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Biomedical subjects

F González Sastre

Publications and source records attributed to F González Sastre.

At least 19 recordsLinked to original sources
PubMed1990

[Evaluation of a new strategy for detecting thyroid dysfunction].

The results of a diagnostic strategy to evaluate thyroid function were assessed. This strategy consists of TSH measurement as the initial biochemical test, assuming that all individuals with normal TSH concentrations are euthyroid and do not require additional measurements of other hormones. The study was carried out in 576 patients whose serum samples had been referred to the laboratory during 4 consecutive weeks for the evaluation of thyroid function. In all cases TSH and free T4 (FT4) concentrations were measured by chemoluminescence, using one tube for each parameter and patient. Total T3 concentrations (T3) were only measured (RIA) in patients with subnormal TSH values, using duplicate samples. With TSH measurement as the initial test, 447 patients (78%) in whom further hormone assessment would not have been required were detected. This rate would have been 75% if FT4 measurement had been adopted as the screening test. In addition, 55 patients with subclinical thyroid dysfunction were identified with TSH measurement. They would have been missed if the screening had been based on FT4 only. T3 measurement only contributed to the identification of one patient with T3 thyrotoxicosis, and it did not provide additional useful information for the diagnostic classification of the remaining patients. The results of these assays show that TSH measurement is the biochemical test of choice as the first step of a strategy to detect thyroid dysfunction. Its use to this end makes the concomitant measurement of other hormonal parameters unnecessary, resulting in a considerable reduction of cost.

Adolescent↗
PubMed1989

[Analysis of adenosine deaminase and its subfractions as a diagnostic parameter in tuberculous pleural effusion].

In this paper we present the results of a study about the diagnostic utility of Adenosine Deaminase (ADA) determination for diagnosing the tuberculous pleural effusion. We carried out this study in 71 patients who came to our Hospital and were diagnosed for pleural effusion. The ADA determination was made in sera and pleural effusion of all these patients. Also we determined how much of this ADA activity was linked to microsomes or not (soluble ADA), by ultracentrifugation as a separative method. Taking as a base the data obtained and using 43 U/l as cutoff point, the Diagnostic Sensitivity of ADA determined in pleural liquid calculated was 1. This means that all patients with tuberculous pleural effusions had ADA activities higher than 43 U/l in their pleural liquid. On the other hand, Diagnostic Specificity was of 0.83. This was due to the existence of 10 false positives: 2 malignancies, 3 empyemas, 1 postpneumonia, 1 secondary to thromboembolic pulmonary disease, 1 secondary to rheumatoid arthritis and 2 of unknown origin. Results obtained show the utility, with some limitations, of ADA determination in pleural liquid in order to diagnose tuberculous pleural effusions. Neither ADA determination in sera nor quantity of ADA linked to microsomes or solubles ADA in pleural liquid seem to have great clinical interest.

Adenosine Deaminase↗
PubMed1979

[Gm1 gangliosidosis types 1 and 2 (author's transl)].

Two cases of gangliosidosis due to aggregates of Gm1 are described. The first patient was a female infant with noticeable retardation in psychomotor development, coarse facies, hepatomegaly, and X-rays showing skeletal anomalies in the large bones, vertebral column, cranium and ribs. She died at the age of 10 months of a septic condition. The second patient was a male infant; deterioration in psychomotor development was first noticed 8 months after birth and this progressed slowly to arrive at a vegetative state with convulsions and myoclonus. The child died at the age of 4 years. There were no signs of enlargement of visceral organs but a cherry red stain was observed in the ophthalmologic examination. In the first case, necropsy revealed the presence of a deposit substance in the histiocytes of the hepatic sinusoids, spleen, pancreas, thymus, septi and pulmonary alveoli, intestinal lamina propria, epithelial cells of the renal glomeruli, and in the neurons and glial cells of the brain. The same deposits were observed only in the neurons and glial cells in the second case. Ultrastructural examination showed the presence of typical cytoplasmic membranous bodies in the central nervous system of both patients. The beta-galactosidase activity in the urine of both patients during life was zero. There was a higher than normal total amount of gangliosides in brain tissue samples from both (1906.7 and 2459.9 NANA/g respectively) as compared with normal values (724.0). This increase was proportional to the rise in Gm1 ganglioside (76.8 and 89.6 percent molar respectively) as compared to control (27.0). These clinical, morphologic, and biochemical data characterize both types 1 and 2 of gangliosidosis due to Gm1 aggregates.

Cerebral Cortex↗
PubMed1977

[Gangliosidosis GM1. Clinical, radiologic, biochemical and histological studies in two cases (author's transl)].

Two cases of Gangliosidosis GM1 are presented. They are a child who showed psychomotor backward and generalized osteoporosis, died at 16 months, and a girl studied because of psychomotor backward when she was less than a year. This girl showed radiological vertebrae alterations similar to mucopolysaccharidosis and died when she was 7 years old. The enzymatic determinations in serum and cultured fibroblasts showed beta-galactosidase deficiency in both cases. Important storage of cerebral gangliosides with increase of the percentage of GM1 was also found in both cases. Histological alterations were found in some other organs besides the brain.

Brain↗
PubMed1977

[GM2 gangliosidosis diagnosis and carriers detection by fractionation of N-acetyl-beta-D-hexosaminidase by electrophoresis on cellulose acetate gel (author's transl)].

A method is described for the fractionation of GM2 gangliosidosis diagnosis and carriers detection by fractionation of N-acetyl-beta-D-Hexosaminidase by electrophoresis on cellulose acetate gel. The hexosaminidase activity is resolved into three bands that are quantified by a densitometric procedure. The methods is applied to normal controls, normal pregnant women, patients of Tay-Sachs disease, heterozigous carriers of Tay-Sachs disease, amniotic fluid, uncultured amniotic cells. The results are compared with those obtained by the "heat inactivation method".

Amniotic Fluid↗