2 research outputs found

    Farmacoepidemiologia no Brasil: evolução e perspectivas Pharmacoepidemiology in Brazil: evolution and prospects

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    O presente trabalho apresenta o desenvolvimento da farmacoepidemiologia no Brasil. Enfatiza o papel dos programas de educação continuada em farmacologia coordenados pelo professor Carlos Lacaz, autor do primeiro livro brasileiro sobre doenças iatrogênicas. Ressalta o papel do programa de formação em farmácia clínica da Organização Pan-Americana de Saúde, onde vários profissionais brasileiros tiveram o primeiro contato com o Programa de farmacovigilância por Monitorização Intensiva Hospitalar. Refere também às primeiras teses de doutorado sobre medicamentos defendidas na Universidade de São Paulo. Relata a tentativa da Divisão de Medicamentos do Ministério da Saúde do Brasil de se direcionar para a farmacovigilância. Tece considerações sobre a I Oficina de Trabalho sobre medicamentos organizada pelas Secretarias Municipal e Estadual de Saúde de São Paulo. Enfatiza a criação da Sociedade Brasileira de Vigilância de Medicamentos, e sua importância como estimuladora da farmacoepidemiologia. Analisa o impulso do setor dinamizado pela implantação dos Centros de Informações de Medicamentos, no país. Conclui que já existem condições para se incrementar a pesquisa farmacoepidemiológica no Brasil.<br>This work recovers the historical development of pharmacoepidemiology in Brazil. The role played by the following events is particularly dealt with the influence of the pharmacological education programs coordinated by professor Carlos Lacaz, author of the first Brazilian textbook on iatrogenic diseases; the clinical pharmacy program offered by the Pan-American Health Organization, which provided a number of Brazilian professionals their first contact with the Program of Drug Surveillance by Intensive Hospital Monitoring; the first doctoral on drugs presented at São Paulo University; the attempt of the Division of Medicine of the Brazilian Health Ministry to include Pharmacovigilance among its more important aims. Also the founding of the Brazilian Association for Drug Surveillance are reported. Emphasis is also placed on the implementation of several Drug Information Centers in Brazil, and the new thrust thus provided to Drug Epidemiology. Finally, conclusions are drawn on the conditions for gathering efforts already available in universities and health service agencies nationwide in order to implement pharmacoepidemiological research in Brazil

    Prolactin induces adrenal hypertrophy

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    Although adrenocorticotropic hormone is generally considered to play a major role in the regulation of adrenal glucocorticoid secretion, several reports have suggested that other pituitary hormones (e.g., prolactin) also play a significant role in the regulation of adrenal function. The aim of the present study was to measure the adrenocortical cell area and to determine the effects of the transition from the prepubertal to the postpubertal period on the hyperprolactinemic state induced by domperidone (4.0 mg kg-1 day-1, sc). In hyperprolactinemic adult and young rats, the adrenals were heavier, as determined at necropsy, than in the respective controls: adults (30 days: 0.16 ± 0.008 and 0.11 ± 0.007; 46 days: 0.17 ± 0.006 and 0.12 ± 0.008, and 61 days: 0.17 ± 0.008 and 0.10 ± 0.004 mg for treated and control animals, respectively; P < 0.05), and young rats (30 days: 0.19 ± 0.003 and 0.16 ± 0.007, and 60 days: 0.16 ± 0.006 and 0.13 ± 0.009 mg; P < 0.05). We selected randomly a circular area in which we counted the nuclei of adrenocortical cells. The area of zona fasciculata cells was increased in hyperprolactinemic adult and young rats compared to controls: adults: (61 days: 524.90 ± 47.85 and 244.84 ± 9.03 µm² for treated and control animals, respectively; P < 0.05), and young rats: (15 days: 462.30 ± 16.24 and 414.28 ± 18.19; 60 days: 640.51 ± 12.91 and 480.24 ± 22.79 µm²; P < 0.05). Based on these data we conclude that the increase in adrenal weight observed in the hyperprolactinemic animals may be due to prolactin-induced adrenocortical cell hypertrophy
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