There exists a complex relationship between liver and thyroid hormones. Liver plays an important role in the activation, inactivation, transportation, and metabolism of thyroid hormones. At the same time, thyroid hormones also affect hepatocytes activity and liver metabolism, such as lipid and bilirubin metabolism. Importantly, thyroid hormone levels often change abnormally in patients with liver cirrhosis. Therefore, studying the change of thyroid hormone levels in patients with liver cirrhosis has a certain clinical value for assessing the severity, prognosis, diagnosis and treatment. This paper reviews the research progress on the relationship between liver cirrhosis and thyroid hormone.
Bilirubin ; Humans ; Liver/metabolism* ; Liver Cirrhosis/metabolism* ; Thyroid Hormones/metabolism*

Adsorption ; Bilirubin ; metabolism ; Liver, Artificial ; Plasma Exchange ; methods

Non-alcoholic fatty liver disease (NAFLD) is a metabolic-related disorder induced by multiple factors and mainly characterized by excessive fat buildup in hepatocytes. With the consumption of a Western-style diet and obesity prevalence in recent years, the incidence of NAFLD has gradually increased, becoming an increasingly serious public health problem. Bilirubin is a heme metabolite and a potent antioxidant. Studies have demonstrated that bilirubin levels have an inverse correlation with the incidence rate of NAFLD; however, which form of bilirubin plays the main protective role is still controversial. It is considered that the main protective mechanisms for NAFLD are bilirubin antioxidant properties, insulin resistance reduction, and mitochondrial function. This article summarizes the correlation, protective mechanism, and possible clinical application of NAFLD and bilirubin.
Humans ; Non-alcoholic Fatty Liver Disease/metabolism* ; Bilirubin ; Antioxidants ; Obesity/complications* ; Hepatocytes/metabolism* ; Liver/metabolism*

Animals ; Bilirubin ; toxicity ; Brain ; drug effects ; metabolism ; Nitric Oxide ; metabolism ; Rabbits

Bilirubin ; Child ; Duodenogastric Reflux ; diagnosis ; Esophageal Diseases ; diagnosis ; Esophagus ; metabolism ; Gastroesophageal Reflux ; diagnosis ; Humans

Adolescent ; Bilirubin ; metabolism ; Child ; Child, Preschool ; Duodenogastric Reflux ; metabolism ; Esophageal pH Monitoring ; Female ; Humans ; Male ; Stomach ; physiopathology

Daily administration of glucocorticoids for 10 days to dogs resulted in a significant increase in the hepatic bile secretion in response to secretory stimulants. The response of hepatic bile in testosterone-treated animals was not changed and the response was increased in DOCA--treated animals. A significant increase of liver weight was induced by the animals receiving glucocorticoids. Other organ weight was not changed; however, a slight reduction of kidney weight was seen in prednisolone, dexamethasone, and DOCA treated animals and also in animals supplemented with cortisone following adrenalectomy. The presence of large areas of ballooning and vesicular changes of liver cells was seen in glucocorticoid treated animals, particularly in cases of dexamethasone and prednisolone. Both vesicular changes of liver cell and its glycogen content were increased by the repeated administration of prednisolone and reduced by the cessation of treatment. Special stain and liver glycogen determination demonstrated the material distending the liver cell was glycogen. These findings indicate that long term administration of glucocorticoids results in an increase of liver weight and hepatic glycogen content as well as increased bile secretion.
Animal ; Bile/secretion* ; Bile Acids and Salts/metabolism ; Bilirubin/secretion ; Cholagogues and Choleretics/pharmacology ; Dogs ; Glucocorticoids/pharmacology* ; Liver/drug effects* ; Liver/pathology ; Liver Glycogen/metabolism ; Organ Weight ; Substances: ; Bile Acids and Salts ; Cholagogues and Choleretics ; Glucocorticoids ; Liver Glycogen ; Bilirubin

Hematologic investigations for 7 years at the Pediatric Department of Yonsei Medical Center of 52 syphilitic infants were reviewed. A moderate degree of anemia with red cell regeneration was observed in 40 infants (76.0%). Marked. thrombocytopenia but without active bleeding was found in 19 infants, and with active bleeding in 3 infants. A wide range of leukocyte counts, relative lymphocytosis and monocytosis were prominant features. The jaundice was mainly due to unconjugated bilirubin in 6 infants, conjugated as well as unconjugated bilirubin in 8 infants. With therapy, the above abnormal hematologic findings showed marked improvement. Early diagnosis is essential. Prevention and congenital syphilis depend on a high level of clinical suspicion, supported by routine and diagnostic use of laboratory and serologic aids, in the asymptomatic or minimally symptomtaic infants.
Bilirubin/blood ; Blood Cell Count ; Blood Platelets ; Female ; Hemoglobins/metabolism ; Human ; Infant, Newborn ; Reticulocytes ; Syphilis, Congenital/blood*

OBJECTIVETo investigate the mechanism of plasma bilirubin level increase after hepatic ischemia-reperfusion in rats.

METHODSRats were divided into a sham operation group (A group), a 20 min ischemia-reperfusion group (B group) and a 35 min ischemia-reperfusion group (C group). Study time points were 6 hours and 1, 3, and 5 days after the reperfusion. Pathological changes in the livers were studied with histological slides stained with hematoxilin and eosin. Routine biochemistry methods were used to detect the bilirubin level of blood plasma and the bile drained from the ischemic hepatic lobes. RT-PCR was used to analyze the expression of the multidrug resistance-associated protein 2 (MRP2) and mRNA. Immunohistochemistry was used to analyze the localization of MRP2 in the canalicular membrane.

RESULTSB and C groups showed a mild inflammatory reaction without hepatocyte necrosis. At 6 h and 1 day after reperfusion, there was a significant increase of the plasma bilirubin level and a decrease of the bilirubin level of the drained bile in B group. These changes lasted to the day 3 and day 5 in C group. MRP2 mRNA down-regulation was found at 6 h only in the B and C groups. No localization of MRP2 in the canalicular membrane was found but it appeared in "esicules" under the canalicular membrane in C group.

CONCLUSIONSAbsence of MRP2 localization in the canalicular membrane could be the cause of the blood plasma bilirubin level increase after liver ischemia-reperfusion.

Animals ; Bilirubin ; blood ; Liver Diseases ; blood ; Male ; Multidrug Resistance-Associated Proteins ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; blood

Bilirubin ; analysis ; Child ; Electric Impedance ; Esophagus ; metabolism ; Gastroesophageal Reflux ; diagnosis ; therapy ; Humans ; Hydrogen-Ion Concentration ; Surveys and Questionnaires