Résumé
Les patients hospitalisés pour une pathologie sévère peuvent présenter un syndrome de basse T3 associant biologiquement T3 basse, T4 normale ou basse, rT3 augmentée et absence d’augmentation de la thyroid stimulating hormone (TSH). La physiopathologie reste à ce jour complexe et imparfaitement élucidée. L’amplitude des variations biologiques est corrélée à la sévérité de la maladie. La diminution de T4 apparaît comme facteur pronostique, avec pour une T4 inférieure à 4 μg/dl une mortalité de 50 % et pour une T4 inférieure à 2 μg/dl une mortalité de 80 %. Néanmoins, ces modifications sont réversibles avec la guérison de la pathologie sous-jacente. À la phase aiguë de la maladie, le syndrome de basse T3 semble être un mécanisme adaptatif, bénéfique, en réponse à l’hypercatabolisme induit par l’agression. Il peut être lié à un défaut de transport des hormones thyroïdiennes, une captation périphérique accrue, un défaut d’expression ou d’activité des enzymes désiodinases de type 1 et 3. À la phase dite chronique de prise en charge des patients de réanimation, la présence d’un syndrome de basse T3 semble davantage liée à un dysfonctionnement de l’axe hypothalamo-hypophyso-thyroïdien, caractérisé par une diminution de la thyrotropin releasing hormone (TRH), TSH et T3-T4. Il n’est pas complètement acté de savoir si ces modifications sont à considérer comme mécanisme adaptatif, ou au contraire, participant à l’absence de récupération. En effet, à ce stade, l’absence d’anabolisme pourrait participer à l’atrophie musculaire, pérennisant la dépendance ventilatoire. Cependant, la prescription d’hormones thyroïdiennes ou de TSH n’améliore pas le pronostic. L’intérêt d’une perfusion de TRH en association à la growth hormone (GH) en phase chronique reste à confirmer.
Abstract
Patients admitted to the intensive care unit with life-threatening diseases may develop low T3 syndrome including low T3, normal or low T4, increased rT3, and the absence of increase in the thyroid stimulating hormone (TSH) levels. The pathophysiology of low T3 syndrome is still imperfectly understood. The intensity of biological alterations seems correlated to the disease severity. Decrease in T4 appears as a possible prognosticator, with a 50%-mortality rate if T4 is less than 4 μg/dl and 80%-mortality rate if less than 2 μg/dl. However, all the biological alterations are reversible as soon as the underlying disease has been treated. In the acute phase, the low T3 syndrome appears to be beneficial as an adaptive mechanism in response to the aggression-induced hypercatabolism, explained by several mechanisms like abnormal transport and increased peripheral uptake of thyroid hormones and altered expression and activity of type 1 and 3 desiodinase enzymes. During the chronic phase of patient’s care, low T3 syndrome is more related to the hypothalamic-pituitary-thyroid axis dysfunction, characterized by a decrease in thyrotropin releasing hormone (TRH), TSH and T3-T4 hormones. Whether these changes should be considered as related to an adaptive mechanism or not, even their role in the lack of recovery from the syndrome is unknown. Accordingly, the absence of anabolism contributes to muscle atrophy, prolonging the patient’s dependence on the ventilator. The prescription of thyroid hormones or TSH does not improve the final prognosis. A possible benefit of TRH infusion in combination with the growth hormone (GH) in the chronic phase needs to be confirmed.
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Cet article correspond à la conférence faite par l’auteur au congrès de la SRLF 2015 dans la session : Pathologies endocriniennes et métaboliques en réanimation.
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Maxime, V., Annane, D. Syndrome de basse T3. Réanimation 24 (Suppl 2), 291–296 (2015). https://doi.org/10.1007/s13546-014-0939-4
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DOI: https://doi.org/10.1007/s13546-014-0939-4