High thyroglobulin (Tg) concentrations in fatal traumatic brain injuries.

It is well known that under physiological conditions, the Tg molecule is the substrate for the hormones triiodothyronine and thyroxine. Its function outside the thyroid gland is unknown. Under certain pathologic conditions, an increase in Tg concentrations in the blood can occur, a phenomenon that is used in the clinical diagnosis of certain thyroid disorders. However, fatal traumatic brain injuries (TBI) can also produce a raised Tg concentration in blood. In such cases, mean (n=151) Tg concentrations of 405.8+/-353.3 ng/mL have been observed, with the values in 57% of these cases exceeding 200 ng/mL. Since it was possible to rule out specifically any thyroid disorders in these cases, the raised values may be explained by the effect of TSH in the spectrum of the "hypothalamic-pituitary-thyroid axis." This assumption has been substantiated by immunohistochemical tests for TSH and Tg. Compared with the controls (sudden unnatural deaths: Tg 23.3+/-27.6 ng/mL), the raised Tg values in the TBI cases were usually accompanied by a reduction in the intensity of immunohistochemical reactions relating to TSH and Tg. The hypophysis showed evidence of significant damage with morphologic changes such as edema, hemorrhages, and focal necrosis in association with reduced TSH levels.