LH:mIU/mL FSH: mIU/mL PRL:(ng/mL)
Follicular phase 0.8 – 10.5 3.0 – 12.0
Midcycle 18.4 – 61.2 8.0 – 22.0
Luteal phase 0.8 – 10.5 2.0 – 12.0
Postmenopausal 8.2 – 40.8 35.0 – 151.0 1.5 – 18.5
Men 0.7 - 7.4 1.0 – 14.0 1.8 – 17
Plasma, serum or urine can be used for LH and FSH
measurements. Both hormones are stable for 8 days
at room temperature and for 2 weeks at 4°C; for longer
periods, the specimen should be stored frozen at or below
–20°C. Because of episodic, circadian and cyclic variations
in the secretion of gonadotrophins, a meaningful clinical
evaluation of these hormones may require determinations
in pooled blood specimens, multiple serial blood
specimens, or timed urine specimens (Fig. 24.22).
Serum is the specimen of choice for PRL assays and can
be stored at 4°C for 24 hours. Freezing is preferred for
maintaining long-term stability. Specimens should be
collected 3 to 4 hours after the patient has awakened,
since PRL levels rise rapidly during sleep and peak in early
morning hours. Emotional stress, exercise, ambulation,
and protein ingestion also elevate PRL levels. As PRL is
secreted episodically, multiple sampling techniques may
be advantageous (e.g. pooling equal volumes of sera from
specimens drawn at 6 to 18 min intervals).
The ranges will differ from laboratory to laboratory and
depend on the reference preparation used for the standards.
The range of values is plotted on a logarithmic scale.
Measured values differ significantly, depending on the
laboratory and immunoassay system employed (Fig. 24.23).
FIG. 24.21: Epitype characterization
The dotted line represents the clinically important lower range
Hyperprolactinemia is defined as consistently elevated
Prolactin levels in the absence of pregnancy or postpartum
lactation and is considered as pituitary disorder.
Prolactin is a pituitary hormone that plays a role in a
variety of reproductive functions. It is essential for normal
production of breast milk following childbirth. Also, it
negatively modulates the secretion of pituitary hormones
responsible for gonadal function.
Common causes: Pituitary tumors, usually prolactinomas,
which are under 10 mm in diameter.
Primary hypothyroidism, due to increased TRH
resulting in increased TSH and Prolactin.
Ingestion of certain drugs, including phenothiazine,
certain high blood pressure medicines (a-methyldopa),
tranquilizers and opioids, anti nausea drugs, oral
Chronic kidney failure and other medical conditions.
Also associated with hypogonadotropinism and
Symptoms of Hyperprolactinemia
¾ Headaches and visual difficulties
¾ Loss of libido and sexual profency in men
¾ Lowered levels of LH and FSH
¾ Symptoms of estrogen deficiency (such as those of
menopause—hot flashes, dyspareunia), even in case of
¾ Signs of increased levels of androgens in women.
Basal Prolactin level can adequately be used to gauge
pituitary tumor size and be followed over time.
Serum FSH, LH and estradiol—usually low to normal in
¾ TSH to rule out hypothyroidism.
¾ CT or MRI to identify microadenomas.
¾ Visual-field examination—in case of macroadenomas
(>10 mm diameter) or any patient electing medical
clinically important lower range
Schematic representation of the range of basal serum prolacting levels (ng/ml)
observed in various pathologic and pharmacologic states
For patients >100 ng/mL of prolactin and normal CT/MRI
or patients with only microadenomas—Bromocriptine or
Exogenous estrogen, in some cases, to combat low
The adrenal cortex produces four major groups of
hormones: (i) glucocorticoids (cortisol, cortisone), (ii)
androgens (androstenedione, dehydroepiandrosterone),
(iii) Mineralocorticoids (aldosterone, deoxycorticosterone,
corticosterone), and (iv) estrogens and progesterone.
Adrenal corticosteroid production is controlled by
of the system. Aldosterone is under minimal control of
ACTH, and its secretion is mainly influenced by volume
receptors, angiotensin II and potassium concentration.
The plasma cortisol, in turn, regulates ACTH secretion.
The direct feedback mechanism does not seem operative
Cortisol-binding globulin (CBG) avidly binds cortisol
and corticosterone and is the main carrier protein at
normal concentrations. Estrogens increase CBG are
inactive but are in equilibrium with free unbound steroid.
The mineralocorticoids increase reabsorption of sodium
and chloride, increased excretion of potassium, and
allow an exchange of intracellular potassium with
extracellular sodium. Aldosterone is most effective in this
regard. The glucocorticoids affect protein, carbohydrate,
and fat metabolism, raising blood glucose, increasing
gluconeogenesis and protein catabolism (with resulting
osteoporosis), metabolising hepatic fat depots, decreasing
tubular reabsorption of urates, increasing uropepsin
secretion, and lyzing eosinophils and lymphocytes.
Clinical Disorders of Adrenal Steroids
1. Acute: Addisonian crisis, Waterhouse-Friderichsen syndrome
2. Chronic: Addison’s disease.
1. Principal glucocorticoids: Cushing’s syndrome.
2. Principal androgen excess: Adrenogenital syndrome in females, macrogenitosomia in males.
3. Aldosterone excess: Primary hyperaldosteronism.
Methods of Evaluation of Glucocorticoids and
Evaluation of adrenocortical function may depend upon:
(i) physical examination, noting particularly pigmentation
of the skin and mucous membranes, pubic and axillary
hair growth, blood pressure and the presence of edema,
(ii) determination of serum sodium, potassium, chloride,
CO2, urea and protein, (iii) X-ray studies of the bones for
osteoporosis and of the adrenal region, with or without
retroperitoneal pneumography and tomography, (iv)
determination of blood and urine levels of 17-ketosteroids,
pregnanetriol, and pregnenetriolone, (v) specific function
tests such as the water loading test and the response of
hormone excretion levels to stimulation by exogenous
ACTH, inhibition of ACTH production by corticosteroids,
or inhibition of 11-β hydroxylation by metyrapone; and
(vi) in the absence of interfering factors, the number of
circulating eosinophils, normally between 100 and 300/ml,
varying inversely with adrenocortical activity.
Urinary 17-Hydroxycorticosteroids, 17-Ketosteroid
Excretion, Ketogenic Steroids, or Free Cortisol
adrenocortical activity. Paraldehyde, quinine, colchicine,
iodides, sulfamerazine, and chlorpromazine interfere with
The test, hence, reflects the activity of the adrenal
cortex and the gonads in the male and the adrenal cortex
in the female. There is a diurnal variation in excretion of
17-hydroxycorticosteroids and 17-ketosteroids of adrenal
origin. The contribution of testosterone metabolites to the
ketosteroids in the urine is minimal.
meprobamate administration. These drugs should be
stopped for several days before urine collection.
The patient should not be receiving androgens or cortisol
when specimens are collected. Testosterone propionate is
excreted in the urine and is measured as 17-ketosteroids,
methyltestosterone does not appear in the urine.
776 Concise Book of Medical Laboratory Technology: Methods and Interpretations Method
A 24 hours urine specimen is collected in a jug containing
5 mL of 2% thymol glacial acetic acid.
High levels of excretion of both 17-hydroxycorticosteroids,
17-ketosteroids, ketogenic steroids, and urinary-free
cortisol are found in adrenocortical carcinoma and
adrenocortical hyperplasia, and of 17-ketosteroids and
pregnanetriol in the adrenogenital syndrome. Low levels
of excretion are found in hypopituitarism. Addison’s
disease, myxedema, and occasionally in anorexia nervosa.
Average-Sodium diet Serum SI units
Supine 3–10 ng/dL 0.14–1.9 nmol/L
pregnant 18–100 ng/dL 0.5–2.8 nmol/L
Nonpregnant 5–30 ng/dL 0.14–0.8 nmol/L
Adult male 6–22 ng/dL 0.17–0.61 nmol/L
1 week–12 months 1–60 ng/dL 0.03–4.43 nmol/L
Age 1–3 years 5–60 ng/dL 0.14–1.7 nmol/L
Age 3–11 years 5–70 ng/dL 0.14–1.9 nmol/L
Age 11–15 years <5–50 ng/dL <0.14–1.4 nmol/L
Norm urine 2–26 mg/24 h 5.6–73 nmol/day
Urinary sodium Plasma renin µg/day nmol/day
<30 nmol/day 5–24 Al/mL/h 35–80 97–220
20–50 nmol/day 2–7 Al/mL/h 13–33 36–91
50–100 nmol/day 1–5 Al/mL/h 5–24 14–66
100–150 nmol/day 0.5–4 Al/mL/h 3–19 8–53
This cholesterol-derived hormone is the most potent
of the mineralocorticoids. Its foremost physiologic
effect is that of regulating the transport of ions across
cell membranes, especially those of renal tubules. This
hormone causes the retention of sodium and chloride and
the elimination of potassium and hydrogen. The second
is the maintenance of blood pressure. Minute quantities
will depress the urinary and salivary sodium to potassium
ratio primarily because of diminished sodium excretion.
The three main factors that apparently affect aldosterone
system appears to be the major mechanism that controls
extracellular fluid by regulation of aldosterone secretion.
Potassium loading results in increased aldosterone levels,
whereas a potassium-deficient diet in the presence of
aldosterone excess will result in a lowered aldosterone level.
Increased concentrations of potassium in the blood plasma
directly stimulate adrenal production of the hormone. The
ACTH may affect aldosterone production in conditions
of acute stress, burns, hemorrhage, and other pathologic
conditions. Under physiologic conditions, ACTH seems to
have little effect on aldosterone production.
1. A 24 hours urine specimen is obtained.
2. Urine should ideally be refrigerated during collection.
3. Venous blood specimen is added to a heparinized or
EDTA vial. Separate the cells from plasma immediately.
Specimen should be obtained in the morning after the
patient has been upright for at least 2 hours.
4. Specify and record the source of the specimen (e.g.
Diuretic agents, progestational agents, estrogens, and
liquorice should be discontinued 2 weeks prior to test. The
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