Subarachnoid metastases from a prolactinoma

Plangger, C; Twerdy, K; Grunert, V.; Weiser, G

doi:10.1055/s-2008-1054208

Cited by 15 publications

(7 citation statements)

References 4 publications

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“…With the addition of our 15 cases, 3 of which were previously published, a total of 64 cases of pituitary carcinoma have been reported in the literature published in English to date 1‐51. Forty‐eight (74%) were hormone‐producing, whereas the remaining seventeen (26%) were considered endocrinologically "nonfunctioning."…”

Section: Discussionmentioning

confidence: 99%

“…To date, 52 such cases have been reported in the literature published in English. 1‐51 These include 16 (30%) prolactin (PRL)‐producing tumors,1‐1315 (28%) adrenocorticotropic hormone (ACTH)‐producing tumors,13‐25 6 (10%) growth hormone (GH)‐producing tumors,29‐34 1 (2%) thyroid‐stimulating hormone (TSH)‐producing tumor,35 1 (2%)gonadotropin‐producing tumor,36 and 13 (30%) "nonfunctioning" tumors 30, 37‐51…”

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Pituitary carcinoma

Pernicone

Scheithauer

Sebo

et al. 1997

Cancer

353

110

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BACKGROUND Pituitary carcinomas are rare adenohypophysial neoplasms, the definition, diagnosis, therapy, and prognosis of which are controversial. METHODS Pituitary carcinomas were defined as primary adenohypophysial neoplasms with documented craniospinal and/or systemic metastases. The authors report a clinicopathologic study of 15 examples examined by light microscopy, immunohistochemistry, and image analysis. Both proliferative activity and p53 tumor suppressor gene expression were studied. RESULTS The study group consisted of 15 patients, including 8 males and 7 females ranging in age from 34‐71 years (mean, 56 years). Of these patients, seven had adrenocorticotropic hormone (ACTH)‐producing tumors (four in the context of Nelson's syndrome), seven had prolactin‐producing tumors, and one had a nonfunctioning tumor. No evidence of diabetes insipidus was seen in any case. Fourteen tumors were initially considered macroadenomas. Of the ten cases for whom tumor extent was known, all had invasive tumors. The interval from the initial diagnosis of adenoma to that of carcinoma ranged from 0.3 to 18.0 years (mean, 6.6 years; median, 5.0 years); the longest mean interval (15.3 years) occurred for patients with Nelson's syndrome. The latency was twice as long for ACTH‐producing tumors as for prolactin (PRL) cell tumors (9.5 vs. 4.7 years). All carcinomas showed a greater tendency toward systemic metastasis than craniospinal metastasis; the rate of systemic metastasis was 71% for PRL cell tumors and 57% for ACTH‐producing tumors. Thirteen percent of tumors showed both patterns of metastasis. Fully 50% of primary tumors and the majority of metastases showed nuclear pleomorphism and/or hyperchromasia. The mean mitotic, MIB‐1, and proliferating cell nuclear antigen indices for primary tumors and metastases were as follows: 2/10 high‐power field (hpf), 2.6% and 11%, respectively; 6/10 hpf, 7.8% and 16%, respectively. Staining for p53 protein was noted in 57% of primary tumors and 88% of metastatic tumors; a relative increase in p53 expression in metastases was noted in 83%. All but one of the primary and metastatic tumors were aneuploid. The most common treatments were radiation therapy and, for PRL cell carcinomas, dopamine agonist administration. Both treatments provided only palliation. Eighty percent of the patients died of metastatic disease 7 days to 8 years after the diagnosis of carcinoma; of these, 66% died within 1 year. At last follow‐up, 20% of patients were alive with metastases 9‐18 months after diagnosis. CONCLUSIONS Nearly all pituitary carcinomas present as functioning, microscopically atypical or mitotically active, invasive macroadenomas. By definition, after an interval related to their immunotype, all metastasize. The tumors show a greater tendency toward systemic metastasis than craniospinal metastasis and are associated with poor prognosis. Radiation and dopamine agonist therapy generally provide only palliation. Proliferation indices and p53 expression tend to be higher in metastases than in ...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Pituitary carcinoma

Pernicone

Scheithauer

Sebo

et al. 1997

Cancer

353

110

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“…In some cases, metastases only manifested during autopsy (14,18,20,21). Intracranial metastases were reported in the frontal lobe (7,9,12,18,19,22,23,27,33,34), parietaloccipital lobe (6,22,29), temporal lobe (10,18,24,28,33), cerebellum (4,8,12,14,29,38), cerebellopontine angle (5,18,31), brainstem (17,20,28,38), and subarachnoid space (9,14,20). Less commonly involved areas were the cranial nerves (20,27) and the orbital space (15,18,28,35).…”

Section: Discussionmentioning

confidence: 99%

Malignant prolactinoma: case report and review of the literature

Kars

Roelfsema²,

Romijn³

et al. 2006

eur j endocrinol

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Pituitary carcinomas are extremely rare. In general, the initial clinical, biochemical, and histological characteristics are of minimal utility in distinguishing benign adenomas from pituitary carcinomas. We describe a 63-year-old woman with a macroprolactinoma, who presented with diplopia and blurred vision. This unusual initial presentation and the subsequent aggressive clinical course, with diffuse local and distant intramedulary metastases, prompted us in retrospect to make a detailed analysis of the therapeutic interventions and histology. In addition, we reviewed all available literature on published cases of malignant prolactinoma and detailed their epidemiological, clinical, and histopathological characteristics. In brief, it is postulated that pituitary carcinomas arise from the transformation of initially large, but benign, adenomas. Unusual and/or atypical clinical manifestations appear to occur more frequently. In vivo, the development of dopamine agonist resistance in invasive macroprolactinoma is indicative of malignancy and should prompt the clinician to perform a biopsy of the tumor. For pituitary tumors that exhibit high mitotic activity, increased Ki-67 and/or p53 immunoreactivity, it may be useful to denote these tumors as 'atypical' prolactinomas to raise the possibility of future malignant development.European Journal of Endocrinology 155 523-534

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“…17,[24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41] Although the diagnosis has not yet been established by a biopsy of the temporal lobe lesion, the positive p53 (see below), the secondary nonresponse to BRC, and the occurrence of a second lesion fluctuating in size with PRL levels are highly suggestive of malignancy. Since histology of the primary tumor is unreliable, pituitary tissue markers have recently become available that are helpful in predicting an adenoma's potential for recurrence and invasive or malignant behavior.…”

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confidence: 99%

Cabergoline in prolactinomas

Fierz

Kaufman

Lee³

et al. 1999

Neuro-Ophthalmology

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Cabergoline is a potent, D2-selective new dopamine agonist with a half-life of 65 hours. We report two cases and review the literature on cabergoline in prolactinomas. Cabergoline appears to be more effective and better tolerated than bromocriptine, compliance may be improved, and costs are comparable. In cases of bromocriptine failure, unusually high starting doses of cabergoline may be necessary. Cabergoline may eventually replace bromocriptine as the drug of choice in prolactinomas.

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Subarachnoid metastases from a prolactinoma

Cited by 15 publications

References 4 publications

Pituitary carcinoma

Pituitary carcinoma

Malignant prolactinoma: case report and review of the literature

Cabergoline in prolactinomas

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