JRSM >
Volume 96, Number 1 >
Pp. 27-28
Department of Endocrinology, Southampton University Hospitals NHS Trust,
Southampton SO16 6YD, UK
1 Department of Neurosurgery, Southampton University Hospitals NHS Trust,
Southampton SO16 6YD, UK
2 Department of Neuroradiology, Southampton University Hospitals NHS Trust,
Southampton SO16 6YD, UK
Correspondence to: Dr Mike Masding, Diabetes Centre, Poole Hospital, Longfleet Road, Poole BH15 2JB, UKE-mail: mmasding{at}poole-tr.swest.nhs.uk
The pituitary gland enlarges physiologically in pregnancy, mainly because of lactotroph hyperplasia1. Pre-existing pituitary tumours can likewise increase in size2, but compressive effects may be due to displacement rather than enlargement.
CASE HISTORY
A woman of 29 was referred to the endocrine clinic for investigation and management of oligomenorrhoea and infertility. Adrenal function was normal, she was euthyroid, and visual fields were normal to confrontation. Investigations suggested anovulatory cycles in the presence of adequate oestrogens (serum prolactin 430 mU/L [normal range 150-800], testosterone 1.4 nmol/L [0.3-2.5], sex hormone binding globulin 130 nmol/L [30-90], oestradiol 300 pmol/L; a menstrual bleed followed administration of medroxyprogesterone acetate 10 mg daily for 5 days). She was treated with clomiphene 50 mg on days 5-10 of the cycle and became pregnant that month.
At 18 weeks' gestation she noticed abnormal vision in the left eye. On examination acuity was reduced on the left (6/12 compared with 6/5), with a central scotoma, loss of vision in the temporal field and an afferent pupil defect on the affected side. An MRI scan showed a pituitary mass extending into the suprasellar cistern, displacing and stretching the optic chiasm (Figure 1). The vertical height of the lesion was 2.0 cm. Serum prolactin, measured several times, had risen by about 100 mU/L—no more than is usual in pregnancy. Other endocrine investigations were likewise normal so she was diagnosed as having a non-functioning pituitary tumour. The obstetric team were reluctant for her to undergo pituitary surgery in the early middle trimester since, if surgery precipitated labour, the fetus would not be viable.
|
The presentation in pregnancy was thought to be due to upward displacement of the tumour by physiological pituitary enlargement; thus dopamine agonist therapy might allow surgery to be deferred. She was started on bromocriptine (5 mg on day 1, 5 mg twice daily on day 2 and 5 mg three times daily thereafter). Five days after the beginning of treatment the visual symptoms had disappeared, and on a repeat MRI scan the optic chiasm was no longer compressed, although there was negligible change in the size of the tumour (Figure 2). The visual fields returned to normal. Bromocriptine therapy was continued and the pregnancy proceeded without incident; a healthy child was born at 39 weeks' gestation.
|
Postpartum, the patient was keen to breast-feed and elected to stop her bromocriptine. Within 2 days the visual field defect returned and she then underwent transsphenoidal decompression of the tumour. On histological examination it proved to be a pituitary adenoma in which only about 5% of cells stained for prolactin and growth hormone. Postoperative endocrine assessment gave normal results except for hypoadrenalism. A year later she had an uncomplicated pregnancy.
COMMENT
We suspect that the beneficial effect of bromocriptine was achieved by an effect on the physiologically enlarged pituitary. A prolactinoma would be expected to respond to this agent3, but this patient's tumour was non-secretory; although 5% of cells stained for prolactin, serum prolactin concentrations were normal before and after pregnancy. 8-16% of non-secretory pituitary adenomas do respond to dopamine agonist therapy, so a direct effect cannot be ruled out; however, the rapidity of the therapeutic response makes this unlikely.
This is not the first report of successful use of bromocriptine to relieve compression of the optic chiasm by a non-secretory pituitary adenoma. In the previous cases, however, the effect was thought to be due to tumour shrinkage4,5. Grossman and colleagues suggest that in these circumstances dopamine agonists work by shrinkage of normal lactotrophs, and recommend only temporary use (for about 2 weeks) before surgery6. We could find no other cases where the physiological lactotroph hyperplasia of pregnancy had caused upward displacement of a clinically silent pituitary tumour.
REFERENCES
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  A. K Demetriades, A. W McEvoy, and M. Powell Lymphocytic hypophysitis J R Soc Med, May 1, 2003; 96(5): 257 - 258. [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
