SFEBES2009 Poster Presentations Endocrine tumours and neoplasia (39 abstracts)
Temozolomide-induced regression of hepatic metastases in a pituitary corticotroph carcinoma with low O6-methylguanine-DNA methyltransferase expression
Hannah Burton 1 , Anand K Annamalai 1 , Andrew Dean 2 , Kalman Kovacs 3 , Nagui Antoun 4 , Ramez W Kirollos 5 , Helen L Simpson 1 , Sarah J Jeffries 6 , Neil G Burnet 6 & Mark Gurnell 1
1Institute of Metabolic Science, Addenbrooke’s Hospital, Cambridge, UK; 2Department of Histopathology, Addenbrooke’s Hospital, Cambridge, UK; 3Department of Pathology, St Michael’s Hospital, University of Toronto, Toronto, Canada; 4Department of Radiology, Addenbrooke’s Hospital, Cambridge, UK; 5Department of Neurosurgery, Addenbrooke’s Hospital, Cambridge, UK; 6Department of Oncology, Addenbrooke’s Hospital, Cambridge, UK.
Background: Pituitary carcinoma occurs in ~0.2% of resected pituitary tumours, and carries a poor prognosis (mean survival <4 years), with standard chemotherapeutic regimens showing limited efficacy. However, recent evidence suggests that temozolomide, an orally active alkylating agent used principally in the management of glioblastoma, may also be effective in controlling aggressive/invasive pituitary adenomas/carcinomas. Low levels of expression of the DNA-repair enzyme MGMT, as assessed by immunohistochemistry, predicts temozolomide responsiveness. Here, we report a case of a pituitary corticotroph carcinoma with hepatic metastases, which responded clinically, biochemically and radiologically to temozolomide therapy.
Case report: A 65-year-old man presented as an emergency with frontal headache and evolving bilateral 3rd nerve palsies. Imaging showed a sellar-based mass with parasellar and suprasellar extension. At transphenoidal surgery a necrotic ACTH-staining pituitary adenoma was resected. There were no features of Cushing’s syndrome clinically or biochemically, and hydrocortisone replacement was required post-operatively. No residual tumour was identified on post-operative MRI and the patient elected for surveillance follow-up.
However, 2 years later he developed clinical and biochemical evidence of ACTH-dependent Cushing’s syndrome. Pituitary MRI showed no evidence of tumour regrowth and, although a peripheral CRH test suggested a corticotroph origin, IPSS did not demonstrate a central: peripheral gradient. Further imaging with CT and FDG-PET revealed multiple hepatic lesions, and subsequent biopsy confirmed metastatic ACTH-staining pituitary carcinoma. MGMT expression was very low in both the primary pituitary tumour and hepatic metastases.
Temozolomide therapy was commenced (200 mg/m2 daily for five consecutive days every 28 days) and has been well tolerated. ACTH levels have fallen from a peak of 5685 to 2318 ng/l after 5 cycles, with CT demonstrating regression of the hepatic lesions. Metyrapone and ketoconazole were also used to help control hypercortisolism and the patient has undergone pituitary radiotherapy to mitigate against the potential risk of local tumour recurrence.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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