Clinical Aspects

Abnormalities of the anterior pituitary stem from a number of causes. Trauma to the anterior pituitary can occur often by mechanical pressure from tumors. The anterior pituitary may decline in function because there has been trauma to the delicate stalk connecting the pituitary to the hypothalamus and the releasing hormone concentrations in the pituitary become inadequate. Tumors of individual cell types may arise and produce high amounts of one or two anterior pituitary hormones, or hormones that act like them, ectopically. Detection of primary abnormal functioning at the pituitary level is easier now due to the availability of many of the releasing hormones that make evocator tests possible (see Chapter 3). In cases of inadequate availability of a pituitary hormone, the target gland hormone can be supplied (e.g., Cortisol for inadequate ACTH supply).

Autoimmune diseases are an important consideration. In Graves' disease, an antibody is produced, apparently directed against the lipid component of the TSH receptor. In binding to the receptor, adenylate cyclase is activated and the thyroid responds as if TSH were there. Unfortunately, thyroid hormone does not negatively feed back on the autoantibody production as it does with TSH production and hyperthyroidism develops. Treatment usually involves ablating the function of the thyroid gland and maintaining normal subsequent hormone levels by replacement therapy.

Two situations will be discussed briefly: those resulting in hypofunction of the anterior pituitary and those resulting in hyperfunction of the anterior pituitary. Many anterior pituitary hormones may be affected in "panhypopituitarism." There is usually an order to the loss of hormonal secretions in hypopituitarism. GH deficiency occurs early followed by LH, FSH, and TSH, and ACTH deficiences are not visualized until later on. One rarely sees PRL deficiency. In the case of AVP deficiency, one can conclude that the problem resides primarily in the hypothalamus. In this disease, the function or access of the pituitary to the hypothalamic releasing hormones is destroyed by trauma, tumors, or vascular insufficiency. Such conditions are eventually corrected by surgical intervention if a tumor and by administration of the terminal hormones, whichever are required, such as the sex hormones, glucocorticoids, or thyroid hormone. Fortunately, evocator tests with purified releasing hormones (e.g., GnRH) and anterior pituitary hormones are available to localize the center of the disturbance as being in the hypothalamus, pituitary, or terminal gland. A particular disease important to development is dwarfism, which can occur because of a deficiency of GH, often beginning at infancy. Other anterior pituitary hormones may be affected in this disease. Primary hypothyroidism, for example, can produce substantial inhibition of the release of GH, resulting in dwarfism. Human growth hormone can be used to treat GH hypo-secretion, but it is presently available in limited quantity. Presumably the cloned gene product will help in the treatment of dwarfism. Other conditions are associated with hypofunctions in ACTH and TSH, and in some cases the results are not severe. ACTH deficiency is substituted therapeutically. There has become an increasing availability of releasing hormones for clinical testing and diagnosis. This advance makes it possible to specifically localize malfunctions in the hy-pothalamus-pituitary-end organ axis.

Overproduction of pituitary hormones can occur when tumors ectopically produce a pituitary hor-mone(s). Disease states occur with excessive prolactin and growth hormone overproduction, leading to gigantism during growth (epiphyseal cartilages are open) or to acromegaly if epiphyseal cartilages are fused. Overproduction of prolactin leads to galactorrhea and amenorrhea in the absence of acromegaly

5. Anterior Pituitary Hormones

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