British Medical Journal

Here's a report published in the British Medical Journal about my case - seems I was quite a find! There's a lot of medical terminology in there, so feel free to highlight the easier to understand bits by clicking the button below.

Spontaneous Endocrine Cure Of Gigantism Due To Pituitary Apoplexy


An 11 year old, tall boy presented with symptoms typical of pituitary apoplexy. A large necrotic and haemorrhagic tumour was removed, which was shown to be an adenoma secreting growth hormone and prolactin. Subsequent treatment comprised cranial irradiation and hormone replacement. Eighteen months after operation growth was static and plasma growth hormone and prolactin concentrations were undetectable.

Pituitary apoplexy is caused by infarction or haemorrhage, or both, into a pituitary tumour. The symptoms and signs are usually typical, with the sudden onset or worsening of headache, vomiting, visual deterioration, fever, drowsiness, and coma. There may be evidence of previous pituitary dysfunction such as acromegaly, Cushing's syndrome, or hyperprolactinaemia. The condition commonly presents as a neurosurgical emergency requiring prompt decrompression of the pituitary mass to restore vision. This decrompression not only relieves pressure on vital intercranial structures but also confirms the presence of a haemorrhagic necrotic tumour characteristic of the condition. Pituitary apoplexy has been reported as occurring in 5-10% of patients with pituitary tumour.

We report results of clinical and endocrine studies in a tall boy who developed symptoms of acute raised intracranial pressure after pituitary apoplexy associated with a pituitary adenoma secreting growth hormone and prolactin.

Case Report
An 11 year old boy presented with severe frontal headache, vomiting, fever, and blurred vision of 12 days' duration. Intermittent headaches over several months had been treated as migraine. Rapid growth had started at age 8, but the rate had slowed during the previous year. On examination he was tall (169cm; +3SD over the normal mean), but there no obvious signs of acromegaly. He was pale, febrile, yet fully conscious. He had decreased visual acuity, bilateral optic atrophy, and a bitemporal hemianopia. Blood pressure was normal. There was no gynaecomastia, but he had galactorrhoea on expression; he was in early puberty. The cerebro-spinal fluid was normal.

Radiography of the skull showed an enlarged pituitary fossa; computed tomography showed a mass that enhanced homogeneously, filling much of the pituitary fossa, with some suprasella extension. Preoperative serum thyroxine concentration was 57 nmol/l (4.4ug/100ml) (normal 60-150 nmol/l (4.7-11.7 ug/100ml)); triidothyronine 1.2 nmol/l (0.8ng/ml) (normal 1.2-3.1 nmol/l (0.8-2.0 ng/ml)); thyroid stimulating hormone < 2.5mU/l (normal <5mU/l) diurnal plasma cortisol < 28 nmol/l (<1.0ug/100ml); random serum growth hormone during sleep 1.8mU/1; and plasma testesterone 1.4 nmol/l (0.4 ng/ml) (prepubertal). There was no response to thyroid stimulating hormone, gonadotrophin, or prolactin to combined stimulation with thyroid releasing hormone and leteinising hormone releasing hormone. The table shows the plasma glucose, insulin, and growth hormone concentrations in response to an oral glucose load (1.75g/kg). Glucose tolerance was normal with an early, exaggerated insulin response at 30 minutes; growth hormone concentration were consistently low.

A large necrotic and haemorrhagic pituitary tumour that compressed the optic nerves on both sides was removed via a right frontotemporal craniotomy. Histological examination showed an acidophillic adenoma with numerous foci of calcification. Immunoperoxidase staining was positive for growth hormone and prolactin antibodies. His vision recovered postoperatively. He was given cranial irradiation and hormone replacement treatment with desmopressin, thyroxine and cortisone acetate. Growth was static 18 months after surgery, and plasma growth hormone and prolactin concentrations were undetectable.

Plasma concentrations of glucose, insulin, and growth
hormone in response to oral glucose load of 1.75 g/kg (75g)

Time (h) Glucose (mU/l) Insulin (mU/l) Growth Hormone (mU/l)
0 3.8 9.7 1.4
0.5 4.7 12.5 1.2
1.0 4.0 12.1 1.2
2.0 3.8 37.8 1.3
3.0 3.4 33.4 1.9
4.0 3.1 12.9 2.5
Conversion : SI to traditional units - Glucose: 1 nmol/1 18mg/100ml.

Pituitary apoplexy associated with gigantism in childhood is rare. Our patient is the youngest patient with pituitary apoplexy to have been reported on. Impairment of the infundibular circulation by impaction of the of the enlarging tumour at the diaphragmatic notch may cause infarction or haemorrhage, or both, into the pituitary gland.