Brain injury · 2007
Histologic study of the human pituitary gland in acute traumatic brain injury.
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Salehi Fateme, Kovacs Kalman, Scheithauer Bernd W, Pfeifer Eric A, Cusimano Michael
Аннотация
PURPOSE: Approximately 25% of patients with traumatic brain injury (TBI) may develop partial or complete hypopituitarism. The causative mechanisms involved in its development are not clear. To the authors' knowledge, there have been no recent morphologic studies of the pituitary following TBI.
METHODS: To characterize the resultant histologic changes, this study investigated the pituitaries of 42 patients who died following a motor vehicle accident, all from the Mayo Tissue Registry. Twelve patients died instantly at the scene of the accident (Group I) whereas 30 survived between 3 hours and 7 days (Group II). All pituitary specimens were obtained at autopsy, formalin-fixed and paraffin-embedded. Hematoxylin-eosin sections cut in horizontal or sagittal plane were examined light-microscopically.
RESULTS: No infarction was noted in the pituitary specimens from group I. In group II, 13 of 30 (43%) showed acute infarcts of varying size. The extent of infarction in group II ranged from focal to sub-total necrosis involving 90% of the adenohypophysis.
CONCLUSIONS: Underlying adenohypophysial pathology in patients dying after TBI is acute infarction. Loss of large numbers of adenohypophysial cells causes reduced secretion of adenohypophysial hormones and may contribute to post-traumatic hypopituitarism.
METHODS: To characterize the resultant histologic changes, this study investigated the pituitaries of 42 patients who died following a motor vehicle accident, all from the Mayo Tissue Registry. Twelve patients died instantly at the scene of the accident (Group I) whereas 30 survived between 3 hours and 7 days (Group II). All pituitary specimens were obtained at autopsy, formalin-fixed and paraffin-embedded. Hematoxylin-eosin sections cut in horizontal or sagittal plane were examined light-microscopically.
RESULTS: No infarction was noted in the pituitary specimens from group I. In group II, 13 of 30 (43%) showed acute infarcts of varying size. The extent of infarction in group II ranged from focal to sub-total necrosis involving 90% of the adenohypophysis.
CONCLUSIONS: Underlying adenohypophysial pathology in patients dying after TBI is acute infarction. Loss of large numbers of adenohypophysial cells causes reduced secretion of adenohypophysial hormones and may contribute to post-traumatic hypopituitarism.