Hormone Treatment in
Transsexuals
Henk Asscheman, MD
and Louis J.G. Gooren, MD
Henk Asscheman and
Louis J.G. Gooren are both affiliated with the Division of
Andrlogy/Endocrinology, Free University Hospital, Amsterdam. Please send all
correspondence to: Professor Louis J.G. Gooren, Free University Hospital, P0.
Box 7057, 1007 MB Amsterdam, the Netherlands.
© 1992 by The Haworth
Press, Inc. All rights reserved.
INTRODUCTION
Except for the sex
chromosomes and gonads all bodily differences between men and women must be
attributed to the actions of sex hormones. While the inherent tendency of the
prenatal human organism is to develop along female lines, prenatal
differentiation as a male depends on testicular hormones (Mullerian-inhibiting
hormone and testosterone and its derivates). The wider bony pelvis in girls in
comparison with boys, is probably dependent on local effects of prenatal
ovarian estrogen production. There is no known fundamental difference in
sensitivity to the biological action of sex steroids on the basis of the
genetic patterns of 46,XY and 46,XX.
The prepubertal period
is hormonally relatively quiescent (Conte, Grumbach, Kaplan & Reiter,
1980). The hormones of puberty accentuate sex differences. Testosterone and its
potent derivate 5alpha-dihydrotestosterone (DHT) induce penile growth and
secondary sex characteristics as sexual hair, deepening of the voice, a
muscular build and the greater average height in males in comparison to the
females. In girls, estrogens in conjunction with progestagens induce breast
formation and a fat distribution predominantly around the hips; subcutaneous
fat padding produces a softness of the body configuration and of the skin. The
skin in women is further generally less oily than in men; the latter on the
basis of activation of the sebaceous glands by androgens.
Fundamental to sex
reassignment treatment is the acquisition to the fullest extent possible of the
sex characteristics of the other sex. With the exception of the internal and
external genitalia, these characteristics are contingent of the biological
effects of the respective sex steroids. Therefore (semi)synthetic sex steroids
are indispensable tools in sex reassignment treatment. The use of cross-gender
hormone treatment is associated with a better outcome (Hamburger, 1969; Leavitt
et al., 1980).
The "two year
real-life test" (Money & Ambinder, 1978) is pivotal in
diagnostic-therapeutic approach of gender dysphoria. It allows both the
gender-dysphoric subject and the psychologist/physician to examine whether sex
reassignment relieves the burden of gender dysphorla. The emerging physical
changes associated with cross-gender sex hormone treatment will facilitate the
assumption of the role as a member of the other sex both in private life and in
society.
The attempt to induce
cross-gender sex characteristics in transsexuals-generally biologically
normally differentiated males and females in their adult years-can be
subdivided into two aspects:
1. Annihilation of sex characteristics of
the original sex.
2. Induction of sex characteristics of the
sex one reckons oneself to belong to.
1. Unfortunately, the
annihilation of sex characteristics of the original sex is incomplete. In
male-to-female transsexuals, there is no mode of treatment to revert earlier
effects of androgens on the skeleton. The greater height, the shape of the
jaws, the size and shape of the hands and feet, and the narrow width of the
pelvis can not be redressed once they have reached their final size at the end
of puberty. Conversely, the relative lower height in female-to-male
transsexuals (in the Netherlands an average of 12 cms) and the broader hip
configuration will not change under the influence of hormonal treatment.
2. While in the
majority of female-to-male transsexuals, a complete and inconspicuously
masculine development can be induced with androgenic hormones, the effects of
feminizing hormone treatment in male-to-female transsexuals can be objectively
unsatisfactory with regard to reduction of male-type of facial/beard hair and
induction of breast development.
Transsexuals often
expect and sometimes demand rapid and complete changes immediately after the
start of the hormonal therapy. The induced effects of cross-sex hormones are,
however, limited and appear only gradually. Before starting hormone treatment a
clear discussion of the possible changes and the limits in an individual
patient, is indispensable in order to prevent unrealistic expectations. In the
next and following sections we describe the effects of cross-gender hormones
separately for male-to-female and female-to-male transsexual subjects.
Which Hormones and
Which Dose?
For each of the above
mentioned aspects of hormone treatment exists a large array of (semi) synthetic
sex steroids. There are no solid literature data to prove certain hormonal drugs
superior in efficacy to others. Only two published studies give an indication
of the value of different hormone schedules in the treatment of transsexuals,
but the results are far from conclusive (Meyer et al., 1981 & 1986). The
choice of hormonal drugs in the treatment of transsexualism depends on
availability (national regulations, pharmaceutical marketing), local
traditions, side effects, route of administration, cost and folk belief (in
particular from the side of the transsexual subject and his/her peer group, but
also from the physician). Optimal dosages of these drugs have not yet been
established.
The first effects of
the cross-gender sex hormones appear already after 6 to 8 weeks (Futterweit,
1980). Voice changes in female-to-male transsexuals and the development of
painful breast noduli in male-to-female transsexuals are the first
manifestations. Thereafter the changes take over 6 to 24 months and even longer
before they are complete (beard growth may take 4 to 5 years in
androgen-treated female-to-male transsexuals).
Cross-Sex Hormone
Treatment in Male-to-Female Transsexuals
Annihilation of Male
Characteristics
In male-to-female
transsexuals suppression of the original sex characteristics can be obtained by
compounds that exert directly or indirectly an antiandrogenic effect. Androgens
are for their production dependent on stimulation by the pituitary hormone
luteinizing hormone (LH) which, in turn, is stimulated by the hypothalamic
hormone luteinizing hormone-releasing hormone (LHRH). The biological action of
androgens is contingent on their interaction with hormone receptors in the
body's tissue cells. Interference with any of these mechanisms will lead to a
decline of the biological action of androgenic hormone. Some of the drugs that
will be listed have a dual action in this respect (Table 1).
TABLE 1. Hormones
Used in Cross-Gender Hormone Treatment of Transsexualism
Antiandrogens:
LHRH analogues leuprorelin Lucrin depotR 3.75 mg/months s.c.
triptorelin Decapepty1-CRR 3.75 mg/months i.m
Interference with
testosterone or DHT production:
spironolactone
AidactoneR 100-200 mg/day p.o.
finasteride
not registered
flutamide
EulexinR 250 mg t.i.d., p.o.
Antlgonadotroplc: cyproterone acetate AndrocurR 100-150
mg/day p.o.
medroxyprogesterone
proveraR 5-10 mg/day p.o.
Depo-ProveraR
150 mg/month i.m.
FarlutaiR
5-10 mg/day p.o.
Farlutal
depotR 100 mg/month i.m.
Androgenreceptor
blockers:
cyproterone
acetate AndrocurR 100-150 mg/day p.o.
nilutamide
AnandronR 300 mg/day p.o.
spironolactone
AldactoneR 100-200 mg/day p.o.
Estrogens:
ethinyl
estradlol LynoraiR 100 µg/day p.o.
conjupted
estrogens premarinR 5-10 mg/day p.o.
17ß
estradlol progynovaR 2-4 mg/day p.o.
Progynon
depotR 10 mg/2 weeks to 100
mg/month i.m.
Estraderm
TTSR 50-100 µg/day tramdermally
estriol
SynapauseR 4-6 mg/day p.o.
Androgens:
testosterone
esters TestoylronR 250 mg/2 weeks 1.m.
sustanonR
250 mg/2 weeks i.m.
testosterone
undecanoate AndrinlR 160-240 mg/day p.o.
1. Suppression of
gonadotropins (the pituitary hormones) that stimulate testicular and ovarian
hormone production can be achieved by LHRH analogues: triptorelin and
leuprorelin 3.75 mg/4 weeks are available as injectables. Their cost is
prohibitive; a major side effect is hot flashes of the type that postmenopausal
women experience. There is no reported experience with these drugs in
transsexuals. Also cyproterone acetate, progestagens and high dose estrogens
suppress gonadotropins by their negative feedback action. Progestagens are
available in the form of medroxyprogesterone acetate (ProveraR) as a parenteral
drug (150 mg/6 weeks) or oral drug (5-10 mg/day). They probably also interfere
with the androgen receptor.
2. interference with
the production of testosterone or its conversion to the potent metabolite
5alpha-dihydrotestosterone (DHT) can be exercised by drugs like spironolactone
(AldactoneR) 100-200 mg/day. Finasteride is a potent 5 alpha-reductase
inhibitor preventing the conversion of testosterone to DHT and therewith
reducing its biological effect.
3. Drugs that
interfere with receptor binding of androgens (or in the future with
postreceptor mechanisms) have been used success-fully. Cyproterone acetate
(AndrocurR) 100 mg/day orally or 300 mg/month intramuscularly and less
effectively medroxyprogesterone acetate have also antigonadotropic action. The
"pure" antiandrogens nilutamide (AnandronR) 300 mg/day and flutamide
(Eulexin 250 mg, three times a day) are potent drugs. They are less suited as
monotherapy since by their interference with the negative feed-back action of
androgens, they stimulate gonadotropin production and subsequently androgen
production. Spironolactone has also receptor-blocking properties.
Of all the above
drugs side-effects have been reported. Some are inherent in the interference
with the biological action of androgens like a reduction of muscle mass and
power and of the hemoglobin content. Some patients will complain of loss of
energy and vitality to straightforward depression. The antiandrogen we have
extensively used is cyproterone acetate (100mg/day). Side effects encountered
are those mentioned above. Our alternative drug is spironolactone. Several
studies have demonstrated its efficacy in transsexuals and in hirsute women
alike. It has also an antihypertensive effect, since the drug was designed as a
diuretic.
We have limited
experience with nilutamide and LHRH antagonists. Medroxy-progesterone acetate
has been widely used in the USA also in sex offenders. It is a satisfactory
drug also in the view of the mild side effects and the costs. A randomized
double-blind clinical trial to establish the best suited antiandrogen compound
in transsexuals has not been performed so far.
Following orchiectomy
we try to reduce or terminate antiandrogen therapy. Sexual hair growth is
clearly dependent on androgens for its initiation and it would be logical to
believe that antiandrogens are redundant following orchiectomy. Though not
verified by research data, patients claim that also after orchiectomy their
sexual hair growth is still reduced by antiandrogens. Due to the much shorter
life cycle of sexual hair on the trunk, arms and legs as compared to the face
and the greater density of hair follicles in the beard area, beard growth is
not reduced to a cosmetically acceptable degree by antiandrogens. Other
measures like depilation by electrolysis are needed. Those subjects who are
young enough to have no significant beard development or whose racial
background provides them with little or no beard development, are not in need
of antiandrogens for this purpose.
Induction of Female
Characteristics
The principal
feminizing hormones are estrogens. Estrogens alone can induce most typical
female characteristics as has been shown in cases of Turner syndrome in which
the ovaries fall to produce hormones. A second sex steroid produced by the
ovaries is progesterone. It prime function is to prepare the uterine mucosa for
nidation. Its feminizing effect is probably limited, but effects of breast
tissue have been described. Meyer et al. (1986) found no difference in breast
hemicircumference between male-to-female transsexuals who had used estrogens
only and those who had used both estrogens and progestagens, but this study was
not a randomized double-blind clinical investigation.
It has been suggested
that "unopposed action of estrogens" (by progestagens) would
constitute a risk factor for carcinomas of the breast and there are
epidemiological data in support of this. On the other hand studies in users of
oral contraceptives have suggested that progestagens play a role in breast
cancer development, though oral contraceptives overall are associated with a
reduced risk of breast cancer. Three cases of breast carcinomas in
male-to-female transsexuals have been published but it is difficult to arrive
at statistically reliable conclusions on risks since the total number of users
is unknown and no data are available on what estrogens and how long these three
subjects have been taking this medication. Of note is the fact that breast
carcinomas have not been observed in men with prostatic carcinoma taking high
doses of estrogens but the follow-up may have been too short in view of their
lethal disease. Male-to-female transsexuals should be informed about this risk
factor. As with the general female population, they should receive information
on self-examination of their breasts. At medical checkups their breasts should
be physically examined and if palpation is suspect, mammography and eventually
biopsy should follow. The fact that transsexuals have often breast implants may
impede physical (self)examination of the breast. In our population of more than
500 hormonally treated male-to-female transsexuals (follow-up 0-20 years with
an estimated median of 6.5 years) we have not come across a case of breast
carcinoma.
In terms of
estrogenic effects there is no superior estrogen. The choice depends mainly on
availability, costs and the preference of the subject. Careful clinical studies
on side effects in the form of randomized double-blind placebo-controlled
studies with different estrogens are non-existent. The chemical formula and the
route of administration lead to substantial differences in characteristics of
estrogenic drugs. All oral estrogens first pass the liver after intestinal
absorptidn and exert an effect on liver metabolism, evidenced by their effects
on lipids, clotting factors and renin The liver metabolism of estrogen is also
related to the chemical formula of the estrogen. Ethinyl estradiol is slowly
metabolized whereas l7beta-estradiol is broken down rather rapidly, explaining
the 10-20 fold difference in daily dosage. Concomitant drug use
(anti-epileptics) may induce a more rapid metabolism of estrogens.
1. Ethinyl estradiol
(LynoralR), 50 µg orally twice (or more) daily, is the most potent estrogenic
drug. It is a chemical modification of 17ß-estradiol, the main estrogen of the
body, and it is slowly metabolized by the liver, but has a large effect on
other metabolic pathways in the liver. It is very cheap, easily available
worldwide and often used by male-to-female transsexuals because it can be
obtained from women friends or without prescription in many countries as the
oral contraceptive pill (always combined with progestagens). In the current
estradiol assays its presence is not measured but the resulting suppression of
gonadotropins suggests its use. A specific assay for ethinyl estradiol is
commercially available.
2.
"Natural" estrogens, which are not natural but metabolized estrogens
from other species (pregnant mare urine) are more appropriately called
conjugated estrogens (PremarinR and other brands). Active dose in
postmenopausal women is 0.625-1.25 mg, but for cross-gender hormone therapy the
active dose is 5-10 mg (Meyer et al., 1986). They are largely metabolized at
first liver passage. It is said that they have less side effects than other
estrogens. However, the supporting scientific evidence is very weak and in
trials of secondary prevention of myocardial infarction in men, conjugated
estrogens in a dose of 2.5 and 5 mg orally per day are clearly associated with
an increased risk of thrombosis. Paradoxically, low doses appear to reduce the
risk of cardiovascular disease in postmenopausal women.
3. 17ß-Estradiol (or
in short estradiol) is the most potent of the three forms of native estrogens
in the human body. It is produced synthetically and can be administered orally
(progynovaK, EstrofemR, ZumenonR 2-4 mg per day) metabolized in great part at
first liver passage, intramuscularly (progynon-DepotR 20-200 mg per month) or
transdermally (Estraderm TI'SR 100 µg, patches are replaced twice weekly). In
particular, this latter form is very promising because of its low number of
estrogen-induced side effects.
However, its efficacy
in cross-gender hormone treatment has not been fully determined (a study is in
progress at our clinic). A considerable number of patients (±10%) have skin
problems at the application site and its sticking qualities can be a problem in
patients that perspire easily or in a hot climate. Another obstacle is the
price (US$ 1.00 per day), it is the most expensive estrogen therapy.
4. Estriol (Synapause
E3R, OvestinR 2-6 mg orally per day) is a less potent native estrogen that is
used in postmenopausal women for atrophic vaginitis and for urinary problems.
In cross-gender hormone treatment high doses are necessary and estriol has no
advantages over estradiol for this indication.
In our clinic ethinyl
estradiol 100 µg orally per day has been the standard treatment for all
male-to-female transsexuals until recently. With the introduction of
transdermal estrogen we have changed our policy because of the frequent
occurrence of thromboembolism in patients over 40 years of age (12%, Asscheman,
Gooren & Eklund, 1989). All new male-to-female transsexuals older than 40
years are treated with Estraderm TTSR 100 µg two patches per week from the
start. Younger patients are offered the same possibility but they are informed that
their risk of thromboembolism is much lower (2.1%) and ethinyl estradiol 100 µg
is proposed as an alternative. Intramuscular estrogen depots are not routinely
given for two reasons. First, in case of side effects, not infrequent with
estrogen therapy, it can take weeks before the serum levels of estradiol have
normalized and second, male4o-female transsexuals tend to abuse estrogens under
the wrong assumption "the more the better." We have seen subjects who
used 800 mg progynon~DepotR, intramuscularly, per week with sometimes serious
side effects (Gooren, Assies, Asscheman, de Slegte & van Kessel, 1988).
With oral administration abuse is also not uncommon, but the doses are not so
extreme.
After sex
reassignment surgery we try to reduce the dose to a minimum that produces no
clinical symptoms of sex hormone deficiency, but no lower than the minimum dose
that protects against osteoporosis. In postoperative patients all kinds of
estrogen substitution therapy are used depending on the personal preference of
the transsexual patient and the lack of clinical symptoms of estrogen
deficiency or side effects. Practically, this is similar to the estrogen
treatment of postmenopausal women with some advantages: there is no need for
progestagens and no risk of endometrial carcinoma.
Cross-Sex Hormone
Treatment in Female-to-Male Transsexuals
Annihilation of
Female Characteristics
The effects of
estrogens on physical characteristics cannot be annihilated by antihormones.
Antiestrogens administered to eugonadal women stimulate gonadotropin and
subsequently ovarian hormone secretion. Theoretically, LHRH antagonists could
be used. The objections have been mentioned earlier.
Transse~uals very
much appreciate that their menstrual periods are terminated. This can be
accomplished by progestagens with their antigonadotropic properties:
medroxyprogesterone acetate (ProveraR, FarlutaiR) 5 mg 1 ~ 2 tablets/day or 150
mg intramuscularly/3 months, lynesterol (OrgametrjiR) 5 mg or norethisterone
(Primolut NR) 5 mg both 1 or 2 tablets/day. Androgens to be discussed in the
next section have in high dosages also antigonadotropic action. There is no
clear advantage in the combination of the two hormones unless androgens alone
suppress menstrual bleeding in-sufficiently.
Induction of Male Characteristics
Androgens exert a
powerful effect on the virilization process but completion may take as long as
24 years and sometimes even longer. The individual outcome depends on genetic
factors both familial and racial. The degree of hairiness of siblings is a fair
predictor of the virilization process.
To be used are
testosterone esters 200-250 mg/2 weeks intramuscularly. Their brand names vary
from place to place (SustanonR, TestovironR). As oral androgens testosterone
undecanoate can be mentioned (AndriolR) 160-240 mg/day, not available in the
USA. With the latter preparation, menstrual bleeding is insufficiently
suppressed in 50% of the patients and addition of a progestagen is required.
The use of oral androgens with an alkyl group in the 17a position of the
molecule is obsolete due to its hepatotoxicity. Oral androgens as mesterolone
and fluoxymesterone are too weak for the induction of virilization.
In approximately
50-60% of the female-to-male transsexuals acne will occur. In 10-15% it is rather
serious requiring dermatological treatment. It is now certain that androgen
treatment has an unfavorable effect on the lipid profile. It places
female-to-male transsexuals in the risk category of men. Therefore they must be
advised not to smoke, to exercise moderately and to prevent over-weight and
high blood pressure.
Effects of
Cross-Gender Hormones in Male to-Female Transsexuals
Annihilation of the
male pattern is possible for a number of secondary sex characteristics but only
to a limited extent. Reduction of androgen-dependent hair growth with
cyproterone acetate and ethinyl estradiol is fairly effective on the trunk and
the limbs, but has a very limited success m the face. The body hair does not
disappear but following suppression of androgen-dependent growth, the hair
becomes less coarse and less visible, resembling the vellus hair on the female
body in certain body regions. If hairlessness of the body is desired, only
electrolysis is effective. Waxing and shaving can result in temporary hairlessness,
which can be prolonged by the decrease in hair growth associated with estrogen
and antiandrogen treatment. The beard hairs also become thinner and softer
after several years of hormone use. Unfortunately, once the beard growth has
fully developed and regular shaving is necessary, the result of antiandrogens
alone is cosmetically unacceptable. Only electrolysis is effective in
eliminating beard growth. In a few patients who had started treatment before
developing visible hair growth, electrolysis could be avoided. After starting
hormone treatment, male type scalp hair loss (masculine alopecia) ceases.
Re-growth of scalp hair on bald areas is incomplete and of the vellus type.
Hairstyle, hair implants or artificial hair techniques ("weaving,"
partial wigs) can successfully mask the masculine alopecia while hormones can
at best make a minor contribution.
Penis length is not
reduced by hormones, but due to its almost continuous flaccid state and an
increase in lower abdominal fat, may appear reduced. Spontaneous erections are
suppressed within 3 months but during erotic arousal erections still occur in
the majority of our patients, evidencing the relative androgen-independence of
this type of erection. Testicular volume is reduced by 25% within the first
year of hormone use. This reduction is appreciated as a sign of progress and
also makes hiding of the male genitals easier.
Induction of female
characteristics is quite variable. In the initial phase of estrogen therapy,
subareolar nodules which can be painful (Futterweit, 1980), are common. The
breast size can be quantified by measuring the maximum hemicircumference over
the nipple with a flexible ruler (either in the supine position or sitting
which is our method). The increase in breast size evolves gradually with often
periods of growth and periods of apparent standstill. The mean
hemicircumference after 1 year is 10 cm in the supine position and 14 cm in the
sitting position (the latter varies from 4 to 22 cm in our patients) and
reaches its maximum after 18 to 24 months. In our patients the mean value is 18
cm, but it can vary from 4 to 28 cm. For comparison: in biological females it
varies from 12 to 36 cm with a mean of 22 cm (own unpublished observations in a
small number of these women). The values in male-to-female transsexuals are
several centimeters less than in biological women. Moreover, the width of the
male thorax is in general larger than that of the female thorax. Consequently,
the proportional effect is judged as unsatisfactory by almost 50% of the
male-to-female transsexual subjects. The majority of those unsatisfied requests
surgical breast implants. In more than 50% of the male-to-female transsexuals,
the estrogen-induced breast size is judged as satisfactory by the transsexual
subject herself, obviating breast surgery. In a small number of subjects
unilateral or bilateral subcutaneous mastectomy has been performed because of
pubertal gynecomastia. The hormonal effect on operated breasts is nil. In the
latter cases early breast implants are indicated, but we prefer to wait at
least one year before recommending any surgery including breast surgery.
In male-to-female
transsexuals, estrogens do not affect the pitch of the voice, and a low voice
can be a great handicap. Speech therapy is necessary to achieve a more feminine
vocal range. Vocalcord surgery does not obviate the need for speech therapy in
almost all cases, but the resulting higher pitched voice facilitates a female
public presentation.
The subcutaneous and
intra-abdominal fat distribution is sex steroid-dependent. Males preferentially
accumulate fat in the upper abdomen ("apples") and females around the
hips ("pears"). Estrogen treatment results generally in more fat
around the hips but this is not the rule and can vary largely. Skeletal
structures like jaws, size of hands and form of the pelvis do not change with
the estrogen and/or antiandrogen treatment.
Not infrequently
male-to-female transsexuals complain of a dry skin and fragile nails. This is a
consequence of the reduction in sebaceous gland activity following antiandrogen
treatment. Avoidance of detergents and application of ointment is mostly
helpful.
Effects of
antiandrogens alone or in combination with estrogens on the mood and the
emotional functioning are often reported by our patients and their partners.
Defmitive scientific proof in transsexuals that they are hormone-related is not
available, but it is likely. In view of the consistency of these subjective
reports and some studies in hypogonadal patients after substitution with
appropriate hormones, an effect of hormones on the brain and consequently on
brain functions like mood, is highly plausible.
Effects of
Cross-Gender Hormones in Female-to-Male Transsexuals
Generally the
virilization process proceeds subjectively and objectively in a satisfactory
way and female-to-male transsexuals are pleased with it. It has no effect on
their breast size. An oily skin and acne may become a problem. In comparison to
other men they are rather short, but a short man is less conspicuous than a
tall woman. The clitoris enlarges in all subjects though in a different degree.
It sometimes suffices to have vaginal intercourse with a female partner, but
that is not the rule. Most subjects indicate an increase of their libido
following androgen treatment. Like male-to-female transsexuals female-to-male
transsexuals must continue androgen treatment after ovariectomy to prevent hot
flashes, loss of male characteristics and above all osteoporosis.
SIDE EFFECTS OF
CROSS-GENDER HORMONE
Few systematic
studies on side effects of cross-gender hormone treatment in transsexuals have
been published. Meyer et al. (1986) found in 90 transsexuals only liver enzyme
abnormalities and mild elevations of serum cholesterol and triglycerides. Case
reports have described pulmonary embolism, cerebral thrombosis, myocardial
infarction, prostatic metaplasia, and breast cancer in estrogen-treated
male-to-female transsexuals and recurrent myocardial infarction in a
female-to-male transsexual treated with androgens.
In 1989 we published
a retrospective study on mortality and morbidity in 303 male-to-female and 122
female-to-male transsexuals who have been treated and followed at our clinic
for 6 months to more than 13 years (Asscheman, Gooren & Eklund, 1989).
Mortality in male-to-female transsexuals was 6-fold in-creased compared with
the general population. This was in particular due to suicide and death by
unknown cause. No deaths occurred in the female-to-male group but the median
age was much lower. Side effects were common m the male-to-female transsexual
patients. Significant increases were observed for venous thrombosisi pulmonary
embolism, depressive mood changes, hyperprolactinemia and elevated liver
enzymes in the male-to-female transsexual patients. In the female-to-male group
acne (12.3%) and weight increases > 10% (17.2%) were the main side effects.
Many side effects were reversible with appropriate therapy or temporary
discontinuation of hormones.
The occurrence of
serious side effects (e.g., the prevalence of thromboembolic disease of 2.1% in
patients below 40 years of age and 12% in patients above 40 years) was,
however, not rare. In view of the needs of transsexuals these side effects
present a difficult dilemma in hormonal gender reassignment. At present no firm
guidelines can be given. The cornerstone of the decision to prescribe
cross-gender hormones remains with the explanation of the possible side effects
to the patients and careful clinical judgment.
Efforts to reduce the
risk of thromboembolic events by transdermal administration of estrogen are
very promising but not conclusive at this moment. Further follow-up of this
relatively young population to disclose long-term side effects is required.
CONCLUSION
Hormones are
indispensable tools for the induction and maintenance of the characteristics of
the sex the transsexual reckons him/herself to belong to. Following sex
reassignment surgery they are hypogonadal and they must receive in principle
lifelong hormone replacement in the same fashion as other hypogonadal patients.
The main goal is to prevent future osteoporosis manifesting itself in the fifth
and higher decades of their lives.
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Last Update: 10
January 1998 by Winni Daniels
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