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Journal ArticleDOI

Tumor Necrosis Factor: A Putative Mediator of the Sick Euthyroid Syndrome in Man

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TLDR
The results suggest that TNF is involved, either directly or indirectly, in the pathogenesis of the sick euthyroid syndrome.
Abstract
Tumor necrosis factor-alpha (TNF) is believed to be an important mediator in many diseases that are associated with the sick euthyroid syndrome. To investigate the effect of TNF on thyroid hormone metabolism, we performed a controlled study in six healthy postabsorptive males, in whom plasma thyroid hormones and TSH were sequentially measured after iv bolus injections of recombinant human TNF (50 micrograms/m2) and isotonic saline. During the 10.5-h study TNF produced the characteristic changes in circulating thyroid hormones and TSH observed in the sick euthyroid syndrome. Compared with the control experiment, TNF induced significant decreases in T3 (-36 +/- 2%; saline, -20 +/- 3%; P less than 0.05) and TSH levels (-68 +/- 3%; saline, -44 +/- 8%; P less than 0.05) and a significant increase in rT3 values (+48 +/- 11%; saline, -12 +/- 7%; P less than 0.05). T4 and free T4 index were not affected by TNF. Free T4 showed a mean transient increase of 18% in five subjects (nonsignificant), which occurred synchronically with a transient 3.5-fold rise in circulating FFA levels. Our results suggest that TNF is involved, either directly or indirectly, in the pathogenesis of the sick euthyroid syndrome.

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Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases.

TL;DR: The goal of this review is to place the exciting advances that have occurred in understanding of the molecular biology of the types 1, 2, and 3 (D1, D2, and D3, respectively) iodothyronine deiodinases into a biochemical and physiological context.
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Leptin prevents fasting-induced suppression of prothyrotropin-releasing hormone messenger ribonucleic acid in neurons of the hypothalamic paraventricular nucleus.

TL;DR: Fasted animals showed significant reduction in plasma total and free T4 and T3 levels compared with controls, that were restored toward normal by the administration of leptin, and the possibility that leptin may have an important role in the neuroendocrine regulation of the thyroid axis was raised.
Journal ArticleDOI

Dangerous Dogmas in Medicine: The Nonthyroidal Illness Syndrome

TL;DR: The condition has been called the euthyroid sick syndrome, but an alternative designation, which does not presume the metabolic status of the patient, is nonthyroidal illness syndrome (NTIS), which seems a preferable name in light of present knowledge and will be used in this review.
Journal ArticleDOI

Anticytokine Strategies in the Treatment of the Systemic Inflammatory Response Syndrome

TL;DR: It is concluded that based on animal studies and preliminary clinical trials, strategies to block IL-1 or TNF may benefit patients with the syndrome, although thorough clinical trials have not been completed.
References
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TL;DR: Use of summary measures to analyse serial measurements, though not new, is potentially a useful and simple tool in medical research.
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Shock and tissue injury induced by recombinant human cachectin.

TL;DR: It appears that a single protein mediator (cachectin) is capable of inducing many of the deleterious effects of endotoxin.
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Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia

TL;DR: Protection against shock, vital organ dysfunction, persistent stress hormone release and death was conferred by administration of antibodies 2 h before bacterial infusion, indicating that cachectin is a mediator of fatal bacteraemic shock and suggesting that antibodies against Cachectin offer a potential therapy of life-threatening infection.
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Cachectin: more than a tumor necrosis factor.

TL;DR: The metabolic impact of infectious and neoplastic disease states has long been known to clinicians and may provoke a severe wasting diathesis, in which negative calorie and nitrogen balance lead to death despite the absence of a large parasite or tumor burden.
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