In one sentence The same excess of growth hormone makes a child a giant and an adult acromegalic, because height can increase only while the growth plates are open.
One hormone, three pictures — the growth plate decides which
Growth hormone is released by the anterior pituitary, the front lobe of the gland that sits in a bony hollow at the base of the brain. Its main task in childhood is to lengthen the skeleton, and it can do that only while the epiphyseal plates — the layers of cartilage near the ends of the long bones — are still open. Those plates fuse at the end of puberty, and once they have fused no amount of growth hormone can add height.
That single fact explains this whole section. Excess growth hormone that starts before fusion produces gigantism, a child who grows far beyond the expected range. Excess that starts after fusion produces acromegaly: the bones can no longer lengthen, but they thicken, and the soft tissues and internal organs enlarge. Deficiency before fusion produces proportionate short stature, sometimes called pituitary dwarfism, and this is the form that responds to hormone replacement.
The usual cause is a pituitary adenoma, a tumour that is nearly always benign. So the two questions to ask are always the same: which hormone, and at what age did it go wrong?
A boy of 12 who is already taller than his father may have gigantism, while a man of 45 whose ring and shoe size have grown but not his height has acromegaly.
Why can excess growth hormone no longer make an adult taller?
Show the answer
Because the epiphyseal growth plates have fused, so the long bones cannot lengthen; the excess instead thickens bone and enlarges soft tissue and organs.
Read detailed explanations
- The GH–IGF-1 axis: why the hormone is measured indirectly
Growth hormone does not travel in a steady stream. It leaves the anterior pituitary in short bursts several times a day, and the largest burst arrives during deep sleep, so a single daytime venous sample is almost meaningless: a healthy person may have a high value at one hour and an undetectable one two hours later. The hypothalamus above the gland conducts this rhythm with two opposing signals, growth-hormone-releasing hormone, which stimulates release, and somatostatin, which inhibits it.
Growth hormone then works in two directions. It binds receptors on liver cells, which respond by secreting insulin-like growth factor 1, commonly shortened to IGF-1; this mediator carries most of the effect on cartilage, where it drives the chondrocytes of the growth plate to multiply and so lengthen the bone. Growth hormone also acts directly on fat and muscle, mobilising fat and opposing insulin, which is why glucose intolerance is part of the disease and not a coincidence.
Because IGF-1 has a much longer half-life and its blood level is fairly stable across the day, it is the integrated marker measured first, and a raised IGF-1 in an adult with the right appearance is strong evidence of excess. Confirmation uses the oral glucose suppression test: after a glucose load, growth hormone should fall to a low nadir, and in acromegaly the somatotroph adenoma ignores the signal and the value fails to suppress. Imaging then localises the lesion.
Two practical consequences follow for nursing. Because release is pulsatile, the timing of the sample matters, and a level drawn at the wrong moment can mislead the team. Because IGF-1 is the mediator, it is the integrated marker used first; treatment, by contrast, targets the growth hormone receptor, and pegvisomant is the antagonist used when surgery and somatostatin analogues have not controlled the disease.
- Mass effect: reading the visual fields and recognising apoplexy
Anatomy, not histology, explains the second half of pituitary disease. The gland occupies the sella turcica, a depression in the sphenoid bone, roofed by a fold of dura called the diaphragma sellae, and the optic chiasm lies directly above it. A tumour that expands upward therefore stretches the chiasm from below and destroys the crossing fibres that arise from the nasal retina of each eye. The result is the classic bitemporal hemianopia: each eye loses the temporal, outer half of its field, so the patient may walk into a doorframe on one side and still read a newspaper normally with either eye tested alone, because the defect becomes obvious only when both fields are charted. A lesser asymmetry produces a bitemporal quadrantanopia, and a patient may be quite unaware of any loss until it is tested formally.
Lateral extension reaches the cavernous sinus, where the oculomotor, trochlear and abducens nerves run on their way to the muscles of the eye, so the patient develops diplopia, ptosis and an eye that will not turn fully.
The most feared complication is pituitary apoplexy: sudden haemorrhage or infarction into an adenoma, giving a violent headache, rapidly failing vision, vomiting and sometimes a picture of acute cortisol insufficiency with shock, because the remaining normal gland is destroyed and cortisol disappears from the circulation. That shock is not hypovolaemia, and thyroid hormone does not fall acutely because thyroxine has a half-life of about a week; it is treated first with immediate parenteral hydrocortisone together with fluids. Apoplexy is a neuroendocrine emergency. The patient needs immediate corticosteroid replacement, urgent imaging and neurosurgical decompression, and the nurse who dismisses the headache as migraine risks the organ that matters most in this disease — sight.
This anatomy also explains two habits of safe care: visual acuity and fields are charted at every review of a patient with a known adenoma, and any new headache, any new double vision and any nasal discharge of clear fluid are reported rather than filed away.
- Surgery and the drugs that are easy to mix up
Treatment decisions follow the tumour, and the nurse who understands the operation and the drugs prevents much of the harm. Pituitary surgery is usually endonasal and transsphenoidal: the surgeon reaches the sella through the sphenoid sinus, so there is no cranial incision, but there is a direct route between the nose and the cerebrospinal fluid. That route explains the two things watched for afterwards. A watery, salty discharge from the nose, especially when the patient bends forward, suggests cerebrospinal rhinorrhoea and is reported at once, because meningitis can follow; epistaxis, or the urge to sniff and blow the nose, can dislodge the graft or the packing. Urine output may also rise sharply in the first day or two if the posterior pituitary or its stalk is disturbed, so hourly output is charted and the pattern is noted rather than the total alone.
Many patients need perioperative hydrocortisone, and after total removal they require lifelong replacement of thyroxine, hydrocortisone and testosterone or oestrogen, together with a written sick-day plan: during vomiting or fever the oral dose is increased, or injectable hydrocortisone or glucagon is used, because the body can no longer mount a stress response of its own.
The drugs are easy to confuse. Bromocriptine and cabergoline are dopamine agonists, not antagonists, and they shrink prolactinomas, often restoring fertility, which means contraception must be discussed with a woman who does not wish to conceive. Octreotide and lanreotide are somatostatin analogues, not growth hormone analogues, and they reduce growth hormone release; they may also be given before operation to improve the patient’s condition. Pegvisomant works differently again, blocking the growth hormone receptor, and is reserved for acromegaly that remains uncontrolled.
Radiotherapy has become far more precise, using stereotactic and fractionated techniques that spare the surrounding brain, but its effect appears over years, so it is a plan for the future and never a treatment for a crisis. Finally, because growth hormone excess raises the risk of colonic polyps and sleep apnoea, follow-up includes surveillance colonoscopy and sleep assessment, not hormone levels alone.