausa (TRHM), o Departamento de Endocrinologia Feminina da SBEM reuniu um grupo de especialistas para fazer uma revisão bibliográfica e selecionar trabalhos nos quais a metodologia adotada demonstrasse rigor científico. Os FE têm ações estrogênicas e antiestrogênicas, predominantemente sobre os receptores de estrogênios (E) beta, com potência estrogênica muito inferior à do estradiol. O conteúdo de FE nas suas fontes vegetais é variável, dependendo da forma de cultivo, safra, armazenamento e industrialização. Também a conversão dos precursores em fitormônios ativos no organismo humano tem grande variabilidade individual. A maior parte das pesquisas com FE é realizada in vitro ou com animais de laboratório, nem sempre podendo ser extrapoladas para humanos. Com relação à síndrome do climatério, alguns estudos sugerem discreta melhora dos fogachos, sem modificação do ressecamento vaginal ou das alterações do humor. No metabolismo lipídico, alimentação rica em soja, mas não isoflavonas isoladamente, promove redução do colesterol total, do LDL-col e dos triglicerídeos, mas não elevam o HDL-col, como os E, e podem causar aumento da lipoproteína (a), que os E contribuem para diminuir. Embora alguns estudos de curta duração sugiram aumento da densidade mineral óssea com uso de isoflavonas, não há demonstração de redução de fraturas. Conclui-se que não há evidências convincentes que justifiquem o uso de FE ou alimentação rica em soja como alternativa para a TRHM.
The hypothalamic-pituitary-adrenal (HPA) axis seems to play an important role in obesity and Type 2 diabetes (DM). The aim of the present study was to determine the adrenal volume in obese patients with DM in comparison to obese non-diabetic patients. Eleven diabetic obese and 19 non-diabetic obese women were sequentially invited to take part in the study. Computed tomography (CT) scan of the abdomen was performed to determine adrenal volume, visceral (VF) and sc fat (SCF). Daily urinary free cortisol (UFC) was used as a measure of integrated cortisol production. In the diabetic patients, hemoglobin A1c was measured as an index of metabolic control. Compared to nondiabetic controls, patients with diabetes had a significantly higher total adrenal volume (4.29+/-1.50 vs 2.95+/-1.64; p=0.03). A highly significant correlation was detected between VF and VF/SCF ratio and total adrenal volume in the whole group (r=0.36, p=0.04 and r=0.48, p=0.008, respectively). This study, therefore, suggests an association between abdominal obesity, enlarged adrenals and Type 2 diabetes. These findings support the hypothesis that an increased activity of the HPA axis in obese subjects may be involved in the pathogenesis of Type 2 diabetes.
RESUMOA incidência de doença cardiovascular aumenta consideravelmente após a menopausa. Um dos motivos para o crescente risco cardiovascular parece ser determinado pela síndrome metabólica, da qual todos os componentes (obesidade visceral, dislipidemia, hipertensão arterial e distúrbio do metabolismo glicídico) se associam à maior incidência de coronariopatia. Após a menopausa, a sín-drome metabólica é mais prevalente do que na pré-menopausa, podendo ter importante papel na ocorrência de infarto do miocárdio e outras morbidades ateroscleróticas e cardiovasculares. A obesidade, componente primordial da síndrome metabólica, se associa ainda ao aumento da incidência de câncer de mama, endométrio, intestino, esôfago e rim. O tratamento da síndrome metabólica se baseia na mudança de hábitos de vida e, quando necessário, no emprego de medicação dirigida aos seus componentes. Na presença de sintomas de síndrome do climatério, a terapia hormonal, quando indicada, concorrerá também para a melhora da síndrome metabólica. Arq Bras Endocrinol Metab. 2014;58(2):91-6Descritores Menopausa; síndrome metabólica; terapia hormonal da menopausa; resistência insulínica; estrogênios ABSTRACTThe incidence of cardiovascular disease increases considerably after the menopause. One reason for the increased cardiovascular risk seems to be determined by metabolic syndrome, in which all components (visceral obesity, dyslipidemia, hypertension, and glucose metabolism disorder) are associated with higher incidence of coronary artery disease. After menopause, metabolic syndrome is more prevalent than in premenopausal women, and may plays an important role in the occurrence of myocardial infarction and other atherosclerotic and cardiovascular morbidities. Obesity, an essential component of the metabolic syndrome, is also associated with increased incidence of breast, endometrial, bowel, esophagus, and kidney cancer. The treatment of metabolic syndrome is based on the change in lifestyle and, when necessary, the use of medication directed to its components. In the presence of symptoms of the climacteric syndrome, hormonal therapy, when indicated, will also contribute to the improvement of the metabolic syndrome. Arq Bras Endocrinol Metab. 2014;58 (2) INTRODUÇÃO A s doenças cardiovasculares são a maior causa de mortalidade em ambos os sexos e sua incidência em mulheres no menacme é menor do que nos homens de mesma idade, diminuindo progressivamente essa diferença com o envelhecimento e o advento da menopausa (1). Considerando-se apenas o sexo feminino, o estudo de Framingham mostrou que a incidência anual de doença cardiovascular em mulheres com menos de 55 anos na pré-menopausa, quando comparada à de mulheres, na mesma faixa etária, nas quais já ocorrera a menopausa, foi cerca de 50% menor (2). A falência ovariana parece, portanto, ser um divisor de águas, em termos de risco cardiovascular.Um dos fatores que aumentam o risco de mortalidade, em homens e mulheres, é a síndrome metabólica. A Third National Health and Nutrition Examination Survey (NH...
It has already been demonstrated that insulin resistance (IR) is associated with the stimulation of erythroid progenitors and with increased levels of inflammation markers. Therefore, IR should also be associated with increased red blood cell (RBC) and white blood cell (WBC) count. The aim of this study is to demonstrate that IR is independently associated with altered hematological parameters in a Brazilian sample. We analyzed laboratorial exams from 925 subjects. All data on hematological parameters, insulin resistance (Homeostasis Model Assessment [HOMA]) and lipid levels were included in the analysis. Demographic information included age and gender. HOMA correlated positively with RBC (r= 0.17, p< 0.001), plasma hemoglobin concentrations (r= 0.14, p< 0.001), hematocrit value (r= 0.15, p< 0.001) and WBC (r= 0.17, p< 0.01). Subjects in the upper quartile of IR had higher levels of plasma glucose, fasting insulin, triglycerides, hematocrit, hemoglobin, RBC and WBC count than those in the lower quartile. In conclusion, IR seems to be associated with alterations in several hematological parameters. These hematological alterations may be considered an indirect feature of the IR syndrome. Já foi demonstrado que a resistência à insulina (RI) está associada com a estimulação de progenitores eritrocitários e com níveis aumentados de marcadores inflamatórios. Desta maneira, a RI pode também estar associada o aumento de hemácias e leucócitos. Esse estudo objetivou demonstrar que a RI está independentemente associada com a alteração de parâmetros hematológicos em uma amostra da população brasileira. Nós analisamos exames laboratoriais de 925 indivíduos, incluindo todos os dados de parâmetros hematológicos, resistência insulínica (homeostasis model assessment -HOMA) e níveis lipídicos. Informação demográfica incluiu idade e gênero. HOMA correlacionou-se positivamente com a contagem de eritrócitos (r= 0,17; p<0,001), a concentração de hemoglobina (r= 0,14; p<0,001), o hematócrito (r= 0,15; p<0,001) e a contagem de leucócitos (r= 0,17; p<0,01). Indivíduos no quartil superior de RI tinham níveis mais elevados de glicemia, insulina de jejum, triglicérides, hematócrito, hemoglobina e contagem de leucóci-tos e eritrócitos do que aqueles no quartil inferior. Em conclusão: a RI parece estar associada com alterações em diversos parâmetros hematológicos. Essa alterações hematológicas podem ser consideradas um achado indireto da síndrome de resistência insulínica.
OCT is a new method that can help the evaluation of ME in diabetic patients. It can be used not only to diagnose the lesion, but also to follow up the patients during treatment. High levels of haemoglobin A1c might be associated with the presence of ME. Diabetic complications (nephropathy and neuropathy) are associated with retinopathy but not with macular edema.
There is a considerable interindividual variation in L-thyroxine [3,5,3',5'-tetraiodo-l-thyronine (T4)] dose required for thyrotropin (thyroid-stimulating hormone) suppression in patients with differentiated thyroid cancer. To investigate whether uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)-mediated T4 glucuronidation in liver affects T4 dose, we genotyped 101 patients for the common UGT1A1-53(TA)n polymorphism and compared T4 doses among patients having zero (5/6 and 6/6 genotypes), one (6/7 genotype), or two (7/7 and 7/8 genotypes) copies of the low-expression (TA)7 and (TA)8 alleles. A significant trend for decreasing T4 dose with increasing number of copies of (TA)7 and (TA)8 (P=0.037) and significant difference in T4 dose across the UGT1A1-53(TA)n genotypes (P=0.048) were observed, despite considerable overlap of T4 doses among different genotypes. These results are consistent with reduced T4 glucuronidation in patients with low-expression (TA)7 and (TA)8 alleles and provide the first evidence for association between UGT1A1-53(TA)n and T4-dose requirement for thyroid-stimulating hormone suppression in a natural clinical setting.
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