Adrenocorticotropic hormone-producing pituitary carcinoma with intracranial metastases.

BACKGROUND: Pituitary carcinomas are rare and challenging clinical entities. Because of the paucity of cases, there is limited information in the literature on how best to diagnose and treat pituitary carcinomas. METHODS: We review the literature and describe a woman who presented with an adrenocorticotropic hormone (ACTH)-secreting pituitary macroadenoma that later evolved into a carcinoma with intracranial metastases. RESULTS: A 39-year-old woman presented at age 27 with classic findings of Cushing's syndrome and a pituitary macroadenoma. Her initial treatment was transsphenoidal surgery, during which we confirmed an ACTH-secreting pituitary neoplasm. For 5 years, she was asymptomatic before her first recurrence. During the next 6 years, she underwent four transsphenoidal surgeries and two craniotomies. After each surgery, there was some reduction in the size of the macroadenoma but the residual tumor mass would rapidly enlarge. Immunochemical staining was positive for ACTH, and a stain for Ki-67 antigen showed a high mitotic index. Eleven years after her initial presentation, magnetic resonance imaging revealed bilateral hippocampal and tempero-occipital masses. The patient's health continued to deteriorate, largely from complications of severe hypercortisolemia, and she died from sepsis. At postmortem, the hippocampus and tempero-occipital lobe masses proved to be a pituitary tumor with positive ACTH staining. CONCLUSIONS: Pituitary carcinomas are rare, may present many years after diagnosis of a primary pituitary adenoma, and should be suspected in patients with persistent or recurrent disease. Reliable histopathologic ways to distinguish between carcinoma and adenoma are difficult because the features of hypercellularity, nuclear pleomorphism, and mitotic figures are not always helpful.

Metabolic complications and increased cardiovascular risks as a result of androgen deprivation therapy in men with prostate cancer.

Prostate cancer is one of the most common malignancies in men. Charles Huggins and Clarence V. Hodges reported the androgen dependence of prostate cancer in 1941. That led to the utilization of androgen deprivation therapy as an important therapeutic modality to treat prostate cancer. Androgen deprivation therapy has additional systemic effects that include sexual dysfunction, psychological changes and more important are the metabolic changes. Metabolic changes in particular include insulin resistance, increase fat mass and low-density lipoprotein cholesterol, and induce type 2 diabetes. In this review we will focus on the cardiovascular risk associated with androgen deprivation therapy that includes the mechanisms involved.