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[ACNERR]

INTRODUCTION

The effects of hormones in acne are most notable in women. Androgens such as
dihydrotestosterone (DHT) and testosterone, the adrenal precursor dehydroepiandrosterone
sulfate (DHEAS), estrogen, and other hormones, including growth
hormone or insulin-like growth factors (IGFs), may each be important. It is likely
that the hormones affecting the sebaceous gland are both taken up from the
serum in addition to being made locally within the gland.
Hormonal therapy is an option in women whose acne is not responding to
conventional treatment or if signs of endocrine abnormalities are present. The greatest
therapeutic benefit from hormonal therapy is achieved in combination with
other effective anti-acne medications. This chapter focuses on the role of hormones
in acne, the clinical presentation of adult female acne, the work-up of a suspected endocrine abnormality, and the available options for hormonal therapy.




ANDROGENS IN ACNE

Both clinical observation and experimental evidence confirm the importance of
androgens in the pathophysiology of acne. The majority of circulating androgens
are produced by the gonads and the adrenal gland. Androgens can also be produced
locally within the sebaceous gland from the adrenal precursor hormone, DHEAS.
The main androgens that interact with the androgen receptor are testosterone
and DHT. Androgen receptors are found in the basal layer of the sebaceous gland
and the outer root sheath keratinocytes of the hair follicle (1,2).DHTis approximately
five to 10 times more potent than testosterone in its interaction with the androgen
receptor.
An essential role for androgens in stimulating sebum production is supported
by several lines of evidence. For example, the development of acne in the prepubertal
period has been associated with elevated serum levels of DHEAS, a precursor for
testosterone (3,4). Androgen-insensitive subjects who lack functional androgen
receptors do not produce sebum and do not develop acne (5). Tumors of the
ovary or the adrenal that produce androgens are often associated with the
development of acne. Systemic administration of testosterone and dehydroepiandrosterone
increases the size and secretion of sebaceous glands (6), and we know
that severe acne is often associated with elevated serum androgens (7,8).

Androgen Metabolism Within the Skin

Acne may be mediated by serum androgens, locally produced androgens, or a combination
of both. Insights have been gained regarding the local metabolism of
androgens within sebaceous glands (9). Such insights may be of benefit in the
design of new acne therapies. The skin and sebaceous gland are capable of
producing and metabolizing androgens (9). DHEAS is the major adrenal androgen
precursor. It circulates in the blood stream in relatively high levels compared with
other hormones with the exception of cortisol. In fact, in for review, see
Ref. postmenopausal women, all sex steroids made in the skin are from adrenal
steroid precursors, especially DHEA. Secretion of this precursor steroid by the
adrenals decreases progressively from age 30 to less than 50% of its maximal
value at age 60 (10). The enzyme 3b -hydroxysteroid dehydrogenase (3b -HSD)
acts on DHEA to convert it to androstenedione (Fig. 1). This conversion may take
place in the adrenal gland and tissues such as the sebaceous gland, where activity
of the 3b -HSD enzyme has been identified by several investigators (11–13). The
reversible conversion of androstenedione into testosterone is then catalyzed in
the human skin by 17b -HSD, a member of the short chain alcohol dehydrogenases
that are related to retinol metabolizing enzymes (14–18). This is a reversible
enzyme that can oxidize and reduce both androgens and estrogens. It is responsible
for converting the weak androgen androstenedione into the more potent androgen
testosterone. It can also interconvert weak and potent estrogens such as estrone
and estradiol. The 17b -HSD enzyme may represent a regulatory point in androgen
and estrogen metabolism within the skin.
DHT is produced from testosterone within peripheral tissues such as the skin
by the action of the 5a -reductase enzyme. Two isozymes of 5a -reductase have been
identified (19). The type 1 isozyme is active within the sebaceous gland (20,21). The
type 2 isozyme is most active in the prostate gland, where it can be inhibited by
drugs such as finasteride. Activity of 5a-reductase and 17b -HSD exhibits regional
differences depending upon the source of the sebaceous glands (9). In skin that is
prone to acne, such as facial skin, activity of the type 1 5a-reductase in sebaceous
glands is greater than in sebaceous glands obtained from nonacne-prone skin
(20). This implies that more DHT is being produced in sebaceous glands from
facial skin compared with other areas of the body that are not prone to develop
acne. The net effect of the activity of these two enzymes is the greater production
of potent androgens such as testosterone and DHT within sebaceous glands of
facial areas, which may in part account for the development of acne in these areas.


The Sebaceous Gland Is a Steroidogenic Tissue

The skin and sebaceous glands are capable of synthesizing cholesterol de novo from
acetate (22–24). Although this cholesterol is utilized in cell membranes, in the formation
of the epidermal barrier, and is secreted in sebum, its use as a substrate for
steroid hormone synthesis had not been established until recently. In order for
steroid synthesis to occur, cholesterol needs to be translocated from the outer to
the inner mitochondrial membrane. This process is regulated by the steroidogenic
acute regulatory protein (25). Additional enzymes and cofactors needed to convert
cholesterol into a steroid include P450 cholesterol side chain cleavage, adrenodoxin
reductase, cytochrome P450c17, and steroidogenic factor-1. Expression of each of
these proteins was found in human facial skin, sebocytes, and in a recently developed
simian virus (SV) 40-immortalized human sebocyte cell line (SEB-1) (26).
These data demonstrate that the skin is in fact a steroidogenic tissue. The clinical
significance of this finding in mediating androgenic skin disorders such as acne,
hirsutism, or androgenetic alopecia remains to be established.

ESTROGENS IN ACNE

Very little is known about the role of estrogens in modulating sebumproduction. Any
estrogen given systemically in sufficient amounts will decrease sebum production.
The dose of estrogen required to suppress sebum production, however, is greater
than the dose required to suppress ovulation (27). The major active estrogen is estradiol,
which is produced from testosterone by the action of the enzyme aromatase.
Aromatase is active in the ovary, adipose tissue, and other peripheral tissues. Estradiol
can be converted to the less potent estrogen, estrone, by the action of the 17b -HSD
enzyme. Both aromatase and 17b -HSD are present in the skin (17,28). Estrogens
may act by severalmechanisms; theymay: (i) directly oppose the effects of androgens
locallywithin the sebaceous gland, (ii) inhibit the production of androgens by gonadal
tissue via a negative feedback loop on pituitary gonadotrophin release, and (iii)
regulate genes that negatively influence sebaceous gland growth or lipid production.
GROWTH HORMONE AND INSULIN-LIKE GROWTH FACTORS IN ACNE
Growth hormone is secreted by the pituitary gland. It acts on the liver and peripheral
tissues to stimulate the production of IGFs, formerly known as somatomedians.
There are two forms of IGF, termed IGF-1 and IGF-2. IGF-1 is the more prevalent
growth factor. It has been hypothesized that growth hormone may be involved in
the development of acne (29). Acne is most prevalent in adolescents during a
time when growth hormone is maximally secreted and serum levels of IGF-1 are
highest. In addition, IGF-1 can be produced locally within the skin, where it can
interact with receptors on the sebaceous gland to stimulate its growth. Furthermore,
conditions of growth hormone excess such as acromegaly are associated with seborrhea
and the development of acne. In some tissues, the actions of IGF-1 can be
mediated by androgens. It is possible that androgens may influence IGF-1 action
in the sebaceous gland as well.

CLINICAL PRESENTATION OF ADULT FEMALE ACNE

For reasons that are not understood, the distribution of facial acne in many adult
females differs from that seen in adolescents and in males. Many adult women
Hormonal Influences in Acne 85
note that acne localizes to the lateral face, chin, and neck (Fig. 2). Oftentimes, acne
in these women is not necessarily widespread or severe, but rather it may be
low-grade, persistent, and consist of a few isolated deep-seated tender nodules.
Many women note flares of their acne just prior to their menstrual period with
reports ranging from 27–60% to 70% of women (30–32). One study has been published
that provides quantitative documentation of acne lesion counts over the
menstrual period (33). In this study of women, who were followed over two menstrual
cycles, 63% showed a 25% increase in inflammatory acne lesions prior to the
menstrual period. Some women may feel that intermittent acne therapy prior to
their menstrual period may be beneficial. There is no evidence for this approach.
Since most acne therapy is designed to prevent the formation of lesions and since
this process often takes several weeks, it seems unlikely that intermittent therapy
would be beneficial. For this reason, it is important to have patients use their medications
consistently and to avoid spot treatment.

WHEN TO SUSPECT AN ENDOCRINE DISORDER IN ACNE PATIENTS


Although hormones influence acne, most acne patients do not have an endocrine
disorder. Hyperandrogenism should be considered in female patients whose acne
is severe, sudden in its onset, or is associated with hirsutism, or irregular menstrual
periods. Additional clinical signs of hyperandrogenism include Cushinoid features,
increased libido, clitoromegaly, deepening of the voice, acanthosis nigricans, or
androgenetic alopecia. Women with hyperandrogenism may also have insulin
resistance. They are at risk for the development of diabetes and cardiovascular
disease. It is therefore important for the long-term health of these patients to identify
hyperandrogenism so that they can receive appropriate therapy from an endocrinologist
or gynecologist.

SCREENING FOR AN ENDOCRINE DISORDER

A medical history and physical examination should be performed that is directed
toward eliciting any symptoms or signs of hyperandrogenism. Screening laboratory
tests for hyperandrogenism include a serum DHEAS, total testosterone, free testosterone,
and luteinizing hormone/follicle-stimulating hormone (LH/FSH) ratio.
These tests should be obtained apart from the time of ovulation in order to avoid
the surge of hormones associated with ovulation. From a practical standpoint, it
may be easiest to suggest that women have these tests performed either just prior
to or during the menstrual period. It is important to note that if a patient is on
oral contraceptives at the time of hormonal testing, an underlying hyperandrogenemia
may be masked. This does not occur with antiandrogens such as cyproterone
or spironolactone. Therefore, it is best that patients discontinue oral contraceptives
four to six weeks prior to the endocrine evaluation.
Excess androgens may be produced by either the adrenal gland or the ovary.
Serumlevels ofDHEAS can be used to screen for an adrenal source of excess androgen
production. Patientswith a serumDHEAS greater than 8000 ng/mL (units may differ
depending upon the laboratory)may have an adrenal tumor and should be referred to
an endocrinologist for further evaluation. Some adrenal tumorsmay also produce testosterone.
Values ofDHEAS in the range of 4000 ng/mLto 8000 ng/mLmay be associated
with congenital adrenal hyperplasia, which is most commonly due to a partial
deficiency in the 21-hydroxylase or 11-hydroxylase enzyme in the adrenal gland.

Such an enzyme deficiency results in the shunting of steroids fromthe cortisol biosynthetic
pathway into the androgen biosynthetic pathway.
An ovarian source of excess androgens can be suspected in cases where the
serum total testosterone is elevated. Serum total testosterone in the range of
150 ng/dL to 200 ng/dL or an increased LH/FSH ratio (greater than 2 to 3) can
be found in cases of polycystic ovary disease. This condition is a spectrum and is
often, but not always, associated with irregular menstrual periods, reduced fertility,
obesity, insulin resistance, or hirsutism. Greater elevations in serum testosterone
may indicate an ovarian tumor and appropriate referral should be made. In some
cases, there can be modest elevations in both DHEAS and testosterone. A serum
level of 17-hydroxypregneneolone can be obtained to discern between an ovarian
or adrenal source of androgens. If 17-hydroxypregneneolone is elevated, it indicates
an adrenal source of excess androgens, most often secondary to late onset congenital
adrenal hyperplasia. Of note is that there is a significant amount of variation in
an individual’s serum androgen levels. In cases where abnormal results are
obtained, it is recommended to repeat the test before proceeding with therapy or
a more extensive work-up.
Questions arise as to the importance of a pelvic ultrasound in the diagnosis of
polycystic ovarian syndrome. This test can be nonspecific, in that women with
normal androgens may have ovarian cysts and conversely, women with hyperandrogenism
and other findings associated with polycystic ovarian syndrome
may not have ovarian cysts at the time of pelvic ultrasound. For this reason, the
diagnosis of polycystic ovarian syndrome is more heavily based upon the serum
hormonal profile and associated clinical findings.
In the majority of women with acne, serum androgens are completely normal,
yet these women will in fact respond if treated with hormonal therapy. Studies have
shown that, as a group, women with acne may have higher levels of serum DHEAS,
testosterone, and DHT than those without acne (7,34). However, although higher,
these laboratory values may still be within the normal range. Serum levels of
DHEAS, DHT, and IGF-1 are reported to correlate positively with acne lesion
counts in women, whereas androstenedione and DHEAS correlate with lesion
counts in men (35). Reduction of serum androgens or inhibition of their action, as
obtained with oral contraceptives or antiandrogens, respectively, can lead to
improvement in acne in women with normal serum androgen levels.

OPTIONS FOR THE HORMONAL THERAPY OF ACNE IN WOMEN


Once the decision has been made to initiate hormonal therapy, the various options
to choose from include: (i) androgen receptor blockers, or antiandrogens (this class
of drugs block the effect of androgens on the sebaceous gland); (ii) inhibitors of
androgen production by the ovary or adrenal gland such as oral contraceptives
or glucocorticosteroids, respectively; or (iii) in the future, it may be possible to
inhibit the activity of androgen metabolizing enzymes in the skin or sebaceous
gland itself.

Agents that Block the Androgen Receptor

Within the class of androgen receptor blockers, therapeutic options include spironolactone,
cyproterone acetate, and flutamide. In the United States, spironolactone is
the most commonly used drug, although flutamide is also available.
Hormonal Influences in Acne 87

Spironolactone

Oral spironolactone decreases sebum excretion rate by 30% to 50%. Recommended
doses are 50 to 100 mg taken with meals (36,37). However, many women with
sporadic outbreaks of inflammatory lesions or isolated cysts respond well to
25 mg twice daily and some even respond to just 25 mg a day. These low doses
in healthy young women are generally well-tolerated. However, if this drug is
used in older women who may have other medical problems, or if higher doses
are used for conditions such as hirsutism or androgenetic alopecia, serum electrolytes
should be monitored. Side effects of spironolactone include breast tenderness
and menstrual irregularities. Additionally, it is important that pregnancy be
avoided during treatment with spironolactone due to the potential for abnormalities
of the male fetal genitalia such as hypospadias.

Cyproterone Acetate

Cyproterone acetate is available in many parts of the world, but not in the United
States. It possesses dual activity in that it serves as a progestogen in oral contraceptives
in addition to its direct inhibition of the androgen receptor. It can be given in
doses of 2 to 100 mg per day as a single agent, in which case there can be improvement
in 75% to 90% of women with acne. Cyproterone acetate, however, is most
commonly used in the form of an oral contraceptive combined with ethinyl estradiol
in varying doses (38). Numerous clinical studies support the efficacy of these
oral contraceptive preparations in women with acne.

Flutamide

Flutamide is apotent nonsteroidal antagonist of the androgenreceptor. Althoughmost
commonly used to treat prostate cancer, flutamide has been reported to be efficacious
in the treatment of acne, hirsutism, and androgenic alopecia (39). It can be given in
doses of 250 mg twice daily in combinationwith an oral contraceptive. Fatal hepatitis
has been reportedwith this drug. Liver function tests should bemonitoredand serious
consideration should be given to the risk/benefit ratio of its use in acne (40). Additionally,
because it is an antiandrogen, pregnancy issues are a concern.
Inhibitors of Adrenal Androgen Production
Another option in hormone therapy is to block the production of androgens either
by the adrenal gland or ovary, which can be accomplished through the use of lowdose
glucocorticoids or oral contraceptives, respectively.

Glucocorticoids

Low-dose glucocorticoids are most commonly used to treat patients with late onset
congenital adrenal hyperplasia, which is an inherent defect in the 21-hydroxylase
or the 11-hydroxylase enzyme. This defect causes a block in the cortisol biosynthetic
pathway, which results in a buildup of steroid precursors that are shunted into the
androgen biosynthetic pathway. Low-dose prednisone (2.5 to 5 mg a day, at bedtime)
can be used. Low doses of dexamethasone can also be used, but the risk of adrenal
suppression is higher. To ascertain if therapy with glucocorticoids is having the
desired effect, serum DHEAS can be monitored for a decrease or normalization of
the level of DHEAS. To check for adrenal suppression, an adrenocorticotrophin
hormone (ACTH) simulation test can be performed. This consists of injecting
88 Thiboutot
ACTH and assessing the plasma cortisol 30 minutes later. If plasma cortisol has risen
by an appropriate amount, the adrenal gland is not suppressed.

Inhibition of Ovarian Androgen Production

Gonadotropin-Releasing Agonists

Androgen production in the ovary can also be blocked by gonadotropin-releasing
hormone agonists such as buserelin, nafarelin, or leuprolide. These gonadotropinreleasing
agonists block ovulation by interrupting the cyclic release of FSH and LH
fromthe pituitary. These drugs are efficacious in acne and hirsutism, and are available
as injectable drugs or nasal spray. However, in addition to suppressing the production
of ovarian androgens, these drugs also suppress the ovarian production of estrogens,
thereby eliminating the function of the ovary. Thus, the patient could develop menopausal
symptoms and suffer from hypoestrogenism. Headaches can also develop, as
well as the occurrence of bone loss, due to the reduction in estrogen.

Oral Contraceptives

Oral contraceptives generally contain an estrogen (most commonly ethinyl estradiol)
and a progestin. In their early formulations, oral contraceptives contained
over 100 mg of estrogen. In these and higher doses, estrogens themselves can suppress
sebum production. Estrogens also act on the liver to increase the synthesis of
sex hormone-binding globulin that binds testosterone and lowers the circulating
levels of free testosterone. In addition, oral contraceptives inhibit the ovarian production
of androgens by suppressing ovulation. This, in turn, decreases serum
androgen levels and reduces sebum production. The concentrations of estrogen
in oral contraceptives have decreased over the years from 150 to 35 mg, and in
the most recent forms, to 20 mg, in order to reduce the side effects associated
with estrogen (41). Oral contraceptives containing low doses of estrogen are
listed in Table 1.

Progestins

The progestins contained in oral contraceptives include estranges and gonanes,
which are derivatives of 19-nortestosterone, cyprotereone acetate, and a novel progestin,
drosperinone. Members of the estrane and gonane class of progestins
(Table 2) can cross-react with the androgen receptor, which can lead to increased
androgenic effects and could aggravate acne, hirsutism, or androgenic alopecia.
These progestins can also cause changes in lipid metabolism and can increase
serum glucose, leading to glucose intolerance, as well as possibly interfering with
the beneficial effect of estrogen on the sex hormone-binding globulin. However,
the third generation progestins, including norgestimate, desogestrel, and gestodene,
are more selective for the progesterone receptor rather than the androgen
receptor. The biological relevance of these differences, however, is uncertain. For
TABLE 1 Oral Contraceptives Containing Low Doses of Estrogen
Ethinyl estradiol 20 mg/Levonorgestrel 0.1 mg (AlesseTM)
Ethinyl estradiol 20, 10 mg/Desogestrel 0.15 mg (MircetteTM)
Ethinyl estradiol 20, 30, 35 mg/norethindrone 1.0 mg (Estrostepw)
Ethinyl estradiol 20 mg/norethindrone acetate 1.0 mg (Lo-Estrinw 1/20)
Ethinyl estradiol 20 mg/drospirenone 3.0 mg (YazTM)

Hormonal Influences in Acne


For years, it has been known that almost all oral contraceptives are beneficial in the
treatment of acne (42). It is possible that some women are more sensitive to the
androgenic effects of a progestin, but it is more likely that the effect of progestin
may be offset by estrogen. All oral contraceptives, regardless of the type of progestin,
will inhibit serum androgen levels. Moreover, although some progestins might
be more androgenic than others, there is an increase in sex hormone-binding globulin
with the use of any oral contraceptives and an improvement of the acne in
women who are treated with them.
Drospirenone is a novel progestin that is derived from 17a-spironolactone. It
possesses antiandrogenic and antimineralocorticoid activity, which can be of
benefit in androgenic-related conditions such as acne and hirsutism and in the
estrogen-related fluid retention associated with some oral contraceptives (43).

ORAL CONTRACEPTIVES STUDIED IN ACNE


Many oral contraceptives have been studied in the treatment of acne (Table 3).
These include those containing ethinyl estradiol in combination with cyproterone
acetate (Diane, Dianette), ethynodiol diacetate (Demulen), levonorgestrel
(TriPhasil, Alesse), norgestimate (Ortho Tri-Cyclenw), desogesterel (Desogen),
and drosperinone (Yasmin, Yaz). Numerous studies point to the efficacy of
ethinyl estradiol/cyproterone acetate oral contraceptives (Diane and Dianette) in
the treatment of acne. Reductions in inflammatory lesion count on the order of
50% to 75% have been reported (44,45). Two large studies involving a total of
approximately 500 women with moderate acne were conducted with ethinyl
estradiol 35 mg/norgestimate (Ortho Tri-Cyclen). Improvement in inflammatory
lesions, total lesions, and global assessment was noted with this oral contraceptive
after six months of treatment (46,47). There was a 50% to 60% improvement in
inflammatory lesions. Decreases in serum free testosterone and an increase in sex
hormone-binding globulin were noted in the active group. Two large, six-month,
placebo-controlled trials (350 and 371 women, respectively) were conducted

TABLE 2 Progestins: 19-Nortestosterone Derivatives
Estranes Gonanes
Norethindrone Norgestrel
Norethindrone acetate Levonorgestrel
Ethynodiol diacetate Desogestrel
Gestodene
Norgestimate

TABLE 3 Oral Contraceptives Studied in Acne
Demulen (ethinyl estradiol 35 mg/ethynodiol diacetate)
Diane, Dianette (ethinyl estradiol 50, 35 mg/cyproterone acetate)
Estrostep (ethinyl estradiol 20, 25, 30 mg/norethindrone)
Alesse (ethinyl estradiol 20 mg/levonorgestrel)
Ortho Tri-Cyclen (ethinyl estradiol 35 mg/norgestimate)
Desogen (ethinyl estradiol 30 mg/desogestrel)
Yasmin (ethinyl estradiol 30 mg/drospirenone)
Yaz (ethinyl estradiol 20 mg/drospirenone)
Triphasil (ethinyl estradiol 30 mg, 40 mg/levonorgestrel)
90 Thiboutot
using ethinyl estradiol 20 mg/levonorgestrel (Alesse) in the treatment of acne
(48,49).

In each study, the oral contraceptive demonstrated significantly greater
reduction in acne lesion counts and improvement in global assessment scores compared
with placebo. The reduction in inflammatory lesion count was on the order of
47%. A study of 128 women with mild-to-moderate acne compared the efficacy of
ethinyl estradiol 30 mg/drospirenone (Yasmin) and ethinyl estradiol 35 mg/cyproterone
acetate (Diane-35) in the treatment of acne for nine cycles (50). Both treatments
produced comparable reductions in acne lesion counts, with an
approximate 60% reduction in inflammatory lesion count. Both treatments also
reduced sebum production and yielded comparable increases in sex hormonebinding
globulin. Two large placebo-controlled studies involving a total of approximately
593 women with moderate acne, found improvement in inflammatory
lesions, total lesions, global assessment, and quality of life in women who were
treated for six months with a triphasic oral contraceptive that contains doses of
20 to 35 mg of ethinyl estradiol in combination with 1.0 mg norethindrone acetate
(Estrostep) (51). In these studies, inflammatory lesion counts were reduced by
approximately 47% (51).
Oral contraceptives that have been approved for the treatment of acne in the
United States include ethinyl estradiol 35 mg/norgestimate (Ortho Tri-Cyclen)
ethinyl estradiol 20 to 35 mg/norethindrone acetate (Estrostep), and ethinyl estradiol
20 mg/drospirenone (Yaz).

ORAL CONTRACEPTIVES AND ANTIBIOTICS

The concern regarding oral contraceptives and antibiotics is essentially theoretical,
owing to the action of broad-spectrum antibiotics, which reduce the gut flora bacteria
and thus may result in decreased absorption of estrogen. This could lead to a
possible reduction in the efficacy of oral contraceptives, although pharmacokinetic
studies suggest that serum levels of estrogen are unaffected by antibiotics such as
tetracycline, doxycycline, and others (52,53). Nevertheless, there have been very
few reports in the literature of pregnancies associated with the use of antibiotics
in conjunction with oral contraceptives (54,55). Existing reports have focused on
tetracycline, and the incidence was 1.2 to 1.4 pregnancies/100 woman years of
use of the oral contraceptive. These data are no greater than the background
failure rate of oral contraceptives (54,55).

NEWER FORMS OF CONTRACEPTIVES

Recently, newer forms of contraceptives have been developed, such as contraceptive
patches, vaginal rings, and injectable combination hormones. Each of these is
designed to suppress ovulation and in this regard will lower the ovarian production
of androgens. As of yet, these formulations have not been studied in the treatment
of acne. The contraceptive patch (Ortho Evra) contains 20 mg of ethinyl estradiol
and 150 mg of the progestin, norelgestromin. The patch is worn for three weeks
and removed for one week, during which time menstrual bleeding will occur.
The advantages of this formulation are better patient compliance, dosing that is
not affected by gastrointestinal disturbances, and more consistent serum levels of
estrogen serum levels compared to oral dosing (56). The vaginal ring (NuvaRing)
is a contraceptive vaginal ring that releases 15 mg of ethinyl estradiol and 120 mg
of the progestin, etonogestrel. It is placed within the vagina for three weeks and
removed for one week. In one study, the incidence of irregular bleeding was less
compared with an oral combination contraceptive (57). An injectable combination
of estradiol cypionate and medroxyprogesterone acetate (Lunelle) has been developed.
This is given as a monthly contraceptive injection. Contraceptive efficacy was
shown to be comparable to a triphasic oral contraceptive containing ethinyl estradiol
and norethindrone (Ortho 7/7/7) (58).

APPROACH TO HORMONAL THERAPY IN FEMALE ACNE

Hormonal therapy is an excellent option for treatment of women whose acne is not
responding to conventional therapy. If there are signs of hyperandrogenism, an
endocrine evaluation is indicated, consisting of tests such as DHEAS, total- and
free-testosterone, and an LH/FSH ratio. Although hyperandrogenism is an indication
for hormonal therapy, women with normal serum androgen levels also
respond well to treatment. The mainstays of hormonal therapy include oral contraceptives
and spironolactone. Other agents to choose from include cyproterone
acetate, flutamide, and glucocorticoids. Hormonal agents work best as part of a
combination regimen including topical retinoids or topical or oral antibiotics
depending upon the severity of the acne. In some women, the additional of hormonal
therapy has improved acne to the point where subsequent treatment with isotretinoin
was no longer necessary. As more is learned about the hormones involved
in acne, their source of production and the mechanisms by which they influence
sebaceous gland growth and sebum production, new opportunities will arise for
the development of novel therapies aimed at the hormonal aspects of acne.

ABSTRACT TAKEN FROM:ACNE AND ITS THERAPY,EDITED BY GUY F. WEBSTER,ANTHONY V. RAWLINGS

[Yankulov]

Very useful info. Can you find some scientific information about teenage hormonal acne? Do you thing "Acne and its therapy" contains some sort of information about teens acne?

[jokerj]

great info!
yes, id liek to know about teenage acne and hormones as well

[sowet]

That info is all great but WHY THE HELL ARE ONLY WOMEN TREATED FOR HORMONAL ACNE.!!!!! I AM A GUY AND I BET MY HORMONES ARE WHACK!!! YET EVERYWHERE ON THIS FORUM PEOPLE COORELATE HORMONAL ACNE TO WOMEN!!!!! ANYONE GOT ANY SUGGESTIONS?!>!!?!? (yes the caps was necessary I am very angry and upset).

[bryan]

That info is all great but WHY THE HELL ARE ONLY WOMEN TREATED FOR HORMONAL ACNE.!!!!!

Because men who use systemic antiandrogens and/or estrogens will get nasty side effects.

.

[radikal]

That info is all great but WHY THE HELL ARE ONLY WOMEN TREATED FOR HORMONAL ACNE.!!!!! I AM A GUY AND I BET MY HORMONES ARE WHACK!!! YET EVERYWHERE ON THIS FORUM PEOPLE COORELATE HORMONAL ACNE TO WOMEN!!!!! ANYONE GOT ANY SUGGESTIONS?!>!!?!? (yes the caps was necessary I am very angry and upset).

how will you like your man tits, hmmm?
Someone who posted on this forum a few months ago had in fact gone through a sex change, partly due to acne.

[sie]

Has anyone ever had a look at this:

Fisher DA. Desideratum dermatologicum—cause and control of premenstrual acne flare. Int J Dermatol. 2000;39:334-336


I don't know if it would be interesting or not, because I don't have access to see it online. Any avid researchers out there had a peak and willing to give a briefing???

THX!

[jokerj]

Has anyone ever had a look at this:

Fisher DA. Desideratum dermatologicum—cause and control of premenstrual acne flare. Int J Dermatol. 2000;39:334-336


I don't know if it would be interesting or not, because I don't have access to see it online. Any avid researchers out there had a peak and willing to give a briefing???

THX!

i'd love to know about this as well!

[Choof_Chomper]

DHT is the main factor causing acne. People with acne have higher levels of dht and theoretically lower levels of regular testosterone since testosterone and other steroid hormone derivatives have certain anabolic/androgenic ratios. This is also probably why people with acne tend to be more skinny and have a harder time inducing muscular hypertrophy to a large extent because they possess lower amounts of anabolic(tissue-building) hormones. Although androgens are somewhat synergistic with anabolics and influence anabolism to some extent. DHT also causes body hair, voice deepening, high sex drive and increased aggressiveness in humans.

[jokerj]

i wonder if theres a way to lower all the effects of dht without lowering the sex drive...

[Choof_Chomper]

i wonder if theres a way to lower all the effects of dht without lowering the sex drive...

when you figure that one out let me know LOL

[bryan]

i wonder if theres a way to lower all the effects of dht without lowering the sex drive...

Keep in mind that a big study from a couple of years ago found no beneficial effect on acne from suppressing the DHT in sebaceous glands.

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[Choof_Chomper]

i wonder if theres a way to lower all the effects of dht without lowering the sex drive...

Keep in mind that a big study from a couple of years ago found no beneficial effect on acne from suppressing the DHT in sebaceous glands.

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lol DHT isnt found in sebaceous glands its a circulating androgen that is largely responsibe for sebaceous activity.

[bryan]

lol DHT isnt found in sebaceous glands its a circulating androgen that is largely responsibe for sebaceous activity.

LOL! DHT sure as hell IS found in sebaceous glands! For your information, sebaceous glands are rich in the 5a-reductase type 1 enzyme, and they have plenty of DHT. You need to start doing a bit of research before talking about things you know nothing about.

Here's another little tidbit of information for you: there's some good scientific evidence indicating that circulating DHT (DHT in the bloodstream, in other words) doesn't play much of a role as an endocrine hormone. It's mainly LOCALLY GENERATED DHT which has an androgenic effect on sebaceous glands, hair follicles, etc. If you wish, I can go over the evidence supporting that view, but you really need to start researching this stuff yourself.

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[Choof_Chomper]

lol DHT isnt found in sebaceous glands its a circulating androgen that is largely responsibe for sebaceous activity.

LOL! DHT sure as hell IS found in sebaceous glands! For your information, sebaceous glands are rich in the 5a-reductase type 1 enzyme, and they have plenty of DHT. You need to start doing a bit of research before talking about things you know nothing about.

Here's another little tidbit of information for you: there's some good scientific evidence indicating that circulating DHT (DHT in the bloodstream, in other words) doesn't play much of a role as an endocrine hormone. It's mainly LOCALLY GENERATED DHT which has an androgenic effect on sebaceous glands, hair follicles, etc. If you wish, I can go over the evidence supporting that view, but you really need to start researching this stuff yourself.

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calm down mr. squiggles. first of all androgen receptors are located in non tissue specific areas. yes that means the skin as well. in fact areas like the hair, prostate and skin which convert testosterone to DHT experience up to 3 times as much androgenicity as muscle tissue itself.endocrine relates to hormone secretion- testosterone and dht are hormones so obviously they wouldnt signal themselves to self-release lol. I also wouldnt be accusing others of not knowing anything especially when they tell you the basic mechanism of acne.

[bryan]

endocrine relates to hormone secretion- testosterone and dht are hormones so obviously they wouldnt signal themselves to self-release lol.

Find a good book on biology (preferably one focusing on endocrinology), and find out what the difference is between an ENDOCRINE hormone and an AUTOCRINE hormone. DHT is considered to be more of an autocrine hormone, meaning that it has an androgenic effect mainly in the tissues where it's actually generated. The relatively smaller number of DHT molecules which make it into the bloodstream are excreted fairly rapidly, which is part of the explanation for why it doesn't have much of an endocrine effect.

Other than that one sentence, the rest of what you wrote has no relevance to what we were discussing.

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[Choof_Chomper]

endocrine relates to hormone secretion- testosterone and dht are hormones so obviously they wouldnt signal themselves to self-release lol.

Find a good book on biology (preferably one focusing on endocrinology), and find out what the difference is between an ENDOCRINE hormone and an AUTOCRINE hormone. DHT is considered to be more of an autocrine hormone, meaning that it has an androgenic effect mainly in the tissues where it's actually generated. The relatively smaller number of DHT molecules which make it into the bloodstream are excreted fairly rapidly, which is part of the explanation for why it doesn't have much of an endocrine effect.

Other than that one sentence, the rest of what you wrote has no relevance to what we were discussing.

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and what was the point of stating where dht is generated? no relevance either. I can generate it in my anus and it could still cause acne if there were sebaceous glands there

[bryan]

and what was the point of stating where dht is generated? no relevance either. I can generate it in my anus and it could still cause acne if there were sebaceous glands there

The point of stating where DHT is generated was to refute your claims that systemic DHT (in the bloodstream, in other words) affects sebaceous glands, and that there is no DHT in sebaceous glands. You need to learn that (1) sebaceous glands are rich in 5a-reductase type 1, hence DHT; and (2) DHT mainly affects the cells where it is generated; which explains why (3) the DHT which _does_ affect sebaceous glands is the DHT generated within those same sebaceous glands. Do you understand now?

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[Choof_Chomper]

The point of stating where DHT is generated was to refute your claims that systemic DHT (in the bloodstream, in other words) affects sebaceous glands, and that there is no DHT in sebaceous glands. You need to learn that (1) sebaceous glands are rich in 5a-reductase type 1, hence DHT; and (2) DHT mainly affects the cells where it is generated; which explains why (3) the DHT which _does_ affect sebaceous glands is the DHT generated within those same sebaceous glands. Do you understand now?

do you know how DHT is formed? tesosterone from the gonads and adrenals secreted into the bloodstream enter the sebaceous glands and bind to the 5a-reductase enzyme that converts it to DHT. then this binds to the androgen receptors. you need testosterone in the bloodstream to be able to generate DHT. its fully dependant on it

[bryan]

do you know how DHT is formed? tesosterone from the gonads and adrenals secreted into the bloodstream enter the sebaceous glands and bind to the 5a-reductase enzyme that converts it to DHT. then this binds to the androgen receptors. you need testosterone in the bloodstream to be able to generate DHT. its fully dependant on it

That's correct. You got it exactly right this time!

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