A case of thyroid crisis complicated with acute hepatic failure.

Inoue, Tatsuki; Tanigawa, Keiichiro; Furuya, Hiroshi; Nakano, Akinobu; Notsu, Kazumi; NOTE, Shinya; Kato, Yuzuru; Nagaoka, Saburo

doi:10.2169/naika.77.564

Cited by 16 publications

(10 citation statements)

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“…The formation of condensed chromatin bodies observed in vitro in liver nuclei exposed to proteins released by T3‐treated mitochondria (Fig. 8A,B) seems to be analogous to nuclear irregularity and ballooning of nuclei reported previously in liver histologic results of thyrotoxic patients 1–8. The in vitro observations support our hypothesis of a direct action of T3 on mitochondria, and also corroborate our in vivo findings of T3‐induced disruption of mitochondrial integrity and release of apoptogenic proteins by mitochondria.…”

Section: Discussionsupporting

confidence: 90%

“…This study has provided insights into the pathogenesis of liver dysfunction associated with severe hyperthyroidism. No firm evidence has been provided on the nature of the hepatic injury in existing literature on hyperthyroidism 1–8. Data from this study suggest that hyperthyroidism induces apoptosis in the liver.…”

Section: Discussionmentioning

confidence: 60%

“…There is increasing evidence that apoptosis plays a major role in various pathologic conditions. Earlier, morphologic changes in the liver of patients with thyrotoxicosis were attributed to necrotic cell death 3, 4. However, at the time, the process of apoptosis had not been investigated.…”

Section: Discussionmentioning

confidence: 99%

“…Thyroid hormone (TH) affects all tissues and modulates the rate of metabolic activity. Liver damage in hyperthyroid patients has been extensively reported since Habershon's original report in 1874 1–5. Liver function becomes compromised in 45% to 90% of thyrotoxic patients; in most cases, the changes in the liver are characterized by some degree of fatty infiltration, and by cytoplasmic vacuolization, nuclear irregularity, and hyperchromatism in hepatocytes 6, 7.…”

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confidence: 99%

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Severe hyperthyroidism induces mitochondria-mediated apoptosis in rat liver

et al. 2004

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Thyrotoxicosis may be associated with a variety of abnormalities of liver function. The pathogenesis of hepatic dysfunction in thyrotoxicosis is unknown, but has been attributed to mitochondrial dysfunction. We studied the effect of altered thyroid function on the apoptotic index in rat liver. Extensive DNA fragmentation and significantly increased caspase-3 activity (P < .001) and caspase-9 activation (P < .005) were observed in hyperthyroid rat liver; cell death by apoptosis was confirmed. In hyperthyroid rat liver, 60% of mitochondria exhibited disruption of their outer membranes and a decrease in the number of cristae. These findings, along with significant translocation of cytochrome c and second mitochondriaderived activator of caspases to cytosol (P < .005), suggest activation of a mitochondrialmediated pathway. However, no change in the expression levels of Bcl-2, Bax, and Bcl-x L were found in hyperthyroidism. For in vitro experiments, rat liver mitochondria were isolated and purified in sucrose density gradients and were treated with triiodothyronine (T3; 2-8 M). T3 treatment resulted in an abrupt increase in mitochondrial permeability transition. Using a cell-free apoptosis system, the apoptogenic nature of proteins released from mitochondria was confirmed by observing changes in nuclear morphologic features and DNA fragmentation. Proteins released by 6 M T3 contained significantly increased amounts of cytochrome c (P < .01) and induced apoptotic changes in 67% of nuclei. In conclusion, using in vivo and in vitro approaches, we provide evidence that excess T3 causes liver dysfunction by inducing apoptosis, as a result of activation of a mitochondria-dependent pathway. Thus, the results of this study provide an explanation for liver dysfunction associated with hyperthyroidism. ( T hyroid hormone (TH) affects all tissues and modulates the rate of metabolic activity. Liver damage in hyperthyroid patients has been extensively reported since Habershon's original report in 1874. [1][2][3][4][5] Liver function becomes compromised in 45% to 90% of thyrotoxic patients; in most cases, the changes in the liver are characterized by some degree of fatty infiltration, and by cytoplasmic vacuolization, nuclear irregularity, and hyperchromatism in hepatocytes. 6,7 The pathogenesis of hepatic dysfunction in severe hyperthyroidism is unknown. Possible thyroid-liver interactions include liver damage secondary to the systemic effects of excess thyroid hormone, direct toxic effects of thyroid hormone on the liver, an association of intrinsic liver disease and intrinsic thyroid disease involving autoimmune mechanisms, changes in thyroid hormone metabolism secondary to intrinsic liver disease, and subclinical physiologic effects of thyroid hormone on functions of the liver. 5 The hepatic injury associated with hyperthyroidism varies from mild liver dysfunction associated with nonspecific histologic changes to severe central hepatic ischemia.Ultrastructural and functional changes in mitochondria, such as enlargement, a mass ...

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Severe hyperthyroidism induces mitochondria-mediated apoptosis in rat liver

et al. 2004

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“…Das Leberversagen kann eine seltene Komplikation einer thyreotoxischen Krise sein [12].Schilddrüsenhormone haben auf den hepatischen Stoffwechsel großen Einfluss und Erhöhungen von Leberenzymen,Ikterus sowie eine Hepatomegalie werden bei Hyperthyreose auch unabhän-gig von einer Herzinsuffizienz häufig gefunden [1,7,9]. Gleichzeitig hat natürlich eine Therapie mit Thionamiden oder Kaliumperchlorat einen potenziell lebertoxischen Effekt.…”

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Die thyreotoxische Krise

Reschke

Lehnert

2003

Der Internist

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Besides the typical and in this case severe signs of hyperthyroidism the thyrotoxic crisis is characterized by additional signs and symptoms such as fever, cardiac involvement (tachycardia, arrhythmia, heart failure) and central nervous impairment eventually leading to coma. Additional diseases and comorbidities impair the diagnostic process and may mask the symptoms of thyrotoxicosis. If undiagnosed, this situation harbors a mortality of approximately 90%. The precise knowledge of typical (and atypical) symptoms is mandatory in order to rapidly recognize this situation and to initiate pharmacological treatment and/or surgery. An experienced endocrinologist should always be involved in this decision process.

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Thyroid storm in a patient with fulminant hepatic failure

et al. 2010

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This manuscript describes a 28-year-old patient with a history of Graves' disease who was transferred to Tulane University Hospital with fulminant hepatic failure. He reported associated nausea, vomiting, anorexia, as well as jaundice and abdominal discomfort for a period of 3 weeks prior to his admission. His thyroid function tests on admission were TSH, 0.013 μU/mL; T3, 94.9 μU/mL; T4, 9.37 μU/mL; Free T4, >6 μU/mL. His liver function tests were characteristic of hepatic failure. The patient underwent an emergent liver transplant. His surgery was complicated by heart failure and acute respiratory distress syndrome. Given the patients clinical presentation and laboratory results, a diagnosis of thyroid storm was made and a decision was made to proceed with an emergent thyroidectomy. The posttransplant multiorgan dysfunction was rapidly reversed by prompt thyroidectomy and decisive management. The patient was discharged from the hospital with normal thyroid and liver function tests.

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A case of thyroid crisis complicated with acute hepatic failure.

Cited by 16 publications

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Severe hyperthyroidism induces mitochondria-mediated apoptosis in rat liver

Severe hyperthyroidism induces mitochondria-mediated apoptosis in rat liver

Die thyreotoxische Krise

Thyroid storm in a patient with fulminant hepatic failure

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