Due to the pulsatile nature of GH release, a reference range is not appropriate
Growth hormone secretion by the pituitary is controlled both by growth hormone releasing hormone (GHRH) and somatostatin, an inhibitory hormone. The pituitary releases growth hormone, which acts on the liver to produce insulin-like growth factor 1(IGF-1, somatomedin C). IGF-1 is responsible for the growth promoting effects of growth hormone. Growth hormone also has metabolic effects such as stimulation of lipolysis and inhibition of carbohydrate metabolism. Growth hormone secretion is episodic and pulsatile and is stimulated by sleep, exercise, stress (hypoglycemia), dopamine, certain amino acids, GHRH, beta-blockers, and glucagon.
The second most common tumor of the pituitary gland is a GH (growth hormone) cell adenoma. If excess growth hormone secretion occurs prior to epiphyseal closure this results in gigantism, while in adults it results in acromegaly. The major clinical manifestations of growth hormone excess include:
Acral enlargement (skin, subcutaneous tissue and skeletal overgrowth) is seen in all patients. This is usually recognized by increases in ring, glove, or shoe sizes. Also, since this is a tumor of the pituitary gland, it can cause visual defects and hypopituitarism.
The most useful tests for the diagnosis of acromegaly are the growth hormone response to an oral glucose load and measurement of insulin-like growth factor 1 (somatomedin). Although elevated growth hormone measurements in the fasting state are consistent with the diagnosis of acromegaly, they are not diagnostic because nonspecific effects such as stress can also elevate growth hormone levels. However, failure to suppress growth hormone to undetectable levels following a 75g oral glucose tolerance test confirms the diagnosis of acromegaly especially if it is coupled with an elevated level of IGF-1. Pituitary imaging studies are useful in localizing the tumor.
Growth hormone deficiency in adults is present when one of the following conditions are met:
When GH deficiency is diagnosed, a CT or MRI search for a CNS lesion should be considered. Thyroid status should also be determined, because hypothyroidism can induce reversible GH deficiency. Random measurements of GH are usually uninformative because basal GH levels are normally low and do not differentiate patients who are deficient from those who are not. Therefore, to diagnose GH deficiency, stimulated GH measurements must be assessed. Stimulated GH tests are obtained first by using physiologic stimulants such as exercise or sleep or pharmacologic stimulants such as clonidine. When using exercise, GH is measured immediately upon completion of 20 minutes of exercise and again at 40 minutes. When using sleep, GH is measured 60 minutes after the patient falls asleep. When using clonidine, 5 ug/kg is given orally and GH is measured 90 minutes later.
Another approach to screening for GH deficiency is to measure insulin-like growth factor-1. In GH deficiency, IGF-1 should be suppressed because GH stimulates its synthesis. Because IGF-1 does not have diurnal variation, it can be measured on a random sample.
Please note this test is not UKAS accredited
Specimen Labelling Procedure