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Thyroid function after thermal trauma
Scandinavian Journal of Plastic and Reconstructive Surgery
|January 1, 1981
Summary
Thyroid hormone levels, including triiodothyronine (T3) and thyroxine (T4), were studied in burn patients. Results suggest thyroid hormones do not cause post-burn hypermetabolism but may be depleted at the cellular level.
Area of Science:
- Endocrinology
- Trauma Medicine
- Metabolic Research
Background:
- Burn injury triggers significant metabolic changes, including hypermetabolism.
- Thyroid hormones play a crucial role in regulating metabolism, but their specific role in post-burn hypermetabolism is not fully understood.
Purpose of the Study:
- To investigate thyroid function and hormone levels in patients with thermal injuries.
- To determine if altered thyroid hormone concentrations contribute to post-traumatic hypermetabolism in burn patients.
Main Methods:
- Prospective study analyzing thyroid function in 12 thermally injured patients over 4-6 weeks.
- Measured serum concentrations of triiodothyronine (T3), reverse triiodothyronine (rT3), thyroxine (T4), TSH, TBG, and TBPA.
- Controlled for potential interference from blood and plasma transfusions.
Main Results:
- Serum T3 was suppressed, and rT3 was increased, leading to a subnormal T3/rT3 ratio initially.
- Thyroxine and free T4-index remained normal; free T3-index was within normal range.
- TSH was initially low but increased over time; TBG varied normally, while TBPA was subnormal.
Conclusions:
- Thyroid hormones are not the primary cause of post-traumatic hypermetabolism in burn injury.
- Findings suggest a depletion of metabolically active thyroid hormones at the cellular level following burn trauma.