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Sexual Precocity in a 16-Month-Old
! `) M* U$ I5 g |. t3 m, nBoy Induced by Indirect Topical; h2 K, [- x) m* e/ ?
Exposure to Testosterone
, U6 v: [+ E+ r7 _; dSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& C5 U6 ~, Z# P6 r# W5 K# d
and Kenneth R. Rettig, MD1
/ Z# B1 Z& `& h sClinical Pediatrics2 w' V& b7 u, E& q/ B- m
Volume 46 Number 6$ T A2 I0 P& q- M3 |7 n; B# w; S
July 2007 540-5432 f; s. R6 p4 l' |+ G1 Y
© 2007 Sage Publications
+ s2 L0 G; v( E7 t, t/ N& {7 h4 x10.1177/0009922806296651; L4 a2 O+ S& e' M0 M! r) @
http://clp.sagepub.com2 z2 _) Q8 ?: U! w
hosted at) r, ~3 K' {9 j" d6 U4 y
http://online.sagepub.com' f, E1 T) ^4 w0 B( x5 z$ O
Precocious puberty in boys, central or peripheral,
" c4 `! \! a& u# F uis a significant concern for physicians. Central
" e- f4 E7 s! y h! Gprecocious puberty (CPP), which is mediated
' r5 r9 X' D. E: L1 _) n, athrough the hypothalamic pituitary gonadal axis, has6 d7 i: }9 X; ?/ b+ Z- G
a higher incidence of organic central nervous system
8 k+ ^6 t+ c: @* U0 t( Mlesions in boys.1,2 Virilization in boys, as manifested
' O! {& X# N9 \4 ^) Hby enlargement of the penis, development of pubic
9 ^+ O6 D! e$ N ~hair, and facial acne without enlargement of testi-
I; e; J- _0 ^6 {. O) Gcles, suggests peripheral or pseudopuberty.1-3 We) Y `4 I; s( @
report a 16-month-old boy who presented with the1 \% A% I# X3 E
enlargement of the phallus and pubic hair develop-; ^% Z& |: t. C6 R( ~: ~
ment without testicular enlargement, which was due( ]+ t* d' z3 Q$ ? s7 M
to the unintentional exposure to androgen gel used by
: E, B1 C8 U- p }' N" A1 P- ?8 @the father. The family initially concealed this infor-( J2 W' t$ x7 p- U4 v/ Y0 T
mation, resulting in an extensive work-up for this, [; u1 i. q; |0 [# N! \% ~7 E: S
child. Given the widespread and easy availability of
k. X0 ^$ F7 G& K1 Ytestosterone gel and cream, we believe this is proba-
7 x8 ~4 G' f7 H$ N: t8 Y' Ibly more common than the rare case report in the
# ^7 s- w$ \ g- }literature.4; v8 \0 X6 S6 z( ~( ]6 g
Patient Report
6 c! ^- C. u( X" t) C" y& kA 16-month-old white child was referred to the
8 `, K5 h' W4 e; Wendocrine clinic by his pediatrician with the concern; T. `" J! Z6 U0 }. P
of early sexual development. His mother noticed
' G+ W# Q9 q8 l, H8 }$ {light colored pubic hair development when he was
b- k% J0 ]5 [% ~From the 1Division of Pediatric Endocrinology, 2University of; B2 P7 ?, e2 G# K
South Alabama Medical Center, Mobile, Alabama.
0 @$ g2 c' H* U6 w2 H* uAddress correspondence to: Samar K. Bhowmick, MD, FACE,3 C" S/ \" R1 ^0 H! T! b
Professor of Pediatrics, University of South Alabama, College of
+ |8 f/ A9 F9 D. KMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: Z% }% Z% w2 m# Fe-mail: [email protected].
5 d& e! K" B2 labout 6 to 7 months old, which progressively became
5 j+ Q6 ^: s, Y# udarker. She was also concerned about the enlarge-& q" a* ^. l2 e- c
ment of his penis and frequent erections. The child
% v; p0 h5 t7 A# K; ^2 W; c( Vwas the product of a full-term normal delivery, with
8 O# Z6 D8 S1 Fa birth weight of 7 lb 14 oz, and birth length of( V; `( u/ Z) o" `2 Y
20 inches. He was breast-fed throughout the first year" v; g( R) E# `+ Y% c0 |( w! G& f8 H3 `
of life and was still receiving breast milk along with
9 _* U1 X/ W5 S4 G1 dsolid food. He had no hospitalizations or surgery," u1 C7 b) C4 k; y3 i0 `
and his psychosocial and psychomotor development
5 K' u+ K$ J9 f0 W9 ywas age appropriate.
2 \+ {; w# |; N# v2 nThe family history was remarkable for the father,: `$ Z! x) X; _" Q( C
who was diagnosed with hypothyroidism at age 16,
) @7 V0 ^ C/ k* x/ D9 _ @2 Xwhich was treated with thyroxine. The father’s
# O: B# E$ ?) X8 f, K7 L# {' |height was 6 feet, and he went through a somewhat3 D z. q: v5 J$ s P$ E: X
early puberty and had stopped growing by age 14.
6 E2 p+ L3 Q! X, U) ZThe father denied taking any other medication. The
5 ]1 y k% C- `4 M6 ^# T6 `child’s mother was in good health. Her menarche7 l! }6 L, N" P! E* b" i- E3 @
was at 11 years of age, and her height was at 5 feet
6 V& s3 I. d. k) H7 z5 inches. There was no other family history of pre-9 h- A- Z4 E4 m% r+ o
cocious sexual development in the first-degree rela-$ U9 L1 v, Y; s5 `0 u6 C
tives. There were no siblings.1 ~9 A) H" m( _
Physical Examination, t t& f+ p, l% h1 x
The physical examination revealed a very active,* @: A& I* T8 n7 F6 N, ]) c* U( U
playful, and healthy boy. The vital signs documented
+ z: O/ ?& [/ K( z2 n& _a blood pressure of 85/50 mm Hg, his length was
$ ^# x) ?! t9 E6 l& N9 I8 `90 cm (>97th percentile), and his weight was 14.4 kg
9 v( E! ? T$ N3 S$ G5 p(also >97th percentile). The observed yearly growth9 f5 l4 q/ J$ d9 e' c( r
velocity was 30 cm (12 inches). The examination of
9 k6 [# ?+ b7 [, `, M7 Dthe neck revealed no thyroid enlargement.
K* t9 H7 P! ?The genitourinary examination was remarkable for
8 T( c7 G$ V- }& R9 Lenlargement of the penis, with a stretched length of
' @/ m3 ~0 [$ G% r( r! s5 v8 cm and a width of 2 cm. The glans penis was very well
: Q# {+ v7 N$ c2 L8 N ?developed. The pubic hair was Tanner II, mostly around
8 i5 A7 |$ b/ x) q, z5401 I2 { Y* p3 ]1 x4 s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* ]8 G: S0 J# v% \* g+ N/ Wthe base of the phallus and was dark and curled. The- U; n' k4 X+ n( R! H
testicular volume was prepubertal at 2 mL each.
1 Z+ x/ Y- Y+ u! ^5 xThe skin was moist and smooth and somewhat6 O0 T1 E1 F1 d4 O1 d& h
oily. No axillary hair was noted. There were no7 B- k$ ^5 `- d5 r
abnormal skin pigmentations or café-au-lait spots.( w; o; T2 Q; Y# f3 i3 D& o0 U
Neurologic evaluation showed deep tendon reflex 2+ _6 d9 q |8 v9 {2 v
bilateral and symmetrical. There was no suggestion2 [( E6 d5 b7 k6 Z" G. |5 o
of papilledema.. q$ b* t+ S0 w* L: E4 ^7 P* |
Laboratory Evaluation; V. S! M$ S$ j* ]) J
The bone age was consistent with 28 months by Y; L5 i: Y4 C# p
using the standard of Greulich and Pyle at a chrono-6 v6 `/ v/ ]3 c1 h2 h" d' E
logic age of 16 months (advanced).5 Chromosomal9 a/ {$ N* U1 `5 Z+ B; m/ {
karyotype was 46XY. The thyroid function test
4 O+ x& u# F: @showed a free T4 of 1.69 ng/dL, and thyroid stimu-
. Z3 a: n5 w/ U, f% y9 blating hormone level was 1.3 µIU/mL (both normal).( S8 \ v) c) t- k. u- [4 t* L
The concentrations of serum electrolytes, blood
' S! U/ w2 H1 c. J6 Z2 aurea nitrogen, creatinine, and calcium all were
- ]( l( R7 c7 Bwithin normal range for his age. The concentration
4 r+ P: r7 y9 ?+ o8 w0 Q! Z* j( Dof serum 17-hydroxyprogesterone was 16 ng/dL
) t5 E. K' Z2 n(normal, 3 to 90 ng/dL), androstenedione was 20
2 a% Y/ O9 ] M0 Dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- E& d3 T: E/ h( ~: U& w
terone was 38 ng/dL (normal, 50 to 760 ng/dL),) K, V, }9 B" U2 T. {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
; L9 N6 M/ d5 o& O" N8 _& c49ng/dL), 11-desoxycortisol (specific compound S)& [; S$ ]& c1 b) V
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* B; a/ b% s2 E3 i5 t% f8 T7 f
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 z, F8 O& ~3 ?! q
testosterone was 60 ng/dL (normal <3 to 10 ng/dL), d: g, Q( ~5 A
and β-human chorionic gonadotropin was less than' y4 W) m: x4 @" Z! q7 {, v
5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 d, o; S' C- n( }3 G& s# lstimulating hormone and leuteinizing hormone
# [7 G% `# L6 g& h2 t+ }9 n7 Jconcentrations were less than 0.05 mIU/mL, p6 b! \ m9 P" M2 c
(prepubertal).
4 G; q; ^. [+ jThe parents were notified about the laboratory4 q& Y T( c4 R S9 T |3 j
results and were informed that all of the tests were
6 I5 w. e; h+ O7 E" |normal except the testosterone level was high. The+ L/ A; o( D+ }
follow-up visit was arranged within a few weeks to( b0 k' ?& G. ^3 h& j# {
obtain testicular and abdominal sonograms; how-8 l4 _3 E& W: x. Z- s
ever, the family did not return for 4 months.! I1 v4 k. r3 J
Physical examination at this time revealed that the
" z5 }( }' p) z* ]child had grown 2.5 cm in 4 months and had gained+ e+ N4 I2 V. {' f, N4 e+ h8 U
2 kg of weight. Physical examination remained- m9 n( u/ F) Y0 j
unchanged. Surprisingly, the pubic hair almost com-
. v. F9 M+ Z) hpletely disappeared except for a few vellous hairs at
) G, i( i, G. Qthe base of the phallus. Testicular volume was still 2
8 A) ^1 f5 a9 ?0 {* ^& d3 QmL, and the size of the penis remained unchanged.# W5 c; y' K& q0 P
The mother also said that the boy was no longer hav-
" ]4 J9 _0 s* Z, Uing frequent erections.: s4 d8 i: M8 S
Both parents were again questioned about use of1 E M9 N' |% t
any ointment/creams that they may have applied to8 V" I& a0 H' T
the child’s skin. This time the father admitted the: t: Z; B. ?7 Q; y. Q
Topical Testosterone Exposure / Bhowmick et al 541
5 {; v( R2 `+ `6 {use of testosterone gel twice daily that he was apply-0 J( n: P3 j$ r1 U5 f# B
ing over his own shoulders, chest, and back area for+ p" Z( w) g( ^& `! ~9 \7 u
a year. The father also revealed he was embarrassed
; E: p+ P1 Y) ?% q0 a8 F/ V: Xto disclose that he was using a testosterone gel pre-
( S4 r: }4 {) {, B. pscribed by his family physician for decreased libido1 }6 n* Y0 _" n8 D0 s! j5 w
secondary to depression.
; D& J( i: @ P0 ~6 d! dThe child slept in the same bed with parents.
- r9 s: O7 r8 ]. U, W3 HThe father would hug the baby and hold him on his5 r2 a: X8 y5 ]. S6 {
chest for a considerable period of time, causing sig-, S* V7 @ M$ Z1 V% t5 h
nificant bare skin contact between baby and father.
0 m' [( @6 e. P+ b3 cThe father also admitted that after the phone call,7 G y$ b2 D. L1 Q, c* ~
when he learned the testosterone level in the baby( ^# U' @: u$ D; f5 B
was high, he then read the product information
* I/ E& r; S$ s* Upacket and concluded that it was most likely the rea-
/ I3 p7 d! L5 A. J8 c3 R1 gson for the child’s virilization. At that time, they7 I. y) p/ N0 ^3 K
decided to put the baby in a separate bed, and the
, w6 @" e. q: g) Hfather was not hugging him with bare skin and had
* A, A- {* _0 T) n0 sbeen using protective clothing. A repeat testosterone7 {% Z: U( i6 D, K3 w) Y2 {
test was ordered, but the family did not go to the4 z; J6 ]6 n! E% r
laboratory to obtain the test.
K9 h- J- {2 d7 |1 cDiscussion
" l7 h" U' h c. QPrecocious puberty in boys is defined as secondary, y! l& p: ]* C5 g4 i5 ^
sexual development before 9 years of age.1,4
* ?! b6 m' x# l6 J+ e2 n9 b$ e7 bPrecocious puberty is termed as central (true) when3 u8 `. W$ r& h! T; c1 Y' Y; Y- ~) u
it is caused by the premature activation of hypo-( H& M. L( n; I& C
thalamic pituitary gonadal axis. CPP is more com-
& O7 t7 ] L% v6 J# B9 Rmon in girls than in boys.1,3 Most boys with CPP
4 D3 ^, G! a( amay have a central nervous system lesion that is
0 Y% O U4 h8 Z6 V8 ], Kresponsible for the early activation of the hypothal-
0 m, W2 j4 M; a+ P. f3 n- Namic pituitary gonadal axis.1-3 Thus, greater empha-1 a8 p3 T* ~+ T) |% S
sis has been given to neuroradiologic imaging in8 v$ J x y6 L% z1 M7 r" c# ?" L
boys with precocious puberty. In addition to viril-/ Q& E$ N! P6 a. p' {2 I# q
ization, the clinical hallmark of CPP is the symmet- t& m: ~7 r3 B( u
rical testicular growth secondary to stimulation by
/ B/ R! K! D- N/ S" V6 p, [/ W1 tgonadotropins.1,3
; m) i( l8 ^9 x, f" @Gonadotropin-independent peripheral preco-
& Q! u+ I: U* B- O( lcious puberty in boys also results from inappropriate
1 D7 Z3 u& Y+ {androgenic stimulation from either endogenous or4 `6 o5 i/ W5 y
exogenous sources, nonpituitary gonadotropin stim-$ ?4 n7 s* _+ z5 F Q
ulation, and rare activating mutations.3 Virilizing
' ^" k7 v9 y% ?- P- kcongenital adrenal hyperplasia producing excessive
, t2 y9 y6 L$ _3 Q6 e5 H; T7 Badrenal androgens is a common cause of precocious
5 }: R) n$ E u5 E% {8 X* T) Lpuberty in boys.3,4* V% t8 X8 b, Q4 Q; V* L5 F# z( `$ n
The most common form of congenital adrenal p9 e; C. d) x' T W* ~
hyperplasia is the 21-hydroxylase enzyme deficiency.) {8 |! `$ {4 j0 ~- ]$ R4 z: C) I
The 11-β hydroxylase deficiency may also result in/ c) J4 n4 C5 }) l
excessive adrenal androgen production, and rarely,5 }* q, x+ @9 Z' S( S) }
an adrenal tumor may also cause adrenal androgen
! m8 ~+ I p z# |9 xexcess.1,3
* V6 U% s4 q" f' a8 z, tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& U, U1 b N! R9 [3 D4 y' z542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 W. W$ c0 Q% L( U4 D9 F, KA unique entity of male-limited gonadotropin-7 O- S9 k$ {5 y z# P
independent precocious puberty, which is also known
' I& y/ I) \8 y' {/ H" o& |6 q0 @as testotoxicosis, may cause precocious puberty at a- I7 W" ? S( R' d% ~
very young age. The physical findings in these boys
2 B6 [) U! p* ], p9 x5 Twith this disorder are full pubertal development,
B- U! U7 T6 Q" H# J( M2 A. t8 q' fincluding bilateral testicular growth, similar to boys
) ^7 x" l3 @5 u( e" Twith CPP. The gonadotropin levels in this disorder
, k1 h8 T3 p; |. D: Y- R% Rare suppressed to prepubertal levels and do not show
9 D$ A5 P: S' l; T9 J5 g! m1 cpubertal response of gonadotropin after gonadotropin-8 U) W1 ?% d" C7 P+ I0 q/ @
releasing hormone stimulation. This is a sex-linked; _6 B8 x$ a5 f3 `# } Y
autosomal dominant disorder that affects only
% c3 d; I1 p+ g$ d4 c1 t! M6 Mmales; therefore, other male members of the family3 l% S% B: s6 u! S) Y4 t
may have similar precocious puberty.33 ~2 O3 L3 I& q" ]; b; X) e1 j
In our patient, physical examination was incon-, l, u! r& }$ O5 O. a; b4 _
sistent with true precocious puberty since his testi-/ m) M! G* U; w( o
cles were prepubertal in size. However, testotoxicosis
# |5 {* a0 D: R9 n: _3 F7 |was in the differential diagnosis because his father9 T' m2 S8 ^$ y% H8 t
started puberty somewhat early, and occasionally," W% c0 I* q9 z
testicular enlargement is not that evident in the
5 D* u, n6 d' g r, O+ }beginning of this process.1 In the absence of a neg-0 P* N" ~7 h- {5 j" S( _) Y4 o
ative initial history of androgen exposure, our+ O% ]0 s& h2 B+ x3 P+ H% G F% U
biggest concern was virilizing adrenal hyperplasia,
5 _- s/ [4 Z9 h6 W5 f0 zeither 21-hydroxylase deficiency or 11-β hydroxylase
. d1 `4 t) P3 qdeficiency. Those diagnoses were excluded by find-
* P. J& [2 K. j: ying the normal level of adrenal steroids.) V' H; X' ~; |2 z, S" w3 t) d9 E7 N
The diagnosis of exogenous androgens was strongly+ S) r( x1 N$ [
suspected in a follow-up visit after 4 months because' m3 W% C- U- T( k. |- R( i
the physical examination revealed the complete disap-* }$ g- g& f6 U
pearance of pubic hair, normal growth velocity, and6 V( T# j4 I# y% B
decreased erections. The father admitted using a testos-
6 C2 _5 R8 [1 z) g. Q! ^terone gel, which he concealed at first visit. He was
P0 v! g& w+ d& n- j8 Husing it rather frequently, twice a day. The Physicians’8 G: n! m6 Y$ J! _ ?7 U
Desk Reference, or package insert of this product, gel or
. q- L, |+ l$ p3 g$ @7 f+ \1 lcream, cautions about dermal testosterone transfer to7 b( ?3 o4 I, b. W
unprotected females through direct skin exposure.
8 a& e- C1 J8 v) O, ~Serum testosterone level was found to be 2 times the
% N- x- U, K. C+ t. }4 S' M( Lbaseline value in those females who were exposed to+ [$ P9 o o! {" L7 V
even 15 minutes of direct skin contact with their male
6 v# `& M/ V, `2 N* [partners.6 However, when a shirt covered the applica-& i; G9 ?1 } q z' s) n) b
tion site, this testosterone transfer was prevented.
: ~9 z9 ^4 o# @3 YOur patient’s testosterone level was 60 ng/mL,! U! D5 D4 p! z' f O" j* Q
which was clearly high. Some studies suggest that; O# g% a, } }- {- i8 W5 ~
dermal conversion of testosterone to dihydrotestos-
- c) M# N3 n T& rterone, which is a more potent metabolite, is more5 S$ L5 l5 K; Q8 y' W, v
active in young children exposed to testosterone; \' u: Z* f( r5 f. W* _# D; g
exogenously7; however, we did not measure a dihy-
" Y p$ C$ j4 D" _3 z) Cdrotestosterone level in our patient. In addition to
' Q- m3 X) y5 {4 @* O- i3 Gvirilization, exposure to exogenous testosterone in
3 @- b$ r0 j* B2 c6 b* |( R; bchildren results in an increase in growth velocity and# G5 E4 L8 A+ G" K( D7 G. n( U
advanced bone age, as seen in our patient.2 `7 x( m7 O& b1 a @/ O% V! |
The long-term effect of androgen exposure during0 h- h# @, i6 N# A) p0 |. B$ X
early childhood on pubertal development and final7 \! v+ y J2 V4 X+ Y; i6 y; ~
adult height are not fully known and always remain3 `% o; y# h! Q) Y0 e8 h* l, B
a concern. Children treated with short-term testos-9 ^, `3 N6 C/ M N4 X, u
terone injection or topical androgen may exhibit some
. G9 q% }% J1 H: ~( `' [acceleration of the skeletal maturation; however, after0 K% e, v) r) o% p
cessation of treatment, the rate of bone maturation. c. U0 O& b3 e4 g1 C% I" E P
decelerates and gradually returns to normal.8,9/ |% c) u: @; G4 u; X
There are conflicting reports and controversy
( b* x/ R) K9 i7 wover the effect of early androgen exposure on adult9 ]* _5 w3 I/ D( k9 E1 o! i
penile length.10,11 Some reports suggest subnormal4 D3 j: ?1 r. O4 w$ U
adult penile length, apparently because of downreg-5 Q; q0 N# P1 ?: K0 t- L
ulation of androgen receptor number.10,12 However,
5 \" w) u9 O2 B* H3 S, X* @Sutherland et al13 did not find a correlation between L( u3 }7 {* ?4 V
childhood testosterone exposure and reduced adult
5 Y& f, P2 ?3 v) Zpenile length in clinical studies.
X( c( I4 e" A6 eNonetheless, we do not believe our patient is
/ H0 T' S" H+ x4 s0 J8 }going to experience any of the untoward effects from- k' \: G4 S! Y* f# |7 b/ K. ?
testosterone exposure as mentioned earlier because! H8 }- i; g( B9 ]7 }# @( w
the exposure was not for a prolonged period of time.
( w1 M2 r$ x- s% m/ OAlthough the bone age was advanced at the time of! G% e5 S0 [4 A" x" q
diagnosis, the child had a normal growth velocity at
6 D2 e' q1 j t" E9 N- S6 ~the follow-up visit. It is hoped that his final adult( _- H5 p9 T4 y4 m0 Y( X! N
height will not be affected.
6 C8 G* Q, E2 g zAlthough rarely reported, the widespread avail-- _) a- s7 t [: v- E/ a% N$ t& O, |
ability of androgen products in our society may
) \; G$ x8 Z% T$ x V* X: nindeed cause more virilization in male or female& ]2 D! h' v4 c
children than one would realize. Exposure to andro-
5 W( E# [+ }3 u' Qgen products must be considered and specific ques-
/ i1 s# t1 O" w. Z& @) A- `tioning about the use of a testosterone product or
# L. ~* |9 r& b1 ?gel should be asked of the family members during7 i3 w7 P+ l- i! }1 e5 {
the evaluation of any children who present with vir-0 E! f4 J6 C- Z& z
ilization or peripheral precocious puberty. The diag-
9 A7 P7 `- P4 l$ V1 P4 Dnosis can be established by just a few tests and by
5 C0 S+ r! y d6 k* f+ Eappropriate history. The inability to obtain such a h4 }& y* {5 T6 T5 ~( D" M
history, or failure to ask the specific questions, may0 ~* F" d9 j R/ W
result in extensive, unnecessary, and expensive
, \, f3 g9 {; G; G4 {$ Sinvestigation. The primary care physician should be8 N t! C* F; l D. s' O
aware of this fact, because most of these children
_; p. A8 R- f, {) x9 b$ ^) l7 nmay initially present in their practice. The Physicians’
. Z8 H, F" C$ N' {Desk Reference and package insert should also put a
5 O1 M. T! C9 g) P/ k; ewarning about the virilizing effect on a male or
) U0 B4 B R' t) ^& a7 hfemale child who might come in contact with some-: T, U1 [4 X* U3 C/ ]0 [
one using any of these products.
0 y F) u/ k0 c% n0 @7 R& G8 Z7 NReferences
& ^4 x" a! A- [# I5 [1. Styne DM. The testes: disorder of sexual differentiation
( F" I- D0 L7 U8 d' i% qand puberty in the male. In: Sperling MA, ed. Pediatric
2 U. p, ~/ e$ j+ eEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% X# b/ n7 d- ` U. k; D2 f2002: 565-628.' G: w" Q5 \* m/ U- ^2 g! E' a: R
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% v7 c O$ P Z; h3 apuberty in children with tumours of the suprasellar pineal |
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