Pfeifer, Eric A.

Following traumatic brain injury (TBI) approximately 25% of patients develop partial or complete hypopituitarism (HP). In our previous histologic study we found no changes in the pituitaries of patients who died instantly after TBI (Group I). In 43% of patients who survived 1‐7 days acute pituitary infarcts were apparent (Group II). In the present work, 3 group I and 7 group II pituitaries with infarcts were selected for histological and immunohistochemistry (IH) evaluation. IH was performed for adenohypophyseal hormones by the streptavidin‐biotin‐peroxidase method. In group I pituitaries, no histological changes were found and IH showed normal distribution and intensity for GH, PRL, ACTH, TSH, FSH, LH and α‐subunit (α‐SU). In group II pituitaries acute infarct (size range: 10% to 80%) was evident. IH in the non‐necrotic areas revealed no significant change. In the area of early necrosis the dying cells were still immunopositive (IP) for GH, PRL, ACTH, TSH, FSH, LS, and α‐SU. Even in the necrotic cells with loss of cell membrane, nuclear pyknosis, rhexis and lysis IP cytoplasms were still apparent indicating that hormone release is affected by ischemia. Subsequently the intensity of IP cells gradually decreased and IP granules leaked out from the necrotic cells and were seen extracellularly. In conclusion infarction and loss of adenohypophyseal cells may contribute to HP but other factors should also be considered.