Hepatitis Acute Fulminant and Thyrotosicosis
Autor(a) principal: | |
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Data de Publicação: | 2017 |
Tipo de documento: | Artigo |
Idioma: | por |
Título da fonte: | Revista Científica da Faculdade de Medicina de Campos |
Texto Completo: | https://www.fmc.br/ojs/index.php/RCFMC/article/view/37 |
Resumo: | Herein, we present the case of a female patient, 44 years old, who was transferred to the intensive care center (ICU) of the Hospital das Clínicas in Belo Horizonte/MG, with abdominal pain, nausea, vomiting, jaundice and fever, anorexia, loss of appetite, whose symptoms began 30 days ago. She has a history of hypothyroidism being treated irregularly with T4 for the last five years and stopped the treatment when the current symptoms appeared. She presented T3 (7.26 pg/mL) VN: 2.77 to 5.07; TSH (0.214 IU/mL) VN: 0.465. Transaminases AST (977 U/L) VN: 15 to 46; ALT (795 U/L) VN:13 to 69; bilirubin total (4.12 mg/dL) VN: 0.2 to 1.3; direct bilirubin (30 mg/dL) VN: up to 0.25. She was maintained without anti-thyroid and was started on propranolol at a dosage of up to 480 mg/day. An MRI abdominal exam presented cholangiocarcinoma with free abdominal fluid, suggestive of being related to the inflammatory process. There was non-specific thickening of the gallbladder and bilateral pleural effusion. The serology exam for Hepatitis A, B, and C was negative. There was liver function deterioration and high levels of thyroid hormones were maintained. The patient suffered an acute fulminant hepatic failure and was immediately submitted to a hepatic transplant. After the procedure the liver (explant) was sent for anatomopathological study; histopathologic findings included the presence of an extensive area of necrosis of the liver parenchyma. The remaining septa showed mononuclear inflammatory infiltrates (MNII). Therefore, it was concluded that chronic hyperthyroidism can exacerbate and perpetuate acute fulminant hepatic failur and that regular medicinal treatment, together with clinically routine laboratory exames could prevent serious complications, permitting successful therapy in patients with hyperthyroidism. |
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Hepatitis Acute Fulminant and ThyrotosicosisHEPATITE AGUDA FULMINANTE E TIREOTOXICOSETireoideHepatiteFígadoInflamaçãoTireotoxicoseInflammationThyroidLiverThyrotoxicosisHepatitisHerein, we present the case of a female patient, 44 years old, who was transferred to the intensive care center (ICU) of the Hospital das Clínicas in Belo Horizonte/MG, with abdominal pain, nausea, vomiting, jaundice and fever, anorexia, loss of appetite, whose symptoms began 30 days ago. She has a history of hypothyroidism being treated irregularly with T4 for the last five years and stopped the treatment when the current symptoms appeared. She presented T3 (7.26 pg/mL) VN: 2.77 to 5.07; TSH (0.214 IU/mL) VN: 0.465. Transaminases AST (977 U/L) VN: 15 to 46; ALT (795 U/L) VN:13 to 69; bilirubin total (4.12 mg/dL) VN: 0.2 to 1.3; direct bilirubin (30 mg/dL) VN: up to 0.25. She was maintained without anti-thyroid and was started on propranolol at a dosage of up to 480 mg/day. An MRI abdominal exam presented cholangiocarcinoma with free abdominal fluid, suggestive of being related to the inflammatory process. There was non-specific thickening of the gallbladder and bilateral pleural effusion. The serology exam for Hepatitis A, B, and C was negative. There was liver function deterioration and high levels of thyroid hormones were maintained. The patient suffered an acute fulminant hepatic failure and was immediately submitted to a hepatic transplant. After the procedure the liver (explant) was sent for anatomopathological study; histopathologic findings included the presence of an extensive area of necrosis of the liver parenchyma. The remaining septa showed mononuclear inflammatory infiltrates (MNII). Therefore, it was concluded that chronic hyperthyroidism can exacerbate and perpetuate acute fulminant hepatic failur and that regular medicinal treatment, together with clinically routine laboratory exames could prevent serious complications, permitting successful therapy in patients with hyperthyroidism.Paciente feminino, 44 anos transferida para o centro de terapia intensiva (CTI) do Hospital das Clínicas de Belo Horizonte/MG, com quadro de dor abdominal, náuseas, vômitos, icterícia e febre, anorexia, inapetência, iniciado há 30 dias. História de hipotireoidismo e tratamento irregular com T4 há cinco anos; interrompeu a medicação quando iniciou o quadro atual. Apresentava T3 (7,26 pg/ml) VN.: 2,77 a 5,07; TSH (0,214 mU/L) VN: 0,465. Transaminases AST (977 U/L) VN.:15 a 46; ALT (795 U/L) VN.:13 a 69; bilirrubina total (4.12 mg/dL) VN.: 0.2 a 1.3; bilirrubina direta (30 mg/dL) VN.: até 0.25. Foi mantida sem anti- tireoidiano e iniciado propranolol até dose de 480 mg /dia. Exame de ressonância magnética abdominal e colangio com líquido livre abdominal, sugestivo de estar relacionado ao processo inflamatório. Espessamento inespecífico da vesícula biliar. Derrame pleural bilateral. Sorologia para o vírus da hepatite A, B e C negativo. Ocorreu piora da função hepática e manutenção de níveis elevados de hormônios tireoidianos. A paciente evoluiu para um quadro de hepatite aguda fulminante, imediatamente submetida ao transplante hepático. Após procedimento o fígado (explante) foi enviado para estudo anatopatológico; os achados histopatológicos incluíram a presença de extensa área de necrose do parênquima hepático. Nos septos remanescentes, mostravam-se infiltrados inflamatórios mononucleares (IIMM). Conclui-se, portanto, que o hipertireoidismo crônico pode exacerbar e perpetuar a disfunção hepática aguda fulminante e que o tratamento medicamentoso regular aliado aos exames laboratoriais de rotina clínica poderão prevenir complicações graves, permitindo uma terapêutica bem sucedida em pacientes com hipertireoidismo.Faculdade de Medicina de Campos (FMC)2017-07-31info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.fmc.br/ojs/index.php/RCFMC/article/view/3710.29184/1980-7813.rcfmc.37.vol.12.n1.2017Scientific Journal of the Medical School of Campos; Vol. 12 No. 1 (2017); 26-32Revista Científica da Faculdade de Medicina de Campos; v. 12 n. 1 (2017); 26-321980-7813reponame:Revista Científica da Faculdade de Medicina de Camposinstname:Faculdade de Medicina de Campos (FMC)instacron:FMCporhttps://www.fmc.br/ojs/index.php/RCFMC/article/view/37/139Copyright (c) 2017 Revista Científica da Faculdade de Medicina de Camposinfo:eu-repo/semantics/openAccessMiranda, Carla Paixão2017-12-12T17:30:29Zoai:ojs.www.fmc.br:article/37Revistahttps://www.fmc.br/ojs/index.php/RCFMC/PRIhttps://www.fmc.br/ojs/index.php/RCFMC/oai||revista@fmc.br1980-78131980-7813opendoar:2017-12-12T17:30:29Revista Científica da Faculdade de Medicina de Campos - Faculdade de Medicina de Campos (FMC)false |
dc.title.none.fl_str_mv |
Hepatitis Acute Fulminant and Thyrotosicosis HEPATITE AGUDA FULMINANTE E TIREOTOXICOSE |
title |
Hepatitis Acute Fulminant and Thyrotosicosis |
spellingShingle |
Hepatitis Acute Fulminant and Thyrotosicosis Miranda, Carla Paixão Tireoide Hepatite Fígado Inflamação Tireotoxicose Inflammation Thyroid Liver Thyrotoxicosis Hepatitis |
title_short |
Hepatitis Acute Fulminant and Thyrotosicosis |
title_full |
Hepatitis Acute Fulminant and Thyrotosicosis |
title_fullStr |
Hepatitis Acute Fulminant and Thyrotosicosis |
title_full_unstemmed |
Hepatitis Acute Fulminant and Thyrotosicosis |
title_sort |
Hepatitis Acute Fulminant and Thyrotosicosis |
author |
Miranda, Carla Paixão |
author_facet |
Miranda, Carla Paixão |
author_role |
author |
dc.contributor.author.fl_str_mv |
Miranda, Carla Paixão |
dc.subject.por.fl_str_mv |
Tireoide Hepatite Fígado Inflamação Tireotoxicose Inflammation Thyroid Liver Thyrotoxicosis Hepatitis |
topic |
Tireoide Hepatite Fígado Inflamação Tireotoxicose Inflammation Thyroid Liver Thyrotoxicosis Hepatitis |
description |
Herein, we present the case of a female patient, 44 years old, who was transferred to the intensive care center (ICU) of the Hospital das Clínicas in Belo Horizonte/MG, with abdominal pain, nausea, vomiting, jaundice and fever, anorexia, loss of appetite, whose symptoms began 30 days ago. She has a history of hypothyroidism being treated irregularly with T4 for the last five years and stopped the treatment when the current symptoms appeared. She presented T3 (7.26 pg/mL) VN: 2.77 to 5.07; TSH (0.214 IU/mL) VN: 0.465. Transaminases AST (977 U/L) VN: 15 to 46; ALT (795 U/L) VN:13 to 69; bilirubin total (4.12 mg/dL) VN: 0.2 to 1.3; direct bilirubin (30 mg/dL) VN: up to 0.25. She was maintained without anti-thyroid and was started on propranolol at a dosage of up to 480 mg/day. An MRI abdominal exam presented cholangiocarcinoma with free abdominal fluid, suggestive of being related to the inflammatory process. There was non-specific thickening of the gallbladder and bilateral pleural effusion. The serology exam for Hepatitis A, B, and C was negative. There was liver function deterioration and high levels of thyroid hormones were maintained. The patient suffered an acute fulminant hepatic failure and was immediately submitted to a hepatic transplant. After the procedure the liver (explant) was sent for anatomopathological study; histopathologic findings included the presence of an extensive area of necrosis of the liver parenchyma. The remaining septa showed mononuclear inflammatory infiltrates (MNII). Therefore, it was concluded that chronic hyperthyroidism can exacerbate and perpetuate acute fulminant hepatic failur and that regular medicinal treatment, together with clinically routine laboratory exames could prevent serious complications, permitting successful therapy in patients with hyperthyroidism. |
publishDate |
2017 |
dc.date.none.fl_str_mv |
2017-07-31 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://www.fmc.br/ojs/index.php/RCFMC/article/view/37 10.29184/1980-7813.rcfmc.37.vol.12.n1.2017 |
url |
https://www.fmc.br/ojs/index.php/RCFMC/article/view/37 |
identifier_str_mv |
10.29184/1980-7813.rcfmc.37.vol.12.n1.2017 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.none.fl_str_mv |
https://www.fmc.br/ojs/index.php/RCFMC/article/view/37/139 |
dc.rights.driver.fl_str_mv |
Copyright (c) 2017 Revista Científica da Faculdade de Medicina de Campos info:eu-repo/semantics/openAccess |
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Copyright (c) 2017 Revista Científica da Faculdade de Medicina de Campos |
eu_rights_str_mv |
openAccess |
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application/pdf |
dc.publisher.none.fl_str_mv |
Faculdade de Medicina de Campos (FMC) |
publisher.none.fl_str_mv |
Faculdade de Medicina de Campos (FMC) |
dc.source.none.fl_str_mv |
Scientific Journal of the Medical School of Campos; Vol. 12 No. 1 (2017); 26-32 Revista Científica da Faculdade de Medicina de Campos; v. 12 n. 1 (2017); 26-32 1980-7813 reponame:Revista Científica da Faculdade de Medicina de Campos instname:Faculdade de Medicina de Campos (FMC) instacron:FMC |
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Faculdade de Medicina de Campos (FMC) |
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FMC |
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FMC |
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Revista Científica da Faculdade de Medicina de Campos |
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Revista Científica da Faculdade de Medicina de Campos |
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Revista Científica da Faculdade de Medicina de Campos - Faculdade de Medicina de Campos (FMC) |
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