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Biomedical subjects

W Nicolau

Publications and source records attributed to W Nicolau.

At least 37 records · Page 2Linked to original sources

Spironolactone-reversible rickets associated with 11 beta-hydroxysteroid dehydrogenase deficiency syndrome.

A 7-year-old girl had growth retardation, hypertension, and hypokalemic alkalosis. Baseline serum aldosterone concentration and plasma renin activity were low and unresponsive to sodium deprivation and to orthostatic changes. Baseline serum progesterone, 17-hydroxyprogesterone, 11-deoxycortisol, and cortisol levels were normal and adequately responsive to ACTH stimulation. No steroid was found abnormally elevated. A diagnosis of 11 beta-hydroxysteroid dehydrogenase deficiency was established on the basis of elevated urinary tetrahydrocortisol plus allotetrahydrocortisol/tetrahydrocortisone ratio, determined by gas chromatography-mass spectrometry. Evaluation of bone mineral metabolism and parathyroid function, and skeletal radiographs, revealed the presence of rickets and secondary hyperparathyroidism. Treatment with spironolactone alone for 2 months corrected hypertension, hypokalemic alkalosis, and all laboratory and radiologic evidence of rickets and hyperparathyroidism, resulting in acceleration of growth rate. The response to spironolactone suggests that a hypermineralocorticoid state is responsible for the hypertensive syndrome and that rickets and hyperparathyroidism could be a consequence of excess mineralocorticoid activity.

11-beta-Hydroxysteroid Dehydrogenases↗

Peripheral blood T and B lymphocytes, in vitro stimulation with phytohemagglutinin, and sensitization with 2,4-dinitrochlorobenzene in Grave's disease.

The percentage and absolute numbers of thymos-dependent (T) and thymos-independent (B) peripheral blood lymphocytes, the in vitro response of lymphocytes to phytohemagglutinin (PHA), and the sensitization with 2,4dinitrochlorobenzene (DNCB) was studied in 26 patients with hyperthyroidism due to Graves' disease. The results showed a normal percentage of both T and B cells and increased absoluted numbers of total lymphocytes in patients compared with 30 healthy controls. The in vitro response to PHA was normal in most patients with the exception of 5 of them who showed an impaired response. All patients developed a reaction of delayed hypersensitivity to DNCB. Our study indicated that there is no general abnormality in cell-mediated immunity in Graves' disease.

Adolescent↗

Effect of iodized oil on iodine content, thyroglobulin maturation and on biochemical constituents of endemic goitre in brazil.

The biochemical and morphological changes in thyroid glands were studied in 5 patients with endemic goitre in the region before and one year after the administration of iodized oil. Each patient received a tracer dose of 125-I 3-5 weeks before the biopsy and another tracer of 131-I 12 h before surgery. It was observed that: 1. Iodine deficient goitrous glands had more protein per gram of tissue and that this was corrected by iodination. 2. The goitrous glands exhibited a higher relative proportion of particulate iodoprotein that incorporates more labelled iodine in relation to time of labelling. This abnormal situation is reverted to normal by iodination. 3. A significantly higher proportion of T3 + T4 is synthetized by the glands treated with iodized oil. 4. The increased amount of 127-I per gram of tissue is followed by an increased iodination level of thyroglobulin. 5. The ultracentrifugal pattern of proteins observed for iodine deficient glands differed from the iodinated glands, indicating a failure of maturation of thyroglobulin and possibly a greater than normal degree of heterogeneity. 6. The shift in sedimentation pattern was clearly induced by the increased degree of iodination, as shown by the iodized oil injection. 7. The increased cellularity and the higher rate of protein synthesis in the goitrous glands are reverted to normal after the iodized oil injection.

Biopsy↗