calcium, phosphorus, and parathyroid hormone in
the blood circulation. Further diagnostic proce-
dures to determine the cause of the hyperparathy-
roidism may include ULTRASOUND of the neck to
evaluate the parathyroid glands, as well as tests of
kidney function and X-rays to evaluate bone struc-
ture and density. Treatment for parathyroid ade-
noma or parathyroid hyperplasia typically involves
surgery to remove the affected parathyroid gland,
which permanently ends the oversecretion. Most
people recover fully and without residual conse-
quences 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). Hypothy-
roidism causes the HYPOTHALAMUS to increase
THYROTROPIN-RELEASING HORMONE(TRH) secretion in
an attempt to increase the thyroid gland’s produc-
tion of thyroid hormones. TRH also stimulates the
pituitary gland to release prolactin. Hyperpro-
lactinemia may also result from a prolactin-secret-
ing ADENOMA of the pituitary gland, a
noncancerous tumor also called a prolactinoma.
Numerous medications may interfere with the
endocrine cascades by suppressing DOPAMINE, a
HORMONEthat “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 lacta-
tion. The cascading effects begin with the hypo-
thalamus and carry through the endocrine cascade
to the gonads (sex glands) Elevated levels of pro-
lactin in the blood circulation shut off the hypo-
thalamus’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 TESTOSTERONEby the
OVARIES, TESTICLES, andADRENAL GLANDS.
In women the primary symptoms of hyperpro-
lactinemia 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 DYSFUNCTIONand HYPOGONADISMresulting
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 pro-
lactin. The results of these tests determine the fur-
ther course of diagnostic procedures, which may
include MAGNETIC RESONANCE IMAGING(MRI) of the
head to evaluate the possibility of prolactinoma or
ULTRASOUNDof 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 thyro-
toxicosis, in which the THYROID GLANDoverpro-
duces 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-
THALAMUSproduces THYROTROPIN-RELEASING HORMONE
(TRH). TRH stimulates the anterior lobe of the PITU-
ITARY GLANDto release THYROID-STIMULATING HORMONE
(TSH). TSH stimulates the thyroid gland to synthe-
size TRIIODOTHYRONINE(T 3 ) and THYROXINE(T 4 ), the
major active thyroid hormones, as well as several
minor or precursor (inactive) thyroid hormones.hyperthyroidism 139