Bocio multinodular tóxico por intoxicación con monóxido de carbono / Toxic multinodular goiter due to poisoning by carbon monoxide

RESUMEN Paciente masculino de 53 años con antecedentes de alergia, trabajador artesanal que realiza serigrafías, con alta exposición a productos químicos que, al someterse a altas temperaturas desprenden gran cantidad de vapor. Acude a consulta refiriendo que desde aproximadamente 2 meses antes presenta decaimiento con calambres musculares, palpitaciones, enrojecimiento de la cara y, aumento de tamaño de la glándula tiroides. Se diagnostica un bocio multinodular tóxico, por cifras hormonales elevadas. Se realiza ultrasonido de tiroides que informa bocio multinodular, una biopsia por aspiración con aguja fina, con atipia de significado incierto, y lesión folicular del tiroides. Se separa de su centro de trabajo y se logra revertir la sintomatología a los 15 días del tratamiento. Frecuentemente aparecen enfermedades asociadas a intoxicaciones por químicos y medicamentos, donde la presencia de hipertiroidismo no es habitual. Se requiere una anamnesis exhaustiva y exámenes complementarios específicos para un diagnóstico y tratamiento adecuados(AU)

ABSTRACT 53 years old male patient with a history of allergy; he works as a craft worker (producing serigraphs) very exposed to chemicals, which when subjected to high temperatures emit large amount of steam. The patient attends to the consultation referring that from approximately 2 months before he has been presenting weakness with muscle cramps, palpitations, flushing of the face and, increase in the size of the thyroid glands. It is diagnosed by the high hormonal figures a toxic multinodular goiter. Thyroid ultrasound is performed that shows multinodular goiter; it is also conducted a biopsy by fine-needle aspiration resulting in atypia of uncertain significance, and follicular lesion of the thyroid. The patient was separated from his workplace and there were reversed the symptoms after 15 days of treatment. Frequently appear diseases associated to poisonings caused by chemicals and medicines, where the presence of hyperthyroidism is not usual. It requires a comprehensive anamnesis and complementary tests that are specific for a proper diagnosis and treatment(AU)

Bone disease in thyrotoxicosis.

Thyrotoxicosis, a clinical syndrome characterized by manifestations of excess thyroid hormone, is one of the commonly-recognised conditions of the thyroid gland. Thyrotoxicosis causes acceleration of bone remodelling and though it is one of the known risk factors for osteoporosis, the metabolic effects of thyroxine on bone are not well discussed. Studies show that thyroid hormones have effects on bone, both in vitro and in vivo. Treatment of thyrotoxicosis leads to reversal of bone loss and metabolic alterations, and decreases the fracture risk. There are limited studies in India as to whether these changes are fully reversible. In this review we discuss about the effects of thyrotoxicosis (endogenous and exogenous) on bone and mineral metabolism, effects of subclinical thyrotoxicosis on bone and mineral metabolism and effects of various forms of treatment in improving the bone mineral density in thyrotoxicosis.

Amiodarona e tireotoxicose: relatos de casos / Amiodarone and thyrotoxicosis: case reports / Amiodarona y tirotoxicosis: relatos de casos

Relata-se que a disfunção tireoidiana induzida pela amiodarona afeta de 2 a 24 por cento dos usuários. Embora seja fácil tratar o hipotireoidismo induzido pela amiodarona, o desenvolvimento da tireotoxicose leva a uma abordagem difícil na maioria dos casos. O objetivo deste estudo é descrever três casos diferentes de pacientes com tireotoxicose induzida por amiodarona e discutir os aspectos clínicos e laboratoriais, e as diferentes abordagens para esses casos. É essencial avaliar cuidadosamente os pacientes antes e durante o tratamento com amiodarona, tendo em vista que o diagnóstico e o tratamento imediato dessa condição são cruciais em pacientes com alto risco cardiovascular.

Amiodarone-induced thyroid dysfunction has been reported to affect 2-24 percent of users. Despite the easy management of amiodarone-induced hypothyroidism, the development of thyrotoxicosis leads to a difficult approach in most cases. The aim of this study is to describe three different cases of patients with amiodarone-induced thyrotoxicosis and discuss the clinical and laboratorial aspects, and the different approaches to them. It is essential to carefully evaluate patients before and during amiodarone therapy, since the prompt diagnosis and treatment of this condition is essential in patients with high cardiovascular risk.

Se relata que la disfunción tiroidea inducida por la amiodarona afecta de 2 a 24 por ciento de los usuarios. Aunque sea fácil tratar el hipotiroidismo inducido por la amiodarona, el desarrollo de la tirotoxicosis lleva a un abordaje difícil en la mayoría de los casos. El objetivo de este estudio es describir tres casos diferentes de pacientes con tirotoxicosis inducida por amiodarona y discutir los aspectos clínicos y de laboratorio, y los diferentes abordajes para esos casos. Es esencial evaluar cuidadosamente los pacientes antes y durante el tratamiento con amiodarona, teniendo en vista que el diagnóstico y el tratamiento inmediato de esa condición son cruciales en pacientes con alto riesgo cardiovascular.

Tumores hipofisários secretores de TSH: relato de dois casos e revisão da literatura / TSH-secreting pituitary tumors: two case reports and literature review

INTRODUÇÃO: Tumores hipofisários secretores de hormônio estimulante da tireoide (TSH), tireotropinomas, são raros e correspondem a menos de 2 por cento de todos os adenomas da hipófise. Manifestam-se clinicamente com sintomas e sinais de tireotoxicose, eventualmente associados a sintomas compressivos, sobretudo visuais, devido ao efeito de massa do tumor. Esses tumores se caracterizam pela presença de níveis séricos elevados de hormônios tireoidianos e níveis séricos elevados, ou inapropriadamente normais, de TSH. Frequentemente, ao diagnóstico, há relato de tratamento prévio cirúrgico, medicamentoso e/ou ablativo, por hipótese de hipertireoidismo primário por doença de Graves. OBJETIVO: Relatar dois casos de tireotropinomas acompanhados na Unidade de Neuroendocrinologia do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HC-FMUSP) e revisar a literatura visando ao manejo desta afecção. CONCLUSÃO: Na presença de hormônios tireoidianos elevados e níveis de TSH inapropriadamente normais ou elevados, a possibilidade de adenoma hipofisário produtor de TSH deve ser considerada com vistas à realização da terapia adequada.

INTRODUCTION: TSH-secreting pituitary adenomas are rare pituitary functioning tumors accounting for less than 2 percent of the pituitary adenomas. The clinical feature consists of thyrotoxicosis occasionally associated to tumoral symptoms due to mass effect. The biochemical feature consists of elevated thyroid hormones levels and normal or high TSH concentrations. This disease is often wrongly diagnosed as Grave's disease, and the ablative therapy is frequently conducted prior to the diagnosis. OBJECTIVE: To report two cases followed in the Neuroendocrine Unit of Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo and to review the literature aiming at the management of this affection. CONCLUSION: In the presence of elevated thyroid hormone levels associated with inappropriate normal or increased TSH levels, the possibility of a TSH-secreting pituitary adenoma should be considered for the proper medical treatment.

Aspectos patogênicos e clínicos do bócio multinodular / Pathogenic and clinical aspects of multinodular goiter

O bócio multinodular (BMN) é definido como um aumento da glândula tireóide secundário à proliferação multifocal de tireócitos e caracteriza-se pela heterogeneidade no crescimento e função das células foliculares. O BMN é considerado uma neoplasia benigna da tireóide. É uma doença comum, com aumento da prevalência em áreas com deficiência de iodo, sendo este o principal fator etiológico ambiental. A patogênese desta disfunção tireoidiana ainda não está inteiramente elucidada. Nesta revisão serão abordados os principais mecanismos envolvidos na patogênese, seguidos das implicações clínicas dessa patologia.

Multinodular goiter (MNG) is defined as an enlargement of the thyroid gland that is characterized by heterogeneity in growth and function of thyroid follicular cells. MNG is now considered a true thyroid neoplasm. It is a common disease, with higher prevalences in iodine deficiency areas. Iodine deficiency is the main environmental etiologic factor for MNG. The pathogenesis of multinodular goiter is not yet fully clarified. The purpose of this review is to summarize the current knowledge of MNG with respect to the pathology, etiologic and clinical characteristics.

Ultrassonografia quantitativa do fígado em gatos com tirotoxicose induzida / Quantitative ultrasond of the liver in cats with induced thyrotoxicosis

Este estudo avaliou ultrassonograficamente o fígado de gatos submetidos à tirotoxicose induzida pela técnica de histograma dos níveis de cinza com o objetivo de melhor avaliar possíveis alterações hepáticas decorrentes do excesso de hormônios tiroidianos. Para isto, foram utilizados nove gatos hígidos, adulto-jovens, que receberam diariamente 150μg/kg de levotiroxina sódica, por 60 dias. O histograma hepático não demonstrou diferença estatística ao nível de 5% de significância entre os momentos avaliados; entretanto, as variações dos valores das variáveis estudadas sugeriram a promoção de aumento da heterogeneidade e diminuição da ecogenicidade do parênquima hepático quando comparado ao momento inicial. A avaliação citopatológica e histopatológica revelou quadro de hepatite tirotóxica em todos os animais

This study evaluated ultrasonographically the liver of cats submitted to induced thyrotoxicosis by the technique of gray-level histogram with the objective of better evaluating the possible hepatic alterations decurring from the excess of the thyroid hormones. For that, there were used nine adult-young healthy cats, which received daily 150ìg/kg of sodic levotiroxin, for 60 days. The hepatic histogram has not demonstrated statistical differences in the 5% level of significance between the evaluated moments; however, the variations of the studied variables’ values suggested an increasing of the heterogeneity and a decreasing of the echogenicity of the hepatic parenchyma when compared to the initial moment. The cytopathologic and histopathologic evaluations have shown of a clinical picture of thyrotoxic hepatitis in all the animals

Espectro clinicopatológico de las tiroiditis

El espectro clinicopatológico de las tiroiditis abarca, desde la rara tiroiditis aguda o supurativa hasta la más rara tiroiditis de Riedel. Las tiroiditis subaguda y silente (y su variante postpartum) también son enfermedades no comunes, mientras que la tiroiditis crónica autoinmune o enfermedad de Hashimoto resulta la tiroiditis y la enfermedad autoinmune órgano específica más frecuente, responsable de la mayor parte de los casos de hipotiroidismo. Efectivamente, en las áreas geográficas no deficientes en yodo, la mayor parte de los desórdenes tiroideos se deben a enfermedad autoinmune. La autoinmunidad como fenómeno primario juega un papel trascendente en la etiopatogenia de la tiroiditis crónica autoinmune, la tiroiditis silente-postpartum y la tiroiditis de Riedel y, sólo un rol secundario en la tiroiditis subaguda. Posiblemente, las infecciones virales causan la tiroiditis subaguda, mientras que los gérmenes piógenos y hongos son responsables de la tiroiditis supurativa. Las tiroiditis autoinmunes y la tiroiditis subaguda se acompañan comúnmente de disfunción tiroidea. Se conoce como “tiroiditis destructiva” al proceso inflamatorio tiroideo acompañado de destrucción y tirotoxicosis transitoria.

En estos casos, la disfunción tiroidea adopta usualmente el patrón de “tiroiditis bifásica”, en la que secuencialmente, la tirotoxicosis pasajera va seguida de hipotiroidismo transitorio y recuperación. Desórdenes con diferente etiopatogenia, como la tiroiditis subaguda, la tiroiditis silente y la enfermedad de Hashimoto, son responsables de los fenómenos fisiopatológicos similares que dan origen a la tiroiditis bifásica. El dolor en la tiroides adquiere relevancia en la tiroiditis subaguda y en la tiroiditis supurativa y, sólo raramente, está presente en la tiroiditis silente o en la exacerbación aguda de la enfermedad de Hashimoto. En la mayor parte de los casos, es posible establecer el diagnóstico de la tiroiditis mediante la historia clínica, las pruebas de función tiroidea y los estudios isotópicos y ecosonográficos. La biopsia tiroidea por aspiración con aguja fina permite resolver los casos dudosos. Esta revisión del “Espectro clínico-patológico de las tiroiditis”, resulta una síntesis de la información bibliográfica y la experiencia lograda con las tiroiditis a través de un enfoque clínico integral.

Clinical-pathological spectrum of thyroiditis comprises from the rare acute o suppurative thyroiditis as far as the rarest Rieldel’s thyroiditis. Also, subacute and silent thyroiditis (and it postpartum variant) are non common diseases, while autoimmune chronic thyroiditis or Hashimoto’s disease results the most frequent thyroiditis and organ-specific autoimmune disorder, that is responsible for most part of hypothyroidism cases. Effectively, in iodine-replete geographic areas, most persons with thyroid disorders have autoimmune disease. Autoimmunity as primary phenomenon plays a transcendent role in etiopathogeny of chronic autoimmune thyroiditis, silent-postpartum thyroiditis and Riedel’s thyroiditis and only a secondary role in subacute thyroiditis. Probably, viral infections cause subacute thyroiditis, while pyogenic germs and fungus are responsible for suppurative thyroiditis. Commonly, autoimmune and subacute thyroiditis are associated with thyroid dysfunction. It is known as “destructive thyroiditis”, the thyroidal inflammatory process that is joined to destruction and transient thyrotoxicosis.

Usually, thyroid dysfunction in these cases adopt “biphasic thyroiditis” pattern, in which sequentially, transient thyrotoxicosis is followed by transient hypothyroidism and recovery. Disorders with different etiopathogeny as subacute thyroiditis, silent thyroiditis and Hashimoto’s thyroiditis are responsible of similarly physiopathologic phenomenons that originated biphasic thyroiditis. Pain in the thyroidal gland is relevant in subacute and suppurative thyroiditis and, rarely is present in silent thyroiditis or in acute exacerbation of Hashimoto’s thyroiditis. In most of the cases, it is possible to establish the diagnosis of thyroiditis through clinical history, thyroidal function tests, isotopic studies and ecosonography. Thyroid fine needle biopsy resolves doubtful cases. This review about “Clinical-pathological spectrum of thyroiditis”, results from the synthesis of bibliographic information and the experience obtained with thyroiditis through and integral clinic focus.