Thyroid Hormones in Comatose Patients with Traumatic Brain Injury

Tenedieva, V D; Потапов, А. А.; Gaitur, E.; Amcheslavski, V. G.; Micrikova, L. V.; Tenedieva, N. D.; Voronov, V. G.

doi:10.1007/978-3-7091-6346-7_80

Cited by 6 publications

(4 citation statements)

References 12 publications

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“…Abnormal thyroid hormone levels are noticed after TBI (Woolf et al, 1988;Tenedieva et al, 2000) and are known to normalize during the recovery. Central hypothyroidism is reported in 5-15% (Powner et al, 2006) of patients in the acute phase following TBI.…”

Section: Thyroid Hormonementioning

confidence: 99%

Systemic manifestations of traumatic brain injury

Gaddam

Buell

Robertson

2015

Handbook of Clinical Neurology

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Section: Thyroid Hormonementioning

confidence: 99%

Systemic manifestations of traumatic brain injury

Gaddam

Buell

Robertson

2015

Handbook of Clinical Neurology

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“…Mocchegiani et al (15) observed no difference in plasma thyroxin (T4) and thyrotropin (TSH) levels among injured patients, but Tenedieva et al (10) found that T3 and T4 levels continued to fall in patients with contusion, epidural, and subdural hematomas.…”

Section: Discussionmentioning

confidence: 99%

Onychomycosis with thyroid dysfunction after traumatic brain injury. A case report

Yazeedi¹,

Venkatachalam²,

Serheed³

et al. 2009

International Journal on Disability and Human Development

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Traumatic brain injury can cause endocrine dysfunction, particularly in the pituitary and thyroid. Onychomycosis is a frequent fungal disorder of nails and toes in normal adults and can be associated with hypothyroidism. We present a 35 years old, Chinese male who was affected by Onychomycosis, hypothyroidism, and severe traumatic brain injury (TBI). Onychomycosis was present before TBI in one finger only but deteriorated during the acute stage of TBI, and improved significantly only after the introduction of thyroid treatment.

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“…Cytokine release within the CNS as well as in the periphery is now an accepted component of the pathophysiology of TBI with IL-6 playing a particularly important role [40]. Experimental investigations and clinical studies demonstrated an interrelation between cytokines such as IL-1, IL-6, or TNF and the low T 3 syndrome [4,5,8,9,16]. Recently, such a role of cytokines in the pathogenesis of low T 3 syndrome has been challenged.…”

Section: Discussionmentioning

confidence: 99%

Low T3 Syndrome in Head-Injured Patients is Associated with Prolonged Suppression of Markers of Cell-Mediated Immune Response

et al. 2005

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European Journal of Trauma Ab stractPurpose: To clarify the association between disturbed thyroid hormone metabolism (low T 3 syndrome) and release of cytokines and markers of cell-mediated immune response. Material and Methods: Concentrations of cytokines as well as of thyroid hormones were determined in 32 patients suffering from severe traumatic brain injury: interleukin-(IL-)1, IL-6, IL-10, tumor necrosis factor, transforming growth factor-(TGF-)β, soluble interleukin-2 receptor (sIL-2R), neopterin, and β 2 -microglobulin (β2m) in serum and cerebrospinal fluid; triiodothyronine (T 3 ), free T 3 , thyroxine (T 4 ), free T 4 , thyrotropin, thyroxine-binding globulin, and albumin in serum. Additionally, clinical parameters were assessed: Glasgow Coma Score, CT scan, intracranial pressure, Glasgow Outcome Score, and occurrence of pneumonia. Results: Among 31 patients with a low T 3 syndrome, those with additional low serum T 4 levels (n = 13) showed a prolonged suppression of serum β2m, neopterin, and sIL-2R, and a higher secondary increase of serum β2m, neopterin, and TGF-β, as well as lower T 3 levels (all p < 0.05). These patients also had a longer stay in the intensive care unit (34 ± 6 days vs. 22 ± 12 days; p = 0.008). Increased levels of β2m correlated with a preceding decrease of thyrotropin (cerebrospinal fluid: r = -0.53; p = 0.004; serum: r = -0.41; p = 0.029). Associations of thyroid hormone metabolism with either other cytokines or with clinical parameters were not detected. Conclusion:These results show that low T3 syndrome is a very common pathophysiological feature after severe traumatic brain injury. The association of a low T 3 syndrome in combination with low serum T 4 levels, with an altered time course of markers of cell-mediated immunity led the authors to hypothesize that a disturbed thyroid hormone metabolism may be interrelated with a prolonged cellular immune dysfunction after traumatic brain injury.

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Thyroid Hormones in Comatose Patients with Traumatic Brain Injury

Cited by 6 publications

References 12 publications

Systemic manifestations of traumatic brain injury

Systemic manifestations of traumatic brain injury

Onychomycosis with thyroid dysfunction after traumatic brain injury. A case report

Low T3 Syndrome in Head-Injured Patients is Associated with Prolonged Suppression of Markers of Cell-Mediated Immune Response

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