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Sexual Precocity in a 16-Month-Old
0 F. l& s7 m/ p, ~Boy Induced by Indirect Topical
$ `3 e% i9 ]( WExposure to Testosterone
. `( V; O; e& ?Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 k# d3 W9 i0 g8 C: H- V
and Kenneth R. Rettig, MD10 ~ ?' y2 I$ q
Clinical Pediatrics
$ y6 \1 U+ H( g& y2 cVolume 46 Number 6
' u. @/ p3 Z+ `' I. ^' |4 f- @July 2007 540-543
4 }. Z2 b; @) i# G© 2007 Sage Publications
& c6 ]& N+ c$ c1 {3 _5 R10.1177/0009922806296651/ \( U3 n0 Z6 {) ?" m6 r/ V
http://clp.sagepub.com4 t/ ]- m% A) @7 S' s5 Z+ ^
hosted at
4 {, u/ ?/ v0 q2 c/ x1 E3 whttp://online.sagepub.com
1 T9 S' a v: @( `) NPrecocious puberty in boys, central or peripheral,/ N: h8 \, l5 f' Q S9 Q
is a significant concern for physicians. Central
, u4 O( B$ k5 u, P# R5 {precocious puberty (CPP), which is mediated
2 C k- Q4 b' M/ Dthrough the hypothalamic pituitary gonadal axis, has; m4 X4 m0 T* t4 I! L i
a higher incidence of organic central nervous system/ }+ V' a9 P( Y! M& h
lesions in boys.1,2 Virilization in boys, as manifested1 t: f) Z& r! f) a! s4 t
by enlargement of the penis, development of pubic* C0 Z5 ~- O/ ~6 k
hair, and facial acne without enlargement of testi-) _- Y3 g, q; q# H' P
cles, suggests peripheral or pseudopuberty.1-3 We2 o1 d g. N R6 m: [
report a 16-month-old boy who presented with the% X( \. B9 Z5 Z3 ~
enlargement of the phallus and pubic hair develop-6 I& i. P b) A/ x8 t s
ment without testicular enlargement, which was due+ G9 @& P$ K/ w J" U% r
to the unintentional exposure to androgen gel used by L+ C& U- @" R2 I7 t! v3 H
the father. The family initially concealed this infor-
2 Q9 D: R9 T/ @$ m4 y/ i& ~# H1 ymation, resulting in an extensive work-up for this
+ e; t4 e% Y+ Nchild. Given the widespread and easy availability of" C. J. W7 I7 [: n2 \7 `. V
testosterone gel and cream, we believe this is proba-! I, T, C" a+ k
bly more common than the rare case report in the6 d+ |. A- p8 \2 F4 v& [
literature.4
2 w! y* T' L; W$ \/ f/ W/ U6 OPatient Report
+ Z- _5 _$ D; }$ S _A 16-month-old white child was referred to the: x6 f, |8 t: K% e) S
endocrine clinic by his pediatrician with the concern
' V" \+ H. i1 B. l5 l: y8 u+ g( Xof early sexual development. His mother noticed
/ t0 V1 G3 t& X7 k( P0 w- J1 Rlight colored pubic hair development when he was+ p7 v2 I' `1 M( c3 J# g5 y2 J
From the 1Division of Pediatric Endocrinology, 2University of$ D5 L4 M9 e% f% d& n
South Alabama Medical Center, Mobile, Alabama.
$ A0 I/ Y; }# m4 y* MAddress correspondence to: Samar K. Bhowmick, MD, FACE,
; _; v) S6 X0 Z& X% j2 A( wProfessor of Pediatrics, University of South Alabama, College of
2 X0 u- T- `9 N: A6 D( eMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 z( _5 X! t' Z- L! v te-mail: [email protected].3 j8 W: p1 t& G8 A# H
about 6 to 7 months old, which progressively became2 {9 I: c) ?: q1 s8 v
darker. She was also concerned about the enlarge-9 O b% t! X& n9 o: g3 }( V! n
ment of his penis and frequent erections. The child
: |, {5 b- f; I& swas the product of a full-term normal delivery, with
' P9 B& O" [* m* s) l# W! j# j( ma birth weight of 7 lb 14 oz, and birth length of
# E5 C, _$ E0 ^' H8 B: f20 inches. He was breast-fed throughout the first year
) x$ B2 I+ C& O5 w' Dof life and was still receiving breast milk along with7 h( {' O- y0 j# W( l
solid food. He had no hospitalizations or surgery,
$ Y8 d1 i# A4 P( \/ @and his psychosocial and psychomotor development
4 O3 ^3 j( @4 h& E+ [! L; I: ~was age appropriate.
8 U9 j( n( ]+ u. F- @4 `The family history was remarkable for the father,+ ~# I6 F! q% d( o4 p2 G- `
who was diagnosed with hypothyroidism at age 16,; N# @2 y! b8 l* Y. T
which was treated with thyroxine. The father’s% l+ q% k8 ^, d. ^+ H. c
height was 6 feet, and he went through a somewhat: a/ y/ t- p2 Q& [) q
early puberty and had stopped growing by age 14.
% H! D, I4 |/ q% YThe father denied taking any other medication. The
0 `& ^) k$ t T0 q% `/ Zchild’s mother was in good health. Her menarche
! F# R# ~# q5 xwas at 11 years of age, and her height was at 5 feet& v: Q8 k9 g2 e7 z+ G' ^1 z) c7 T
5 inches. There was no other family history of pre-
( W Q: N! d2 x6 }6 y! ]+ wcocious sexual development in the first-degree rela-
1 y9 \7 J' t. f1 W$ `. {tives. There were no siblings.
7 R; x( f/ X- Q1 E, KPhysical Examination
$ F1 W# r9 N7 i+ aThe physical examination revealed a very active,
& E% f. F( G$ g* D+ g3 xplayful, and healthy boy. The vital signs documented
+ f2 M* P2 Q, ?/ [, ]: Ya blood pressure of 85/50 mm Hg, his length was
5 I8 B s5 A, \- I90 cm (>97th percentile), and his weight was 14.4 kg. q3 M0 l& i- j- }& t/ O
(also >97th percentile). The observed yearly growth
, A+ C& ~& w7 n0 Pvelocity was 30 cm (12 inches). The examination of5 Y3 M1 i2 i! t2 G$ R. n
the neck revealed no thyroid enlargement.* r5 B" b2 j# A$ D+ G
The genitourinary examination was remarkable for+ D. z2 Q8 {4 x( P5 Y6 k7 ~9 B( T
enlargement of the penis, with a stretched length of/ e0 E/ x! a' ]9 q0 s
8 cm and a width of 2 cm. The glans penis was very well1 l" k& r9 C3 @& _* L# h
developed. The pubic hair was Tanner II, mostly around
& X) J1 R7 I. x4 L2 L540
" q1 O5 N, ?( p8 Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; c2 H8 {9 W* z0 {9 m1 p2 ~* f
the base of the phallus and was dark and curled. The
! d/ X" p& {9 Btesticular volume was prepubertal at 2 mL each.3 u5 T3 c6 |& A% O; B7 i
The skin was moist and smooth and somewhat
2 `* i3 R+ C' i) V: d) c" Foily. No axillary hair was noted. There were no b9 R g2 k* }7 o M- S7 Y
abnormal skin pigmentations or café-au-lait spots.: P1 ?! E& J, a2 x$ g) J
Neurologic evaluation showed deep tendon reflex 2+, C! F: i+ j4 Y8 v. ]
bilateral and symmetrical. There was no suggestion( u2 n6 M1 X, u, t9 h4 i$ r- q
of papilledema.
) W' a# i; l) ^8 g" o, dLaboratory Evaluation8 y, `& C4 M* g/ y/ A' n$ R- a
The bone age was consistent with 28 months by
) ?! d) Y# x/ ~7 t8 y3 G, Qusing the standard of Greulich and Pyle at a chrono-- E) y! Q6 e3 W! W- b2 ^
logic age of 16 months (advanced).5 Chromosomal
4 Y! E; f: s) {: m1 H5 rkaryotype was 46XY. The thyroid function test
0 J* t: _4 b" Zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 I' _1 W4 x# m: h8 ^lating hormone level was 1.3 µIU/mL (both normal).! A( a8 D b0 c' q. W
The concentrations of serum electrolytes, blood
5 @" g- ~1 H5 ^5 F# \8 Aurea nitrogen, creatinine, and calcium all were
& {9 L) I3 G) ]! V- Gwithin normal range for his age. The concentration
7 p, P( @2 e! q, I* S* l$ Vof serum 17-hydroxyprogesterone was 16 ng/dL
3 m a( ]3 D& u c(normal, 3 to 90 ng/dL), androstenedione was 20( H4 ^0 b2 g; ?3 c/ a
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 x* c# t9 j) g6 {7 g" Z( I6 G
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 T! y M5 {* x" odesoxycorticosterone was 4.3 ng/dL (normal, 7 to4 {+ W1 _* l# u6 `$ t
49ng/dL), 11-desoxycortisol (specific compound S)
( @* B7 L3 J0 s: @was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 M9 s' U; _' Y8 ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. l/ y5 |$ W/ |; N. O: ^$ h: h* |) ]
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),# a+ G: ]2 r) a4 u
and β-human chorionic gonadotropin was less than+ p% S9 j8 c6 W Y" O% K- x1 e, a
5 mIU/mL (normal <5 mIU/mL). Serum follicular0 [- Z7 m2 f6 h
stimulating hormone and leuteinizing hormone0 ^8 Q2 J, W; L$ J+ \, m
concentrations were less than 0.05 mIU/mL; d$ C y8 S4 i5 _- m/ O7 ~
(prepubertal).+ @* X8 A3 E0 u$ ?
The parents were notified about the laboratory# L6 x b3 ^" k, ~7 i( g7 J% S2 Q
results and were informed that all of the tests were
% r- }0 ?: F5 Y! `5 Inormal except the testosterone level was high. The- B U0 S# C! E$ c* {
follow-up visit was arranged within a few weeks to
4 k4 s6 e( Q8 r: Q1 x6 Uobtain testicular and abdominal sonograms; how-) o! \* ]$ j1 E2 N
ever, the family did not return for 4 months.; u- e" t% i7 |$ T
Physical examination at this time revealed that the
! q+ e% t; V/ m2 ~& i( Gchild had grown 2.5 cm in 4 months and had gained) f4 h! W: d& g7 a; ?, N
2 kg of weight. Physical examination remained
! t) {* D: A7 F% \5 Qunchanged. Surprisingly, the pubic hair almost com-- i9 X4 S* d# g/ s1 t+ X
pletely disappeared except for a few vellous hairs at% ~3 G. D3 E2 u1 i0 |
the base of the phallus. Testicular volume was still 2
6 y6 ?2 Z9 ], q- W( d. [mL, and the size of the penis remained unchanged.2 L! ?1 ^: p0 t8 n. ~5 R: e3 q( Z
The mother also said that the boy was no longer hav-
* k6 ]8 Q6 C" P: Oing frequent erections.( x \" z) _) f) i- s" o8 ~) m5 e
Both parents were again questioned about use of
0 o* v( d, F- }% j% cany ointment/creams that they may have applied to% ^, b% f& H2 p" h
the child’s skin. This time the father admitted the! U0 ~4 B! h, x. G* d9 a
Topical Testosterone Exposure / Bhowmick et al 541
; f( ]) j5 g2 N g1 F# _use of testosterone gel twice daily that he was apply-
8 T m4 n0 O4 L: I4 Bing over his own shoulders, chest, and back area for+ Z' o+ S1 [0 \! n$ b' O# j
a year. The father also revealed he was embarrassed: Y& W1 E+ V* m
to disclose that he was using a testosterone gel pre-
) |0 M; _% R' h/ z2 n1 ascribed by his family physician for decreased libido
0 I( S; S( A% O( esecondary to depression.
6 Y. l( z7 |! QThe child slept in the same bed with parents.% `* z7 ~, m' S- k2 f2 i
The father would hug the baby and hold him on his
0 j) X8 Z0 W f8 C+ t# | Schest for a considerable period of time, causing sig-
# n9 ?' G6 T$ G" A( `& x3 J: S" Cnificant bare skin contact between baby and father.
! n& n g- V, L& `- {5 b9 ^( YThe father also admitted that after the phone call,( r( Q) w8 p8 j$ G/ x
when he learned the testosterone level in the baby
) b4 B( G# B7 ^5 b$ J* Lwas high, he then read the product information
6 T. J: b3 h1 P: Y ipacket and concluded that it was most likely the rea-
/ t. S: R; q- p5 N7 K, A9 B3 L& Y/ ^son for the child’s virilization. At that time, they
- Y4 r+ M+ r' i+ M( T5 pdecided to put the baby in a separate bed, and the% @# N3 a; n7 K' w0 z
father was not hugging him with bare skin and had
V6 b* U+ Z, \5 g1 tbeen using protective clothing. A repeat testosterone
% k- j1 K# A/ btest was ordered, but the family did not go to the4 A" k7 _1 O7 T7 q# L" f- A
laboratory to obtain the test.
" R' z7 t+ e0 W3 l; dDiscussion
) {: Y) R- W0 R2 q9 {! {Precocious puberty in boys is defined as secondary+ e% \$ U& o3 i ^) m, e6 }$ t( y8 k
sexual development before 9 years of age.1,4) u) _$ A0 n: K( L
Precocious puberty is termed as central (true) when- J% f9 N. N+ r' Q
it is caused by the premature activation of hypo-4 v3 l" u |% g$ i; [ Y% ~
thalamic pituitary gonadal axis. CPP is more com-3 o+ V% d& s/ w
mon in girls than in boys.1,3 Most boys with CPP
1 Y6 Z: K) e0 z h! g" ^* lmay have a central nervous system lesion that is- E& g# V q& V1 v3 ?5 X9 v8 X* D
responsible for the early activation of the hypothal-
2 ]3 p/ ^& ?7 `. yamic pituitary gonadal axis.1-3 Thus, greater empha-
: Y Q, F' A# Y zsis has been given to neuroradiologic imaging in
. X: p$ k1 o) q6 wboys with precocious puberty. In addition to viril-7 K% c8 W1 I+ A: s2 L
ization, the clinical hallmark of CPP is the symmet-; y @7 V1 e/ m
rical testicular growth secondary to stimulation by
. v2 b z z& w! agonadotropins.1,3
2 }0 I$ b0 ^% M7 l2 {+ wGonadotropin-independent peripheral preco-
! Q5 i9 \3 @: Z/ O' _" u. Scious puberty in boys also results from inappropriate$ _; G4 n8 G6 s
androgenic stimulation from either endogenous or$ \ P1 ?" x2 F, ?' [* b" Q4 ~4 {
exogenous sources, nonpituitary gonadotropin stim-
9 A5 }' ^( ~+ m; Q* n# mulation, and rare activating mutations.3 Virilizing
; `! Q) j: U! Y9 Xcongenital adrenal hyperplasia producing excessive& H" i3 @8 E5 X& s( H/ m: c' G! F
adrenal androgens is a common cause of precocious
% V" w: U# L4 k; M) j8 Apuberty in boys.3,48 W1 [" f" P3 W Q: X4 f# j/ h
The most common form of congenital adrenal
! E! m& ]" d5 I# }7 shyperplasia is the 21-hydroxylase enzyme deficiency.
5 m2 c" V. M# C4 R7 hThe 11-β hydroxylase deficiency may also result in
7 J) C. w/ Z- B* L, f& fexcessive adrenal androgen production, and rarely,3 }3 [! Q1 z: z
an adrenal tumor may also cause adrenal androgen
* s- v( k/ ?6 _7 l mexcess.1,3- a; B* J0 l0 \ I5 ?9 n
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ L" u: @& s' B5 h$ j542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 H- H( Y7 Z+ x5 p. NA unique entity of male-limited gonadotropin-
, c0 x( Q& ^7 Y8 _' xindependent precocious puberty, which is also known
# C- ]- s0 ?& s% x# sas testotoxicosis, may cause precocious puberty at a
/ Z: I) z6 G$ x6 ^' U! [very young age. The physical findings in these boys
1 b, I: G' n, x$ k& H- Wwith this disorder are full pubertal development,
- q: e! {" q6 m# `, I+ @% H8 r8 pincluding bilateral testicular growth, similar to boys
]( A. [) t' Ewith CPP. The gonadotropin levels in this disorder
( G* Y% }& I& ?: r* Sare suppressed to prepubertal levels and do not show
) v- a4 w4 `4 R0 Cpubertal response of gonadotropin after gonadotropin-
* d) w9 l2 G: ] s( h5 creleasing hormone stimulation. This is a sex-linked
- j) N+ Q8 q- s3 p- \' ]# R iautosomal dominant disorder that affects only+ [8 \- D0 Z' f$ P4 \ h9 s$ z' }
males; therefore, other male members of the family2 ~/ j+ V( U9 f6 d' o" ~
may have similar precocious puberty.3
) |9 o# a* b1 V L% k. NIn our patient, physical examination was incon-$ x5 u0 N# g F
sistent with true precocious puberty since his testi-& k+ Y' [: ?5 m
cles were prepubertal in size. However, testotoxicosis
8 z6 C/ ^2 F" g) \* I) Q+ [5 cwas in the differential diagnosis because his father7 L4 l* q6 n" V/ o+ N8 {; z. Q
started puberty somewhat early, and occasionally,
w4 f6 P" r' i* dtesticular enlargement is not that evident in the
) r3 G+ j& a; z0 M: d! abeginning of this process.1 In the absence of a neg-
6 \5 b/ K$ Y( i% o+ a8 aative initial history of androgen exposure, our: r7 ?8 R4 Q: ^. j5 o( h& i
biggest concern was virilizing adrenal hyperplasia,# `. e5 L- c# |
either 21-hydroxylase deficiency or 11-β hydroxylase
" ]+ S3 \/ T9 y' W" d, W$ l Qdeficiency. Those diagnoses were excluded by find-
1 s. K; q4 t8 E7 zing the normal level of adrenal steroids.
. l z; d) ]5 R6 i; x/ SThe diagnosis of exogenous androgens was strongly
% S0 L, L8 _- A0 d% |9 Lsuspected in a follow-up visit after 4 months because
' b. l" f5 U3 Z, Mthe physical examination revealed the complete disap-# e$ |) K$ C& Z# C/ T+ O: l ^. G
pearance of pubic hair, normal growth velocity, and) V' X% x5 K8 r2 d
decreased erections. The father admitted using a testos-' `. o# E5 H8 s) x) R5 Y6 c
terone gel, which he concealed at first visit. He was6 s) j4 \' N- D2 f+ D
using it rather frequently, twice a day. The Physicians’6 r0 W- @7 d3 J( K: q7 Q
Desk Reference, or package insert of this product, gel or! G. \& o1 H: u4 Q( @
cream, cautions about dermal testosterone transfer to& ?& S& j* h; N
unprotected females through direct skin exposure.- i6 _ F% R. v/ y# P
Serum testosterone level was found to be 2 times the
) t z R. w4 G2 A I8 Q" Xbaseline value in those females who were exposed to7 N0 h* b& K3 d& ~ B6 n2 l1 L7 o
even 15 minutes of direct skin contact with their male
! Y- `8 @# V/ l$ N/ k8 v. r( [% r6 epartners.6 However, when a shirt covered the applica-
! n3 i( ]! D/ w2 U; w. ition site, this testosterone transfer was prevented.. g2 Q9 M; B8 o0 Q3 z
Our patient’s testosterone level was 60 ng/mL,
, k2 v4 ]. p( F- _which was clearly high. Some studies suggest that- D2 {7 M" t2 j4 W$ R& i) X
dermal conversion of testosterone to dihydrotestos-" j7 k4 m$ |, v% l( ]1 _
terone, which is a more potent metabolite, is more% {' y$ I" o% A# ?7 F# ?
active in young children exposed to testosterone
$ D; N' c4 v: G8 u0 j& Texogenously7; however, we did not measure a dihy-2 M/ E, C' e: Z; W8 v) ]8 c: j
drotestosterone level in our patient. In addition to
5 C! [ I, z, @# @: {, \/ Rvirilization, exposure to exogenous testosterone in
, f0 `8 \$ O) _. m7 ?( J9 O8 W- q5 w/ Pchildren results in an increase in growth velocity and
# _0 q( b* R; D* x5 Dadvanced bone age, as seen in our patient.5 n; W5 P5 {8 I, t3 Y
The long-term effect of androgen exposure during
3 M3 C$ u4 k; s# ]3 V! dearly childhood on pubertal development and final- g1 n& }/ ~! f' S
adult height are not fully known and always remain
% `0 @! y: U# \a concern. Children treated with short-term testos-# o: ? K4 m4 N
terone injection or topical androgen may exhibit some
0 b) D( i! P. W$ c4 N% lacceleration of the skeletal maturation; however, after7 ~- S& F2 k; Y+ W
cessation of treatment, the rate of bone maturation7 E* f3 z$ j, V$ N6 I, Q S
decelerates and gradually returns to normal.8,9; x! t, m' C' Q( Z6 \5 y, L g
There are conflicting reports and controversy9 |; \9 C) y& C% p8 O
over the effect of early androgen exposure on adult; F: f2 N& h7 o+ i7 k7 a
penile length.10,11 Some reports suggest subnormal
5 s2 q8 O' S4 v( Y5 x$ \% J( d, ladult penile length, apparently because of downreg-" d! c) H5 [$ [: _9 O( f
ulation of androgen receptor number.10,12 However,4 m: j7 `3 h! G% l% S
Sutherland et al13 did not find a correlation between5 O) r" p7 u' q m; U# L
childhood testosterone exposure and reduced adult; p: z& R- K W4 V$ _
penile length in clinical studies., h9 R3 ?9 L# Y4 I0 \, ?" p
Nonetheless, we do not believe our patient is* H+ ?" c8 C4 A u2 ]5 f
going to experience any of the untoward effects from
* `, \( I( w. r. m! o+ g6 ]2 p0 ~testosterone exposure as mentioned earlier because. {. Z9 T. ~: D: B0 ^& u% t
the exposure was not for a prolonged period of time.
1 Z; J3 g& q' m1 M3 a/ i. c# M! ZAlthough the bone age was advanced at the time of! d$ k9 M6 q$ I4 e0 L
diagnosis, the child had a normal growth velocity at1 c5 z4 T A. @/ d/ o% W; @" E
the follow-up visit. It is hoped that his final adult" }% c( ^* m. U ]
height will not be affected.
* p5 V/ P ?6 H% EAlthough rarely reported, the widespread avail-
* J8 ?( c' ~. t5 l. f% m5 ?& jability of androgen products in our society may
$ G! o( c5 j2 j j, L" hindeed cause more virilization in male or female/ b) d& H l' j/ y7 R4 | ]5 n
children than one would realize. Exposure to andro-% W l: j4 \3 O1 g2 Y) q1 i6 z
gen products must be considered and specific ques-
7 n, F0 H* k3 h; v4 Gtioning about the use of a testosterone product or
" m8 |# o! ~) U! n9 tgel should be asked of the family members during
- P6 A# ]9 @7 f- O b: Zthe evaluation of any children who present with vir-+ X, G' \% i$ Q9 O0 k
ilization or peripheral precocious puberty. The diag- N# z8 d5 l1 F' o
nosis can be established by just a few tests and by
# _# \0 V$ a9 Pappropriate history. The inability to obtain such a
& n$ k4 }$ z$ T" O4 T) Whistory, or failure to ask the specific questions, may& [- c+ N, z! E: ?) D7 j
result in extensive, unnecessary, and expensive5 C! K n U/ `/ v5 w5 a, m
investigation. The primary care physician should be- d% b( j. v4 l# T f
aware of this fact, because most of these children) k2 }0 J# Q7 P3 M# m3 M; H
may initially present in their practice. The Physicians’
4 _* t7 z6 H) n3 k, |Desk Reference and package insert should also put a
, v n7 D( \1 n$ w8 Z0 b; u# nwarning about the virilizing effect on a male or
8 p* t, I( g% m% Yfemale child who might come in contact with some-
7 k6 l+ k7 K6 None using any of these products.
5 Q) v3 q7 q3 x2 d" @! u6 sReferences
9 |: x6 |; w7 E7 e1 H1. Styne DM. The testes: disorder of sexual differentiation9 a6 J" P. D0 R& l8 ?
and puberty in the male. In: Sperling MA, ed. Pediatric! I3 i! I6 i# `0 k# K2 D
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( u. `7 i* V, O7 @9 O+ u
2002: 565-628.+ e1 j3 N& G( T* N6 M0 D4 F4 ]/ J
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* f/ K: a5 k% t; [; V+ Bpuberty in children with tumours of the suprasellar pineal |
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