Abstract
This study aimed to investigate the usefulness of the thyroid-related hormones as markers of acute systemic hypoxia/ischemia to identify deaths caused by asphyxiation due to neck compression in human autopsy cases. The following deaths from pathophysiological conditions were examined: mechanical asphyxia and acute/subacute blunt head injury; acute/subacute non-head blunt injury; sharp instrument injury as the hemorrhagic shock condition; drowning as alveolar injury; burn; and death due to cardiac dysfunction. Blood samples were collected from the left and right cardiac chambers and iliac veins, and serum triiodothyronine (T3), thyroxine (T4), thyroglobulin (Tg), and thyroid-stimulating hormone (TSH) levels were measured using electrochemiluminescence immunoassays. Two types of thyroid cell lines were used to confirm independent thyroid function under the condition of hypoxia (3% O2). The human thyroid carcinoma cell line (HOTHC) cell line derived from human anaplastic thyroid carcinoma and the UD-PTC (sample of the second resection papillary thyroid carcinoma) cell line derived from human thyroid papillary adenoma, which forms Tg retention follicles, were used to examine the secretion levels of T3, T4, and Tg hormones. The results showed a strong correlation between T3 and T4 levels in all blood sampling sites, while the TSH and Tg levels were not correlated with the other markers. Serum T3 and T4 levels were higher in cases of mechanical asphyxia and acute/subacute blunt head injury, representing hypoxic and ischemic conditions of the brain as compared to those in other causes of death. In the thyroid gland cell line, T4, T3, and Tg levels were stimulated after exposure to hypoxia for 10–30 min. These findings suggest that systemic advanced hypoxia/ischemia may cause a rapid and TSH-independent release of T3 and T4 thyroid hormones in autopsy cases. These findings demonstrate that increased thyroid-related hormone (T3 and T4) levels in the pathophysiological field may indicate systemic hypoxia/ischemia.
Highlights
During pathological autopsies, it is very important to distinguish deaths due to acute systemic hypoxia/ischemia caused by asphyxiation due to neck compression from those due to sudden natural causes [1, 2]
The results of this study showed that the T3 levels in several cases of asphyxia and blunt head injury exceeded the measurement range, the levels of other thyroidrelated hormones remained within the range
Asphyxia and acute/subacute head injuries, representing hypoxic and ischemic conditions of the brain were associated with the highest serum T3 and T4 levels at all sampling sites, with the exception being the T4 levels in samples from the left cardiac chamber
Summary
It is very important to distinguish deaths due to acute systemic hypoxia/ischemia caused by asphyxiation due to neck compression from those due to sudden natural causes (e.g., acute ischemic heart disease) [1, 2]. Previous studies examining this issue from the perspective of forensic pathology, biochemistry, and molecular biology [3,4,5] suggested that thyroid hormones could be used as markers of direct physical thyroid gland stimulation following cervical compression [6, 7]. The present study investigated changes in thyroid-related hormone levels in cases of hypoxic ischemia by biochemical analysis
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