Liver changes in patients with hyperthyroidism

Sola, Jesús Javier; Pardo-Mindan, F. J.; Zozaya, J. M.; Quiroga, Jorge; Sangro, Bruno; Prìeto, Jesús

doi:10.1111/j.1600-0676.1991.tb00516.x

Cited by 44 publications

(26 citation statements)

References 9 publications

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“…Sola of five patients with hyperthyroidism that revealed nonspecific changes including mild to moderate intrahepatic cholestasis, lobular inflammation of eosinophilic origin, and Kuppfer cell hyperplasia. There was no correlation between the severity of the histologic damage and thyroid function tests [4,17]. Our patient's liver biopsy demonstrated a predominantly centrizonal cholestasis with hepatocellular degeneration, features in keeping with the previously reported literature.…”

Section: Discussionsupporting

confidence: 76%

Severe cholestatic jaundice secondary to hyperthyroidism

Usta¹,

Massaad²,

Parekh³

et al. 2013

IJCRI

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Introduction:Hyperthyroidism is a known cause of nonspecific abnormalities in liver biochemitries; most commonly mild elevations in serum bilirubin and liver enzymes. Case Report: A case of severe cholestatic jaundice secondary to Grave's disease. The patient is a 28yearoldAfricanAmerican male who presented to the emergency room with chronic diarrhea, weight loss and jaundice. At presentation, his liver enzymes were elevated in a cholestatic pattern and his bilirubin was 21.4 mg/dL. Upon treatment with propranolol and propylthouracil, his diarrhea, pruritus, jaundice, and liver enzymes quickly improved. His bilirubin returned to normal over a period of two months. Conclusion: While severe intrahepatic cholestasis and jaundice due to hyperthyroidism is rare, the diagnosis should be considered in patients presenting with manifestations of liver disease, as appropriate treatment of hyperthyroidism results in resolution of jaundice.

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Section: Discussionsupporting

confidence: 76%

Severe cholestatic jaundice secondary to hyperthyroidism

Usta¹,

Massaad²,

Parekh³

et al. 2013

IJCRI

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“…Even if this can originate from bone and/or liver, the concomitant increase of ␥-GT and bilirubin is an index of cholestasis (10). The histological features observed in the course of cholestasis are similar to the nonspecific changes seen in hepatic injury, in addition to centrilobular intrahepatocytic cholestasis (49). The early reports of patients developing a spectrum of pathological changes from focal necrosis with fatty change to cirrhosis can be attributed to untreated hyperthyroidism (11).…”

Section: Discussionmentioning

confidence: 82%

Thyroid hormone inhibits biliary growth in bile duct-ligated rats by PLC/IP₃/Ca²⁺-dependent downregulation of SRC/ERK1/2

Fava¹,

Ueno²,

Glaser³

et al. 2007

American Journal of Physiology-Cell Physiology

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.-The role of the thyroid hormone agonist 3,3Ј,5 L-tri-iodothyronine (T3) on cholangiocytes is unknown. We evaluated the in vivo and in vitro effects of T3 on cholangiocyte proliferation of bile duct-ligated (BDL) rats. We assessed the expression of ␣ 1-, ␣2-, ␤1-, and ␤2-thyroid hormone receptors (THRs) by immunohistochemistry in liver sections from normal and BDL rats. BDL rats were treated with T3 (38.4 g/day) or vehicle for 1 wk. We evaluated 1) biliary mass and apoptosis in liver sections and 2) proliferation in cholangiocytes. Serum-free T3 levels were measured by chemiluminescence. Purified BDL cholangiocytes were treated with 0.2% BSA or T3 (1 M) in the absence/presence of U-73122 (PLC inhibitor) or BAPTA/AM (intracellular Ca 2ϩ chelator) before measurement of PCNA protein expression by immunoblots. The in vitro effects of T3 (1 M) on 1) cAMP, IP3, and Ca 2ϩ levels and 2) the phosphorylation of Src Tyr139 and Tyr530 (that, together, regulate Src activity) and ERK1/2 of BDL cholangiocytes were also evaluated. ␣ 1-, ␣2-, ␤1-, and ␤2-THRs were expressed by bile ducts of normal and BDL rats. In vivo, T3 decreased cholangiocyte proliferation of BDL rats. In vitro, T3 inhibition of PCNA protein expression was blocked by U-73122 and BAPTA/AM. Furthermore, T3 1) increased IP3 and Ca 2ϩ levels and 2) decreased Src and ERK1/2 phosphorylation of BDL cholangiocytes. T3 inhibits cholangiocyte proliferation of BDL rats by PLC/IP3/Ca 2ϩ -dependent decreased phosphorylation of Src/ERK1/2. Activation of the intracellular signals triggered by T3 may modulate the excess of cholangiocyte proliferation in liver diseases.

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“…Mild histological changes are common [46] , but cases of fulminant hepatic failure with centrizonal necrosis have been described [46,47] . Long term untreated hyperthyroidism can ultimately lead to cirrhosis [48] . Quantitative 99mTc-HIDA cholescintigraphy in hyperthyroid rats without a gallbladder showed accelerated bile flow to the duodenum [21] .…”

Section: Livermentioning

confidence: 99%

Consequences of dysthyroidism on the digestive tract and viscera

Daher¹,

Yazbeck²,

Jaoude³

et al. 2009

WJG

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Thyroid hormones define basal metabolism throughout the body, particularly in the intestine and viscera. Gastrointestinal manifestations of dysthyroidism are numerous and involve all portions of the tract. Thyroid hormone action on motility has been widely studied, but more complex pathophysiologic mechanisms have been indicated by some studies although these are not fully understood. Both thyroid hormone excess and deficiency can have similar digestive manifestations, such as diarrhea, although the mechanism is different in each situation. The liver is the most affected organ in both hypo-and hyperthyroidism. Specific digestive diseases may be associated with autoimmune thyroid processes, such as Hashimoto's thyroiditis and Grave's disease. Among them, celiac sprue and primary biliary cirrhosis are the most frequent although a clear common mechanism has never been proven. Overall, thyroidrelated digestive manifestations were described decades ago but studies are still needed in order to confirm old concepts or elucidate undiscovered mechanisms. All practitioners must be aware of digestive symptoms due to dysthyroidism in order to avoid misdiagnosis of rare but potentially lethal situations.

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Liver changes in patients with hyperthyroidism

Cited by 44 publications

References 9 publications

Severe cholestatic jaundice secondary to hyperthyroidism

Severe cholestatic jaundice secondary to hyperthyroidism

Thyroid hormone inhibits biliary growth in bile duct-ligated rats by PLC/IP₃/Ca²⁺-dependent downregulation of SRC/ERK1/2

Consequences of dysthyroidism on the digestive tract and viscera

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Liver changes in patients with hyperthyroidism

Cited by 44 publications

References 9 publications

Severe cholestatic jaundice secondary to hyperthyroidism

Severe cholestatic jaundice secondary to hyperthyroidism

Thyroid hormone inhibits biliary growth in bile duct-ligated rats by PLC/IP3/Ca2+-dependent downregulation of SRC/ERK1/2

Consequences of dysthyroidism on the digestive tract and viscera

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Thyroid hormone inhibits biliary growth in bile duct-ligated rats by PLC/IP₃/Ca²⁺-dependent downregulation of SRC/ERK1/2