Showing papers by "Niki Karavitaki published in 2008"

Surgical debulking of pituitary macroadenomas causing acromegaly improves control by lanreotide.

Abstract: Summary Background Macroadenomas causing acromegaly are cured surgically in only around 50% of patients. Primary medical treatment with somatostatin analogues has been suggested to be a means of treating patients with a potentially poor surgical outcome. Previous retrospective studies have also suggested that surgical debulking of pituitary tumours causing acromegaly improves control by somatostatin analogues. No prospective study using lanreotide has been carried out thus far to assess whether this is the case. Objective We carried out a prospective study to assess whether surgical debulking of pituitary macroadenomas causing acromegaly improved the subsequent control of acromegaly by the somatostatin analogue lanreotide. Patients and methods We treated 26 consecutive patients [10 males and 16 females – median age 53·5 years (range 22–70)] with macroadenoma causing acromegaly unselected for somatostatin response for 16 weeks with lanreotide, maximizing GH and IGF-I suppression, if necessary, by incremental dosing. Surgical resection was carried out and the patients were re-assessed off medical treatment at 16 weeks following surgery. Those with nadir GH > 2 mU/l in the oral glucose tolerance test (OGTT) and a mean GH in the GH day curve (GHDC) > 5 mU/l were subsequently restarted on lanreotide and the responses were assessed at the same time points as during the preoperative lanreotide treatment. Results GH values fell on lanreotide treatment and prior to surgery they were considered ‘safe’ (mean GH in GHDC 2 mU/l in the OGTT and ‘unsafe’ GH levels (mean GH in GHDC > 5 mU/l); on re-exposure to lanreotide, GH levels fell in all patients and at the end of 16 weeks postsurgery, they were ‘safe’ in three of them (50%) (P 20% shrinkage. Conclusions In this first prospective study using lanreotide, surgical debulking of pituitary tumours causing acromegaly improved subsequent postoperative control by the somatostatin analogue lanreotide. Surgery should, therefore, be considered in patients with macroadenoma causing acromegaly, even if there is little prospect of surgical cure. Lanreotide causes significant pituitary tumour shrinkage in the majority of patients.

What Is the Natural History of Nonoperated Nonfunctioning Pituitary Adenomas

Abstract: Limited information is available on the outcome of clinically nonfunctioning pituitary adenomas (NFAs) in patients who are not operated upon and do not receive radiotherapy for protracted periods. Most reports are of selected cases of incidentally found lesions. Most NFAs escape early detection and are recognized only when large enough to exert pressure on surrounding tissues. This retrospective study was based on 40 patients presenting in the years 1989-2005, 16 with microadenomas and 24 with macroadenomas. All patients had imaging features suggesting pituitary adenoma but no clinical or biochemical evidence of hormonal hypersecretion. Follow-up averaged 42 months. Half of the macroadenomas and 12.5% of microadenomas became larger during follow-up. The 48-month probabilities of tumor enlargement were 44% and 19%, respectively. Of patients whose tumors enlarged, 57% had new or more advanced visual field defects; all of them had macroadenomas. The optic chiasm was involved in 21% of patients, all of whom also had macroadenomas. None of these patients had deteriorating vision. Two-thirds of macroadenomas that increased in size were accompanied by new or worsening visual field defects. In contrast, none of the microadenomas enlarged enough to compromise vision. Neither gender nor age at presentation predicted enlargement of either microadenomas or macroadenomas. In patients with macroadenomas, enlargement was not predicted by the presence of a visual field defect or cavernous sinus invasion at the time of presentation. No patient had symptoms of pituitary apoplexy. The investigators conclude that a policy of "watchful waiting" is reasonable for patients having nonfunctioning pituitary microadenomas, but probably is not safe for those with macro-NFAs.

Collision lesions of the sella: co-existence of craniopharyngioma with gonadotroph adenoma and of Rathke's cleft cyst with corticotroph adenoma.

Abstract: Collision lesions of the sellar region are relatively uncommon. Most contributions include a pituitary adenoma or a cyst/cystic tumor, particularly a Rathke cleft cyst. The association of craniopharyngioma with an adenoma is particularly rare. Among reported cases, some have included secondary prolactin cell hyperplasia due to pituitary stalk section effect. Herein, we report two collision lesions, including a gonadotroph adenoma with adamantinomatous craniopharyngioma and a corticotroph adenoma with Rathke’s cleft cyst. Clinicopathologic correlation and a review of the literature are undertaken.

Craniopharyngiomas. Historical aspects of their management.

Abstract: The history of the management of craniopharyngiomas offers a comprehensive review of the exciting progress in neurosurgery, neuroimaging, neuroendocrinology and radiation oncology during the last century. In this historical note, we present the evolution in management of these most challenging of brain tumours, which, despite the substantial knowledge and expertise gained since the first attempt of surgical removal, remains a subject of considerable debate.

Acromegaly and anaplastic astrocytoma: coincidence or pathophysiological relation?

Abstract: Insulin-like growth factor type I (IGF-I) is an important promoter in the tumorigenesis of several extracranial and intracranial neoplasms. In astrocytic-cell tumors, the role of autocrine and paracrine IGF-I expression in enhancing tumoral progression is well established. However, the influence of systemic IGF-I levels on the clinical behavior of astrocytic neoplasms remains an open subject of research. We report the case of a 28-year-old man who presented simultaneously with acromegaly and an anaplastic astrocytoma, which had rapidly progressed from a low-grade astrocytoma. The coexistence of systemic IGF-I hypersecretion with a quick progression in the histopathological grade of the astrocytoma raises the compelling question of whether the clinical behavior of the astrocytic tumor was influenced by the acromegalic status. The role of IGF-I signaling in the pathogenesis of astrocytic-cell tumors and the experience with therapeutic strategies addressing this pathway in astrocytomas are also discussed.