Τίτλος:
Thyroid hormones alterations during acute liver failure: possible
underlying mechanisms and consequences
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Thyroid hormones are now recognized to change in different disease
states with important consequences on severity and prognosis of disease.
However, little is known about thyroid hormones’ alterations in acute
liver failure (ALF). To study the changes in thyroid hormones and
cardiac thyroid receptors during ALF, we subjected seven female pigs to
surgical liver devascularization. Liver function biochemical markers,
thyroid hormones, endogenous opioids, malondialdehyde (MDA), and
interleukins 1 and 6 were measured in serum for 24 h postoperatively.
Heart biopsies were harvested at the end of the experiment. Baseline
heart biopsies were taken from five additional animals. Serum thyroxin
(T-4) and triiodothyronine (T-3) levels markedly decreased, whereas
free-triiodothyronine and thyroxin-stimulating hormone levels did not
change. T-4 and T-3 levels correlated with the degree of liver failure
and with MDA and interleukin-6 levels. Beta-endorphin levels initially
increased, whereas levels of leucine-enkephalin did not change. Thyroid
hormone receptor-alpha 1 protein expression in the heart decreased
1.6-fold after ALF, whereas myocardial myosin isoform expression
remained unchanged. The downregulation of T-4 and T-3 levels during ALF
seems to correlate well with the severity of disease. This
downregulation related to inflammation and oxidative stress and resulted
in changes in myocardial thyroid receptors.
Συγγραφείς:
Kostopanagiotou, Georgia
Kalimeris, Konstantinos
Mourouzis,
Iordanis
Costopanagiotou, Constantinos
Arkadopoulos, Nikolaos
and Panagopoulos, Dimitrios
Papoutsidakis, Nikolaos
Chranioti,
Aikaterini
Pafiti, Agatha
Spanou, Danai
Smyrniotis,
Vassilios
Pantos, Constantinos
Περιοδικό:
Endocrine Development
Λέξεις-κλειδιά:
Acute liver failure; Thyroid hormone receptor alpha 1; Non-thyroidal
illness syndrome; Lipid peroxidation; Endogenous opioids
DOI:
10.1007/s12020-009-9210-2
