Pituitary
tumours
Introduction
Pituitary tumours account for 8 per cent of all intracranial
tumours.
Historically they were classified according to their staining characteristics
seen on light microscopy. However, the three types (chromophobe, acidophilic and
basophilic) did not correspond closely with the clinical syndromes of pituitary
hypersecretion. The subsequent development of immunological staining techniques
and electron microscopy provided a more refined classification of pituitary
tumours. It is now correct to classify pituitary
tumours according to their
size (microadenomas, mesoadenomas and macroadenomas) and whether they are
endocrine active or inactive (Table 35.5). These features will also
determine their presentation.
Clinical
features
Pituitary tumours arise in the sella tercica and can expand up into the
suprasellar cisterns, compressing the optic chiasm above and resulting in visual
failure — classically a bitemporal hemianopia. Careful assessment of the
visual fields, visual acuity and optic fundi is therefore essential. They may
also invade laterally into the cavernous sinuses on each side, compressing the
third to fourth cranial nerves.
Endocrine
disturbance is due to either hypopituitarisrn or excess secretion of a
particular pituitary hormone. Prolactin secreting tumours are usually found in
younger women and cause loss of libido, infertility, amenorrhoea and
galactorrhoea. Corticotrophin-producing tumours cause Cushing’s disease due to cortisol
excess. The principal features are moon face, abdominal striae, buffalo hump,
hypertension and diabetes mellitus.
Acromegaly
is due to an overproduction of growth hormone. The disease is disfiguring,
causing prognathism and overgrowth of joints, especially in the hands and feet.
Systemic side effects include hypertension, cardiomyopathy, diabetes mellitus,
excessive sweating, arthralgias and lassitude. Haemorrhage into a macroadenoma,
known as pituitary apoplexy, can precipitate an acute presentation with
headache, hypopituitarism and visual failure. Diabetes insipidus, a product of
direct hypothalamic involvement, is usually indicative of a craniopharyngioma
and rarely caused by pituitary tumours.
Investigation
Diagnosis is confirmed by laboratory assessment of pituitary endocrine
function, neuroradiological imaging (Fig. 35.33) and formal visual assessment.
Radioimmunoassay
will identify the hormone being secreted. It is important, particularly with
acute presentations, to exclude a prolactinoma as the majority of these will
respond rapidly to treatment with the dopamine antagonist bromocriptine.
Prolactin levels above 200 ng/ml ate usually diagnostic. Nonfunctioning
macroadenornas may cause hyperprolactinaemia due to distortion of the pituitary
stalk or impingement on the hypothalamus. This is because the latter produces
prolactin-inhibiting factor, which under normal circumstances suppresses
prolactin levels to below 15 ng/ml. Diagnosis of Cushing’s disease is made by
radioimmunoassay of adrenocorticotrophic hormone (ACTH) in the peripheral blood
and petrosal venous sinus sampling.
With
the exception of some patients with Cushing’s disease, MRI of the sella will
confirm diagnosis of an intrasellar mass. The resolution of MRI will also detect
all but the smallest (<2 mm) tumours and any extrasellar extension.
Treatment
Treatment depends on the endocrine disturbance present and the effect of
compression of adjacent neural structures. For prolactinomas, bromocriptine (a
dopamine agonist) is commenced. Surgical excision is reserved for
macroadenomas compressing the optic chiasm, growth hormone secreting tumours
causing acromegaly and ACTH secreting tumours causing Cushing’s disease.
Occasionally surgery is undertaken in patients with prolactinomas not
responding to medical treatment or when unwanted side effects occur. This is
usually performed via a transphenoidal route although the transcranial route can
be employed. The aim is to preserve
Radiotherapy
is used for subtotal resections and for persistent hypersecretion of pituitary
hormones. The long-term follow-up of nonfunctioning pituitary adenomas has shown
a recurrence rate approaching 40 per cent at 10 years indicating that there is
perhaps a more extensive role for this modality and that postoperative patients
should be more closely followed up.