RESUMO
PURPOSE: To describe a case of acute thyroiditis and bilateral optic neuritis associated with SARS-CoV-2 vaccination. METHODS: A single case report from a tertiary referral center. RESULTS: The patient described in the following case report developed acute thyroiditis and bilateral optic neuritis following SARS-CoV-2 vaccination. The patient underwent pulse therapy followed by oral tapering corticosteroid therapy with an improvement of the bilateral disc swelling and the visual field, and recovery of thyroid-stimulating hormone to the normal limits. CONCLUSION: Although the association between immunization and the onset of demyelinating manifestations of the central nervous system is well documented, this is the first reported case of bilateral optic neuritis and acute thyroiditis and subsequent to administration of vaccination against SARS-CoV-2.
Assuntos
Vacinas contra COVID-19/efeitos adversos , COVID-19/prevenção & controle , Neurite Óptica/etiologia , SARS-CoV-2 , Tireoidite/etiologia , Vacinação/efeitos adversos , Doença Aguda , Adulto , Feminino , Glucocorticoides/uso terapêutico , Humanos , Imageamento por Ressonância Magnética , Neurite Óptica/diagnóstico , Neurite Óptica/tratamento farmacológico , Órbita/diagnóstico por imagem , Pulsoterapia , Tireoidite/diagnóstico , Tireoidite/tratamento farmacológico , Tomografia de Coerência Óptica , Acuidade Visual/fisiologiaRESUMO
BACKGROUND: Iodine is essential for thyroid hormone synthesis and is an important regulator of thyroid function. Chronic iodine deficiency leads to hypothyroidism, but iodine excess also impairs thyroid function causing hyperthyroidism, hypothyroidism, and/or thyroiditis. This study aimed to investigate the underlying mechanisms by which exposure to chronic iodine excess impairs pituitary-thyroid axis function. METHODS: Male Wistar rats were treated for two months with NaI (0.05% and 0.005%) or NaI+NaClO4 (0.05%) dissolved in drinking water. Hormone levels, gene expression, and thyroid morphology were analyzed later. RESULTS: NaI-treated rats presented high levels of iodine in urine, increased serum thyrotropin levels, slightly decreased serum thyroxine/triiodothyronine levels, and a decreased expression of the sodium-iodide symporter, thyrotropin receptor, and thyroperoxidase mRNA and protein, suggesting a primary thyroid dysfunction. In contrast, thyroglobulin and pendrin mRNA and protein content were increased. Kidney and liver deiodinase type 1 mRNA expression was decreased in iodine-treated rats. Morphological studies showed larger thyroid follicles with higher amounts of colloid and increased amounts of connective tissue in the thyroid of iodine-treated animals. All these effects were prevented when perchlorate treatment was combined with iodine excess. CONCLUSIONS: The present data reinforce and add novel findings about the disruption of thyroid gland function and the compensatory action of increased thyrotropin levels in iodine-exposed animals. Moreover, they draw attention to the fact that iodine intake should be carefully monitored, since both deficient and excessive ingestion of this trace element may induce pituitary-thyroid axis dysfunction.
Assuntos
Regulação da Expressão Gênica/efeitos dos fármacos , Iodo/intoxicação , Hipófise/efeitos dos fármacos , Intoxicação/fisiopatologia , Glândula Tireoide/efeitos dos fármacos , Tireoidite/etiologia , Animais , Antídotos/uso terapêutico , Iodeto Peroxidase/antagonistas & inibidores , Iodeto Peroxidase/genética , Iodeto Peroxidase/metabolismo , Iodo/química , Iodo/urina , Masculino , Percloratos/uso terapêutico , Hipófise/metabolismo , Hipófise/patologia , Hipófise/fisiopatologia , Intoxicação/metabolismo , Intoxicação/patologia , Intoxicação/prevenção & controle , RNA Mensageiro/metabolismo , Ratos Wistar , Receptores da Tireotropina/antagonistas & inibidores , Receptores da Tireotropina/genética , Receptores da Tireotropina/metabolismo , Eliminação Renal , Compostos de Sódio/uso terapêutico , Iodeto de Sódio/administração & dosagem , Simportadores/antagonistas & inibidores , Simportadores/genética , Simportadores/metabolismo , Glândula Tireoide/metabolismo , Glândula Tireoide/patologia , Glândula Tireoide/fisiopatologia , Tireotropina/sangue , Tireotropina/metabolismo , Tiroxina/sangue , Tiroxina/metabolismo , Testes de Toxicidade Crônica , Toxicocinética , Tri-Iodotironina/sangue , Tri-Iodotironina/metabolismoRESUMO
El término tiroiditis comprende un grupo de enfermedades de la glándula tiroides caracterizado por la presencia de inflamación, abarcando entidades autoinmunes y no-autoinmunes. Pueden manifestarse como enfermedades agudas con dolor tiroideo severo (tiroiditis subaguda y tiroiditis infecciosas), y condiciones en las cuales la inflamación no es clínicamente evidente, cursando sin dolor y presentando disfunción tiroidea y/o bocio (tiroiditis inducida por fármacos y tiroiditis de Riedel). El objetivo de esta revisión es aportar un enfoque actualizado sobre las tiroiditis no-autoinmunes cubriendo sus aspectos clínicos, diagnósticos y terapéuticos.
The term thyroiditis comprises a group of thyroid diseases characterized by the presence of inflammation, including autoimmune and non-autoimmune entities. It may manifest as an acute illness with severe thyroid pain (subacute thyroiditis and infectious thyroiditis), and conditions in which the inflammation is not clinically evident evolving without pain and presenting primarily thyroid dysfunction and/or goiter (drug-induced thyroiditis and Riedel thyroiditis). The aim of this review is to provide an updated approach on non-autoimmune thyroiditis and its clinical, diagnostic and therapeutic aspects.
Assuntos
Humanos , Tireoidite/diagnóstico , Tireoidite/etiologia , Tireoidite/terapia , Tireoidite Subaguda/diagnóstico , Tireoidite Supurativa/diagnóstico , Tireoidite Supurativa/etiologia , Tireoidite Supurativa/terapia , Anti-Inflamatórios não Esteroides/uso terapêutico , Doença Crônica , Interferon-alfa/efeitos adversos , Compostos de Lítio/efeitos adversos , Diagnóstico Diferencial , Glucocorticoides/uso terapêutico , Bócio/complicações , Amiodarona/efeitos adversosRESUMO
The term thyroiditis comprises a group of thyroid diseases characterized by the presence of inflammation, including autoimmune and non-autoimmune entities. It may manifest as an acute illness with severe thyroid pain (subacute thyroiditis and infectious thyroiditis), and conditions in which the inflammation is not clinically evident evolving without pain and presenting primarily thyroid dysfunction and/or goiter (drug-induced thyroiditis and Riedel thyroiditis). The aim of this review is to provide an updated approach on non-autoimmune thyroiditis and its clinical, diagnostic and therapeutic aspects.
Assuntos
Tireoidite , Amiodarona/efeitos adversos , Anti-Inflamatórios não Esteroides/uso terapêutico , Doença Crônica , Diagnóstico Diferencial , Glucocorticoides/uso terapêutico , Bócio/complicações , Humanos , Interferon-alfa/efeitos adversos , Compostos de Lítio/efeitos adversos , Tireoidite/diagnóstico , Tireoidite/etiologia , Tireoidite/terapia , Tireoidite Subaguda/diagnóstico , Tireoidite Subaguda/etiologia , Tireoidite Subaguda/terapia , Tireoidite Supurativa/diagnóstico , Tireoidite Supurativa/etiologia , Tireoidite Supurativa/terapiaRESUMO
A tireotoxicose é um estado hipermetabólico decorrente dos efeitos de níveis teciduais elevados de hormônios tireoideanos (HTs). O hipertireoidismo é a causa mais comum, e decorre do excesso de hormônios produzidos pela tireoide. Outras causas de tireotoxicose ocorrem por produção extratireoideana ou administração exógena de hormônios tireoideanos. A principal causa de tireotoxicose, o bócio difuso tóxico (BDT) de causa autoimune, responsável por até 80% dos casos, é aqui abordado, assim como as demais causas. O tratamento é realizado com drogas antitireoideanas, iodo radioativo ou cirurgia e exige acompanhamento de longo prazo, tanto pela possibilidade de recidivas como do desenvolvimento de hipotireoidismo.
Thyrotoxicosis is a hypermetabolic state due to the effects of high tissue levels of thyroid hormones (TH). Hyperthyroidism is the most common cause and results from excess hormones produced by the thyroid. Other causes of thyrotoxicosis occur extra thyroid production or exogenous administration of thyroid hormones. The main cause of thyrotoxicosis, the diffuse toxic goiter (DTG) of autoimmune cause, accounting for up to 80% of cases, is discussed here, as well as other causes. The treatment is performed with antithyroid drugs, radioactive iodine or surgery and requires long-term follow-up, due to both the possibility of recurrence and the development of hypothyroidism.
Assuntos
Humanos , Masculino , Feminino , Bócio/cirurgia , Bócio/terapia , Hipertireoidismo/diagnóstico , Hipertireoidismo/etiologia , Hipertireoidismo , Antitireóideos/uso terapêutico , Glândula Tireoide/cirurgia , Hormônios Tireóideos/metabolismo , Oftalmopatias/complicações , Radioisótopos do Iodo/uso terapêutico , Tireotoxicose , Tireoidite/etiologiaRESUMO
Factors that should be considered when studying the effect of dietary iodine in the development of thyroid cancer include pathological criteria, diagnostic techniques, screening programs, radioactive fallout, and standard of medical care in the studied population. In most surveys, papillary carcinoma forms the largest group of thyroid malignancies, both before and after iodine prophylaxis where an increase in the papillary:follicular carcinoma ratio is also noted. Undifferentiated carcinomas decrease after salt prophylaxis. In Salta, Argentina, the increasing incidence of clinically significant papillary thyroid cancer and the decrease of undifferentiated carcinoma after iodine prophylaxis are probably due to better access to health centers and consequent earlier detection of differentiated precursor tumors. Autoimmune focal and diffuse or Hashimoto's thyroiditis are linked to dietary iodine. Pathological studies made in different regions indicate that these types of thyroiditis occur more frequently in areas of iodine sufficiency than in areas of iodine deficiency, and increase after iodine prophylaxis both in non-goitrous and iodine-deficient areas like Salta, Argentina. An increase of lymphocytic thyroiditis could be linked to an increased incidence of primary thyroid lymphoma, and thyroiditis is more commonly associated with papillary carcinoma than with other types of thyroid follicular or C-cell derived carcinomas regardless of iodine intake.
Assuntos
Adenocarcinoma Folicular/prevenção & controle , Adenoma/prevenção & controle , Carcinoma Papilar, Variante Folicular/prevenção & controle , Iodo/administração & dosagem , Cloreto de Sódio na Dieta/administração & dosagem , Neoplasias da Glândula Tireoide/prevenção & controle , Tireoidite/etiologia , Adenocarcinoma Folicular/epidemiologia , Adenocarcinoma Folicular/patologia , Adenoma/epidemiologia , Adenoma/patologia , Argentina , Carcinoma Papilar, Variante Folicular/epidemiologia , Carcinoma Papilar, Variante Folicular/patologia , Dieta , Feminino , Bócio Endêmico/complicações , Bócio Endêmico/epidemiologia , Bócio Endêmico/prevenção & controle , Humanos , Iodo/efeitos adversos , Masculino , Modelos Biológicos , Cloreto de Sódio na Dieta/efeitos adversos , Neoplasias da Glândula Tireoide/epidemiologia , Neoplasias da Glândula Tireoide/patologia , Tireoidite/epidemiologia , Tireoidite/patologiaRESUMO
La falla ovárica prematura (FOP), también llamada menopausia precoz, se define como la pérdida de la función cíclica de los ovarios antes de los 40 años de edad y después de la pubertad. Se ha reportado anormalidades endocrinas y autoinmunes asociadas con la FOP y se ha sugerido que las enfermedades tiroideas son comunes. Sesenta y dos mujeres con FOP fueron estudiadas para determinar la frecuencia de trastornos tiroideos, ya que no hay estudios sobre esta asociación en esta región geográfica. La evaluación incluyó historia clínica y examen físico, medición de tiroestimulina (TSH)...
Assuntos
Feminino , Bócio/diagnóstico , Bócio/fisiopatologia , Hipotireoidismo/prevenção & controle , Menopausa Precoce/fisiologia , Tireoidite/etiologiaRESUMO
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 Rieldels thyroiditis. Also, subacute and silent thyroiditis (and it postpartum variant) are non common diseases, while autoimmune chronic thyroiditis or Hashimotos 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 Riedels 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 Hashimotos 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 Hashimotos 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.
Assuntos
Humanos , Fungos/imunologia , Inflamação/patologia , Tireoidite/classificação , Tireoidite/etiologia , Tireoidite/patologia , Tireotoxicose/patologia , Biópsia/métodos , Doença de Hashimoto/patologiaRESUMO
AIMS: We report uncommon histopathological findings in fatal measles infection. METHODS AND RESULTS: We describe the autopsies of four patients who died during a measles outbreak in São Paulo, Brazil, in 1997. Two of the patients were children receiving chemotherapy for non-Hodgkin's lymphoma, one was an adult with acquired immunodeficiency syndrome (AIDS) and the fourth was an apparently healthy woman. All patients had their deaths attributed to measles pneumonia. The autopsies revealed extensive giant cell pneumonia and diffuse alveolar damage, severe acute pancreatitis, necrotizing sialoadenitis and thyroiditis due to measles. Measles antigen was detected in lung tissue using a monoclonal anti-measles antibody. CONCLUSIONS: : Pancreatitis, thyroiditis and sialoadenitis are not previously reported histopathological findings in measles infection. Pancreatitis is a potentially severe complication and should be considered when treating patients with atypical measles.
Assuntos
Sarampo/patologia , Adolescente , Adulto , Pré-Escolar , Evolução Fatal , Humanos , Pulmão/patologia , Linfonodos/patologia , Masculino , Sarampo/complicações , Pâncreas/patologia , Pancreatite/etiologia , Pancreatite/patologia , Sialadenite/etiologia , Sialadenite/patologia , Glândula Submandibular/patologia , Glândula Tireoide/patologia , Tireoidite/etiologia , Tireoidite/patologiaRESUMO
A 23 years old female with Graves' disease initiated a symptomatic treatment with propanolol and then received radioactive iodine (I-311) 370 MBq (10 mCi) as definitive treatment. Three weeks later she was hospitalized because she presented acute radiation thyroiditis. She was discharged after 48 h of treatment, but clinical symptoms and signs persisted for over 30 days, but in less degree. One month later she developed hypothyroidism. There are three therapeutics options for the treatment of Grave's disease (antithyroid drugs, radioiodine and surgery). There are some hospitals in which the use of radioactive iodine is preferred as the first option, without a pretreatment with antithyroid drugs, but this could lead to acute thyroiditis or thyroid storm.