vascular and neural connections such that secretion is not facilitated. Cells in the pars intermedia may secrete MSH (melanocyte-stimulating hormone) which stimulates the

 looking primarily for retarded bone age. Hypopituitarism

must be differentiated from isolated growth hormone

deficiency, where normal pubertal development occurs.

Other causes of short stature must be considered, e.g.

constitutional causes, hypogonadism, hypothyroidism,

and gonadal dysgenesis. Eunuchoid habitus eventually

emerges only in the hypogonadal disorder. Normal

plasma levels are less than 3 ng/mL, after insulin hypoglycemia the level rises to approximately 10–25 ng/mL

within 60 minutes. Caution should be used in the dose

of insulin administered. If hypopituitarism is suspected,

doses of 0.05 units/kg are recommended; the dose can

be increased if insufficient hypoglycemia is achieved.

The infusion of arginine 0.5 g/kg for 30 minutes, can

also increase GH levels to greater than 10 ng/mL in

60–90 minutes. This test has the advantage of not producing

hypoglycemia. Absence of a normal response to these

provocative tests is diagnostic.

Excess

Growth records, changes in soft tissue mass, enlargement

of sella turcica, increased sweating, tufting of phalanges,

vertebral overgrowth and spur formation, and organomegaly are all useful indications of GH excess. Serial

studies of visual fields are essential. While increases in

BMR and serum phosphorus concentration are helpful,

the diagnosis is established by the level of GH and its

response to suppressive maneuvers. Serum GH levels

are greater than 10 ng/mL and are not suppressed after

oral glucose loads. The availability of serum GH levels

makes possible the evaluation of surgical or radiologic

treatment.

The Endocrine System 735

In Brief

Clinical Disorders

1. Deficiency: Dwarfism

2. Excess: Gigantism (prepubertal)

 Acromegaly (postpubertal)

Interfering Factors

1. Increased levels are associated with use of oral contraceptives and estrogens.

2. Decreased levels are associated with obesity and use

of corticosteroids.

CORTICOTROPIN (ACTH)

Actions

This stimulates production of all adrenocortical hormones

(transient stimulatory effect on aldosterone) and causes

hyperplasia of adrenal cortex. In the adrenal, it promotes

increased protein synthesis, accelerates glycolysis and

increases steroidogenesis. Extra-adrenal actions include

mobilization of nonesterified fatty acids from fat depots.

Normally, the amount of circulating ACTH is controlled by

the levels of cortisol in the blood, individual biorhythms

and stress.

Methods of Evaluation

The X-ray of sella turcica should be taken, study

basal excretion of 17-hydroxycorticosteroids, assess

diurnal variation patterns, study plasma cortisol levels.

Corticotropin lack is indicated by:

¾ Failure of adrenocortical function

¾ Low 24 hours urinary excretion of 17 ketosteroids and

17-hydroxycorticosteroids, which increase stepwise in

response to daily corticotropin administration

¾ Failure of hydroxycorticosteroid excretion to increase

following administration of metyrapone, which blocks

the production of cortisol and results in increase of

corticotropin production by the intact hypophysis

¾ Normal or slightly reduced aldosterone excretion

¾ Plasma ACTH levels—normally barely detectable

are markedly increased in adrenal insufficiency and

Cushing’s disease.

SI units

0800 hours, peak 25-100 pg/mL 25-100 ng/L

1800 hours, trough 0-50 pg/mL 0-50 ng/L

Clinical Disorders

Increased Addison’s disease, ectopic ACTH syndrome,

pituitary adenoma, pituitary Cushing’s syndrome,

primary adrenal insufficiency, and stress. Drugs include

amphetamine sulfate, calcium gluconate, corticosteroids,

estrogens, ethanol, lithium carbonate, and spironolactone

(corticotropin-like substances elaborated by malignant

tissue, particularly in the lung, pancreas or prostate, may

also lead to Cushing’s disease).

Decreased primary adrenocortical hyperfunction (due to

tumor or hyperplasia) and secondary hypoadrenalism.

OTHER ANTERIOR PITUITARY HORMONES

TSH

This hormone stimulates the synthesis and secretion of

thyroid hormones. It is a glycoprotein hormone controlled

by feedback from thyroid hormones.

The TSH controls production and release of T3 and T4

at three levels:

¾ The entry of I- into the follicle

¾ The entry of Tg bound T3 and T4 from follicular space

into the lumen

¾ The release of T3 and T4 from Tg with the help of

protease enzyme.

FSH

The target organs for FSH are the testes, in men, and the

ovaries in women. The hormone stimulates the germinal

epithelium in the testes to cause and facilitate the

making of sperm. In women, it stimulates the growth and

development of the follicle. It stimulates the production

of testosterone in men and estrogen and progesterone

in women. Its release from the pituitary is governed by a

negative feedback mechanism involving these steroids.

LH

The male target organ is the testes and the testosterone

producing interstitial cells of Leydig in particular. In

women the target of LH is the developing follicle within

the ovary where it is necessary for ovulation to occur and a

corpus luteum to develop.

LH, FSH—Recommendations for Testing

¾ Irregular menstrual periods—amenorrhea.

¾ Primary and secondary hypogonadism in male and

female

¾ When a female complains of masculinizing features or

a male complains of feminine features

¾ Infertility cases

¾ IVF centers—assisted conception

736 Concise Book of Medical Laboratory Technology: Methods and Interpretations ¾ Monitor LH, FSH levels after LHRH stimulation

¾ LH/FSH ratio is a useful parameter in diagnosis of PCO

(polycystic ovary)

¾ FSH is a good indicator in menopause

¾ In children where they seem to grow faster than their

age or otherwise (precocious and delayed puberty).

Prolactin

This hormone is involved in breast development and

lactation. In concert with estrogen, it prepares the

mammary gland for lactation and then causes the synthesis

of milk. Secretion is regulated by a release inhibiting factor

and suckling may cause the release of prolactin from the

pituitary. It steadily increases during pregnancy, reaching

200 ng/mL in the 3rd trimester and returns to normal in

nonlactating women 2-3 weeks postpartum. In lactating

women 6 months postpartum. It also increases with breast

stimulation, exercise, sleep, and stress.

Prolactin—Recommendations for Testing

¾ Diagnosis of hyperprolactinemia and monitoring the

effectiveness of treatment

¾ When a male complains of impotence, decreased libido

¾ Female complains of irregular menstrual cycle—

amenorrhea

¾ Pituitary tumor (microadenoma or macroadenoma)

¾ Used alone or with LH and FSH for detecting pituitary

dysfunction.

INTERMEDIATE LOBE (PARS INTERMEDIA)

In the adult human, this lobe is diminished with poor

vascular and neural connections such that secretion is not

facilitated. Cells in the pars intermedia may secrete MSH

(melanocyte-stimulating hormone) which stimulates the

activity of melanocytes in the skin.

POSTERIOR PITUITARY (NEUROHYPOPHYSIS)

This portion of the pituitary is really an extension of

the hypothalamus. Neurons with their cell bodies in

the hypothalamus and their terminal portions in the

neurohypophysis release two hormones. Antidiuretic

hormone (ADH) and oxytocin are stored there within the

terminal processes of neurons until the signal to release

them is received.