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Lewis M. Rothman, Joanna Sher, Robert M. Quencer and Michael S. Tenner

P otential extrasellar sites for the development of pituitary adenomas include intracranially the pars tuberalis, 2 and ventral to the sella the body of the sphenoid and the posterior surface of the nasopharynx. 3 A unique case of an adenoma arising ventral to the sella within the sphenoid was reported by Erdheim in 1909. 1 According to Russell this tumor presumably arose within “an embryonic nest at the site of the obliterated craniopharyngeal duct.” To the authors' knowledge, our case is the first reported example of an intracranial ectopic pituitary

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Thomas Mindermann and Charles B. Wilson

P ituitary adenomas differ in cellular derivation, hormonal function, natural history, biological behavior, and therapeutic responsiveness. 19 They exhibit different immunostaining properties depending on their cellular derivation. Based on differences in immunostaining and ultrastructure, Horvath and Kovacs 19 distinguished pituitary adenomas originating from several different cell lines: growth hormone (GH), prolactin (PRL), and mixed GH and PRL cell adenomas; acidophil-stem cell adenomas; mammosomatotroph and corticotroph cell adenomas; silent

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Familial acromegaly with pituitary adenoma

Report of three affected siblings

Kazem Abbassioun, Vahab Fatourehchi, Abbass Amirjamshidi and Nemotallah Aghai Meibodi

F amilial occurrence of pituitary adenomas with or without clinical acromegaly in association with other endocrine-related tumors (multiple endocrine adenomatosis) is a well recognized entity. 6, 8 However, familial cases of isolated acromegaly with pituitary adenoma are extremely rare, 2 and most reports lack biochemical and histological documentation. Recently, hypersomatotropism and acanthosis nigricans were reported in two brothers with pituitary tumors 4 and in uni-ovular twin brothers. 3 We are reporting the cases of three acromegalic brothers with

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Lee B. Jacoby, E. Tessa Hedley-Whyte, Karen Pulaski, Bernd R. Seizinger and Robert L. Martuza

B enign pituitary adenomas are among the most common neurosurgical tumors and account for a diversity of clinical syndromes due to their hormone content and release. Pituitary adenomas may secrete one, several, or no known hormones. While these end-products of pituitary tumors have been extensively studied, the initiating events of tumorigenesis have not. It is not known if most pituitary adenomas arise from single mutations or if most are formed from multiple cells simultaneously stimulated by factors released from the hypothalamus. In the first instance, one

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B. K. Kleinschmidt-DeMasters, Ken R. Winston, David Rubinstein and Mary H. Samuels

P ituitary adenomas occur only rarely in extrasellar sites that are not in continuity with the pituitary. Such sites have included the sphenoid sinus, 8 nasal cavity, 3, 10 petrous temporal bone, 10 and third ventricle. 11 Ectopic growth has been reported in patients with a separate intrasellar pituitary adenoma, suggesting that the ectopic growth arose from dissemination of a primary intrasellar tumor, either spontaneously or following surgical manipulation. 9, 10 In the very rare situation where ectopic pituitary adenomas have been identified without

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Edward H. Oldfield and Marsha J. Merrill

obtained 5 months later showing no evidence of residual tumor. Arguments Supporting the Proposed Mechanism Pituitary Tumors Have High Energy Demand/Consumption The whole-body [ 18 F]-fluorodeoxyglucose (FDG)–positron emission tomography (PET) and pituitary MR images shown in Fig. 2 were obtained in a 62-year-old man in whom mediastinal lymphadenopathy was being investigated. The images demonstrate a pituitary macroadenoma that was not causing symptoms. Assessment indicated that this was a nonfunctioning pituitary adenoma. FIG. 2. This 62-year

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Jason Sheehan, Jessica Rainey, James Nguyen, Ruthie Grimsdale and Shaojie Han

P ituitary adenomas are one of the most common types of intracranial tumors, with autopsy studies demonstrating an incidence of 25%. 1 The biology of pituitary adenomas can vary substantially. Some pituitary adenomas are slow growing, incidentally found, and require no treatment whatsoever. On the other extreme, some pituitary adenomas prove refractory to surgery, radiation, and pituitary-suppressive medications (for example, dopamine receptor agonists and somatostatin analogs) and continue to progress. Pituitary carcinomas occur in 0.2% of patients and may

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William A. S. Taylor, David Uttley and P. R. Wilkins

tumors that retained their original benign histology; 5, 8 this report discusses a further case in which multiple dural metastases appeared in a patient with pituitary adenoma. Case Report This 40-year-old man presented to the neurosurgical unit of the Atkinson Morley's Hospital in 1980 with a history of left visual field loss for the previous 9 months. He had no other symptoms and no significant medical history. Examination An examination revealed that the patient had visual acuity of J4 on the right and J20 on the left with a left upper quadrantic

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Masahiro Izawa, Motohiro Hayashi, Kohtarou Nakaya, Hiroyuki Satoh, Taku Ochiai, Tomokatsu Hori and Kintomo Takakura

P ituitary adenomas have been treated with a variety of modalities, including resection, medication (bromocriptine, somatostatin, cabergoline), fractionated radiotherapy, and stereotactic radiosurgery. The policy at our institution has been that all adenomas should first be treated with resection to reduce volume and to obtain a histological diagnosis. If the initial microsurgical removal is not radical, additional surgery may be considered. However, GKS for pituitary adenomas has played an important role in tumor growth control and improvement or

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James N. Domingue, S. Douglas Wing and Charles B. Wilson

E xtension of the subarachnoid space into the sella turcica, or the empty sella syndrome, has been described in detail. However, only a few patients with pituitary adenomas and coexisting partially empty sellas have been reported. To date this association has been seen in acromegaly, 16, 21, 23 in patients with the Forbes-Albright syndrome (amenorrhea, galactorrhea, pituitary tumor), 21 and recently in a patient with Cushing's syndrome. 8 This paper reports our series of 17 patients with coexisting pituitary adenomas and partially empty sellas discovered