Síndrome metabólico en los cálculos de oxalato cálcico: ¿es tan importante en este tipo de litiasis? / Metabolic syndrome in calcium oxalate stones: Is it so important in this type of lithiasis?

introducción y objetivo Se ha descrito la asociación del síndrome metabólico con la litogénesis, especialmente en cálculos de ácido úrico. El objetivo de este trabajo es analizar la importancia del síndrome metabólico en la litogénesis oxalocálcica. Materiales y métodos Evaluación metabólica de 151 pacientes: parámetros bioquímicos, hormonales y orina de 24horas; características asociadas al síndrome metabólico. Se evaluó la relación entre las características asociadas con el síndrome metabólico y las relacionadas con la litogénesis mediante el coeficiente de correlación de Spearman (CCS), «t» de Student y prueba exacta de Fisher. Resultados El índice de masa corporal promedio (IMC) fue 25,9 (DE 3,7). La mediana de edad fue de 51 años (18,6-84,8) y el 64,9% eran hombres. No hubo diferencias estadísticamente significativas entre hipertensión y estradiol, testosterona, triglicéridos o colesterol (p>0,05). Referente a la glucosa la media fue 114,5 y 93,5mg/dl en pacientes con y sin hipertensión (p=0,000). Los niveles de glucosa, estradiol, testosterona o colesterol no variaron con la proteinuria (p>0,05). La media de triglicéridos fue 185,6 y 108.2mg/dl en pacientes con y sin proteinuria (p=0,001). La hipertensión y la proteinuria no se asociaron (p=0,586). El IMC se correlacionó con el ácido úrico sérico y urinario y la creatinina urinaria. Conclusiones Existen pocas asociaciones entre las características del síndrome metabólico y las anomalías relacionadas con la litogénesis. El síndrome metabólico no parece tener un papel relevante en el desarrollo de cálculos oxalocálcicos (AU)

Introduction and objective The association of metabolic syndrome with lithogenesis has been described, especially in uric acid stones. The aim of the work was to analyze the role of the metabolic syndrome in oxalocalcic lithogenesis. Materials and methods Metabolic evaluation of 151 patients including biochemical, hormonal and 24-urine urine parameters, as well as characteristics associated with metabolic syndrome. The relationship between characteristics associated with metabolic syndrome and those related to lithogenesis was evaluated using Spearman's correlation coefficient (SCC), Student's t test and Fisher's exact test. Results The average body mass index (BMI) was 25.9 (SD 3.7). The median age was 51 years (18.6-84.8) and 64.9% were men. There were no statistically significant differences between hypertension and estradiol, testosterone, triglycerides, or cholesterol (P=.191, .969, .454, .345, respectively). Regarding glucose, mean value was 114.5 and 93.5mg/dl in patients with and without hypertension (P=.000). Glucose, estradiol, testosterone, or cholesterol levels did not vary with proteinuria (P=.518, P=.227, P=.095, P=.218, respectively). Mean triglycerides were 185.6 and 108.2mg/dl in patients with and without proteinuria (P=.001). Hypertension and proteinuria were not associated (P=.586). BMI correlated with serum and urinary uric acid and urinary creatinine. Conclusions There are few associations between the characteristics of metabolic syndrome and abnormalities related to lithogenesis. Metabolic syndrome does not seem to have a relevant role in the development of oxalocalcic stones (AU)

Metabolic syndrome in calcium oxalate stones: Is it so important in this type of lithiasis?

INTRODUCTION AND OBJECTIVE: The association of the metabolic syndrome with lithogenesis has been described, especially in uric acid stones. The aim of the work was to analyze the role of the metabolic syndrome in oxalocalcic lithogenesis. MATERIALS AND METHODS: Metabolic evaluation of 151 patients including biochemical, hormonal and 24-urine urine parameters, as well as characteristics associated with metabolic syndrome. The relationship between the characteristics associated with the metabolic syndrome and those related to lithogenesis was evaluated using Spearman's correlation coefficient (SCC), Student's t test and Fisher's exact test. RESULTS: The average body mass index (BMI) was 25.9 (SD 3.7). The median age was 51 years (18.6-84.8) and 64.9% were men. There were no statistically significant differences between hypertension and estradiol, testosterone, triglycerides or cholesterol (P=.191, .969, .454, .345, respectively). Regarding glucose, the mean was 114.5 and 93.5mg/dl in patients with and without hypertension (P=.000). The levels of glucose, estradiol, testosterone or cholesterol did not vary with proteinuria (P=.518, P=.227, P=.095, P=.218, respectively). The mean triglycerides were 185.6 and 108.2mg/dl in patients with and without proteinuria (P=.001). Hypertension and proteinuria were not associated (P=.586). BMI correlated with serum and urinary uric acid and urinary creatinine. CONCLUSIONS: There are few associations between the characteristics of the metabolic syndrome and the anomalies related to lithogenesis. Metabolic syndrome does not seem to have a relevant role in the development of oxalocalcic stones.

Role of endogenous taurine on the glutamate analogue-induced neurotoxicity in the rat hippocampus in vivo.

The glutamate analogues N-methyl-D-aspartate (NMDA), kainic acid (KA), and quisqualic acid (QA), prepared in different hypertonic media, were perfused in vivo in the hippocampal CA1 field of rats using a microdialysis technique. Extracellular taurine levels, estimated after analysis of the taurine content of dialysates, increased during perfusion of all three agonists but varied according to the osmolarity of the medium. The NMDA-induced increase in extracellular taurine content was only slightly inhibited by perfusion of 150 and 300 mM sucrose. The KA-evoked increase was partially dependent on extracellular osmolarity, because addition of 50 and 150 mM sucrose caused a dose-dependent inhibition that was not augmented using higher sucrose concentrations. QA caused a taurine increase that was totally abolished by addition of 50 mM sucrose. These results indicate that the rise in extracellular taurine level elicited by QA and part of the increase elicited by KA are probably due to a release caused by the cellular swelling that these substances evoke, a finding substantiating the previously proposed osmoregulatory role of taurine. However, almost all the increase in extracellular taurine content caused by NMDA and all the osmotically insensitive part of the KA-evoked rise cannot be explained as release triggered by cell swelling and may reflect a function of taurine other than osmoregulation.

In vivo effects of gamma-aminobutyric acid and beta-alanine on thyrotrophin secretion in the normal and hypothyroid rat.

The effect of pharmacological doses of two amino acids neurotransmitters, gamma-aminobutyric acid (GABA) and beta-alanine (beta-Ala), on thyrotrophin (TSH) secretion was studied in normal and hypothyroid (PTU-treated) male rats. Inhibition of TSH secretion was observed in normal rats treated with the drugs, 30 min after their administration. Hypothyroid animals responded only to GABA administration, decreasing their serum TSH at 30 min. Response to thyrotrophin-releasing hormone (TRH) after 15 min of drug administration was blunted in GABA injected animals, as compared to saline-injected controls. When TRH was injected at the same time as GABA and beta-Ala, the response was significantly lower than in controls. It is suggested that beta-Ala and GABA act at the pituitary by impairing the TSH response to TRH. The possibility that beta-Ala actions may be due to decreased GABA catabolism is considered, since beta-Ala administration increased GABA synaptosomal levels.