Neurosurg. Rev. 15 (1992) 3 1 9 - 3 2 2
H y p o p h y s e a l metastatic hypernephroma mimicking a pituitary adenoma. Case report Shunji Nishio l, Harutoshi Tsukamoto l, Masashi FukuP, and Toshiyuki Matsubara z ~Department of Neurosurgery, Neurological Institute, Faculty of Medicine, Kyushu University, and 2Department of Neurosurgery, Chidoribashi Hospital, Fukuoka, Japan
Abstract
2 Case report
A patient with a remote history of nephrectomy for hypernephroma presented a visual field defect with hypopituitarism. Neuro-imaging studies showed a highly vascularized sellar mass with suprasellar extension. Surgery, which was performed via the subfrontal approach, disclosed the pituitary tumor to be a hypernephroma. Although anterior pituitary involvement is rare, chiasreal compression is much rarer in metastatic pituitary carcinomas, a review of previously reported cases of metastatic pituitary hypernephroma and our own case indicated that pituitary metastasis from this carcinoma, in contrast to other metastatic pituitary tumors, often mimics pituitary adenoma.
A 63-year-old female was admitted to our hospital on September 14, 1990, for evaluation of a bilateral visual field defect. In 1986, four years prior to the patient's present admission, a painless, gross hematuria developed. A computed tomographic (CT) scan revealed a 6 • 5 • 5 cm tumor in the right kidney, and a radical nephrectomy with hilar lymphadenectomy was performed. The pathologic evaluation revealed the renal tumor to be a hypernephroma with no lymph node metastasis. Postoperatively, she remained in good health without any evidence of metastatic disease. Around May 1989, however, the patient noted that her bitemporal visual fields were diminishing.
Keywords: Carcinomatous metastasis, chiasmal compression, hypernephroma, hypopituitarism, pituitary adenoma.
1 Introduction Pituitary metastases from distant primary sites are a well-described complication of neoplastic diseases [13, 18]. In patients with these metastases the most common sites of the primary carcinomas is the lung followed by the prostate and stomach in men, and the breast, lung and stomach in women [19]. In this report, we describe a patient whose hypernephroma reappeared as an isolated pituitary metastasis four years after curative nephrectomy. While an increasing number of cases with metastatic carcinomas of the pituitary are being recognized before death, chiasmal compression and metastatic pituitary hypernephroma are so rare in such cases that such report seemed to us to be pertinent and of interest. 9
1992 by Walter de Gruyter & Co. Berlin. New York
Examination on admission disclosed galactorrhea, bitemporal hemianopsia, bilateral optic pallor, and a decreased visual acuity in the left eye. The patient had slight polyuria with diuresis of 2 . 0 2.5 L/day. Baseline levels of GH, luteinizing hormone, follicle-stimulating hormone, thyroxine, and cortisol were slightly lower than normal, and their responses to provocation tests were poor. Her prolactin level was 99.7 ng/ml (normal: 1 . 4 14.6 ng/ml). Plain skull x-ray disclosed an enlarged sella turcica. A C T scan revealed a large, contrastmedium-enhanced sellar and suprasellar mass. M R I demonstrated the lesion to have signal void areas within the mass, and the tumor was markedly enhanced after the administration of GdDTPA (Figure 1). Cerebral angiography showed enlarged meningohypophyseal trunks and marked tumor staining (Figure 2). The patient had no other clinical evidence of metastatic disease from her primary tumor.
320
Figure 1. MRI scans show linear signal void areas within the sellar and suprasellar mass on Tl-weighted image (left), and marked enhancement of the lesion after administration of Gd-DTPA (right).
The patient underwent a transcranial surgery for decompression of the optic nerve and chiasm. At surgery, a large highly vascular tumor, which occupied the sellar and suprasellar regions, was found. Incision into the tumor yielded profuse bleeding and the surgery ended after biopsy. Her postoperative course was uneventful and her visual field deficit remained unchanged. The patient received radiotherapy to the sellar region (60 Gy) over six weeks. Ten months after the treatment, her visual acuity and field slightly improved, and repeat CT scans of the sella revealed no gross change in the size of the tumor. The histologic examination of the tumor tissues obtained at surgery revealed a sheet-like proliferation of polygonal cells which had abundant clear cytoplasm. The patient's original renal tumor was morphologically indistinguishable from the sellar lesion, and the pituitary tumor was interpreted as a metastasis from the hypernephroma.
3 Discussion
The metastatic potential of hypernephroma is prodigious in that 24 to 57% of patients with this carcinoma demonstrate metastatic disease at initial presentation [2, 9, 16]. The most frequent metastatic sites of this carcinoma are the lung and liver [9, 16], and the incidence of intracranial metastasis ranged from 5.7 to 35% [10, 11]. Metastasis of this carcinoma to the pituitary gland, however, has rarely been reported in the literature [1, 3, 4, 8, 11, 12, 151.
Nishio et al., Metastatic pituitary hypernephroma
Figure 2. Left common carotid arteriograms demonstrate a highly vascularized tumor in the sellar and suprasellar areas.
What is of interest regarding our patient is that at the time of the initial presentation of pituitary tumor there was no evidence of any disseminated metastatic disease. Pituitary metastasis usually develops during the terminal phase of malignant disease [11], and when metastases to the pituitary are evident, they are usually associated with widespread disease [1, 4, 6]. Hypernephromas, however, are known to have a tendency to reappear as isolated metastasis far removed from the primary site and often many years after the curative surgery for the primary tumor [8, 12]. Among the 8 cases with metastatic pituitary hypernephromas, at least 5 had a single intrasellar metastasis, and 3 were diagnosed as having a tumor in the sellar region from 4 to 9 years after the initial diagnosis of renal tumor. Since pituitary metastasis more frequently involves the posterior lobe than the anterior lobe [14, 18], it often manifests itself as a posterior pituitary syndrome or diabetes insipidus [5, 13, 17], which is a rare presenting symptom of pituitary adenoma [11, 14]. On the other hand, hypopituitarism and visual field defect, which are both common manifestations of pituitary adenomas, are rarely recognized in patients with pituitary metastasis [5, 6, 12, 17]. In the case reported here, visual symptoms were the first evidence of metastatic carcinoma, and endocrinological studies revealed the patient to have hypopituitarism. After reviewing the literature, it has become apparent that, as in our case, metastatic renal carcinomas often present as visual disturbances and hypopituitarism and mimic a non-secreting pituitary adenoma. Hypernephromas often grow extremely slowly and have such a 10ng clinical history that they can attain Neurosurg. Rev. 15 (1992)
Nishio et al., Metastatic pituitary hypernephroma sufficient size to compress the optic chiasm and produce hypopituitarism [6]. Preoperative distinction between pituitary aden o m a and metastasis can usually be achieved through a patient history a n d presenting symptoms. A l t h o u g h the presence o f a single pituitary metastasis that appears as the first manifestation o f carcinoma is considered to be an exceptional clinical finding [4, 7, 13], McCoRMICK et al. [14] reported that a b o u t 30% o f patients with metastatic carcinoma to the pituitary h a d no k n o w n malignancy. A m o n g 8 reported cases o f metastatic pituitary h y p e r n e p h r o m a , three were diagnosed as having a pituitary t u m o r before being diagnosed as having a renal tumor. Thus consideration o f a diagnosis of metastatic pituitary h y p e r n e p h r o m a should not be limited only to patients with pre-
321 vious history o f malignancy, diabetes insipidus, rapid progression o f clinical symptoms a n d / o r disseminated metastatic disease [1, 14]. There have been few reports of patients h a r b o r i n g pituitary metastases who have been operated u p o n to decompress the optic nerves and chiasm [3, 4, 6, 14]. F o u r of the 7 patients who had a metastatic h y p e r n e p h r o m a were operated u p o n transsphenoidally, and 3 transcranially. As in our case, profuse bleeding was encountered and removal sufficient for decompression o f the optic pathways could be performed in only 2 out o f 5 cases who h a d displayed visual symptoms. A l t h o u g h every a t t e m p t should be m a d e to preserve visual function, patients with widespread disease m a y be better m a n a g e d with h o r m o n a l replacement and radiation therapy [14].
References
[1] ANNIKO M, P-G LUNDQUIST, C SILFVERSW.~RD, J WERSALL: Hypernephroma metastasis in the pituitary gland. A case report. Arch Otorhinolaryngol 232 (1981) 227--232 [2] BADALAMENTRA, E KREUTZER, RW c l u c K , HW HERR, GV WONG, WR FAIR, G GNECCO, JH GALlClCrf: Surgical treatment of brain metastasis from renal cell carcinoma. Urology 36 (1990) 112-117 [3] BRANCH CL, ER LAWS JR: Metastatic tumors of the sella turcica masquerading as primary pituitary tumors. J Clin Endocrinol Metab 65 (1987) 4 6 9 474 [4] BUONAGUIDIR, M FERDEGHINI,F GAGGIONATO,G TUSlNI: Intrasellar metastasis mimicking a pituitary adenoma. Surg Neurol 20 (1983) 373--378 [5] COHEN MM, S LESSILL:Chiasmal syndrome due to metastasis. Arch Neurol 36 (1979) 565-567 [6] Cox EV: Chiasmal compression from metastatic cancer to the pituitary gland. Surg neurol 11 (1979) 4 9 - 50 [7] DUCHEN LW: Metastatic carcinoma in the pituitary gland and hypothalamus. J Pathol Bacteriol 91 (1986) 247 - 355 [8] EICK J J, KA BELL, MT STEPHAN, HA FUSELIERJR: Metastatic renal cell carcinoma presenting as an intrasellar mass on computerized tomography. J Urol 134 (1985) 128-130 [9] FUSELIER HA JR, SL GUICE, W BRANNAN, MG OCHSNER, KV SANGISETTY, EN BECKMAN, CA BARNES:Renal cell carcinoma: the Ochsner Medical Institution experience (1945-1978). J Urol 130 (1983) 445--448
Neurosurg. Rev. 15 (1992)
[10] GAMACHEFW, JB POSNER:Metastatic brain tumors. In: YOUMANSJR (ed): Neurological Surgery, ed 2, Vol 5. WB Saunders, Philadelphia, 1982, pp 28722898 [11] HORIKOSHIT, S MITSUKA, R KtMURA, A FUICAMACHI, H NUKUI: Renal cell carcinoma metastatic to the hypophysis. Case report. Neurol Med Chir (Tokyo) 28 (1988) 7 8 - 8 2 [12] JAMES RL JR, G ARSENIS, M STOLER, D BARAN: Hypophyseal metastatic renal cell carcinoma and pituitary adenoma. Case report and review of the literature. Am J Med 76 (1984) 337-340 [13] MAx MB, MDF DECK, DA ROTTENBERG:Pituitary metastasis: incidence in cancer patients and clinical differentiation from pituitary adenoma. Neruology 31 (1981) 998-1002 [14] McCORMICKPC, KD POST, AD KANDJI, AP HAYS: Metastatic carcinoma to the pituitary gland. Br J Neurosurg 3 (1989) 71--80 [15] POST K, DL KASDON: Sellar and parasellar lesions mimicking adenoma. In: POST KD, IMD JACKSON, S R~ICHLIN (eds): The Pituitary adenoma. Plenum Publishing Co. New Y o r k - L o n d o n 1980, pp 1 5 9 216 [16] ROCHMAN SC, JA BELLS, SJ KANDZARE Renal cell carcinoma. South Med J 72 (1979) 1 1 - 1 4 [17] TABBARAWS, AM MEnlO, GP AFTIMOS:Metastatic renal cell adenocarcinoma. Proc First Int Sympo on Kidney Tumors. In: Llss A (ed): Progress in clinical and biological research. Vol 100, Alan R Liss. New York. 1982, pp 317-336
322 [18] TEEARSRJ, EM SILVERMAN: Clinicopathologic review of 88 cases of carcinoma metastatic to the pituitary gland. Cancer 36 (1975) 216--220
Nishio et al., Metastatic pituitary hypernephroma
[19] TINDALL GT, DL BARROW: Disorders of the pituitary. CV Mosby. St Louis. 1986, p 108, p 308 Submitted December 9, 1991. Accepted December 20, 1991. Shunji Nishio, M.D. 3-1-1 Maidashi Higashi-ku Fukuoka 812 Japan
Neurosurg, Rev. 15 (1992)
H y p o p h y s e a l metastatic hypernephroma mimicking a pituitary adenoma. Case report Shunji Nishio l, Harutoshi Tsukamoto l, Masashi FukuP, and Toshiyuki Matsubara z ~Department of Neurosurgery, Neurological Institute, Faculty of Medicine, Kyushu University, and 2Department of Neurosurgery, Chidoribashi Hospital, Fukuoka, Japan
Abstract
2 Case report
A patient with a remote history of nephrectomy for hypernephroma presented a visual field defect with hypopituitarism. Neuro-imaging studies showed a highly vascularized sellar mass with suprasellar extension. Surgery, which was performed via the subfrontal approach, disclosed the pituitary tumor to be a hypernephroma. Although anterior pituitary involvement is rare, chiasreal compression is much rarer in metastatic pituitary carcinomas, a review of previously reported cases of metastatic pituitary hypernephroma and our own case indicated that pituitary metastasis from this carcinoma, in contrast to other metastatic pituitary tumors, often mimics pituitary adenoma.
A 63-year-old female was admitted to our hospital on September 14, 1990, for evaluation of a bilateral visual field defect. In 1986, four years prior to the patient's present admission, a painless, gross hematuria developed. A computed tomographic (CT) scan revealed a 6 • 5 • 5 cm tumor in the right kidney, and a radical nephrectomy with hilar lymphadenectomy was performed. The pathologic evaluation revealed the renal tumor to be a hypernephroma with no lymph node metastasis. Postoperatively, she remained in good health without any evidence of metastatic disease. Around May 1989, however, the patient noted that her bitemporal visual fields were diminishing.
Keywords: Carcinomatous metastasis, chiasmal compression, hypernephroma, hypopituitarism, pituitary adenoma.
1 Introduction Pituitary metastases from distant primary sites are a well-described complication of neoplastic diseases [13, 18]. In patients with these metastases the most common sites of the primary carcinomas is the lung followed by the prostate and stomach in men, and the breast, lung and stomach in women [19]. In this report, we describe a patient whose hypernephroma reappeared as an isolated pituitary metastasis four years after curative nephrectomy. While an increasing number of cases with metastatic carcinomas of the pituitary are being recognized before death, chiasmal compression and metastatic pituitary hypernephroma are so rare in such cases that such report seemed to us to be pertinent and of interest. 9
1992 by Walter de Gruyter & Co. Berlin. New York
Examination on admission disclosed galactorrhea, bitemporal hemianopsia, bilateral optic pallor, and a decreased visual acuity in the left eye. The patient had slight polyuria with diuresis of 2 . 0 2.5 L/day. Baseline levels of GH, luteinizing hormone, follicle-stimulating hormone, thyroxine, and cortisol were slightly lower than normal, and their responses to provocation tests were poor. Her prolactin level was 99.7 ng/ml (normal: 1 . 4 14.6 ng/ml). Plain skull x-ray disclosed an enlarged sella turcica. A C T scan revealed a large, contrastmedium-enhanced sellar and suprasellar mass. M R I demonstrated the lesion to have signal void areas within the mass, and the tumor was markedly enhanced after the administration of GdDTPA (Figure 1). Cerebral angiography showed enlarged meningohypophyseal trunks and marked tumor staining (Figure 2). The patient had no other clinical evidence of metastatic disease from her primary tumor.
320
Figure 1. MRI scans show linear signal void areas within the sellar and suprasellar mass on Tl-weighted image (left), and marked enhancement of the lesion after administration of Gd-DTPA (right).
The patient underwent a transcranial surgery for decompression of the optic nerve and chiasm. At surgery, a large highly vascular tumor, which occupied the sellar and suprasellar regions, was found. Incision into the tumor yielded profuse bleeding and the surgery ended after biopsy. Her postoperative course was uneventful and her visual field deficit remained unchanged. The patient received radiotherapy to the sellar region (60 Gy) over six weeks. Ten months after the treatment, her visual acuity and field slightly improved, and repeat CT scans of the sella revealed no gross change in the size of the tumor. The histologic examination of the tumor tissues obtained at surgery revealed a sheet-like proliferation of polygonal cells which had abundant clear cytoplasm. The patient's original renal tumor was morphologically indistinguishable from the sellar lesion, and the pituitary tumor was interpreted as a metastasis from the hypernephroma.
3 Discussion
The metastatic potential of hypernephroma is prodigious in that 24 to 57% of patients with this carcinoma demonstrate metastatic disease at initial presentation [2, 9, 16]. The most frequent metastatic sites of this carcinoma are the lung and liver [9, 16], and the incidence of intracranial metastasis ranged from 5.7 to 35% [10, 11]. Metastasis of this carcinoma to the pituitary gland, however, has rarely been reported in the literature [1, 3, 4, 8, 11, 12, 151.
Nishio et al., Metastatic pituitary hypernephroma
Figure 2. Left common carotid arteriograms demonstrate a highly vascularized tumor in the sellar and suprasellar areas.
What is of interest regarding our patient is that at the time of the initial presentation of pituitary tumor there was no evidence of any disseminated metastatic disease. Pituitary metastasis usually develops during the terminal phase of malignant disease [11], and when metastases to the pituitary are evident, they are usually associated with widespread disease [1, 4, 6]. Hypernephromas, however, are known to have a tendency to reappear as isolated metastasis far removed from the primary site and often many years after the curative surgery for the primary tumor [8, 12]. Among the 8 cases with metastatic pituitary hypernephromas, at least 5 had a single intrasellar metastasis, and 3 were diagnosed as having a tumor in the sellar region from 4 to 9 years after the initial diagnosis of renal tumor. Since pituitary metastasis more frequently involves the posterior lobe than the anterior lobe [14, 18], it often manifests itself as a posterior pituitary syndrome or diabetes insipidus [5, 13, 17], which is a rare presenting symptom of pituitary adenoma [11, 14]. On the other hand, hypopituitarism and visual field defect, which are both common manifestations of pituitary adenomas, are rarely recognized in patients with pituitary metastasis [5, 6, 12, 17]. In the case reported here, visual symptoms were the first evidence of metastatic carcinoma, and endocrinological studies revealed the patient to have hypopituitarism. After reviewing the literature, it has become apparent that, as in our case, metastatic renal carcinomas often present as visual disturbances and hypopituitarism and mimic a non-secreting pituitary adenoma. Hypernephromas often grow extremely slowly and have such a 10ng clinical history that they can attain Neurosurg. Rev. 15 (1992)
Nishio et al., Metastatic pituitary hypernephroma sufficient size to compress the optic chiasm and produce hypopituitarism [6]. Preoperative distinction between pituitary aden o m a and metastasis can usually be achieved through a patient history a n d presenting symptoms. A l t h o u g h the presence o f a single pituitary metastasis that appears as the first manifestation o f carcinoma is considered to be an exceptional clinical finding [4, 7, 13], McCoRMICK et al. [14] reported that a b o u t 30% o f patients with metastatic carcinoma to the pituitary h a d no k n o w n malignancy. A m o n g 8 reported cases o f metastatic pituitary h y p e r n e p h r o m a , three were diagnosed as having a pituitary t u m o r before being diagnosed as having a renal tumor. Thus consideration o f a diagnosis of metastatic pituitary h y p e r n e p h r o m a should not be limited only to patients with pre-
321 vious history o f malignancy, diabetes insipidus, rapid progression o f clinical symptoms a n d / o r disseminated metastatic disease [1, 14]. There have been few reports of patients h a r b o r i n g pituitary metastases who have been operated u p o n to decompress the optic nerves and chiasm [3, 4, 6, 14]. F o u r of the 7 patients who had a metastatic h y p e r n e p h r o m a were operated u p o n transsphenoidally, and 3 transcranially. As in our case, profuse bleeding was encountered and removal sufficient for decompression o f the optic pathways could be performed in only 2 out o f 5 cases who h a d displayed visual symptoms. A l t h o u g h every a t t e m p t should be m a d e to preserve visual function, patients with widespread disease m a y be better m a n a g e d with h o r m o n a l replacement and radiation therapy [14].
References
[1] ANNIKO M, P-G LUNDQUIST, C SILFVERSW.~RD, J WERSALL: Hypernephroma metastasis in the pituitary gland. A case report. Arch Otorhinolaryngol 232 (1981) 227--232 [2] BADALAMENTRA, E KREUTZER, RW c l u c K , HW HERR, GV WONG, WR FAIR, G GNECCO, JH GALlClCrf: Surgical treatment of brain metastasis from renal cell carcinoma. Urology 36 (1990) 112-117 [3] BRANCH CL, ER LAWS JR: Metastatic tumors of the sella turcica masquerading as primary pituitary tumors. J Clin Endocrinol Metab 65 (1987) 4 6 9 474 [4] BUONAGUIDIR, M FERDEGHINI,F GAGGIONATO,G TUSlNI: Intrasellar metastasis mimicking a pituitary adenoma. Surg Neurol 20 (1983) 373--378 [5] COHEN MM, S LESSILL:Chiasmal syndrome due to metastasis. Arch Neurol 36 (1979) 565-567 [6] Cox EV: Chiasmal compression from metastatic cancer to the pituitary gland. Surg neurol 11 (1979) 4 9 - 50 [7] DUCHEN LW: Metastatic carcinoma in the pituitary gland and hypothalamus. J Pathol Bacteriol 91 (1986) 247 - 355 [8] EICK J J, KA BELL, MT STEPHAN, HA FUSELIERJR: Metastatic renal cell carcinoma presenting as an intrasellar mass on computerized tomography. J Urol 134 (1985) 128-130 [9] FUSELIER HA JR, SL GUICE, W BRANNAN, MG OCHSNER, KV SANGISETTY, EN BECKMAN, CA BARNES:Renal cell carcinoma: the Ochsner Medical Institution experience (1945-1978). J Urol 130 (1983) 445--448
Neurosurg. Rev. 15 (1992)
[10] GAMACHEFW, JB POSNER:Metastatic brain tumors. In: YOUMANSJR (ed): Neurological Surgery, ed 2, Vol 5. WB Saunders, Philadelphia, 1982, pp 28722898 [11] HORIKOSHIT, S MITSUKA, R KtMURA, A FUICAMACHI, H NUKUI: Renal cell carcinoma metastatic to the hypophysis. Case report. Neurol Med Chir (Tokyo) 28 (1988) 7 8 - 8 2 [12] JAMES RL JR, G ARSENIS, M STOLER, D BARAN: Hypophyseal metastatic renal cell carcinoma and pituitary adenoma. Case report and review of the literature. Am J Med 76 (1984) 337-340 [13] MAx MB, MDF DECK, DA ROTTENBERG:Pituitary metastasis: incidence in cancer patients and clinical differentiation from pituitary adenoma. Neruology 31 (1981) 998-1002 [14] McCORMICKPC, KD POST, AD KANDJI, AP HAYS: Metastatic carcinoma to the pituitary gland. Br J Neurosurg 3 (1989) 71--80 [15] POST K, DL KASDON: Sellar and parasellar lesions mimicking adenoma. In: POST KD, IMD JACKSON, S R~ICHLIN (eds): The Pituitary adenoma. Plenum Publishing Co. New Y o r k - L o n d o n 1980, pp 1 5 9 216 [16] ROCHMAN SC, JA BELLS, SJ KANDZARE Renal cell carcinoma. South Med J 72 (1979) 1 1 - 1 4 [17] TABBARAWS, AM MEnlO, GP AFTIMOS:Metastatic renal cell adenocarcinoma. Proc First Int Sympo on Kidney Tumors. In: Llss A (ed): Progress in clinical and biological research. Vol 100, Alan R Liss. New York. 1982, pp 317-336
322 [18] TEEARSRJ, EM SILVERMAN: Clinicopathologic review of 88 cases of carcinoma metastatic to the pituitary gland. Cancer 36 (1975) 216--220
Nishio et al., Metastatic pituitary hypernephroma
[19] TINDALL GT, DL BARROW: Disorders of the pituitary. CV Mosby. St Louis. 1986, p 108, p 308 Submitted December 9, 1991. Accepted December 20, 1991. Shunji Nishio, M.D. 3-1-1 Maidashi Higashi-ku Fukuoka 812 Japan
Neurosurg, Rev. 15 (1992)
