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Computed tomographic appearances and clinical features of prolactin-secreting pituitary adenomas in young male patients
ClinicalRadiology (1985) 36, 22%231 © 1985 Royal College of Radiologists
0009-9260/85/404227502 00
Computed Tomographic Appearances and Clinical Features of Prolactin-secreting Pituitary Adenomas in Young Male Patients NICHOLAS
DAUNT*
and PAUL
MOWAT
Department of Radiology, Royal Brisbane Hospital, Brisbane, Queensland, Australia
Prolactin-secreting adenomas, the commonest of the pituitary tumours, are being recognised with increasing frequency in men. Their appearance and behaviour differ from those occurring in women, being typically larger and more aggressive. We describe the clinical features and radiological findings of three prolactinomas in young males and review the literature.
Since the introduction of improved endocrine assays for p r o l a c t i n a n d a b e t t e r u n d e r s t a n d i n g o f its c o n t r o l and mode o f a c t i o n , it h a s b e c o m e i n c r e a s i n g l y recognised that prolactin-secreting tumours are far more common than previously appreciated. It has b e e n e s t i m a t e d t h a t t h e y c o n s t i t u t e as m u c h as 5 0 % o f all p i t u i t a r y a d e n o m a s ( L e a v e n s et al., 1981). Many of them would previously have fallen into the category of non-functioning chromophobe adenomas, but up to 70% of these tumours are prolactin-secreting ( F r a n k s et al., 1975; J a c o b s , 1976). Three young male patients aged 15-20 years with prolactin-secreting adenomas recently presented to us for radiological assessment. We present their case histories and radiological findings and discuss the clinical features and behaviour of these tumours.
CASE REPORTS Case 1. A 15-year-old male presented with a 2-month history of intermittent blurring of vision in his left eye. He gave a history of 7 years of increasingly frequent headaches and excessive weight gain and, more recently, polydipsia of several months duration. Examination revealed a bitemporal hemianopia. Clinically, there was no evidence of any obvious hormone excess or deficiency. An enlarged, expanded pituitary fossa was found on skull radiography. A computed tomography (CT) scan was performed which showed a large, homogeneously enhancing pituitary mass extending into the suprasellar cistern and the left cavernous sinus (Fig. la, b). Bilateral internal carotid angiography showed stretched cavernous carotid segments on both sides, no A1 segment elevation and no evidence of an aneurysm. An exploratory operation revealed a reddish-blue mass which looked like an aneurysm and yielded bright red blood on needling. Only partial removal was possible, the histology showing a chrornophobe adenoma. Hormone assay demonstrated an isolated elevation of prolactln (5670ng/ml; normal level <13 ng/ml) and a testosterone deficiency (5.4 nmolllitre; normal level 10-35 nmol/litre).Bromocriptine was commenced, initially at a dose of 2.5 mg twice daily, then increased to three times daily after 3 weeks. *Present address and address for reprints: N. Daunt, X-Ray Department, Mater Misericordiae Private Hospital, Raymond Terrace, Brisbane, Queensland, Australia.
After 6 months of treatment with bromocriptine, the s e r u m prolactin had fallen to 420ng/ml. A repeat CT scan showed virtual disappearance of the intra- and suprasellar components of the tumour, but with new tumour tissue posterior to the clivus (Fig. lc). The visual fields were normal at follow-up, the main clinical problem being persisting obesity. Case 2. A 17-year-old male presented with a short history of blurred vision in his left eye, and a 1-year history of increasingly frequent headaches. On examination he was found to have a left ptosis and diplopia. He had gained 20kg weight in 4 years. His visual fields were normal. There was evidence of an expanding intrasellar lesion on skull radiography. A CT scan showed a large mass in the pituitary fossa with suprasellar extension, lateral extension into both cavernous sinuses and erosion of the floor of the sella with a soft-tissue mass in the left side of the sphenoid sinus. The tumour exhibited homogeneous density enhancement following injection of contrast medium (Fig. 2a, b). Arteriography by bilateral internal carotid artery injections showed a minor mass effect on the left side. A markedly elevated prolactin (11000 ng/ml) was found. All other hormone assays were normal apart from a low testosterone (7.8 nmol/litre). A sperm count showed deficient numbers with 50% abnormal forms. The bone age was normal. Hypercalcaemia was also present (2.97mmol/litre). Biopsy of the pituitary lesion disclosed a chromophobe adenoma. Treatment was initiated with bromocriptine, 2.5mgnocte, later increased to 7.5 mgt.d.s. A marked fall in prolactm level occurred over 8 months to 340 ng/ml and at follow-up all symptoms and signs had disappeared. A repeat CT scan showed a marked diminution in size of the tumour with virtual disappearance of the extrasellar component (Fig. 2c). During the follow-up period, surgical exploration of the neck revealed a parathyroid adenoma which was removed, with subsequent fall in calcium to a normal level. The combination of a pituitary adcnoma and a parathyroid adenoma is part of the multiple endocrine neoplasia syndrome Type l. Case 3. A 20-year-old male presented with an acute right hemiparesis which resolved almost completely within 1 week. Clinically, no other abnormality was seen. There were no obvious hormone deficiencies or excess and the visual fields were normal. Skull radiographs showed destruction of the dorsum sellae and upper clivus with depression and asymmetry of the floor of the sella. A C T scan was performed which showed a large soft-tissue mass eroding the dorsum sellae, much of the clivus, the petrous apices and the left anterior clinoid process. It extended into the sphenoid and ethmoid sinuses, superiorly into the suprasellar cistern and laterally into the floor of the left middle cranial fossa. Focal calcification was present. The mass exhibited predominantly homogeneous enhancement following injection of contrast medium but with several small cystic or necrotic areas which showed no enhancement (Fig. 3a-c). Initial diagnostic possibilities included a chordoma or an aggressive pituitary tumour. Selective carotid and vertebral arteriography showed a mass effect due to the tumour, but without arterial compression or invasion, and no pathological circulation was identified. A markedly elevated prolactin level (12900ng/ml) and a low testosterone (5.8 nmol/litre) were found. All other hormone levels were normal. Treatment with bromocriptine 2.5mgt.d.s. was started which was later increased to 7.5 mgt.d.s, with a subsequent fall in serum prolactin to 315ng/ml over 9 months. A repeat CT scan showed a marked diminution in tumour size (Fig. 3d). The only remaining clinical problem is mildly diminished sensation in the patient's right hand.
228
CLINICAL RADIOLOGY
(a)
(b)
(c)
Fig. 1 - Case 1. (a) Contrast-enhanced tumour extending to the left parasellar region (L +50, W250). (b) Suprasellar extension (L +50, W 150). (c) Six months post-operatively: the intra- and suprasellar components are no longer in evidence, but there is now some tumour tissue behind the clivus (L +50, W 150).
DISCUSSION The occurrence of prolactin-secreting pituitary adenomas in young women, causing infertility and treatable by bromocriptine, is firmly established. These tumours are usually microadenomas and are difficult to demonstrate due to their small size. The behaviour of these tumours in male patients is significantly different, with a tendency to an aggressive nature and large size on initial investigation (Carter et al., 1978; Grisoli et al., 1980; Leavens et al., 1981). In these series no microadenomas were found. Some cases of smaller adenomas in men are recorded, Vezina (1981) reporting eight of 55 adenomas in men associated with a normal pituitary fossa on plain radiography.
The clinical features which might be expected are due to: 1. the effect of the mass on surrounding structures, 2. the effect of excessive prolactin secretion and 3. the effect of the mass on the production of other pituitary hormones. The effects of the mass on surrounding structures give rise to headaches and visual impairment. Appro x imately 50% of published cases have included visual impairment, usually a bitemporal hemianopia due to chiasmal compression. Headaches are also a common complaint, often being of long duration: one of our patients had a 7-year history of headaches. The presentation of our third case, simulating a vascular accident, is unusual.
229
PROLACTIN-SECRETING PITUITARY ADENOMAS IN YOUNG MALES
(b)
(a)
Fig. 2 - Case 2. (a) Enhancing pituitary tumour with suprasellar and left parasellar extension (L +40, W 150). (b) Coronal reconstruction (L +40, W 150). (c) Follow-up scan after 15 months on bromocriptine. No extrasellar tumour is evident (L +40, W200).
(c)
Hypothyroidism and adrenal insufficiency are uncommon, occurring in about a quarter of reported cases. More common is a low testosterone level, often an isolated deficiency, which reflects compromised FSH/LH secretion. The effects of a low testosterone and those due to a raised prolactin are hard to differentiate clinically. Both can give rise to one or more of the following: loss of libido, impotence, infertility, an abnormal sperm count (Toth, 1981; Ayalon et al., 1982) and obesity, which is often intractable (Nabarro, 1982)_ Galactorrhoea, accelerated puberty and increased bone age occur less frequently (Leavens et al., 1981; Slonim et al., 1982). Our three patients were aged 15, 17 and 20 years. The usual age range of patients with these tumours is about 15-60 years, although they have been reported in 13-year-olds (Schroffner, 1976; Slonim et al., 1982) and one in a 12-year-old (VanMeter et al., 1977). It has been suggested that adenomas in adolescents are more likely to be 'invasive', implymg involvement of contiguous structures but not indicating malignancy (Ortiz-Suarez and Erickson, 1975). Raised prolactin levels may occur with many hypothalamic and pituitary disorders, including nonprolactin-secreting pituitary tumours, and aneurysms, meningiomas, chordomas and craniopharyngiomas can elevate prolactin levels due to their effect on the production of prolactin inhibiting factor or its trans-
mission through the portal vessels. However, repeated values above 100 ng/ml are suggestive and levels above 500ng/ml are virtually diagnostic of a prolactinsecreting tumour (Horrobin, 1980). Attempts have been made to correlate the prolactin level with the aggressiveness of the turnout. It has been suggested that a prolactin level above 335 ng/ml is likely to be due to invasive adenoma (Leavens et al., 1981). Very high levels, above 3000ng/ml, have been equated with tumour invasion of the cavernous sinus (Shucart, 1980). The best treatment for these large, invasive adenomas is controversial. Surgery has only limited success, the prolactin remaining elevated in many instances, suggesting residual turnout tissue. Radiotherapy trials have met with little success; indeed, with high daily fraction dosage the risk of visual failure seems to outweigh the doubtful benefits of this treatment (Harris and Levene, 1976). Bromocriptine is an accepted method of reducing prolactin secretion and, recently, a decrease in turnout size has been reported following this treatment (Ayalon et al., 1982; Chernow et al., 1982), suggesting an actual antitumour effect. All three of our cases have shown a marked decrease in turnout size on medical treatment. It might be anticipated that, following the shrinkage of a tumour by this treatment, it may be more amenable to surgery at a later date.
21
230
CLINICAL RADIOLOGY
(a)
(c)
(b)
(d)
Fig. 3 - Casc 3. (a) Post-contrast coronal reconstruction demonstrating a large pituitary turnout with extensive lobulated suprasellar and left parasellar components with homogeneous enhancement (L +50, W 150). (b) Post-contrast sagittal reconstruction showing posterior and inferior extension of the mass with destruction of the upper part of the clivus (L +50, W 150). (c) Post-contrast scan. Suprasellar component extending into the left temporal lobe. Three small, non-enhancing, low-density necrotic areas are noted (L +50, W 150). (d) Follow-up scan after 9 months shows marked diminution in tumour size with only a small residual left suprasellar mass (L +50, W 150).
PROLACTIN-SECRETING PITUITARY ADENOMAS IN YOUNG MALES
REFERENCES Ayalon, D., Eckstein, N., Hommonai, Z. T., Paz, G. F., Eshel, A. & Reider, I. (1982). Effects of long term treatment with bromocriptine on pituitary prolactinoma in a male. International Journal of Obstetrics and Gynaecology, 20, 481-485. Carter, J. N., Tyson, J. E., Tolis, G., VanVliet, S., Faiman, C. & Friesen, G. (1978). Prolactin secreting tumours and hypogonadism in 22 men. New England Journal of Medicine, 299, 847-852. Chernow, B., Buck, D. R., Early, C. B., Ray, J. & O'Brian, J. T. (1982). Rapid shrinkage of a prolactin secreting pituitary tumour with bromocriptine: CT documentation. American Journal of Neuroradiology. 3, 442-443. Franks, S., Jacobs, H. S. & Nabarro, J. D. N. (1975). Studies of prolactin secretion in pituitary disease. Journal of Endocrinology, 67, 55-62. Grisoli, F., Vincentelli, F., Jaquet, P., Guibot, M., Hassoun, J. & Farnavier, P. (1980). Prolactin secreting adenomas in 22 men. Surgical Neurology, 13, 241-247. Harris, J. R. & Levene, M. B. (1976). Visual complications following irradiation for pituitary adenomas and craniopharyngiomas. Radiology, 120, 167-17i. Horrobin, D. F. (1980). Prolactin, 8, 102-108. Jacobs, H. S. (1976). Prolactin and amenorrhoea. New England Journal of Medicine, 295, 954-956.
231
Leavens, M. E., Samaan, N. A., Larson, D. L., Jessie, R. H. & Byers, R. M. (1981). Prolactin secreting pituitary adenomas. International Advances in Surgical Oncology, 4, 27%310. Nabarro, J. D. (1982). Pituitary prolactinomas. Clinical Endocrinology (Oxford), 17, 129-155. Ortiz-Suarez, H. & Erickson, D. L. (1975). Pituitary adenomas of adolescents. Journal of Neurosurgery, 43, 437-439. Schroffner, W. G. (1976). Prolactin secreting pituitary tumour in early adolescence. Archives of Internal Medicine, 136, 11641165. Shucart, W. A. (1980). Implications of very high serum prolactin levels associated with pituitary tumours. Journal of Neurosurgery, 52, 226-228. Slonim, A. E., Glick, A. D., Island, D. P. & Kasselberg, A. G. (1982). Hyperprolactinaemia associated with advanced puberty in a male. Journal of Pediatrics, 101, 236239. Toth, A. (1981). Abnormal seminal cytology in a patient with a prolactin secreting pituitary adenoma. Fertility and Sterility, 36, 818-820. VanMeter, Q. L., Gavis, F. J., Hayes, J. W. & Wilson, C. B. (1977). Galactorrhoea in a 12 year old boy with a chromophobe adenoma. Journal of Pediatrics, 90, 756-758. Vezina, J. L. (1981). II.Le Prolactinome. Aspects radiologiques de la selle turcique. Neurochirurgie, 27, Suppl. 1.
0009-9260/85/404227502 00
Computed Tomographic Appearances and Clinical Features of Prolactin-secreting Pituitary Adenomas in Young Male Patients NICHOLAS
DAUNT*
and PAUL
MOWAT
Department of Radiology, Royal Brisbane Hospital, Brisbane, Queensland, Australia
Prolactin-secreting adenomas, the commonest of the pituitary tumours, are being recognised with increasing frequency in men. Their appearance and behaviour differ from those occurring in women, being typically larger and more aggressive. We describe the clinical features and radiological findings of three prolactinomas in young males and review the literature.
Since the introduction of improved endocrine assays for p r o l a c t i n a n d a b e t t e r u n d e r s t a n d i n g o f its c o n t r o l and mode o f a c t i o n , it h a s b e c o m e i n c r e a s i n g l y recognised that prolactin-secreting tumours are far more common than previously appreciated. It has b e e n e s t i m a t e d t h a t t h e y c o n s t i t u t e as m u c h as 5 0 % o f all p i t u i t a r y a d e n o m a s ( L e a v e n s et al., 1981). Many of them would previously have fallen into the category of non-functioning chromophobe adenomas, but up to 70% of these tumours are prolactin-secreting ( F r a n k s et al., 1975; J a c o b s , 1976). Three young male patients aged 15-20 years with prolactin-secreting adenomas recently presented to us for radiological assessment. We present their case histories and radiological findings and discuss the clinical features and behaviour of these tumours.
CASE REPORTS Case 1. A 15-year-old male presented with a 2-month history of intermittent blurring of vision in his left eye. He gave a history of 7 years of increasingly frequent headaches and excessive weight gain and, more recently, polydipsia of several months duration. Examination revealed a bitemporal hemianopia. Clinically, there was no evidence of any obvious hormone excess or deficiency. An enlarged, expanded pituitary fossa was found on skull radiography. A computed tomography (CT) scan was performed which showed a large, homogeneously enhancing pituitary mass extending into the suprasellar cistern and the left cavernous sinus (Fig. la, b). Bilateral internal carotid angiography showed stretched cavernous carotid segments on both sides, no A1 segment elevation and no evidence of an aneurysm. An exploratory operation revealed a reddish-blue mass which looked like an aneurysm and yielded bright red blood on needling. Only partial removal was possible, the histology showing a chrornophobe adenoma. Hormone assay demonstrated an isolated elevation of prolactln (5670ng/ml; normal level <13 ng/ml) and a testosterone deficiency (5.4 nmolllitre; normal level 10-35 nmol/litre).Bromocriptine was commenced, initially at a dose of 2.5 mg twice daily, then increased to three times daily after 3 weeks. *Present address and address for reprints: N. Daunt, X-Ray Department, Mater Misericordiae Private Hospital, Raymond Terrace, Brisbane, Queensland, Australia.
After 6 months of treatment with bromocriptine, the s e r u m prolactin had fallen to 420ng/ml. A repeat CT scan showed virtual disappearance of the intra- and suprasellar components of the tumour, but with new tumour tissue posterior to the clivus (Fig. lc). The visual fields were normal at follow-up, the main clinical problem being persisting obesity. Case 2. A 17-year-old male presented with a short history of blurred vision in his left eye, and a 1-year history of increasingly frequent headaches. On examination he was found to have a left ptosis and diplopia. He had gained 20kg weight in 4 years. His visual fields were normal. There was evidence of an expanding intrasellar lesion on skull radiography. A CT scan showed a large mass in the pituitary fossa with suprasellar extension, lateral extension into both cavernous sinuses and erosion of the floor of the sella with a soft-tissue mass in the left side of the sphenoid sinus. The tumour exhibited homogeneous density enhancement following injection of contrast medium (Fig. 2a, b). Arteriography by bilateral internal carotid artery injections showed a minor mass effect on the left side. A markedly elevated prolactin (11000 ng/ml) was found. All other hormone assays were normal apart from a low testosterone (7.8 nmol/litre). A sperm count showed deficient numbers with 50% abnormal forms. The bone age was normal. Hypercalcaemia was also present (2.97mmol/litre). Biopsy of the pituitary lesion disclosed a chromophobe adenoma. Treatment was initiated with bromocriptine, 2.5mgnocte, later increased to 7.5 mgt.d.s. A marked fall in prolactm level occurred over 8 months to 340 ng/ml and at follow-up all symptoms and signs had disappeared. A repeat CT scan showed a marked diminution in size of the tumour with virtual disappearance of the extrasellar component (Fig. 2c). During the follow-up period, surgical exploration of the neck revealed a parathyroid adenoma which was removed, with subsequent fall in calcium to a normal level. The combination of a pituitary adcnoma and a parathyroid adenoma is part of the multiple endocrine neoplasia syndrome Type l. Case 3. A 20-year-old male presented with an acute right hemiparesis which resolved almost completely within 1 week. Clinically, no other abnormality was seen. There were no obvious hormone deficiencies or excess and the visual fields were normal. Skull radiographs showed destruction of the dorsum sellae and upper clivus with depression and asymmetry of the floor of the sella. A C T scan was performed which showed a large soft-tissue mass eroding the dorsum sellae, much of the clivus, the petrous apices and the left anterior clinoid process. It extended into the sphenoid and ethmoid sinuses, superiorly into the suprasellar cistern and laterally into the floor of the left middle cranial fossa. Focal calcification was present. The mass exhibited predominantly homogeneous enhancement following injection of contrast medium but with several small cystic or necrotic areas which showed no enhancement (Fig. 3a-c). Initial diagnostic possibilities included a chordoma or an aggressive pituitary tumour. Selective carotid and vertebral arteriography showed a mass effect due to the tumour, but without arterial compression or invasion, and no pathological circulation was identified. A markedly elevated prolactin level (12900ng/ml) and a low testosterone (5.8 nmol/litre) were found. All other hormone levels were normal. Treatment with bromocriptine 2.5mgt.d.s. was started which was later increased to 7.5 mgt.d.s, with a subsequent fall in serum prolactin to 315ng/ml over 9 months. A repeat CT scan showed a marked diminution in tumour size (Fig. 3d). The only remaining clinical problem is mildly diminished sensation in the patient's right hand.
228
CLINICAL RADIOLOGY
(a)
(b)
(c)
Fig. 1 - Case 1. (a) Contrast-enhanced tumour extending to the left parasellar region (L +50, W250). (b) Suprasellar extension (L +50, W 150). (c) Six months post-operatively: the intra- and suprasellar components are no longer in evidence, but there is now some tumour tissue behind the clivus (L +50, W 150).
DISCUSSION The occurrence of prolactin-secreting pituitary adenomas in young women, causing infertility and treatable by bromocriptine, is firmly established. These tumours are usually microadenomas and are difficult to demonstrate due to their small size. The behaviour of these tumours in male patients is significantly different, with a tendency to an aggressive nature and large size on initial investigation (Carter et al., 1978; Grisoli et al., 1980; Leavens et al., 1981). In these series no microadenomas were found. Some cases of smaller adenomas in men are recorded, Vezina (1981) reporting eight of 55 adenomas in men associated with a normal pituitary fossa on plain radiography.
The clinical features which might be expected are due to: 1. the effect of the mass on surrounding structures, 2. the effect of excessive prolactin secretion and 3. the effect of the mass on the production of other pituitary hormones. The effects of the mass on surrounding structures give rise to headaches and visual impairment. Appro x imately 50% of published cases have included visual impairment, usually a bitemporal hemianopia due to chiasmal compression. Headaches are also a common complaint, often being of long duration: one of our patients had a 7-year history of headaches. The presentation of our third case, simulating a vascular accident, is unusual.
229
PROLACTIN-SECRETING PITUITARY ADENOMAS IN YOUNG MALES
(b)
(a)
Fig. 2 - Case 2. (a) Enhancing pituitary tumour with suprasellar and left parasellar extension (L +40, W 150). (b) Coronal reconstruction (L +40, W 150). (c) Follow-up scan after 15 months on bromocriptine. No extrasellar tumour is evident (L +40, W200).
(c)
Hypothyroidism and adrenal insufficiency are uncommon, occurring in about a quarter of reported cases. More common is a low testosterone level, often an isolated deficiency, which reflects compromised FSH/LH secretion. The effects of a low testosterone and those due to a raised prolactin are hard to differentiate clinically. Both can give rise to one or more of the following: loss of libido, impotence, infertility, an abnormal sperm count (Toth, 1981; Ayalon et al., 1982) and obesity, which is often intractable (Nabarro, 1982)_ Galactorrhoea, accelerated puberty and increased bone age occur less frequently (Leavens et al., 1981; Slonim et al., 1982). Our three patients were aged 15, 17 and 20 years. The usual age range of patients with these tumours is about 15-60 years, although they have been reported in 13-year-olds (Schroffner, 1976; Slonim et al., 1982) and one in a 12-year-old (VanMeter et al., 1977). It has been suggested that adenomas in adolescents are more likely to be 'invasive', implymg involvement of contiguous structures but not indicating malignancy (Ortiz-Suarez and Erickson, 1975). Raised prolactin levels may occur with many hypothalamic and pituitary disorders, including nonprolactin-secreting pituitary tumours, and aneurysms, meningiomas, chordomas and craniopharyngiomas can elevate prolactin levels due to their effect on the production of prolactin inhibiting factor or its trans-
mission through the portal vessels. However, repeated values above 100 ng/ml are suggestive and levels above 500ng/ml are virtually diagnostic of a prolactinsecreting tumour (Horrobin, 1980). Attempts have been made to correlate the prolactin level with the aggressiveness of the turnout. It has been suggested that a prolactin level above 335 ng/ml is likely to be due to invasive adenoma (Leavens et al., 1981). Very high levels, above 3000ng/ml, have been equated with tumour invasion of the cavernous sinus (Shucart, 1980). The best treatment for these large, invasive adenomas is controversial. Surgery has only limited success, the prolactin remaining elevated in many instances, suggesting residual turnout tissue. Radiotherapy trials have met with little success; indeed, with high daily fraction dosage the risk of visual failure seems to outweigh the doubtful benefits of this treatment (Harris and Levene, 1976). Bromocriptine is an accepted method of reducing prolactin secretion and, recently, a decrease in turnout size has been reported following this treatment (Ayalon et al., 1982; Chernow et al., 1982), suggesting an actual antitumour effect. All three of our cases have shown a marked decrease in turnout size on medical treatment. It might be anticipated that, following the shrinkage of a tumour by this treatment, it may be more amenable to surgery at a later date.
21
230
CLINICAL RADIOLOGY
(a)
(c)
(b)
(d)
Fig. 3 - Casc 3. (a) Post-contrast coronal reconstruction demonstrating a large pituitary turnout with extensive lobulated suprasellar and left parasellar components with homogeneous enhancement (L +50, W 150). (b) Post-contrast sagittal reconstruction showing posterior and inferior extension of the mass with destruction of the upper part of the clivus (L +50, W 150). (c) Post-contrast scan. Suprasellar component extending into the left temporal lobe. Three small, non-enhancing, low-density necrotic areas are noted (L +50, W 150). (d) Follow-up scan after 9 months shows marked diminution in tumour size with only a small residual left suprasellar mass (L +50, W 150).
PROLACTIN-SECRETING PITUITARY ADENOMAS IN YOUNG MALES
REFERENCES Ayalon, D., Eckstein, N., Hommonai, Z. T., Paz, G. F., Eshel, A. & Reider, I. (1982). Effects of long term treatment with bromocriptine on pituitary prolactinoma in a male. International Journal of Obstetrics and Gynaecology, 20, 481-485. Carter, J. N., Tyson, J. E., Tolis, G., VanVliet, S., Faiman, C. & Friesen, G. (1978). Prolactin secreting tumours and hypogonadism in 22 men. New England Journal of Medicine, 299, 847-852. Chernow, B., Buck, D. R., Early, C. B., Ray, J. & O'Brian, J. T. (1982). Rapid shrinkage of a prolactin secreting pituitary tumour with bromocriptine: CT documentation. American Journal of Neuroradiology. 3, 442-443. Franks, S., Jacobs, H. S. & Nabarro, J. D. N. (1975). Studies of prolactin secretion in pituitary disease. Journal of Endocrinology, 67, 55-62. Grisoli, F., Vincentelli, F., Jaquet, P., Guibot, M., Hassoun, J. & Farnavier, P. (1980). Prolactin secreting adenomas in 22 men. Surgical Neurology, 13, 241-247. Harris, J. R. & Levene, M. B. (1976). Visual complications following irradiation for pituitary adenomas and craniopharyngiomas. Radiology, 120, 167-17i. Horrobin, D. F. (1980). Prolactin, 8, 102-108. Jacobs, H. S. (1976). Prolactin and amenorrhoea. New England Journal of Medicine, 295, 954-956.
231
Leavens, M. E., Samaan, N. A., Larson, D. L., Jessie, R. H. & Byers, R. M. (1981). Prolactin secreting pituitary adenomas. International Advances in Surgical Oncology, 4, 27%310. Nabarro, J. D. (1982). Pituitary prolactinomas. Clinical Endocrinology (Oxford), 17, 129-155. Ortiz-Suarez, H. & Erickson, D. L. (1975). Pituitary adenomas of adolescents. Journal of Neurosurgery, 43, 437-439. Schroffner, W. G. (1976). Prolactin secreting pituitary tumour in early adolescence. Archives of Internal Medicine, 136, 11641165. Shucart, W. A. (1980). Implications of very high serum prolactin levels associated with pituitary tumours. Journal of Neurosurgery, 52, 226-228. Slonim, A. E., Glick, A. D., Island, D. P. & Kasselberg, A. G. (1982). Hyperprolactinaemia associated with advanced puberty in a male. Journal of Pediatrics, 101, 236239. Toth, A. (1981). Abnormal seminal cytology in a patient with a prolactin secreting pituitary adenoma. Fertility and Sterility, 36, 818-820. VanMeter, Q. L., Gavis, F. J., Hayes, J. W. & Wilson, C. B. (1977). Galactorrhoea in a 12 year old boy with a chromophobe adenoma. Journal of Pediatrics, 90, 756-758. Vezina, J. L. (1981). II.Le Prolactinome. Aspects radiologiques de la selle turcique. Neurochirurgie, 27, Suppl. 1.