What is Hyperpituitarism ?
Hypopituitarism is a complex syndrome marked by metabolic dysfunction, sexual immaturity, and growth retardation (when it occurs in childhood). It results from a deficiency of the hormones secreted by the anterior pituitary gland. The disorder is also known as panhypopituitarism.
Panhypopituitarism refers to a generalized condition caused by partial or complete failure of the gland to produce all six of the vital hormones: corticotropin, thyroid-stimulating hormone (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), and prolactin. Partial hypopituitarism and complete hypopituitarism occur in adults and children; in children, these diseases can cause dwarfism and pubertal delay.
Total loss of all hormones is fatal without treatment, but the prognosis is good with adequate replacement therapy and correction of the underlying causes.
Causes of Hypopituitarism.
The most common cause of primary hypopituitarism is a tumor. Other causes include congenital defects (hypoplasia or aplasia of the pituitary gland); pituitary infarction (most often from postpartum hemorrhage); partial or total hypophysectomy by surgery, irradiation, or chemical agents; and, rarely, granulomatous disease, such as tuberculosis. Occasionally, primary hypopituitarism has no identifiable cause.
Secondary hypopituitarism stems from a deficiency of releasing hormones produced by the hypothalamus. The process may be idiopathic or result from infection, trauma, or tumor.
Signs & Symptoms of Hypopituitarism
Hypopituitarism may present with many different Signs and symptoms. Signs and symptoms of Hypopituitarism depending on which pituitary hormones are deficient. This Topics may include:
Man have Signs and symptoms:
A woman, may Signs and symptoms develop:
In suspected hypopituitarism, evaluation is used to confirm hormonal deficiency caused by impairment or destruction of the anterior pituitary gland. It's also used to rule out disease of the target organs (adrenals, gonads, and thyroid gland) or hypothalamus. Low serum levels of thyroxin, for example, indicate diminished thyroid gland function, but further tests are necessary to identify the source of this dysfunction as the thyroid, pituitary, or hypothalamus.
Radioimmunoassay showing decreased plasma levels of some or all pituitary hormones (except corticotropin, which may require more sophisticated testing, accompanied by target-organ hypofunction, sugests pituitary failure and eliminates target gland disease. Failure of thyrotropin-releasing hormone administration to increase TSH or prolactin concentrations rules our hypothalamic dysfunction as the cause of hormonal deficiency.
Gonadotropin-releasing hormone administered I.V. can be used to distinguish between pituitary and hypothalamic causes of gonadotropin deficiency.
Administering a dopamine antagonist, such as metoclopramide, allows evaluation of the prolactin secretory reserve. In patients with hypopituitarism, increased prolactin levels indicate a lesion in the hypothalamus or pituitary stalk.
Clomiphene, an estrogen antagonist, can also be used as a diagnostic agent.
Diagnosis of dwarfism requires measurement of GH levels in the blood after administration of regular insulin to induce hypoglycemia, or of levodopa, which causes hypotension. These drugs should provoke increased GH secretion. Persistently low GH levels, despite provocative testing, confirm GH deficiency.
Computed tomography scanning, magnetic resonance imaging, or cerebral angiography is used to confirm the presence of intrasellar or extrasellar tumors.
Two provocative tests are also used, but both require careful medical supervision because they may precipitate an adrenal crisis. Oral administration of metyrapone enables detection of the source of low hydroxycorticosteroid levels; the drug blocks cortisol synthesis, which should stimulate pituitary secretion of corticotropin. Insulin administration induces hypoglycemia and stimulates corticotropin secretion. Persistently low levels of corticotropin indicate pituitary or hypothalamic failure.
Replacement of hormones normally secreted by the target glands is the most effective treatment for hypopituitarism and panhypopituitarism. Hormonal replacement includes cortisol, the most important drug; thyroxine; and androgens or cyclic estrogen. Prolactin doesn't need replacement. The patient of reproductive age may benefit from FSH and human chorionic gonadotropin to boost fertility. Free thyroxine levels should be monitored in patients with hypopituitarism, as TSH level becomes an unreliable marker for thyroid replacement.
Somatrem, identical to GH but the product of recombinant DNA technology, has replaced growth hormones derived from human sources. It's effective for treating dwarfism, stimulating growth increases of 4" to 6" (10.2 to 15.2 cm) in the first year of treatment. The growth rate tapers off in subsequent years. After pubertal changes occur, the effects of GH therapy are limited.
Occasionally, a child becomes unresponsive to GH therapy, even with larger doses, perhaps because of antibody formation against the hormone. In such patients, small doses of androgen may again stimulate growth, but extreme caution is necessary to prevent premature closure of the epiphyses. Children with hypopituitarism may also need adrenal and thyroid hormone replacement and, as they approach puberty, sex hormones.
The disorder is not preventable. Awareness of risk may allow early diagnosis and treatment.
There is no known prevention of hypopituitarism, except for prevention of damage to the pituitary/hypothalamic area from injury.
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