Higher Parametric Thyroid Feedback Quantile-based Index is a predictor of type 2 diabetes in a German population sample.

BACKGROUND: Type 2 diabetes has been described to be associated with hypothyroidism but we recently found that a decrease in pituitary sensitivity to thyroid hormone is associated with diabetes, obesity, and the metabolic syndrome.We aim to assess the longitudinal nature of this association in the population-based Study of Health in Pomerania(SHIP) in Germany. MATERIALS AND METHODS: 77% of a population-based sample of 4308 participants between 20 and 79 years was followed for 5 years. We studied 2542 participants without diabetes or thyroid medication at baseline and complete data in the variables of interest. Data of baseline thyroxine(fT4) and thyrotropin(TSH) were used to calculate the Parametric Thyroid Feedback Quantile-based Index(PTFQI), which measures whether TSH remains elevated despite fT4 being high. It uses the average population response as reference. PTFQI association with incidence of type 2 diabetes over 5 years was estimated with Poisson regression models adjusted for age, sex, and body mass index(BMI). RESULTS: Compared with the 1st PTFQI quartile, Incidence Rate Ratios (IRR) for diabetes were 1.54(95% CI 0.97 to 2.46), 1.55(0.94 to 2.57), and 1.97(1.27 to 3.10) for the upper quartiles (p-trend=0.004) after adjusting for age and sex. The association remained statistically significant after additionally adjusting for BMI: 1.64(1.05 to 2.59) for the 4th vs the 1st quartile (p-trend=0.043). CONCLUSIONS: An elevation of the pituitary TSH-inhibition threshold is associated with incident type 2 diabetes independently of BMI. The PTFQI might have clinical potential for prognosis and metabolic status monitoring.

Persistent hypoglycemia due to an IGF-II-secreting malignant pheochromocytoma: a case report and literature review.

A malignant pheochromocytoma with IGF-II-mediated hypoglycemia is reported; although treatment was cumbersome and evolution unfortunate, this diagnosis must be kept in mind when dealing with NICTH's differential diagnosis.

Resistencia a la insulina tipo A, nueva mutación del gen del receptor de la insulina descrita / Resistance to type A insulin: A new mutation of the receptor gene of the insulin described

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Comparación de los efectos inducidos sobre la calciuria por tiazidas y diferentes dosis de sal en la dieta: implicaciones en la práctica clínica / A comparison of induced effects on urinary calcium by thiazides and different dietary salt doses: Implications in clinical practice

Introducción: La restricción de ClNa en la dieta y el tratamiento con tiazidas han sido utilizados en pacientes hipercalciúricos. Objetivos: Conocer la ingesta habitual de sal y la correlación entre natriuria y calciuria con la dieta habitual (B) y tras la modificación de la cantidad de ClNa y la administración de tiazidas. Material y métodos: Diecinueve jóvenes sanos, a los que se les sustituyó su dieta por 2 l diarios de Nutrison(R) Low Sodium (500 mg de Na) durante 2 días. Posteriormente se añadieron cada 2 días 5 g de ClNa ("5", "10" y "15") y durante los 2 últimos días 50 y 100 mg de Higrotona(R) (H50) y (H100). Se determinaron iones, ARP y aldosterona en sangre venosa, así como la natriuria y calciuria. Valoración estadística: se calcula la t de Wilcoxon y la correlación lineal de Pearson. Resultados: Natriuria (mEq/24h): 210,3 ± 87,6 ("B"); 42,7 ± 20,4 ("5"); 135,5 ± 50,6 ("10"); 225,5 ± 56,7 ("15"). Calciuria (mg/24h): 207,8 ± 93,6 ("B"); 172,8 ± 63,1 ("5"); 206,2 ± 87,7 ("10"); 227,4 ± 84,1 ("15"). Correlación positiva entre natriuria y calciuria en "10" (r = 0,47) y en "15" (r = 0,67). Tras Higrotona(R), natriuria: 232,3 ± 50,7; 377 ± 4 (H50); 341,1 ± 68,4 (H100); Ca en orina: 209,8 ± 57,4; 213,2 ± 67,6 (H50); 159,1 ± 52,2 (H100). Conclusiones: La ingesta de sal en la población estudiada es de 14,9 ± 4,9 g/día. Encontramos correlación entre natriuria y calciuria con ingestas de 11,25 y 16,25 g de sal. Con la ingesta habitual, por cada gramo de sal aumenta la calciuria 5,46 mg y con 100 mg de Higrotona(R), la calciuria disminuye 50,7 mg/24 h. Los datos podrían ser de utilidad para el manejo de pacientes con hipercalciuria excretora o hipoparatiroidismo

Introduction: Both dietary restriction of sodium chloride (NaCl) and treatment with thiazides have been used in hypercalciuric patients. Objectives: To calculate regular salt intake and investigate the correlation between natriuresis and urinary calcium with usual diet (B) and after changing the amount of NaCl intake and administration of thiazides. Material and methods: Nineteen healthy young individuals had their diet replaced by 2l of Nutrison(R) Low Sodium (500 mg sodium/day) daily for two days. Then, 5 g of NaCl were added every two days ("5", "10" and "15"), administering 50 mg (H50) and 100 mg (H100) of Higroton(R) on the last two days. Blood sodium, plasma renin activity (PRA) and aldosterone were determined in venous blood samples, as were urinary sodium and calcium. Statistical analysis: Wilcoxon t-test and the Pearson linear correlation were calculated. Results: Urinary Na (mEq/24h): 210.3 ± 87.6 ("B"); 42.7±20.4 ("5"); 135.5±50.6 ("10"); 225.5±56.7 ("15"). Urinary calcium (mg/24h): 207.8±93.6 ("B"); 172.8±63.1 ("5"); 206.2±87.7 ("10"); 227.4±84.1 ("15"). A positive correlation was observed between natriuresis and urinary calcium in "10" (r = 0.47) and "15" (r = 0.67). After Higroton(R), natriuresis: 232.3 ± 50.7; 377 ± 4 (H50); 341.1±68.4 (H100); Ca in urine: 209.8 ± 57.4; 213.2 ± 67.6 (H50); 159.1 ± 52.2 (H100). Conclusions: Salt intake in the population studied was estimated to be 14.9 ± 4.9 g/day with a positive correlation found between sodium and calcium urine output with daily intakes of 11.25 and 16.25g of salt. With the usual intake, for each gram of salt, urinary calcium increased by 5.46 mg/24 h and with 100 mg of Higroton(R) it decreased by 50.7 mg/24h. These data could be useful for the management of patients with excretory hypercalciuria or hypoparathyroidism

A comparison of induced effects on urinary calcium by thiazides and different dietary salt doses: Implications in clinical practice. / Comparación de los efectos inducidos sobre la calciuria por tiazidas y diferentes dosis de sal en la dieta: implicaciones en la práctica clínica.

INTRODUCTION: Both dietary restriction of sodium chloride (NaCl) and treatment with thiazides have been used in hypercalciuric patients. OBJECTIVES: To calculate regular salt intake and investigate the correlation between natriuresis and urinary calcium with usual diet (B) and after changing the amount of NaCl intake and administration of thiazides. MATERIAL AND METHODS: Nineteen healthy young individuals had their diet replaced by 2l of Nutrison® Low Sodium (500mg sodium/day) daily for two days. Then, 5g of NaCl were added every two days («5¼, «10¼ and «15¼), administering 50mg (H50) and 100mg (H100) of Higroton® on the last two days. Blood sodium, plasma renin activity (PRA) and aldosterone were determined in venous blood samples, as were urinary sodium and calcium. STATISTICAL ANALYSIS: Wilcoxon t-test and the Pearson linear correlation were calculated. RESULTS: Urinary Na (mEq/24h): 210.3±87.6 («B¼); 42.7±20.4 («5¼); 135.5±50.6 («10¼); 225.5±56.7 («15¼). Urinary calcium (mg/24h): 207.8±93.6 («B¼); 172.8±63.1 («5¼); 206.2±87.7 («10¼); 227.4±84.1 («15¼). A positive correlation was observed between natriuresis and urinary calcium in «10¼ (r=0.47) and «15¼ (r=0.67). After Higroton®, natriuresis: 232.3±50.7; 377±4 (H50); 341.1±68.4 (H100); Ca in urine: 209.8±57.4; 213.2±67.6 (H50); 159.1±52.2 (H100). CONCLUSIONS: Salt intake in the population studied was estimated to be 14.9±4.9g/day with a positive correlation found between sodium and calcium urine output with daily intakes of 11.25 and 16.25g of salt. With the usual intake, for each gram of salt, urinary calcium increased by 5.46 mg/24 h and with 100mg of Higroton® it decreased by 50.7mg/24h. These data could be useful for the management of patients with excretory hypercalciuria or hypoparathyroidism.

Infarto hipofisario silente de etiología infrecuente / Silent pituitary infarction of an uncommon etiology

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Are proton pump inhibitors a new antidiabetic drug? A cross sectional study.

AIM: To investigate the effect of proton pump inhibitors (PPIs) on glycemic control (HbA1c) in type 2 diabetic patients. METHODS: A cross-sectional study of consecutive in-patients admitted to hospital in any department during the first semester of the year 2010 who had a recent HbA1c measurement. The study excluded those with a diagnosis of hyperglycemic decompensation, diabetic onset or pregnancy. It compared HbA1c levels of those taking PPIs and those not. RESULTS: A total of 97 patients were recruited. The average HbA1C level was 7.0% ± 1.2%. Overall PPI consumption was 55.7%. HbA1c was significantly lower in individuals who took PPIs: -0.6%, 95% CI: -0.12 to -0.83. People who used PPIs with some type of insulin therapy had a HbA1c reduction by -0.8%, 95% CI: -0.12 to -1.48. For the rest of subgroup analysis based on the antidiabetic drug used, PPI consumption always exhibited lower HbA1c levels. CONCLUSION: PPIs seems to be consistently associated with better glycemic control in type 2 diabetes. HbA1c reduction observed is similar to incretin-based therapies.

Levothyroxine therapy and imatinib.

Levothyroxine requirements in patients with hypothyroidism are usually stable. Consequently, thyroid function is usually monitored once or twice yearly. Occasionally, the dose of levothyroxine can be changed by pharmacological reactions. We report the case of a 59-year-old woman who was under levothyroxine therapy for hypothyroidism secondary to subtotal thyroidectomy, with clinical and biochemical euthyroidism, who required an increased dose of levothyroxine after starting imatinib therapy. The patient was diagnosed with chronic myeloid leukemia and imatinib therapy was started. Subsequently, we observed clinical and biochemical hypothyroidism, requiring an increase in levothyroxine dose. Some cases of hypothyroidism after initiation of imatinib therapy in patients with levothyroxine replacement therapy have recently been published. Our case provides further evidence of a reaction between the two drugs. Therefore, we discuss the most likely physiopathological mechanisms contributing to imatinib-induced hypothyroidism in patients under levothyroxine replacement therapy.