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Search Results: 1 - 10 of 12967 matches for " Lenine;Medeiros-Neto "
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Iodine nutrition in Brazil: where do we stand?
Medeiros-Neto, Geraldo;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2009, DOI: 10.1590/S0004-27302009000400014
Abstract: brazilian legislation, since 1955, failed to achieve its objectives because the issue was not properly addressed: iodized salt was only available in endemic areas, at a low amount of 10 mg iodine/kg salt. lack of surveillance and cooperation were common errors. from 1982 to 1992, the inan distributed potassium iodate to the industry free of charge, but it was abolished in 1991. only four years later (1995) was a new law enacted effective in determining that all salt for human use should be iodized at levels established by the health authorities. during the period comprising 1998 to 2004, excessive iodination of salt (40 to 100 mg/kg) could lead to an increased prevalence of chronic autoimmune thyroiditis and iodine-induced hyperthyroidism. in 2003, the content of iodine/kg of salt was lowered to 20 to 60 mg i/kg salt. a national survey of schoolchildren is currently underway and will indicate the changes required for adequate iodine in salt for human use.
Carcinoma papilífero da Tireóide: uma Hidra de sete cabe as?
Medeiros-Neto Geraldo
Arquivos Brasileiros de Endocrinologia & Metabologia , 2003,
Abstract:
Moléstias associadas à carência cr?nica de iodo
Knobel, Meyer;Medeiros-Neto, Geraldo;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2004, DOI: 10.1590/S0004-27302004000100007
Abstract: the thyroid gland promotes its adaptation to iodine deficiency inducing an increase in the iodine uptake followed by a substantial increase in the thyroid gland mass (goiter). simultaneously, there is a preferential t3 secretion by the follicular cell and a persistently elevated serum tsh. laboratory tests, isotopic methods and imaging are routinely used to verify the altered thyroid pathophysiology. in certain populations the presence of goitrogenic natural substances, present in the locally consumed staple food, were found and may add to the pathogenic process. endemic cretinism is usually present when the iodine deficiency is quite low and may present with the neurologic or myxedematous sub-types, frequently associated with deafmutism. in brazil, the prevalence of iodine-deficiency disorders has been evaluated, periodically, with schoolchildren examined for goiter. universal salt iodination was implemented in brazil in the early fifties but recently the system was considered effective for the supply of iodine to the brazilian population.
Relevance of iodine intake as a reputed predisposing factor for thyroid cancer
Knobel, Meyer;Medeiros-Neto, Geraldo;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2007, DOI: 10.1590/S0004-27302007000500007
Abstract: iodine is a trace element that is essential for the synthesis of thyroid hormone. both chronic iodine deficiency and iodine excess have been associated with hypertrophy and hyperplasia of follicular cells, attributed to excessive secretion of tsh. this may be associated to thyroid cancer risk, particularly in women. experimental studies have documented thyroid cancer induction by elevation of endogenous tsh, although in a small number of animals. iodine deficiency associated with carcinogenic agents and chemical mutagens will result in a higher incidence of thyroid malignancy. inadequate low iodine intake will result in increased tsh stimulation, increased thyroid cell responsiveness to tsh, increased thyroid cell egf-induced proliferation, decreased tgfb 1 production and increased angiogenesis, all phenomena related to promotion of tumor growth. epidemiological studies associating iodine intake and thyroid cancer led to controversial and conflicting results. there is no doubt that introduction of universal iodine prophylaxis in population previously in chronic iodine-deficiency leads to a changing pattern of more prevalent papillary thyroid cancer and declining of follicular thyroid cancer. also anaplastic thyroid cancer is practically not seen after years of iodine supplementation. iodine excess has also been indicated as a possible nutritional factor in the prevalence of differentiated thyroid cancer in iceland, hawaii and, more recently, in china. in conclusion: available evidence from animal experiments, epidemiological studies and iodine prophylaxis has demonstrated a shift towards a rise in papillary carcinoma, but no clear relationship between overall thyroid cancer incidence and iodine intake.
Bioequivalência de Prepara??es Comerciais de L-Tiroxina (100 e 200μg): Avalia??o em Pacientes Hipotireóideos Previamente Tireoidectomizados
Camargo, Rosalinda Y.A.;Souza, Jean Jorge S. de;Bezerra, Ana K.M.;Seidenberger, Katia;Tomimori, Eduardo;Cardia, Maria Silvia;Knobel, Meyer;Brand?o, Lenine;Medeiros-Neto, Geraldo;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2002, DOI: 10.1590/S0004-27302002000500006
Abstract: a major issue influencing prescribing patterns of physicians has been the relative bioavailability and bioequivalence of commercial levothyroxine preparations. some studies have suggested similar bioequivalence between various l-t4 tablets while other reports have found differences. some of these studies have been criticized for methodological defects in patients' selection or study design, which have become appreciated only in retrospect. moreover the us pharmacopeia has proposed that commercial tablets of l-t4 should be tested for its dissolution in two different solutions. each manufacturer should periodically test batches of tablets as indicated. in the present study, we have compared serum thyroid function parameters (total t4, total t3, free t4, and serum tsh) in previously totally thyroidectomized patients, without sonographic evidence for reminiscent thyroid tissue in the cervical area. the above parameters were measured, as function of time, for 15 days of either an oral solution of l-t4 (100μg) or tablets of l-t4a and l-t4b (100μg/tablet). there was no significant difference between the various parameters, in relation to time, for each of the different preparations. moreover l-t4a tablets did not differ from l-t4b tablets, when those parameters were tested, either at the concentration of 100 or 200μg/day. we conclude that the two oral formulations of l-thyroxine have similar bioavailability and bioequivalence under the present experimental conditions.
A fun??o gonadal do homem obeso
Lima, Nicolau;Cavaliere, Humberto;Halpern, Alfredo;Medeiros-Neto, Geraldo;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2000, DOI: 10.1590/S0004-27302000000100006
Abstract: in obese men, sex hormone-binding globulin (shbg) as well as total testosterone (tt) levels are decreased. data concerning serum free testosterone (ft) levels in obese men are discordant. ft levels are decreased in only some morbidly obese men consistent with an impairment of the feedback regulatory mechanism. it has been suggested that a functional decrease of lh pulse amplitude and serum lh levels are reflected in their hypoandrogenism. we have studied two groups of obese men (group 1: bmi £ 35kg/m2 and group 2: bmi 3 35.1kg/m2) before and after six months of a low calorie diet (1200kcal/day), every patient received a therapeutic prescription of dexfenfluramine (15mg b.i.d.) that was maintained for six months. plasma insulin levels, serum total testosterone, free testosterone and lh concentrations were obtained before and after weight loss. moderately obese men (bmi = 32.3 ± 1.9kg/m2) presented significantly decreased tt levels (390 ± 120ng/dl) as well as ft (mean ± sd: 16.0 ± 4.8pg/ml) as compared with normal controls. serum lh concentrations (4.5 ± 2.9mlu/ml) were normal. insulin levels were elevated in all patients (46,3 ± 30.1 mu/ml). after weight-loss there was a significant (p < 0.01) increase in tt, ft and lh levels whereas insulin concentrations significantly decreased, in massively obese men (bmi = 43.0 ± 6.7kg/m2) tt (320 ± 110ng/dl), ft (11.0 ± 2.1pg/ml) and lh (3.1 ± 1.3mlu/ml) were decreased and significantly lower as compared with the previous group and normal controls. as expected, after weight loss as expected, tt, ft and lh levels increased significantly while insulin concentrations decreased. we concluded that ft levels are dependent on the degree of obesity, massively obese men (bmi 3 35.1kg/m2) being considered as candidates for consistently low ft levels.
Genética molecular do hipotireoidismo congênito
Knobel, Meyer;Nogueira, Célia Regina;Medeiros-Neto, Geraldo;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2001, DOI: 10.1590/S0004-27302001000100005
Abstract: congenital hypothyroidism (ch) occurs in 1/3000-4000 neonates worldwide and may be classified as permanent or transient. primary ch accounts for the majority of affected children, while secondary and tertiary ch are rare. in iodine-sufficient countries, thyroid dysgenesis (td) is the most frequent cause of ch. hereditary inborn errors of thyroid hormonogenesis account for about 10-20% ch children. environmental, genetic and autoimmune factors have been implicated in the etiology of ch, but in the majority of cases the cause of td remains to be clarified. candidates for playing a pathogenetic role in td are genes involved in thyroid gland ontogeny, such as those of thyroid transcription factors titf1, titf2, pax-8 and the tsh-receptor (tshr). no abnormality in the titf1 gene has yet been found in ch, while mutations in the pax-8 gene were identified in at least 5 neonates with td. loss of function mutations of the tshr gene, although not involved in td, may produce a spectrum of congenital defects ranging from euthyroid hyperthyrotropinemia to overt hypothyroidism with a hypoplastic gland. the cloning of genes implicated in the biosynthesis of thyroid hormones, such as those of thyroperoxidase (tpo) and thyroglobulin (tg), has led to the identification of mutations responsible for some cases of goitrous hypothyroidism due to iodide organification defect or abnormalities in tg synthesis. recently, the molecular basis of the iodide transport defect and pendred?s syndrome were reported, due to mutations, respectively, on the nis and pds genes. in conclusion, we still do not have elucidated the molecular basis of td, the most common of the defects affecting neonates with ch.
Carcinoma insular de tireóide
Pereira, Maria Adelaide A.;Camargo, Rosalinda;Medeiros-Neto, Geraldo;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2000, DOI: 10.1590/S0004-27302000000300011
Abstract: o objetivo dessa apresenta??o é discutir o carcinoma insular da tireóide, uma forma rara de neoplasia com características clínicas e histológicas bastante peculiares. inicialmente, será apresentado o caso seguido de uma breve discuss?o clínica. posteriormente, ser?o discutidos aspectos histológicos e ihqs e os marcadores de agressividade desse tipo de tumor, seguindo-se uma discuss?o aberta com outros membros do servi?o.
Genética molecular do hipotireoidismo congênito
Knobel Meyer,Nogueira Célia Regina,Medeiros-Neto Geraldo
Arquivos Brasileiros de Endocrinologia & Metabologia , 2001,
Abstract: O hipotireoidismo congênito (HC) ocorre, mundialmente, em 1/3000-4000 neonatos e pode ser classificado em permanente ou transitório. O HC primário é responsável pela maioria dos afetados, enquanto o secundário e terciário s o raros. Nos países iodo-suficientes, a disgenesia tireóidea (DT) é a causa mais freqüente de HC. Os defeitos hereditários da síntese hormonal ocorrem em minoria de crian as portadoras de HC. Fatores ambientais, genéticos e auto-imunes concorrem na etiologia do HC, mas na maioria dos casos de DT a causa é obscura. Atribui-se aos genes envolvidos na ontogenia da glandula tireóidea, como os fatores de transcri o TITF1, TITF2, PAX-8 e receptor de TSH (TSHR), fun o patogenética na DT. Até o momento n o foi descrita anormalidade no gene TITF1 como causa de HC, enquanto foram identificadas muta es no PAX-8 em cinco recém-nascidos com DT. Embora n o envolvidas na DT, muta es inativadoras do TSHR podem produzir espectro de defeitos congênitos oscilando entre hipertirotropinemia com eutireoidismo e hipotireoidismo com hipoplasia glandular. A clonagem dos genes envolvidos na biossíntese dos horm nios tireóideos, como o da tireoperoxidase (TPO) e tireoglobulina (Tg), permitiu a identifica o de muta es responsáveis por alguns casos de bócio e hipotireoidismo decorrente de defeito de incorpora o de iodeto ou anormalidades na síntese de Tg. Recentemente, foi demonstrada a base molecular do defeito de transporte ativo de iodeto e da síndrome de Pendred, respectivamente, devidas a muta es no gene NIS (simportador de sódio e iodeto) e no gene PDS (pendrina). Em conclus o, grande parte dos pacientes com HC e DT n o tem esclarecida, ainda, a causa molecular desta síndrome.
Impacto médico-social do tratamento medicamentoso da moléstia de Graves-Basedow em Hospital Público Universitário: avalia??o retrospectiva e proje??o prospectiva de conduta terapêutica
Lima, Nicolau;Knobel, Meyer;Camargo, Rosalinda Y.;Tomimori, Eduardo;Medeiros-Neto, Geraldo;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2005, DOI: 10.1590/S0004-27302005000400017
Abstract: the aim of the present study was to evaluate a new proposal for increasing compliance to the clinical management of patients with graves? disease (gd) in a large and public university hospital. the patients were carefully selected (no previous gd treatment, goiter volume less than 6ml must be living in the metro area of s?o paulo), received medication at no cost, were contacted frequently by the social worker and alerted for the date of consultation and only referred to a single endocrinologist during all phases of treatment. we recruited 229 patients with gd that were initially treated with methimazole (mmi - 60mg q.d) in a single daily dose followed by a combination of mmi (20mg) plus l-t4 (100μg) daily for 24 months. only 83 patients (36.2%) completed the protocol and were subdivided in: group 1 (n= 34) that were in remission for 3 years after discontinuation of the mmi and group 2 (n= 49) that presented recurrence of gd between 2 and 36 months without mmi. predictive factors associated with remission were: decrease of the glandular volume, serum tg< 40ng/ml and normal trab values. we concluded that in spite of a careful protocol planned to increase compliance, more than 60% of patients with gd did not complete the therapeutic trial and were referred for radioiodine treatment. the solution for this low therapeutic success for gd should be the possible identification of factors that would indicate patients that are not inclined to follow a long period of clinical therapy.
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