Search Results
Search for other papers by Emmely M de Vries in
Google Scholar
PubMed
Search for other papers by Eric Fliers in
Google Scholar
PubMed
Search for other papers by Anita Boelen in
Google Scholar
PubMed
Introduction Illness results in profound changes in thyroid hormone (TH) metabolism called the ‘sick euthyroid syndrome’ or ‘nonthyroidal illness syndrome’ (NTIS). NTIS is characterized by decreased serum triiodothyronine (T 3 ) and thyroxine (T 4
Search for other papers by Maria H Warner in
Google Scholar
PubMed
Search for other papers by Geoffrey J Beckett in
Google Scholar
PubMed
. ‘Non-thyroidal illness syndrome (NTIS)’ is now more commonly used to describe the typical changes in thyroid-related hormone concentrations that can arise in the serum following any acute or chronic illness that is not caused by an intrinsic abnormality
Search for other papers by Tatiana Ederich Lehnen in
Google Scholar
PubMed
Search for other papers by Rafael Marschner in
Google Scholar
PubMed
Search for other papers by Fernanda Dias in
Google Scholar
PubMed
Search for other papers by Ana Luiza Maia in
Google Scholar
PubMed
Search for other papers by Simone Magagnin Wajner in
Google Scholar
PubMed
Introduction Nonthyroidal illness syndrome (NTIS), also known as low T3 syndrome, is a clinical condition observed in ill patients characterized by a rapid decrease in serum triiodothyronine (T3) levels accompanied by increased reverse T3 (rT3
Search for other papers by M A Pavia Jr in
Google Scholar
PubMed
Search for other papers by B Paier in
Google Scholar
PubMed
Search for other papers by M I Noli in
Google Scholar
PubMed
Search for other papers by K Hagmüller in
Google Scholar
PubMed
Search for other papers by A A Zaninovich in
Google Scholar
PubMed
Abstract
The effect of in vivo administration of cadmium chloride on the pituitary-thyroidal axis was assessed in 200 g body weight Wistar rats. A dose of 2·5 mg/kg body weight was injected i.v. 24 h before the experiments were initiated. Plasma thyroxine (T4) and tri-iodothyronine (T3) concentrations in cadmium-treated rats were significantly (P<0·01) decreased, whereas plasma TSH failed to increase in response to low T4 and T3. However, the TSH response to TRH and the pituitary content of TSH in these rats were both normal. Cadmium induced a significant (P<0·01) decrease in 4-h thyroidal 131I uptake and in thyroid/plasma radioactivity ratio. The in vitro conversion of T4 to T3 in the pituitary was significantly (P<0·01) blocked by cadmium whereas there was no in vivo effect. Parameters of peripheral T4 kinetics in cadmium-treated rats, such as metabolic clearance rate (P<0·01), fractional turnover rate (P<0·01), absolute disposal rate (P<0·05), urinary clearance (P<0·05) and faecal clearance (P<0·05), were all decreased by cadmium. The lack of response of TSH to low plasma T4 and T3 and the normal response to exogenous TRH in this and in other non-thyroidal illness syndromes produced by other pathologies suggest a decreased stimulation of pituitary thyrotrophs by endogenous TRH.
Journal of Endocrinology (1997) 154, 113–117
Search for other papers by J. Kvetny in
Google Scholar
PubMed
Search for other papers by L. Matzen in
Google Scholar
PubMed
ABSTRACT
Nuclear tri-iodothyronine (T3) binding and thyroid hormone-stimulated oxygen consumption and glucose uptake were examined in mononuclear blood cells from patients with non-thyroidal illness (NTI) in which serum T3 was significantly (P < 0·05) depressed (0·62± 0·12 (s.d.) nmol/l) compared with healthy control subjects (1·45 ± 0·30 nmol/l). Neither serum TSH nor sex hormone-binding globulin differed from that of the control group.
Nuclear T3 binding capacity was increased (P < 0·05) in patients with NTI (10·1 ± 3·0 fmol/100 μg DNA) compared with controls (2·5 ± 0-9 fmol/100 μg DNA). Unstimulated glucose uptake was increased in cells from patients with NTI (2·03 ± 0·49 mmol/l per mg DNA per h, P < 0·01) compared with controls (1·13 ± 0·20 mmol/l per mg DNA per h). Thyroxine-stimulated glucose uptake (stimulated glucose uptake–unstimulated glucose uptake) was increased in cells from patients with NTI (2·06 ± 1·67 mmol/l per mg DNA per h, P < 0·01) compared with controls (0·26 ± 0·1 mmol/l per mg DNA per h), and T3-stimulated glucose uptake was also increased in cells from patients with NTI (1·34 ± 0·81 mmol/l per mg DNA per h, P < 0·05) compared with controls (0·24 ± 0·10 mmol/l per mg DNA per h). In contrast, neither unstimulated nor thyroid hormone-stimulated oxygen consumption differed.
We conclude that both increased nuclear T3 binding and increased thyroid hormone-induced glucose uptake may represent counter-regulatory mechanisms which tend to maintain intracellular homeostasis.
Journal of Endocrinology (1990) 124, 495–499
Search for other papers by Anita Boelen in
Google Scholar
PubMed
Search for other papers by Anne H van der Spek in
Google Scholar
PubMed
Search for other papers by Flavia Bloise in
Google Scholar
PubMed
Search for other papers by Emmely M de Vries in
Google Scholar
PubMed
Search for other papers by Olga V Surovtseva in
Google Scholar
PubMed
Search for other papers by Mieke van Beeren in
Google Scholar
PubMed
Search for other papers by Mariette T Ackermans in
Google Scholar
PubMed
Search for other papers by Joan Kwakkel in
Google Scholar
PubMed
Search for other papers by Eric Fliers in
Google Scholar
PubMed
Introduction During illness, thyroid hormone metabolism changes profoundly. Serum thyroid hormones decrease and the classical negative feedback loop of the hypothalamic–pituitary–thyroid axis is absent. This is known as the nonthyroidal
Search for other papers by A Boelen in
Google Scholar
PubMed
Search for other papers by J Kwakkel in
Google Scholar
PubMed
Search for other papers by W M Wiersinga in
Google Scholar
PubMed
Search for other papers by E Fliers in
Google Scholar
PubMed
Introduction Acute systemic illness induced by bacterial endotoxin (lipopoly saccharide; LPS) administration, results in altered peripheral and central thyroid hormone metabolism, so-called nonthyroidal illness (NTI; Papanicolaou
Search for other papers by E M de Vries in
Google Scholar
PubMed
Search for other papers by H C van Beeren in
Google Scholar
PubMed
Search for other papers by M T Ackermans in
Google Scholar
PubMed
Department of Endocrinology and Metabolism, Hypothalamic Integration Mechanisms, Laboratory of Endocrinology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
Search for other papers by A Kalsbeek in
Google Scholar
PubMed
Search for other papers by E Fliers in
Google Scholar
PubMed
Search for other papers by A Boelen in
Google Scholar
PubMed
Introduction Profound changes occur in the hypothalamus–pituitary–thyroid (HPT) axis during illness and starvation. The nonthyroidal illness syndrome (NTIS) is characterized by decreased serum tri-iodothyronine (T 3 ) and thyroxine (T 4
Search for other papers by J Kwakkel in
Google Scholar
PubMed
Search for other papers by O Chassande in
Google Scholar
PubMed
Search for other papers by H C van Beeren in
Google Scholar
PubMed
Search for other papers by W M Wiersinga in
Google Scholar
PubMed
Search for other papers by A Boelen in
Google Scholar
PubMed
Introduction Lipopolysaccharide (LPS, a bacterial endotoxin) administration is a well-established animal model for non-thyroidal illness (NTI; Boelen et al . 1995 ) via the induction of an acute phase inflammatory response ( Palsson-McDermott & O
Search for other papers by J Kwakkel in
Google Scholar
PubMed
Search for other papers by W M Wiersinga in
Google Scholar
PubMed
Search for other papers by A Boelen in
Google Scholar
PubMed
Introduction Increased serum levels of proinflammatory cytokines have been associated with nonthyroidal illness (NTI; Boelen et al. 1993 ), which is a state of altered thyroid hormone regulation and metabolism during illness
