Hepatic conversion of amino nitrogen to urea nitrogen in hypothyroid patients and upon l-thyroxine therapy

Marchesini, Giulio; Fabbri, Andrea; Bianchi, Giampaolo; Motta, Ewa; Bugianesi, Elisabetta; Urbini, D.; Pascoli, Ana Lúcia; Lodi, Alessandra

doi:10.1016/0026-0495(93)90123-6

Cited by 19 publications

(9 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Decreased hepatic metabolism in hypothyroidism is reflected by reduced oxygen consumption [70] and causes a significant decrease in gluconeogenesis [71] and urea nitrogen production [72] . Myxedema ascites in hypothyroidism is rare and may be a long-standing overlooked and/or isolated sign of the disease [73] .…”

Section: Livermentioning

confidence: 99%

Consequences of dysthyroidism on the digestive tract and viscera

Daher¹,

Yazbeck²,

Jaoude³

et al. 2009

WJG

View full text Add to dashboard Cite

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.

show abstract

Section: Livermentioning

confidence: 99%

Consequences of dysthyroidism on the digestive tract and viscera

Daher¹,

Yazbeck²,

Jaoude³

et al. 2009

WJG

View full text Add to dashboard Cite

show abstract

“…We used the galactose elimination capacity (GEC) to assess hepatocyte cytosol activity (7), the plasma clearance of indocyanine green (ICGCl) to assess hepatic blood flow and excretory liver cell function independently of hepatic blood flow (8), the antipyrine plasma clearance (ApCl) to estimate hepatic microsomal system activity (9), and the functional hepatic nitrogen clearance (FHNC) to assess mitochondrial-cytosolic metabolic capacity for conversion of amino-nitrogen (10).…”

Section: Introductionmentioning

confidence: 99%

Quantitative liver functions in Turner syndrome with and without hormone replacement therapy

et al. 2007

View full text Add to dashboard Cite

Background: Studies have documented elevated levels of liver enzymes in many females with Turner syndrome (TS). Histology has shown a range of changes. Treatment with female hormone replacement therapy (HRT) reduces liver enzymes. Aim: To study quantitative liver functions in TS in detail with and without HRT. Design: Randomized crossover study with active treatment (HRT in TS and P-pill in controls) or no treatment. Subjects: Women with TS (nZ8, age 29.7G5.6 (meanGS.D.) years), verified by karyotype, and agematched controls (C; nZ8, age 27.3G4.9 years). Methods: We determined liver enzymes in blood, used the galactose elimination capacity to assess hepatocyte cytosol activity, plasma clearance of indocyanine green to assess excretory function, antipyrine clearance to estimate microsomal activity, and the functional hepatic nitrogen clearance (FHNC) to assess mitochondrial-cytosolic metabolic capacity for conversion of amino-nitrogen. Results: Liver enzymes were elevated in untreated TS and reduced by HRT. The hepatic capacities for conversion of galactose, indocyanine green, and antipyrine were normal and did not change by HRT.

show abstract

“…In a rat liver model, hypothyroidism was associated with an increased urea synthesis, attributed to an increase in urea cycle enzyme activity 9,19. However, when studied in hypothyroid women, a decreased urea synthesis rate, in comparison with values measured in euthyroidism, was found 20. Inefficient urea synthesis during hypothyroidism, as was demonstrated in vivo, is expected to result in an increased ammonia level.…”

Section: Discussionmentioning

confidence: 88%

Hyperammonemic Coma—Barking Up the Wrong Tree

et al. 2007

View full text Add to dashboard Cite

Hepatic encephalopathy and myxedema coma share clinical features: coma, ascites, anemia, impaired liver functions, and a "metabolic" electroencephalogram (EEG). Hyperammonemia, a hallmark of hepatic encephalopathy, has also been described in hypothyroidism. Differentiation between the 2 conditions, recognition of their possible coexistence, and the consequent therapeutic implications are of utmost importance. We describe a case of an 82-year-old woman with a history of mild chronic liver disease who presented with hyperammonemic coma unresponsive to conventional therapy. Further investigation disclosed severe hypothyroidism. Thyroid hormone replacement resulted in gain of consciousness and normalization of hyperammonemia. In patients with an elevated ammonia level, altered mental status, and liver disease, who do not have a clear inciting event for liver disease decompensation, overwhelming evidence of hepatic decompensation, or who do not respond to appropriate therapy for hepatic encephalopathy, hypothyroidism should be considered and evaluated.

show abstract

Hepatic conversion of amino nitrogen to urea nitrogen in hypothyroid patients and upon l-thyroxine therapy

Cited by 19 publications

References 40 publications

Consequences of dysthyroidism on the digestive tract and viscera

Consequences of dysthyroidism on the digestive tract and viscera

Quantitative liver functions in Turner syndrome with and without hormone replacement therapy

Hyperammonemic Coma—Barking Up the Wrong Tree

Contact Info

Product

Resources

About