Encyclopedia of Health and Medicine

hyperthyroidism 139
calcium, phosphorus, and parathyroid hormone in
the blood circulation. Further diagnostic procedures
to determine the cause of the hyperparathyroidism
may include ULTRASOUND of the neck to
evaluate the parathyroid glands, as well as tests of
kidney function and X-rays to evaluate bone structure
and density. Treatment for parathyroid adenoma
or parathyroid hyperplasia typically involves
surgery to remove the affected parathyroid gland,
which permanently ends the oversecretion. Most
people recover fully and without residual consequences
unless osteoporosis has become significant
and requires subsequent treatment.
See also CALCITONIN; HYPOPARATHYROIDISM; PAGET’S
DISEASE OF THE BONE; SURGERY BENEFIT AND RISK
ASSESSMENT.
hyperprolactinemia A circumstance of elevated
PROLACTIN in the BLOOD circulation that occurs
when the anterior lobe of the PITUITARY GLAND
secretes excessive prolactin. One of the most
common causes of hyperprolactinemia is HYPOTHY-
ROIDISM (underactive THYROID GLAND). Hypothyroidism
causes the HYPOTHALAMUS to increase
THYROTROPIN-RELEASING HORMONE (TRH) secretion in
an attempt to increase the thyroid gland’s production
of thyroid hormones. TRH also stimulates the
pituitary gland to release prolactin. Hyperprolactinemia
may also result from a prolactin-secreting
ADENOMA of the pituitary gland, a
noncancerous tumor also called a prolactinoma.
Numerous medications may interfere with the
endocrine cascades by suppressing DOPAMINE, a
HORMONE that “turns off” prolactin secretion.
Hyperprolactinemia has both direct action and
cascading effects on the endocrine function. The
direct action of prolactin activates the milk ducts
in the breasts, causing milk production and lactation.
The cascading effects begin with the hypothalamus
and carry through the endocrine cascade
to the gonads (sex glands) Elevated levels of prolactin
in the blood circulation shut off the hypothalamus’s
production of GONADOTROPIN-RELEASING
HORMONE (GNRH), which consequently slows the
pituitary gland’s production of LUTEINIZING HORMONE
(LH) and FOLLICLE-STIMULATING HORMONE (FSH). These
events further lead to reduced production of
ESTROGENS, PROGESTERONE, and TESTOSTERONE by the
OVARIES, TESTICLES, and ADRENAL GLANDS.
In women the primary symptoms of hyperprolactinemia
include disturbances of MENSTRUATION
(notably infrequent or absent menstrual periods),
INFERTILITY, and milk production (galactorrhea)
when not pregnant or BREASTFEEDING. In men the
primary symptoms of hyperprolactinemia include
ERECTILE DYSFUNCTION and HYPOGONADISM resulting
from diminished testosterone levels. When the
cause of the hyperprolactinemia is a prolactinoma,
both men and women may experience headaches
and disturbances of vision from pressure the
tumor applies on adjacent structures, such as the
OPTIC NERVE, in the BRAIN.
The diagnostic path begins with blood tests to
measure the levels of key hormones such as the
thyroid hormones, the sex hormones, and prolactin.
The results of these tests determine the further
course of diagnostic procedures, which may
include MAGNETIC RESONANCE IMAGING (MRI) of the
head to evaluate the possibility of prolactinoma or
ULTRASOUND of the neck to assess the thyroid gland.
Treatment targets the underlying cause of the
excessive prolactin secretion, which may require
surgery to remove an adenoma or medications
(dopamine agonists, which suppress prolactin
secretion) to treat prolactinoma, or hormone
replacement therapy to treat hypothyroidism.
Most people recover fully and without residual
consequences after appropriate treatment, though
may require ongoing treatment for the identified
underlying conditions.
See also HYPOPITUITARISM; OSTEOPOROSIS; SURGERY
BENEFIT AND RISK ASSESSMENT.
hyperthyroidism A condition, also called thyrotoxicosis,
in which the THYROID GLAND overproduces
thyroid hormones. The excessive thyroid
hormones accelerate METABOLISM.
In health the endocrine system maintains a
precise balance among the thyroid hormones to
regulate many of the functions of metabolism. The
thyroid hormonal cascade begins when the HYPO-
THALAMUS produces THYROTROPIN-RELEASING HORMONE
(TRH). TRH stimulates the anterior lobe of the PITU-
ITARY GLAND to release THYROID-STIMULATING HORMONE
(TSH). TSH stimulates the thyroid gland to synthesize
TRIIODOTHYRONINE (T 3 ) and THYROXINE (T 4 ), the
major active thyroid hormones, as well as several
minor or precursor (inactive) thyroid hormones.