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The hypothalamus and pituitary gland control the entire endocrine system. The hypothalamus contains several releasing factors that stimulate the pituitary gland to release hormones (Rang & Dale, 1991). Table 1 depicts the role of the hypothalamus and pituitary gland.
Table 1.

The Role of the Hypothalamus and Pituitary Gland

GHRH: growth hormone releasing hormone
PRH: prolactin releasing hormone
CRH: corticotropin releasing hormone
TRH: thyroid releasing hormone
GRH: gonadotropin releasing hormone
GH: growth hormone
PL: prolactin
CH: corticotrophin
TSH: thyroid stimulating hormone
FSH: follicle stimulating hormone
LH: luteinizing hormone

The pituitary is located at the base of the brain. It hangs down from the pituitary stalk and is encased in bone. There are two sections of the pituitary: anterior and posterior. The anterior portion of the pituitary does not have neuronal communication with the hypothalamus. On the other hand, the posterior portion of the pituitary communicates with the hypothalamus resulting in the release of hormones from the pituitary. The pituitary secretes growth hormone (GH), prolactin, corticotrophin, luteinizing hormone, follicle stimulating hormone, thyrotropin, and anti-diuretic hormone (Rang & Dale, 1991).

Panhypopituitarism is the failure to produce several or all hormones (Shimon & Melmed, 1998; Vance, 1994). Causes of panhypopituitarism include trauma; neoplasm; inflammation; infiltration; infection; ischemia, irradiation; developmental, congenital absence of the pituitary; and familial panhypopituitarism (Kohler, 1986; Shimon & Melmed, 1998; Vance, 1994).

Each hormone secreted by the pituitary plays a specific role. The following describes each hormone deficiency, how to diagnose the deficiency, and the treatment.

Growth Hormone

GH exhibits metabolic effects and growth-promoting effects. GH elevates blood glucose during times of hypoglycemia. It causes an increase in protein synthesis and fat utilization during times of stress (Rang, & Dale, 1991). Patients who have GH deficiency often have failure to thrive and are overweight for their statue. Dwarfism is common in GH deficiency (Shimon & Melmed, 1998).


1. Measure insulin-like growth factor-l. This test is not accurate in young children. A normal insulin-like growth factor-I is often present despite GH deficiency (Johnson, 1993).

2. Sleep specimen test. Draw GH levels at baseline and 30 minutes and 60 minutes after the onset of sleep. A rise in GH will be present if there is no deficiency (Johnson, 1993).

3. Exercise test. The patient should fast for more than 4 hours. Measure baseline GH levels. Exercise patient for 20 minutes. Draw GH level immediately after exercise. An increase in GH will be present in the absence of GH deficiency (Johnson, 1993).

4. Arginine infusion. Give 0.5 g/kg IV of arginine. Arginine should be infused over at least 30 minutes. Side effects are related to the rate of infusion. If the patient begins to experience flushing, nausea, vomiting, or headache, decrease the rate of infusion. Arginine should not be pushed intravenously. Arginine should be avoided in patients with renal or hepatic insufficiency (Johnson, 1993; Phelps & Hak, 1996). A patient with GH deficiency will have a GH level of less than 5 ng/ml after the arginine infusion. Patients with a GH level of greater than 10 ng/ml can be ruled out for GH deficiency. Serum GH levels between 5-10 ng/ml after arginine infusions are not specific and cannot diagnose or rule out GH deficiency (Johnson, 1993).

5. Insulin-induced hypoglycemia. Give 0.075 units/kg intravenously of regular insulin. The goal is to get the serum glucose levels to fall below 40 mg/dl. Measure glucose before insulin is given and 20 minutes, 30 minutes, 60 minutes, and 90 minutes after injection (Kohler, 1986). GH levels will be less than 5 ng/ml in a patient with GH deficiency. GH levels greater than 10 ng/ml can rule out GH deficiency. Caution must be used with this test secondary to the risk of hypoglycemia (Johnson, 1993).

Other medications that can be used to test GH deficiency are levodopa, glucagon, and clonidine. GH serum levels should rise to greater than 10 ng/ml to rule out GH deficiency (Kohler, 1986).

Treatment. Somatrem (Protropin[R]) should be given at a dose of 0.05-0.1 mg/kg subcutaneously or intramuscularly three times per week (Benitz & Tatro, 1988; Taketomo, Hodding, & Kraus, 1996). Each 5 mg vial of somatrem should be mixed with 1-5 ml of bacteriostatic sterile water with benzyl alcohol preservative. If patient is less than 1 month old, only reconstitute with preservative free sterile water. Once reconstituted with bacteriostatic sterile water, the same vial can be used for up to 7 days (Phelps & Hak, 1996; Taketomo et al., 1996).


Adrenocorticotrophic hormone (ACTH) stimulates the synthesis and release of glucocorticoids from the adrenal cortex. Patients with ACTH deficiency may experience salt wasting, hyponatremia, hyperkalemia, weakness, fatigue, anorexia, or hypoglycemia. Hypoglycemia is more pronounced in patients who also have GH deficiency (Rang & Dale, 1991; Shimon & Melmed, 1998).


1. Corticotropin stimulation test. Give cosyntropin (Cortrosyn[R]) 0.125 mg intramuscularly or intravenously. Measure serum cortisol levels before injection and 30 minutes and 60 minutes after injection. Serum cortisol levels should be greater than 20 mcg/dl in the absence of ACTH deficiency. Serum cortisol levels less than 10 mcg/dl can diagnose ACTH deficiency. Patients should not receive steroids the day before this test (Kohler. 1986).

2. Insulin-induced hypoglycemia (refer to section in GH deficiency). Cortisol levels will rise greater than 20 mcg/dl if the patient does not have ACTH deficiency. Serum cortisol levels less than 10 mcg/dl indicate ACTH deficiency (Johnson, 1993).

3. Metyrapone. Metyrapone blocks cortisol production. In patients with ACTH deficiency, metyrapone administration will result in failure to increase ACTH and cortisol precursors. This test can precipitate adrenal crisis; therefore, extreme caution must be utilized (Johnson, 1993).


1. Oral hydrocortisone. Give hydrocortisone orally 0.5-0.75 mg/kg/day or 20-25 mg/[m.sup.2]/day. Doses should be divided every 8 hours (Benitz & Tatro, 1988; Johnson, 1993; Taketomo et al., 1996). Hydrocortisone should be given with food or milk to decrease gastrointestinal side effects.

2. Intramuscular/intravenous hydrocortisone. Give hydrocortisone intramuscularly or intravenously 0.25-0.35 mg/kg/day or 12-15 mg/[m.sup.2]/day. Doses can be given can be given once daily in the morning (Benitz & Tatro, 1988; Johnson, 1993; Taketomo et al., 1996). Hydrocortisone sodium succinate has benzyl alcohol as a preservative and should not be used in neonates (Phelps & Hak, 1996).

Thyrotropin Hormone

Thyrotropin hormone is essential for growth. It plays an important role in central nervous system growth and maturation. Thyrotropin hormone also increases the metabolism of carbohydrates, fats, and proteins (Kohler, 1986; Rang & Dale, 1991). Characteristics of thyrotropin deficiency include dry skin, thick tongue, coarse hair, constipation, respiratory depression, and bradycardia (Vance, 1994).


1. Serum thyrotropin. Normal serum thyrotropin (TSH) is 0.4-4.8 mcunits/ml (Johnson, 1993).

2. Free thyroxine index. Normal free thyroxine index is 1.34.2.

3. Serum T3. Normal serum T3 is 85-185 ng/dl.

4. Total T4. Normal total 1-4 is 5-11 mcg/dl.

Treatment. Treatment is based on age and weight (Benitz & Tatro, 1988; Johnson, 1993; Taketomo et al., 1996).

1. If patients is 0-6 months old, start therapy with levothyroxine 8-10 mcg/kg/day (max: 50 mcg).

2. If patient is 6-12 months old, start therapy with levothyroxine 6-8 mcg/kg/day (max: 75 mcg).

3. If patient is 1-5 years old, start therapy with levothyroxine 5-6 mcg/kg/day (max: 100 mcg).

4. If patient is 6-12 years old, start therapy with levothyroxine 4-5 mcg/kg/day (max: 150 mcg).

5. if patient is older than 12 years, start therapy with levothyroxine 2-3 mcg/kg/day (max: 150 mcg).

Antidiuretic Hormone

Antidiuretic hormone (ADH) regulates the reabsorption of water from the kidney (Rang & Dale, 1991). Characteristics of ADH deficiency include diabetes insipidus, dehydration, polyuria, polydypsia, and increased serum osmolality (Shimon & Melmed, 1998).

Diagnosis. The water deprivation test is used to detect ADH deficiency. Fluids should be restricted for at least 7 hours before the test. The following should be measured every hour: body weight, urine specific gravity, and urine volume. Serum sodium, urine osmolality, and serum osmolality should be measured every 2 hours. Dehydration and hypernatremia can result if monitoring becomes haphazard. If the patient loses more than 5% of their initial body weight, the test must be stopped and the patient rehydrated. Normal values which rule out ADH deficiency are as follows: (a) urine osmolality 500-1400 mOsm/L, (b) plasma osmolality 288-291 mOsm/L, (c) plasma osmolality: urine osmolality [is greater than] 2, and (d) urine specific gravity [is greater than] 1.010 (Johnson, 1993).

Treatment. Desmopressin (DDAVP[R]) is given 5 mcg daily intranasally. If intravenous desmopressin is necessary, the dose is one-tenth of the intranasal dose. Doses can be increased to a maximum of 20-30 mcg/day intranasal or 23 mcg/day intravenous. Desmopressin should be stored in the refrigerator (Benitz & Tatro, 1988; Johnson, 1993; Taketomo et al., 1996).

Prolactin and luteinizing/follicle stimulating hormones have little impact on pediatric patients; therefore, discussion has been omitted from this article.


In conclusion, panhypopituitarism is a disease that can affect the entire endocrine system. Hormone deficiencies can affect growth and maturation, mammary gland structure and function, release of glucocorticoids, thyroid function, water reabsorption from the kidney, and ovulation and spermatogenesis. Panhypopituitarism is a treatable disease. Patients can have a normal life with treatment and life-long medical follow-up.

Jodi L. Mann, PharmD, is Consultant Pharmacist, Kroger Long Term Care, Indianapolis, IN.
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Author:Mann, Jodi L.
Publication:Pediatric Nursing
Date:Nov 1, 1999
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