OBJETIVO: Identificar fatores associados a alterações do teste oral de tolerância à glicose (TOTG), independentemente da glicemia de jejum (GJ). SUJEITOS E MÉTODOS: 377 pacientes (53,8 ± 15,2 anos; 77,7% mulheres e IMC = 31,4 ± 5,9 kg/m²), sem história de diabetes melito (DM), foram submetidos ao TOTG e comparados de acordo com o resultado: normal (NGT), intolerantes (IGT) e DM. RESULTADOS: 202 pacientes (53,6%) apresentaram TOTG alterado, sendo identificados 69 com DM (18,3%) e 133 com IGT (35,3%). Na análise multivariada, os fatores, além da GJ, que se associaram (P < 0,05) ao TOTG alterado foram: idade (DM = 58,7 ± 12,9; IGT = 56,7 ± 14,3; NGT = 49,6 ± 15,6 anos), hipertensão arterial (DM = 69,6%; IGT = 63,9%; NGT = 43,4%), GJ (DM = 111,9 ± 9,2; IGT = 103,5 ± 10,3; NGT = 96,6 ± 11,1 mg/dL), HbA1C (DM = 6,1 ± 0,7%; IGT = 6,1 ± 0,5%; NGT = 5,8 ± 0,4%), triglicérides (DM = 179,3 ± 169,9; IGT = 154,2 ± 84,1; NGT = 129,1 ± 71,9 mg/dL), HDL-c (DM = 44,7 ± 9,2; IGT = 47,5 ± 12,3; NGT = 50,6 ± 13,4 mg/dL) e ácido úrico em mulheres (DM = 5,3 ± 1,5; IGT = 5,3 ± 1,3; NGT = 4,7 ± 1,3 mg/dL). CONCLUSÃO: Idade, hipertensão arterial, níveis elevados de triglicérides, de HbA1C e de ácido úrico (em mulheres) e baixos níveis de HDL-c se associam a alterações do TOTG em pacientes com sobrepeso/obesidade, independentemente da GJ.

OBJECTIVE: To identify factors associated with changes in oral glucose tolerance test (OGTT), regardless of fasting glucose (FG). SUBJECTS AND METHODS: 377 patients (53.8 ± 15.2 years, 77.7% women and BMI = 31.4 ± 5.9 kg/m²) with no history of diabetes mellitus(DM), underwent OGTT and compared according to the results: normal (NGT), impaired (IGT) and DM. RESULTS: 202 patients (53.6%) had altered glucose tolerance: 69 with DM (18.3%) and 133 with IGT (35.3%). In multivariate analysis, factors regardless of FG that were associated (P < 0.05) with changes in the OGTT were age (DM = 58.7 ± 12.9; IGT = 56.7 ± 14.3; NGT = 49.6 ± 15.6 years), hypertension (DM = 69.6%; IGT = 63.9%; NGT = 43.4%), FG (DM = 111.9 ± 9.2; IGT = 103.5 ± 10.3; NGT = 96.6 ± 11.1 mg/dL), HbA1C (DM = 6.1 ± 0.7%; IGT = 6.1 ± 0.5%; NGT = 5.8 ± 0.4%), triglycerides (DM = 179.3 ± 169.9; IGT = 154.2 ± 84.1; NGT = 129.1 ± 71.9 mg/dL), HDL-c (DM =44.7 ± 9.2; IGT = 47.5 ± 12.3; NGT = 50.6 ± 13.4 mg/dL) and uric acid in women (DM = 5.3 ± 1.5; IGT = 5.3 ± 1.3; NGT = 4.7 ± 1.3 mg/dL). CONCLUSION: Age, hypertension, elevated triglycerides, HbA1C, uric acid (in women) and low HDL-C are associated with changes in the OGTT patients with overweight / obesity, irrespective of FG.

INTRODUÇÃO: Pesquisa de corpo inteiro após dose terapêutica de (131I) NaI (PCI) associada à tireoglobulina (Tg) sérica, anticorpo antitireoglobulina (anti-Tg) e ultrassom (US) cervical representam os métodos de referência para detecção de carcinoma diferenciado de tireoide (CDT) residual ou metastático. Algumas causas de PCI falsos-positivas, como processos inflamatórios, alguns tumores não tireoidianos e até mesmo cistos renais e sebáceos, são bem conhecidas. MÉTODOS: Neste trabalho, descreveu-se um caso de cisto hepático benigno simulando metástase de carcinoma de tireoide em PCI após dose terapêutica de (131I) NaI. RESULTADOS: Ressalta-se a importância do reconhecimento dos cistos hepáticos benignos como fator complicador do seguimento dos pacientes com câncer de tireoide. CONCLUSÕES: Para minimizar erros de diagnóstico e, consequentemente, na condução dos casos de CDT, é necessário conhecer as possíveis causas de PCI falsos-negativas e positivas.

INTRODUCTION: The follow-up of differentiated thyroid carcinoma (DTC) for detecting persistent or recurrent disease is based on iodine whole body scan (WBS), the evaluation of the tumor marker thyroglobulin (Tg), the anti-thyroglobulin antibody (anti-Tg) and neck ultrasonography (US). Well known false-positive causes of WBS include inflammatory processes, some non-thyroid tumors, kidney or even sebaceous cysts . METHODS: We reported a case of false-positive WBS, after therapeutic dose of (131I) NaI. RESULTS: We enphasize the importance of recognizing benign liver cysts mimicking DTC metastasis. CONCLUSIONS: False-positive and negative results may occur with WBS and must be recognized to avoid mismanagement.

OBJECTIVES: To assess the results of growth hormone on the growth of girls with Turner Syndrome and identify relevant parameters to improve outcomes. METHODS: Growth velocity and final height were studied in a historical cohort of 41 girls, regularly followed up for hormone distribution at three referral centers. The influence of oxandrolone and of estrogens on the final height was analyzed. The girls (initial chronological age=8.9±3.4years; initial bone age=7.0±3.1years) used 0.19 mg/kg/week of growth hormone for 4.0 ± 2.0 years. RESULTS: In the first year, growth velocity increased by 71.5% in 41 girls and 103.4% in those who reached final height (11 girls). The whole group had a gain in the height SDS of 0.8 ± 0.7 (p<0.01) and for those who reached a final height of 1.0 ± 0.8 (p<0.01). Final height (143.6 ±6.3 cm) was 3.9 ± 5.3 cm higher than the predicted height, and the height gain occurred before estrogen therapy. Oxandrolone had no significant influence on height gain. The significant variables contributing to the final height were the duration of growth hormone used and its use prior to starting estrogens, the initial height SDS, and the growth velocity during the first year of treatment. CONCLUSIONS: We concluded that the use of growth hormone significantly increased the final height, which remained lower than the target. Results point to a need for starting growth hormone use as early as possible and to maximize treatment before estrogen replacement. It has been observed that even moderate doses of growth hormone may significantly increase early growth velocity.

Ao contrário da doença de Cushing subclínica, a síndrome de Cushing subclínica de origem adrenal é uma entidade amplamente conhecida. É definida como uma hiperprodução autônoma de cortisol, de leve intensidade, insuficiente para causar sinais clínicos específicos de hipercortisolismo, porém suficiente para levar a alterações bioquímicas detectáveis no eixo hipotálamo-hipófise-adrenal. Apesar de a doença de Cushing representar a grande maioria dos casos de hipercortisolismo, há poucos relatos na literatura sobre doença de Cushing subclínica. Neste trabalho são descritos três casos de doença de Cushing subclínica, causadas por macroadenomas hipofisários corticotróficos, confirmados por estudo imuno-histoquímico, despertando a atenção dos endocrinologistas clínicos para essa entidade e sugerindo que a investigação laboratorial do hipercortisolismo seja incluída em todos os casos de adenomas hipofisários.

Unlike subclinical Cushing’s disease, adrenal subclinical Cushing’s syndrome is widely recognized. It is defined as an autonomous cortisol hyperproduction of mild intensity not causing specific clinical signs, but detectable biochemically as derangements of the hypothalamic-pituitary-adrenal axis function. Although Cushing’s disease accounts for the majority of hypercortisolism states, subclinical Cushing’s disease has been rarely reported. Three cases of subclinical Cushing’s disease due to pituitary corticotrophic macroadenomas, confirmed by immunohistochemistry, are presented in order to underscore its recognition by clinical endocrinologists and to emphasize a diagnostic evaluation of hypercortisolism in all cases of pituitary adenomas.