Thyrotoxicosis is associated with heightened adrenergic activity, arrhythmogenic susceptibility, and procoagulant alterations; yet, its contribution to sudden death outside overt thyroid storm remains incompletely understood. We retrospectively screened 975 consecutive autopsies and identified 7 cases with biochemical evidence of thyroid hormone excess defined by elevated free T3 and/or free T4 levels. Clinical background, medication exposure, thyroid-related biomarkers, including thyroglobulin, thyroid autoantibodies, and interleukin-6, together with detailed histopathological examination of the thyroid gland and the cardiovascular system, were integrated to assess the potential contribution of thyroid hormone excess to the fatal outcome. Targeted genetic analysis was additionally performed in selected cases. Two cases fulfilled clinicopathological criteria for thyroid storm and showed markedly elevated IL-6 concentrations, suggesting severe systemic decompensation. In the remaining cases, death was attributed to structural cardiovascular or cerebrovascular pathology, including intracerebral hemorrhage, acute coronary thrombosis with plaque rupture, hydrocephalus, or presumed arrhythmic mechanisms. Biochemical thyrotoxicosis was observed even in the absence of thyroid-stimulating hormone suppression, and exogenous or treatment-associated thyrotoxicosis was sometimes accompanied by thyroid atrophy rather than hyperplasia. These findings indicate that thyroid hormone excess detected at autopsy represents a clinicopathological spectrum ranging from primary thyroid-driven death to contexts in which thyrotoxicosis functions as a physiological modifier that lowers the threshold for fatal cardiovascular events. Integrative interpretation of biochemical, pathological, and clinical findings may improve the understanding of thyroid hormone–mediated vulnerability in sudden death.

Received: 16 March 2026

Accepted after revision: 08 April 2026

Article published online:
17 April 2026

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