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Introduction
Sex hormones, or steroidal hormones, are important for hair growth.
A lack of one or more of these hormones could lead to a absence
of body hair in adults, but more significantly an over expression
of steroidal hormones and/or a lack of antagonists to steroidal
hormones can result in hirsutism (excessive body hair) and/or the
development of female pattern baldness. Because of this a blood
test to examine hormone levels may be desirable if a tentative diagnosis
of androgen induced hirsutism or androgenetic alopecia is made.
It is rare for a man to suffer from systemic hormone abnormalities,
although hyperandrogenicity in men is possible with some prostate
and adrenal gland disorders. For women pre-menopause the story is
somewhat different. Women may also rarely have an adrenal gland
disorder, but much more common is a disorder of hormone production
in the ovaries. Polycystic ovary syndrome (PCOS) is the most common
problem that leads to a net excessive steroidal hormone activity.
This may be associated with hirsutism, and in more severe cases,
female pattern baldness. One of the simplest methods of diagnosing
PCOS is with a blood test. In many cases of PCOS the hormone and
hormone antagonist levels are altered. However, it is possible to
have PCOS, but to have blood hormone values within the normal ranges.
If a blood test comes back normal, but symptoms still suggest hormones
are involved, doctors may need to resort to ultra sound scanning
of the ovaries to confirm a PCOS diagnosis. A normal blood test
result for a premenopasual woman still does not rule out androgen
action on hair follicles, but it does help to determine if systemic
problems like PCOS are behind the hair problem.
Post menopausal women may experience some degree of androgenetic
alopecia as estrogen, an indirect antagonist of testosterone, diminishes.
In severe cases women may develop a male pattern alopecia presentation
with hairline recession. A blood test can be useful to confirm that
hair loss post menopause is androgen mediated.
A comprehensive blood test (primarily for women) for steroidal
hormones and antagonists would include:
- Sex hormone binding globulin (SHBG)
- Estrogens (usually only the estradiol (E2) form is tested)
- Progesterone
- 17 Hydroxyprogesterone (tested sometimes)
- Dehydroepiandrosterone sulfate (DHEAS) and/or Dehydroepiandrosterone
(DHEA)
- Total testosterone (T)
- Free testosterone (that testosterone which is not bound to other
molecules like SHBG)
- Androstenedione (possibly androstenediol too)
- Prolactin (PRL)
- Follicular stimulating hormone (FSH)
- Lutinizing hormone (LH)
Although dihydrotestosterone (DHT) is the primary promoter of androgenetic
alopecia it is not generally tested because DHT is a relatively
unstable molecule and levels can vary significantly over a short
space of time. In addition, the DHT in the blood stream is not a
particularly good reflection of the DHT in hair follicles. Steroid
hormone responsive hair follicles produce their own DHT through
enzyme conversion of DHEAS and T that they receive through the blood
stream. To define excessive systemic androgen activity doctors look
at the DHEAS, testosterone, and androstenedione results.
Depending on the tentative diagnosis, other tests may be done alongside
steroidal hormone tests. For PCOS, blood is also often tested for
insulin levels to define insulin resistance which can be associated
with PCOS. Thyroid hormones may also be tested as part of the evaluation
as these hormones, though not steroidal in nature nor antagonists
of steroid hormones, can have a significant impact on hair growth.
Note that in terms of understanding hirsutism and androgenetic
alopecia, blood test results only present part of the story. The
blood test results indicate what is going on systemically in terms
of hormone production. A blood test does not provide an insight
into hormonal activity in the skin and hair follicles. Skin and
hair follicles produce their own enzymes that can convert mild androgens
like DHEA into potent androgens like DHT. So it is possible to have
normal blood test results but have significant androgenic activity
in the hair follicles. A normal blood test result does not rule
out a diagnosis of androgen induced hirsutism or androgenetic alopecia.
Standard
test ranges of hormones in women
Note; only the basic adult ranges are listed here. During pregnancy,
or when using hormone contraceptives, normal hormone activity undergoes
significant changes that are not listed below. The values for children
are also significantly different. Normal ranges will be slightly
different in different laboratories as there is no calibration of
the tests between different labs.
|
Hormone / antagonist
|
Estrus cycle / Life stage
|
Value
|
| Progesterone (nanograms per milliliter or nano-moles
per liter) |
Follicular phase |
< 1.5 ng/ml
(< 3.18 nmol/L) |
| |
Mid luteal phase |
3 – 20 ng/ml
(9.54 – 63.6 nmol/L) |
| |
Postmenopausal |
0 – 15 ng/ml |
| 17-Hydroxyprogesterone (nanograms per deciliter
or nano-moles per liter) |
Follicular phase |
20 – 100 ng/dL
(0.6 – 3.0 nmol/L) |
| |
Midcycle peak |
100 – 250 ng/dl
(3 – 7.5 nmol/L) |
| |
Luteal phase |
100 – 500 ng/dl
( 3 – 15 nmol/L) |
| |
Postenopausal |
< 70 ng/dl
(< 2.1 nmol/L) |
| 17-Hydroxypregnenolone (nanograms per milliliter
or nano-moles per liter) |
Pubertal |
44 – 235 ng/ml
(1.3 – 7.1 nmol/L) |
| |
Adult |
53 – 357 ng/ml
(1.6 – 10.7 nmol/L) |
| 18-Hydroxycorticosterone (nanograms per deciliter
or pico-moles per liter) |
Recumbent (morning value) |
22.9 – 27.7 ng/dL
(630 – 762 pmol/L) |
| |
Upright (midday value) |
43.7 – 53.5 ng/dL
(1202 – 1472 pmol/L) |
| Estrone (picograms per milliliter or pico-moles
per liter) |
Follicular phase |
30 – 100 pg/ml
(111 – 370 pmol/L) |
| |
Ovulatory phase |
> 150 pg/ml
(> 555 pmol/L) |
| |
Luteal phase |
90 – 160 pg/ml
(333 – 592 pmol/L) |
| |
Postmenopausal |
20 – 40 pg/ml
(74 – 148 pmol/L) |
| Estriol (nanograms per milliliter or nano-moles
per liter) |
Non pregnant |
< 2 ng/ml
(< 7 nmol/L) |
| |
30 – 32 weeks pregnant |
2 – 12 ng/ml
(7 – 42 nmol/L) |
| |
33 – 35 weeks pregnant |
3 – 19 ng/ml
(10 – 66 nmol/L) |
| |
36 – 38 weeks pregnant |
5 – 27 ng/ml
(17 – 94 nmol/L) |
| |
39 – 40 weeks pregnant |
10 – 30 ng/ml
(35 – 104 nmol/L) |
| Estradiol (picograms per milliliter or pico-moles
per liter) |
Follicular phase |
50 – 145 pg/ml
(184 – 532 pmol/L)
|
| |
Midcycle peak |
112 – 443 pg/ml
(411 – 1626 pmol/L) |
| |
Luteal phase |
50 – 241 pg/ml
(184 – 885 pmol/L)
|
| |
Postmenopausal |
< 59 pg/ml
(< 217 pmol/L) |
| FSH (units per liter) |
Follicular phase |
3.0 – 20.0 U/L |
| |
Ovulatory phase |
9.0 – 26.0 U/L |
| |
Luteal phase |
1.0 – 12.0 U/L |
| |
Postmenopausal |
18.0 – 153.0 U/L |
|
LH (units per liter)
|
Follicular phase |
2.0 –15.0 U/L |
| |
Ovulatory phase |
22.0 – 105.0 U/L |
| |
Luteal phase |
0.6 – 19.0 U/L |
| |
Postmenopausal |
16.0 – 64.0 U/L |
| SHBG (nanomoles per liter) |
Follicular phase |
24 – 200 nmol/L |
| |
Luteal phase |
48 – 185 nmol/L |
| |
Contraceptives |
89 – 379 nmol/L |
| |
Postmenopausal |
46 – 200 nmol/L |
| Dehydroepiandrosterone (DHEA) (nanograms per deciliter
or nano-moles per liter) |
|
130 – 980 ng/dl
(4.5 – 34.0 nmol/L) |
| Dehydroepiandrosterone sulfate (DHEAS) (micrograms
per deciliter) |
Premenopausal |
12 – 535 µg/dl
|
| |
Postmenopausal |
30 – 260 µg/dl |
| Androstenedione (nanograms per milliliter or nano-moles
per liter) |
Premenopausal |
0.8 – 2.3 ng/ml
(2.8 – 8.0 nmol/L) |
| |
Postmenopausal |
0.3 – 0.8 ng/ml
(1.0 – 2.8 nmol/L) |
| Androstenediol (nanograms per milliliter) |
|
0.2 – 2 ng/ml |
| Total testosterone - morning sample (nanograms
per deciliter or nano-moles per liter) |
|
6 – 86 ng/dl
( 0.21 – 2.98 nmol/L) |
| Free testosterone - morning sample (picrograms
per milliliter or pico-moles per liter) |
20 – 40 yr |
0.6 – 3.1 pg/ml
( 20.8 – 107.5 pmol/L) |
| |
41 – 60 yr |
0.4 – 2.5 pg/ml
( 13.9 – 86.7 pmol/L) |
| |
61 – 80 yr |
0.2 – 2.0 pg/ml
( 6.9 – 69.3 pmol/L) |
| Dihydrotestosterone (nanograms per milliiliter
or nano-moles per liter) |
Adult |
6 – 33 ng/ml
(0.2 – 1.1 nmol/L) |
| Cortisol (micrograms per milliliter or nano-moles
per liter) |
Morning sample |
5 – 20 µg/ml
(140 – 552 nmol/L) |
| |
Afternoon sample |
2.5 – 10 µg/ml
(69 – 276 nmol/L) |
| Prolactin (nanograms per milliliter) |
Premenopausal |
2 – 20 ng/ml |
| |
Postmenopasual |
0 – 15 ng/ml |
An
explanation of test results for sex hormones in women
Testosterone - Testosterone levels should be fairly low
in women as compared to men. It is possible for a woman to have
no testosterone production and still be healthy other than perhaps
a diminished sex drive. In healthy women the majority of testosterone
production (up to 70%) is derived from the conversion of DHEAS and
androstenedione by enzymes within the skin. The rest is secreted
direct from the ovaries and adrenal glands. An excess of testosterone,
above the normal range signals a potential problem. Most doctors
would consider a level above 50 ng/dl to be somewhat elevated. Above
100 ng/dl of testosterone in women is symptomatic of some kind of
hyperandrogenism. If the testosterone is over 200 ng/dl an ovarian
ultrasound is used to look for any ovarian tumors. The higher the
testosterone level the more risk of hirsutism or androgenetic alopecia
if there is no corresponding rise in androgen antagonists (estrogens
and SHBG).
Estrogens - Estrogens come in several shapes and sizes but
the common one and the one usually tested for is estradiol (E2).
Estradiol concentrations in women vary considerably depending on
age and the stage of the reproductive cycle. The normal range may
be anywhere between 50-700 picograms per milliliter. At the time
of ovulation the range may be between 100-400 picograms per milliliter.
Estrogens antagonize (cancel out) the actions of androgen hormones
so more estrogen in effect reduces androgen hormone activity. As
such, an estrogen level at the higher end of the normal range is
preferable in terms of reducing susceptibility to androgenetic alopecia.
Currently, there is much debate about how estrogens may directly
act on hair follicles. Hair follicles do express estrogen receptors
so the follicle are directly responsive to estrogen hormone molecules.
However, there is confusion as to what estrogens do to the follicles
- whether they stimulate or inhibit hair growth. There may be a
different response depending on the estrogen type. Abnormally high
estrogen levels on day 3 may indicate existence of a functional
cyst or diminished ovarian reserve - however, there are no reports
of hair loss in association with abnormally high estrogen levels
so the risk of hair loss seems to be a minor one.
Dehydroepiandrosterone (DHEA) - Dehydroepiandrosterone sulfate
(DHEAS) is the sulfated form of Dehydroepiandrosterone (DHEA). DHEA
is a relatively unstable molecule and it mostly gets converted to
DHEAS before circulating in the blood stream. For the purpose of
understanding androgenetic alopecia, DHEA and DHEAS can be regarded
as basically the same thing. If DHEAS is over 700 micrograms per
deciliter, an MRI is ordered to rule out and adrenal tumor. If the
DHEAS is between 500 - 700 micrograms per deciliter, then further
endocrine testing is usually needed to rule out adrenal hyperfunction
such as adrenal hyperplasia. An elevated DHEAS level may be improved
through use of dexamethasone, prednisone, or insulin-sensitizing
medications. DHEA can be converted into more potent androgen forms,
ultimately it can be converted into dihydrotestosterone by enzymes
in the hair follicles. As such, A high DHEA level potentially suggests
an increased susceptibility to hirsutism or androgenetic alopecia
if there is no corresponding rise in androgen antagonists.
Follicle Stimulating Hormone (FSH) - FSH is often used as
a gauge of ovarian reserve. In general, under 6 is excellent, 6-9
is good, 9-10 fair, 10-13 diminished reserve, 13+ very hard to stimulate.
In PCOS testing, the LH:FSH ratio may be used in the diagnosis.
The ratio is usually close to 1:1, but if the LH is higher, it is
one possible indication of PCOS. For healthy hair growth then, the
ratio of FSH to LH should be roughly equal.
Luteinizing Hormone (LH) - A normal LH level is similar
to FSH. An LH that is higher than FSH is one indication of PCOS.
Prolactin - Increased prolactin levels can interfere with
ovulation. They may also indicate further testing (MRI) should be
done to check for a pituitary tumor. Some women with PCOS and associated
hair problems also have hyperprolactinemia.
Progesterone (P4) - An elevated level may indicate a reduced
fertility. A progesterone test is done to confirm ovulation. When
a follicle releases its egg, it becomes what is called a corpus
luteum and produces progesterone. A level over 5 probably indicates
some form of ovulation, but most doctors want to see a level over
10 on a natural cycle, and a level over 15 on a medicated cycle.
There is no mid-luteal level that predicts pregnancy. Some say the
progesterone test may be more accurate if done first thing in the
morning after fasting.
Sex Hormone Binding Globulin (SHBG) - Increased androgen
production often leads to lower SHBG. This is a potential problem
in terms of hair growth as SHBG is an antagonist to testosterone.
SHBG binds to testosterone and renders it inactive. Bound testosterone
cannot interact with androgen receptors on cells so it has no impact
on hair follicles. A reduced SHBG level suggests a possible increase
in susceptibility to hirsutism or androgenetic alopecia. The more
SHBG there is the better in terms of healthy hair growth.
Normal
ranges for hormone tests references
- Fischbach FT. A manual of laboratory and
diagnostic tests. Lippincott, Philadelphia, ISBN: 039755186X.
1998
- Kratz A, Lewandrowski KB. Case records
of the Massachusetts General Hospital. Weekly clinicopathological
exercises. Normal reference laboratory values. N Engl J Med. 1998
Oct 8;339(15):1063-72.
- Pasquali R, Vicennati V, Bertazzo D, Casimirri
F, Pascal G, Tortelli O, Labate AM. Determinants of sex hormone-binding
globulin blood concentrations in premenopausal and postmenopausal
women with different estrogen status. Virgilio-Menopause-Health
Group. Metabolism. 1997 Jan;46(1):5-9.
- Greenspan FS, Baxter JD. Basic & Clinical
Endocrinology. 4th ed. Norwalk: Appleton-Lange, 1994
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