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Biomedical subjects

Gisah A de Carvalho

Publications and source records attributed to Gisah A de Carvalho.

3 recordsLinked to original sources

[Use of lithium carbonate for the treatment of amiodarone-induced thyrotoxicosis].

Among the amiodarone-induced thyroid dysfunctions, thyrotoxicosis is the most troublesome and with the highest rate of morbidity and mortality. Treatment consists in the use of a high dose of anti-thyroid drugs and steroids in an isolated form or in combination. Association of several other drugs have been proposed for the treatment of refractory cases. In this study we report the case of a 40 y.o. patient, with a history of idiopatic dilated miocardiopathy, who developed severe amioradone-induced thyrotoxicosis after heart transplantation. Since the patient did not respond to an initial treatment consisting of a high dose of anti-thyroid drugs combined with steroids, a low dose of lithium carbonate was added for a short period of time, which resulted in normalization of the thyroid function. In this case, the addition of lithium carbonate to the two other drugs resulted in a successful and safety therapy in controlling amiodarone-induced thyrotoxicosis.

Adult↗

[Anaplastic thyroid carcinoma].

Well-differentiated thyroid carcinoma (TC), as papillary and follicular carcinoma, usually follows a relatively benign course after total thyroidectomy and thyroid remnant ablation with 131I. In contrast, anaplastic TC or undifferentiated TC, also derived from the thyroid follicular epithelium, refers to one of the more aggressive human malignancies, which have lost most or all characteristics of the tissue from which it originated. Rapid tumor growth presages early mortality unless combined therapy is aggressively pursued. Definitive curative approach does not exist for most patients. The best approach is still aggressive surgery combined with the associated use of new chemotherapies associated with local external beam radiotherapy.

Carcinoma↗

[Thyroid hormone resistance syndrome].

Resistance to thyroid hormone (RTH) is a syndrome characterized by elevated serum thyroid hormone (TH) levels and elevated or inappropriately normal thyrotropin levels. In general, patients exhibit TH resistance in the pituitary and peripheral tissues. The phenotype of RTH is variable; the affected individuals are clinically euthyroid or even hypothyroid depending on the severity of the mutation, the variable hyposensitivity to TH among individuals as well as in different tissues. In almost all cases the genetic basis of RTH lies in mutation of the carboxyl-terminus of the ss-thyroid hormone receptor. RTH is a dominant disorder, except in one family; most individuals are heterozygous for the mutant allele. New standard techniques and genetically engineered mouse model systems have increased our understanding on TH receptor action, in particular, how mutant thyroid receptors from RTH patients can block wild-type thyroid receptor function (dominant negative activity), and how the mutant receptors can differently affect various tissues and individuals.

Animals↗