Growth hormone is a polypeptide with anabolic effects on protein metabolism and with lipolytic and immunostimulating properties ( Ihornerefal 199.2). It is secreted by pituitary somatotropes in a pulsatile fashion that is believed to result principally from a dynamic interaction between two hypothalamic neuropeptides, the stimulatory growth-hormone-releasing hormone and the inhibitory somatostatin. Growth hormone has direct and indirect anabolic actions; the principal mediator of the latter is insulin-like growth factor I (IGF-I). To a certain extent, growth hormone action is reflected in serum concentrations of IGF-I, which is mainly generated by the liver and bound to six specific binding proteins, predominantly to IGF-binding protein 3. In critically ill patients, serum IGF-I correlates well with conventional nutritional indices such as nitrogen balance. Ihe immunostimulating properties of growth hormone are manifested in direct action on I lymphocytes and indirect effects through IGF-I on neutrophils (Murphy.efa/ 1995).
Growth hormone deficiency is probably the most common endocrine expression of hypopituitarism. Acquired growth hormone deficiency in adulthood results in reduced muscle strength and exercise capacity, reduced thermoregulation and sweating ability, subnormal kidney function, decreased lean body mass and bone mineral density, abnormal thyroid hormone, lipid, and carbohydrate metabolism, myocardial dysfunction, and impaired social well being, and it leads to increased mortality due to cardiovascular disease (De.Boer.et.al 1995). Growth hormone replacement therapy in growth-hormone-deficient adults improves these symptoms.
During prolonged critical illness, growth hormone secretion is characterized by reduced pulse amplitude and sometimes by elevated interpulse levels and is associated with low circulating IGF-I and IGF-binding protein 3 levels ( Van d^ Dopamine infusion further attenuates pulsatile growth hormone secretion and lowers serum IGF-I. Through this endocrine side-effect, prolonged dopamine administration in the critically ill presumably contributes to the maintenance of fat depots and the failure to induce protein anabolism despite optimal feeding. In catabolic conditions requiring new protein synthesis, prolonged suppression of growth hormone secretion may contribute to impaired wound healing, delayed recovery, or atrophy of the enteral mucosa and muscle weakness. Likewise, exogenous and endogenous glucocorticoids and somatostatin may have a deleterious effect on the somatotrope axis, and hence anabolism, in severe illness.
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