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Sexual Precocity in a 16-Month-Old* A7 t; _! ~8 [. v5 E( L7 V# b
Boy Induced by Indirect Topical
! z$ D" X) l8 {4 A' b1 tExposure to Testosterone
9 A; _1 D7 R! n8 ^Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: ?8 S, J2 i' L
and Kenneth R. Rettig, MD1
3 S: U0 I5 Y _Clinical Pediatrics3 c; K, }. E& _, z P1 {8 C3 P
Volume 46 Number 6
/ V+ `1 ?7 U$ d$ qJuly 2007 540-5432 e6 B4 E2 y9 V7 [
© 2007 Sage Publications+ _; f$ x- R: {+ X+ \/ i8 o
10.1177/0009922806296651
* L9 t) M: b9 E: b' Ihttp://clp.sagepub.com
7 H0 n+ J8 w0 khosted at7 D: I L: ^6 v# M
http://online.sagepub.com9 t6 H" [$ ~% z% J6 F) K; {
Precocious puberty in boys, central or peripheral,
9 W, Y' d8 J# p& xis a significant concern for physicians. Central& n, W7 T3 `& `, p; [7 @ i$ l. }
precocious puberty (CPP), which is mediated
& \' M8 s2 c4 D, T4 K& Athrough the hypothalamic pituitary gonadal axis, has, q/ `1 e- e. d# ]7 }
a higher incidence of organic central nervous system% F; o) j6 v/ h4 r2 \* V
lesions in boys.1,2 Virilization in boys, as manifested
f+ y) ~0 q c, L! Dby enlargement of the penis, development of pubic
) r! H) b# o; _3 G2 i W0 [hair, and facial acne without enlargement of testi-- S( P: L; e9 s6 x/ o
cles, suggests peripheral or pseudopuberty.1-3 We. q1 d1 Q1 z7 D+ b2 s1 h, o: y
report a 16-month-old boy who presented with the6 H. D0 {4 f r; n
enlargement of the phallus and pubic hair develop-
: o* w+ s9 C! O# Q) @9 Cment without testicular enlargement, which was due
% u3 [* W3 t! W% Y$ w0 e, x) ?to the unintentional exposure to androgen gel used by
' J" X w9 d# {; k8 rthe father. The family initially concealed this infor-
; U0 s3 v# b) I- n/ ?mation, resulting in an extensive work-up for this
4 @% \2 X! U/ D- g0 j4 d$ _7 _7 Nchild. Given the widespread and easy availability of1 n: i% G/ Q: }+ R8 }2 g, ~
testosterone gel and cream, we believe this is proba-% h. u0 e6 g0 m$ S
bly more common than the rare case report in the
, ~, I" j3 G% l* Z- }literature.4
/ d: k& P1 x2 \6 uPatient Report0 p) ^9 e* _* [' w
A 16-month-old white child was referred to the
3 c* m5 F8 X- P2 ?2 O+ pendocrine clinic by his pediatrician with the concern( v' C! A+ i" M" o3 b3 G( Y8 l6 g' J
of early sexual development. His mother noticed
- {- c* }. ]; k; flight colored pubic hair development when he was+ V4 s! i n$ [1 n) F
From the 1Division of Pediatric Endocrinology, 2University of5 q# }- N6 m5 `/ s; x
South Alabama Medical Center, Mobile, Alabama.
) f8 O+ j: I N& s% s& O& V* y. SAddress correspondence to: Samar K. Bhowmick, MD, FACE,. z2 h, P9 r/ y3 [$ W5 y0 s) A
Professor of Pediatrics, University of South Alabama, College of6 m k+ G1 Q; V
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 I& q2 P" f* A" o' {! w: Y3 De-mail: [email protected].! X$ N# v+ I2 b9 F6 G% p
about 6 to 7 months old, which progressively became' `$ |( @6 o- d g! Y
darker. She was also concerned about the enlarge-7 [7 q. c. x4 _0 S" n1 D1 i
ment of his penis and frequent erections. The child
/ n9 @0 e/ M& r) W6 V/ A/ a: Mwas the product of a full-term normal delivery, with. q) \4 `7 Z* Z N1 S
a birth weight of 7 lb 14 oz, and birth length of% y4 T% k2 I* t- }& s" \) C8 O
20 inches. He was breast-fed throughout the first year
) {- K* B. {9 D0 eof life and was still receiving breast milk along with5 p" N0 \* H" T: n: {3 i3 T Q! f
solid food. He had no hospitalizations or surgery,2 `3 q) `- n; B* A# p7 q7 s
and his psychosocial and psychomotor development
1 F1 r5 O* f( D" |: swas age appropriate.
$ \& V( I% _ i5 v0 q" ]- x* PThe family history was remarkable for the father,) c. |0 p8 @% W4 }
who was diagnosed with hypothyroidism at age 16,& p' _: _) ~5 `% w) J
which was treated with thyroxine. The father’s0 }% X3 j+ K; N! x- x7 A4 M) ^
height was 6 feet, and he went through a somewhat$ X+ h7 v# B% y q
early puberty and had stopped growing by age 14.9 m: ?! @" ^9 R
The father denied taking any other medication. The
' d+ ~) x: `, B* h3 W# D) Lchild’s mother was in good health. Her menarche- o: ?( E' A: ~, q/ @
was at 11 years of age, and her height was at 5 feet
) B% o: C9 H7 x: Q3 k4 \0 p4 U5 inches. There was no other family history of pre-8 f( d0 {6 X4 `9 l" k
cocious sexual development in the first-degree rela-
4 J, }7 N1 D% [; ?- l5 Y) r$ ~tives. There were no siblings.
6 _. k1 ?! ~% c$ c0 b' dPhysical Examination
% }7 C x5 W) `5 W/ eThe physical examination revealed a very active,; e" |+ x' k' d3 D9 ?4 Q" R
playful, and healthy boy. The vital signs documented& L/ x1 [8 z& ?9 G
a blood pressure of 85/50 mm Hg, his length was$ W( x. Q C0 x
90 cm (>97th percentile), and his weight was 14.4 kg
. z$ i* v" V6 u+ c(also >97th percentile). The observed yearly growth
, |8 Y! k- K# Dvelocity was 30 cm (12 inches). The examination of6 Y' z Z0 H d7 o7 t
the neck revealed no thyroid enlargement.1 v6 _% m4 m9 ]2 C+ ? s& y
The genitourinary examination was remarkable for
% v! c$ t( n h1 K. u1 Oenlargement of the penis, with a stretched length of9 q4 S/ y- Y q9 x/ l: j5 E! g
8 cm and a width of 2 cm. The glans penis was very well' v" f: X4 Z3 Z
developed. The pubic hair was Tanner II, mostly around
. i8 e* g5 V4 r2 U' J2 j540
' V w3 Q$ k9 h# {7 u, V# L4 Lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 v4 i. H5 x$ n- l7 E
the base of the phallus and was dark and curled. The/ C8 y) `. H! a! A7 l( {8 a" _
testicular volume was prepubertal at 2 mL each.6 ` S5 S: ~0 Y& n, _/ I
The skin was moist and smooth and somewhat
/ S6 c+ X6 ]. Ooily. No axillary hair was noted. There were no
' z9 [3 B9 o0 h0 q& }5 uabnormal skin pigmentations or café-au-lait spots.
5 k1 ]+ K% b. @: E/ C; P1 t+ i# vNeurologic evaluation showed deep tendon reflex 2+
v; A7 T) h2 N: h0 j: h% xbilateral and symmetrical. There was no suggestion
$ Z$ F c! e! |6 l* V! V8 {of papilledema.) t0 b1 W& j- k5 X: L- U$ r2 c+ K
Laboratory Evaluation
& R, O6 i. z t8 c$ XThe bone age was consistent with 28 months by
# r# O# S1 ~: wusing the standard of Greulich and Pyle at a chrono-4 I- D0 D& m& n- c
logic age of 16 months (advanced).5 Chromosomal1 M* S/ p, u' J \6 ?. z0 M
karyotype was 46XY. The thyroid function test
* `0 y0 X \5 N4 Q- @& Qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
M$ B0 n7 J/ T0 I% a! H( v* {lating hormone level was 1.3 µIU/mL (both normal).7 ^5 I6 L7 d$ Z/ t
The concentrations of serum electrolytes, blood
+ y; f( O5 ]8 P$ E B& @) Kurea nitrogen, creatinine, and calcium all were
0 Y7 i2 O6 R& m+ Owithin normal range for his age. The concentration) o, S ~, O v
of serum 17-hydroxyprogesterone was 16 ng/dL
7 \* n; G; P' `+ l# s1 u8 |6 s(normal, 3 to 90 ng/dL), androstenedione was 20
" X5 M# k7 Q% l, m2 Wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 r! Q: U. a8 k5 w/ h
terone was 38 ng/dL (normal, 50 to 760 ng/dL),/ c2 G! O- d0 T& G' K' N
desoxycorticosterone was 4.3 ng/dL (normal, 7 to4 R% D8 E, |9 Y* n2 u7 w3 I8 U
49ng/dL), 11-desoxycortisol (specific compound S): I' R0 |( x9 X# ~ H& b
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) y5 s& X ]* o, V$ B$ z: Btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# Z6 n& f9 ]$ v: y# N
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 y- X: Z7 O5 \3 L
and β-human chorionic gonadotropin was less than
! z; q% P* q8 C K5 mIU/mL (normal <5 mIU/mL). Serum follicular
4 o. V2 E& b# c! U0 {stimulating hormone and leuteinizing hormone3 |& i, _: S1 V0 {( ^; h6 \& o. d
concentrations were less than 0.05 mIU/mL
8 @* i" C, q2 V% j. P(prepubertal).
( [" X. ]& ]4 S5 lThe parents were notified about the laboratory8 T: ~. r( l6 N/ D3 Z3 A. B8 z
results and were informed that all of the tests were" j; d4 y2 A! P+ p
normal except the testosterone level was high. The" a* A- I) H2 }1 D5 w/ h
follow-up visit was arranged within a few weeks to
& _- g1 I/ w! l/ X. ?2 }obtain testicular and abdominal sonograms; how-
3 g: \3 [' y0 R0 t" }3 A" Jever, the family did not return for 4 months.0 [6 b: f* E6 F
Physical examination at this time revealed that the3 f) I6 z: U5 ?- F9 y) J3 P
child had grown 2.5 cm in 4 months and had gained
8 D- O2 e, i; |5 M2 kg of weight. Physical examination remained! i. _2 a7 g$ O, m* t
unchanged. Surprisingly, the pubic hair almost com-3 k o: w1 k, ?& g
pletely disappeared except for a few vellous hairs at
# x+ y2 k1 _2 }( q6 `; ^9 Z/ r; hthe base of the phallus. Testicular volume was still 20 ~& S+ A3 a @5 b7 w
mL, and the size of the penis remained unchanged.
; Y* m& q4 L) F. N0 V, yThe mother also said that the boy was no longer hav-
9 ^. i, U' [8 ] sing frequent erections.3 ^8 J% c4 A8 h4 A* m5 h
Both parents were again questioned about use of
& ~4 E) U, B5 p8 \any ointment/creams that they may have applied to7 B7 L" ?6 V* C6 U. p
the child’s skin. This time the father admitted the( D, D: U+ u1 a0 a& T) P
Topical Testosterone Exposure / Bhowmick et al 541
7 ~' Q# N4 O7 u- x, Luse of testosterone gel twice daily that he was apply-. u' x9 Y2 ~' L, K |" O
ing over his own shoulders, chest, and back area for, ~$ z1 N( Q+ ^8 v
a year. The father also revealed he was embarrassed
9 H. ?: w; a! |6 `* b( }& }to disclose that he was using a testosterone gel pre-
/ W" |9 L9 {, G9 X# uscribed by his family physician for decreased libido
; F& t; I# M8 F; Jsecondary to depression.
- m9 U( F* Y2 Q4 I; ^ x2 vThe child slept in the same bed with parents.
8 D3 O1 r5 }7 z5 T% c1 GThe father would hug the baby and hold him on his
9 i. G, @) J/ Kchest for a considerable period of time, causing sig-1 p! X3 S0 j1 K6 W" w1 _+ |" d0 u
nificant bare skin contact between baby and father.3 l |% _2 |$ T1 A6 a' a( |, R
The father also admitted that after the phone call,- d9 w5 i5 D. G/ o1 T
when he learned the testosterone level in the baby) {' o, s% a$ A3 @4 R2 j: ^
was high, he then read the product information
2 n2 M2 r+ c- G$ q& _packet and concluded that it was most likely the rea-' \( |7 [ P, c$ s. `9 [
son for the child’s virilization. At that time, they' f+ _2 V) x+ l3 o( b. H( O
decided to put the baby in a separate bed, and the
% ]$ K& S8 Y3 E. Y. q. [8 ?6 Z1 Qfather was not hugging him with bare skin and had
}. K8 b; F2 T% ^6 O: a1 E- tbeen using protective clothing. A repeat testosterone" W8 w1 X. D( n$ l; k* [( L
test was ordered, but the family did not go to the, p% v! _ l6 j- j8 ]/ p
laboratory to obtain the test.8 |# ]( I6 F! O% Y0 B
Discussion
. i! c5 c% J# q: V$ c- DPrecocious puberty in boys is defined as secondary9 C) O' E, N2 f7 [# v
sexual development before 9 years of age.1,4% \( x7 v& P( O8 r5 P# L
Precocious puberty is termed as central (true) when
0 O: i4 L, z3 T- I4 Cit is caused by the premature activation of hypo-
% ^- _+ D6 L( W5 z) w3 X* Zthalamic pituitary gonadal axis. CPP is more com-/ z3 Z" q- Z ?9 y, [9 z
mon in girls than in boys.1,3 Most boys with CPP& d) e: E/ [" z
may have a central nervous system lesion that is
& S, G, u# h* ~responsible for the early activation of the hypothal-
% `$ L8 l8 ^; d+ u* C3 Z* F) Mamic pituitary gonadal axis.1-3 Thus, greater empha-
" m0 t0 ?" s; f4 O9 o: q( psis has been given to neuroradiologic imaging in$ t2 C8 x, E( ^2 y* W" s# O. A% x* Y
boys with precocious puberty. In addition to viril-) D1 P: I. @8 E6 f; R- f
ization, the clinical hallmark of CPP is the symmet-
( m6 d/ [3 i8 F6 s* vrical testicular growth secondary to stimulation by
7 }1 h' _* S, N/ @gonadotropins.1,3
) A/ ~, W( U, ]$ R. e; j! GGonadotropin-independent peripheral preco-$ F: ?$ |8 O& V+ x8 @. Q
cious puberty in boys also results from inappropriate
" P& `; G& j. Tandrogenic stimulation from either endogenous or
4 {/ s2 n. B4 L4 C$ Qexogenous sources, nonpituitary gonadotropin stim-& [: w C3 k" D; w
ulation, and rare activating mutations.3 Virilizing
% f" o+ M7 F5 ]) H5 o/ Lcongenital adrenal hyperplasia producing excessive! O$ {4 J' }" ~9 h4 U
adrenal androgens is a common cause of precocious
4 S) ?) R9 x- ]/ ^) dpuberty in boys.3,4
1 u% w; ]8 D: s. l. e% |The most common form of congenital adrenal3 n: D' w! j+ N. `5 y
hyperplasia is the 21-hydroxylase enzyme deficiency.
% e1 B; R) r* F, U3 S6 f7 r: VThe 11-β hydroxylase deficiency may also result in
' m6 N& h u2 @4 w5 R$ nexcessive adrenal androgen production, and rarely,' ?/ e4 B- y3 i
an adrenal tumor may also cause adrenal androgen
4 O+ s( \- S* c$ j, q. f3 Z7 I$ v% y" |excess.1,3
; h+ ?# _- Z# J/ kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: Q$ L/ I# @+ }5 H" b6 z# S
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 E2 u! O' k0 o' H; L% n F* J, VA unique entity of male-limited gonadotropin-, \! ^" d6 _ T: U* k2 R
independent precocious puberty, which is also known) N% k2 {( G* i
as testotoxicosis, may cause precocious puberty at a
: i8 d$ L. R2 T# I: W! B# y: Uvery young age. The physical findings in these boys
! l; P, ^) A* y- v* x! ^with this disorder are full pubertal development,; d" B5 L0 @% {- I& ~3 o
including bilateral testicular growth, similar to boys
/ u. u1 p% e; T2 cwith CPP. The gonadotropin levels in this disorder
0 ~8 k& z; ]$ u( c rare suppressed to prepubertal levels and do not show% y2 V. n. k# T' S9 \
pubertal response of gonadotropin after gonadotropin-$ I' b: C& T4 \: j( K* d* M8 y
releasing hormone stimulation. This is a sex-linked6 _' }3 K- O* v L
autosomal dominant disorder that affects only2 r, v, n" A1 X! }. K$ M
males; therefore, other male members of the family
( Y& w+ J9 f5 G, i( i5 Z/ S3 rmay have similar precocious puberty.36 H k0 O* B7 z$ u$ \
In our patient, physical examination was incon-0 r% n3 j5 Y+ @9 T( N5 s( x7 G
sistent with true precocious puberty since his testi-
' t: W ]6 w) g/ K# a# }" d6 V, acles were prepubertal in size. However, testotoxicosis
6 I' z% q0 B/ h& Y5 A: Dwas in the differential diagnosis because his father
. y* `3 Z- U& F0 \. q* j2 estarted puberty somewhat early, and occasionally,0 w6 ?1 E$ E. C2 L2 z
testicular enlargement is not that evident in the% B" j" I" |0 ~: r
beginning of this process.1 In the absence of a neg-
. b$ z& \ L% m& Aative initial history of androgen exposure, our+ i; [6 |- S# u |$ c% R
biggest concern was virilizing adrenal hyperplasia,
- k# Y* j. R& ]8 w: I Z5 veither 21-hydroxylase deficiency or 11-β hydroxylase
( _* Z1 o% {" R: A6 }) xdeficiency. Those diagnoses were excluded by find-
) W" E8 F- E7 e+ y. j3 D1 [6 ping the normal level of adrenal steroids.# F( b5 o' o7 v, u4 y
The diagnosis of exogenous androgens was strongly& V! @( }+ N- O
suspected in a follow-up visit after 4 months because
8 W# Q3 r5 A7 G& e) c( ?2 }% N2 Cthe physical examination revealed the complete disap-; M" _: i$ X1 Z$ x; i/ ?
pearance of pubic hair, normal growth velocity, and. m) [2 p" z0 B
decreased erections. The father admitted using a testos-: x6 Z" i: D8 s/ L5 e2 J
terone gel, which he concealed at first visit. He was6 K& d- B C d5 S
using it rather frequently, twice a day. The Physicians’
4 \8 k, C7 m9 ^Desk Reference, or package insert of this product, gel or
, }, u1 [. G; W" }% Z$ Dcream, cautions about dermal testosterone transfer to7 F# I5 h- X+ R1 Z7 y; y
unprotected females through direct skin exposure.
- R4 S* m' h# B3 |; R5 NSerum testosterone level was found to be 2 times the! G; X% o1 b$ {' z1 r$ d; a
baseline value in those females who were exposed to
( ~, H3 Q9 B c" Seven 15 minutes of direct skin contact with their male
5 }* y: w# ]' {6 _1 D3 w1 ^partners.6 However, when a shirt covered the applica-- u2 k [2 ~7 ]7 {2 K
tion site, this testosterone transfer was prevented./ L& r A# A3 p9 D- s( H
Our patient’s testosterone level was 60 ng/mL," V A+ n8 z; E( q C, p3 d5 X
which was clearly high. Some studies suggest that
1 j+ w2 E; h' M" N& z* g C5 Cdermal conversion of testosterone to dihydrotestos-
6 x' M9 h1 n3 J' Wterone, which is a more potent metabolite, is more3 Z% U, d- G: w$ X
active in young children exposed to testosterone
) D6 f3 l X0 j3 R2 v& pexogenously7; however, we did not measure a dihy-
$ d: ~' E! a( _2 X- N. d& bdrotestosterone level in our patient. In addition to9 E: L4 P9 B; S( I4 T
virilization, exposure to exogenous testosterone in6 q5 x4 I$ @* z P; Q2 J6 Z$ }7 \
children results in an increase in growth velocity and3 |4 a9 j+ C+ M5 o' f4 L, V& |+ f
advanced bone age, as seen in our patient.0 e0 ^! Z& r7 g. Q O; ^
The long-term effect of androgen exposure during
* f( i* a) d+ m6 @3 X. _( M9 R; S- ?early childhood on pubertal development and final
# p) }" K$ {1 n# N) h }$ zadult height are not fully known and always remain
|: }$ X8 B9 b! K2 ia concern. Children treated with short-term testos-9 q5 p3 \. N3 x% G: W
terone injection or topical androgen may exhibit some
: m9 c( N0 x5 ^1 b: xacceleration of the skeletal maturation; however, after6 q5 u( L, g4 \( K# e
cessation of treatment, the rate of bone maturation; ]# h2 C1 b( T7 ^
decelerates and gradually returns to normal.8,9
9 v1 j; `! \# o3 `) B- ]+ OThere are conflicting reports and controversy' E1 v: r# d s; \7 p
over the effect of early androgen exposure on adult
+ H* D* S+ _4 q( D$ u" ^+ y, t; mpenile length.10,11 Some reports suggest subnormal5 g# Z6 q% W! {; u9 U0 m
adult penile length, apparently because of downreg-
2 z1 T9 ^3 M3 s# D% E& u3 m; Sulation of androgen receptor number.10,12 However,4 b+ W9 p4 y1 x4 f- x$ j
Sutherland et al13 did not find a correlation between* T' Z0 L. ]/ L" P9 d# M* c; p B7 N
childhood testosterone exposure and reduced adult
+ B4 S! P, l0 Y: [; |7 ipenile length in clinical studies.
. P; Z. _! g: n+ _Nonetheless, we do not believe our patient is
5 D8 C9 s, x; F2 b$ ~going to experience any of the untoward effects from
# l9 B' }9 `9 P7 {" M8 btestosterone exposure as mentioned earlier because
, i: R6 V7 h5 J) A v9 t5 R6 Tthe exposure was not for a prolonged period of time.7 N& a3 W* o7 x1 ~* N8 ?
Although the bone age was advanced at the time of( V/ i9 v/ u8 }: n# v
diagnosis, the child had a normal growth velocity at- ? h2 j# c* b+ t( \
the follow-up visit. It is hoped that his final adult
% `2 u# r/ P4 z% m' |, @! uheight will not be affected.
7 [% ]! e( e5 d2 sAlthough rarely reported, the widespread avail-
9 ^' U# k0 C7 |# eability of androgen products in our society may+ {2 F, t$ w$ y( a2 t1 c1 y
indeed cause more virilization in male or female. w$ N$ D: M# J
children than one would realize. Exposure to andro-
4 o+ W6 U; ^5 ?' J0 @! h! @3 Kgen products must be considered and specific ques-
3 r3 _6 p7 R% n; z+ V6 E3 xtioning about the use of a testosterone product or
$ k* J+ W2 n1 m) g6 Wgel should be asked of the family members during F- g R, E* w$ J6 z
the evaluation of any children who present with vir-% ]$ c s; z5 L
ilization or peripheral precocious puberty. The diag-/ ]4 x5 z" m# Y
nosis can be established by just a few tests and by
6 p( m0 y' @% }$ f0 }1 ^3 Sappropriate history. The inability to obtain such a- d( g. s; l) i& E. ^, p
history, or failure to ask the specific questions, may
5 i% V- q" T8 hresult in extensive, unnecessary, and expensive
9 x$ I J4 j0 J. r; Vinvestigation. The primary care physician should be+ w0 f, X( P+ t: U
aware of this fact, because most of these children
% `' R: T/ ^- I: B/ i/ X ^0 Qmay initially present in their practice. The Physicians’* M. j5 o; x& }% H7 S3 R- s3 R
Desk Reference and package insert should also put a* Z1 a4 x2 q# Y& D
warning about the virilizing effect on a male or7 ?/ H+ }* y! J: [- n
female child who might come in contact with some-4 y. v7 q- f9 g0 d* F
one using any of these products./ C' X, i9 ^0 ]. P
References
& P" [. Q' x: s: Z) l' U% Y W1. Styne DM. The testes: disorder of sexual differentiation
; D! ?' g9 s L& r) Z) E7 h) {and puberty in the male. In: Sperling MA, ed. Pediatric
% n( \- h5 c% s1 w* R' q( WEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
z: ]: _5 x- U; S9 g- d2002: 565-628.) e7 }. O- L3 ^; c% Y9 m- |
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 m9 a# {5 B* Y
puberty in children with tumours of the suprasellar pineal |
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