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Sexual Precocity in a 16-Month-Old
( ~! f4 F, _6 f6 ^1 ]Boy Induced by Indirect Topical
* ~( |, {% B i9 ?& D% ^! vExposure to Testosterone
1 i2 d1 ~3 k# E" K) }2 t# lSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
/ t8 X! t6 `" P5 b/ ~8 {% Xand Kenneth R. Rettig, MD1
* F7 }2 U5 H% M1 FClinical Pediatrics
* n$ ]8 H# r. x! RVolume 46 Number 65 G& Q; d: l0 i" _; m# K/ v
July 2007 540-543- s- }) \& A1 N N9 x3 J
© 2007 Sage Publications
9 V# u) E# F! ` n- S10.1177/00099228062966513 U* z5 a4 Z* D9 G, ^9 \$ L0 _ ^- y' H5 J
http://clp.sagepub.com
. n' `3 D& q# F5 I% v8 h( V; Q Xhosted at% ?" r) y/ l+ q9 k, }# O3 x' w ~
http://online.sagepub.com& _: G! \) I$ R* ]0 V: D
Precocious puberty in boys, central or peripheral,3 T: u3 P7 e2 p* C
is a significant concern for physicians. Central# d" |5 S! J0 q
precocious puberty (CPP), which is mediated
) [) E6 r/ u/ gthrough the hypothalamic pituitary gonadal axis, has8 @+ W1 Q- r. ]9 m
a higher incidence of organic central nervous system
* D/ G% z, z hlesions in boys.1,2 Virilization in boys, as manifested# i+ m7 h. p% ?& K J6 K( u
by enlargement of the penis, development of pubic
# @/ A! j( l7 |: E9 Z. Phair, and facial acne without enlargement of testi-
1 |6 ?, D4 y4 X# Z3 t! |cles, suggests peripheral or pseudopuberty.1-3 We
# ^( S. h9 j/ ?, \report a 16-month-old boy who presented with the1 z( b- u+ E7 ?3 |5 K! Z2 v
enlargement of the phallus and pubic hair develop-
" I+ s; g4 G3 a$ Z* Nment without testicular enlargement, which was due
+ ~1 e# x5 r' I- `% Cto the unintentional exposure to androgen gel used by
3 U C. t2 @" `/ @2 i2 S# d. T9 rthe father. The family initially concealed this infor-
& a( q. j7 k/ L/ ~& cmation, resulting in an extensive work-up for this& b8 ?/ b' b3 R4 s- F: A2 d. [, b% ?4 S
child. Given the widespread and easy availability of' I. d( d* Q9 n* I1 K# B
testosterone gel and cream, we believe this is proba-7 Z% h3 b3 \2 ?4 q
bly more common than the rare case report in the
: {1 F n. d* j( V+ Jliterature.4
. g" C' j% ~$ V; Z) gPatient Report
. ?2 f! {* }6 a' Z- k/ d5 ?; A AA 16-month-old white child was referred to the+ m0 Y* }( @8 x2 s
endocrine clinic by his pediatrician with the concern4 L: u# X# d. B9 C
of early sexual development. His mother noticed6 F) M' n, e: h9 U/ r4 Q! c
light colored pubic hair development when he was
! [4 v# c. g) z; t: n$ xFrom the 1Division of Pediatric Endocrinology, 2University of) G6 z/ ?) u! T, Z4 k" d
South Alabama Medical Center, Mobile, Alabama.& ]7 h0 i# w- @. {+ L
Address correspondence to: Samar K. Bhowmick, MD, FACE,
. n; I: J3 P, {* Q, RProfessor of Pediatrics, University of South Alabama, College of& ]/ |# I6 t! _7 V& {+ l9 G7 N9 R
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! y9 o; A$ P! s: D1 a) Ie-mail: [email protected].
; j* m% d/ M+ o, Eabout 6 to 7 months old, which progressively became
: i/ B: J) O) v( Udarker. She was also concerned about the enlarge-0 i" i) `8 W6 K8 y3 \
ment of his penis and frequent erections. The child+ [9 m! \& [: M ? z7 G: T( k
was the product of a full-term normal delivery, with& g* o; P) p* L" h7 z
a birth weight of 7 lb 14 oz, and birth length of/ X' q6 X: `, y, m/ j
20 inches. He was breast-fed throughout the first year2 F' m" Z1 ^( Z* o# l
of life and was still receiving breast milk along with
; X( m4 _& c; n/ X/ r/ S' h# Vsolid food. He had no hospitalizations or surgery,
, G& q r, y* x' {and his psychosocial and psychomotor development
. r0 u9 |9 W/ o9 z( G$ ywas age appropriate.
3 i h' h6 @- w0 n/ ]) }3 ]2 A9 |The family history was remarkable for the father,
! L6 d: m7 @* ]0 V7 L1 K2 ?who was diagnosed with hypothyroidism at age 16,
2 s9 k4 k' N( \* i7 ~- Z, jwhich was treated with thyroxine. The father’s
0 ~$ [2 N- A* X, ?# e, [9 Kheight was 6 feet, and he went through a somewhat) S1 B5 C) }+ J4 h; R" [- k
early puberty and had stopped growing by age 14.# x. Z& m5 I" Z: G
The father denied taking any other medication. The5 m9 l+ s8 |1 o/ r6 w$ O' x1 s
child’s mother was in good health. Her menarche+ e% r' ~% W7 O8 l
was at 11 years of age, and her height was at 5 feet
1 }% s w0 s: Q6 t) s/ ^5 inches. There was no other family history of pre-" D6 s. }, W4 o% V' `
cocious sexual development in the first-degree rela-6 N. D7 v$ w) a' p9 _
tives. There were no siblings.: r4 y$ D6 e9 J% N. R! _
Physical Examination
9 e7 A' ~$ r6 Y5 wThe physical examination revealed a very active,3 h8 {/ K9 u! ^ t1 \1 Q+ P5 L
playful, and healthy boy. The vital signs documented* F7 ?+ V: S6 [) @
a blood pressure of 85/50 mm Hg, his length was
. J8 o) D" Y7 u& S1 E' g90 cm (>97th percentile), and his weight was 14.4 kg
6 p5 O" j$ s# K) W1 }(also >97th percentile). The observed yearly growth
& `: |0 m( H8 C/ S, vvelocity was 30 cm (12 inches). The examination of
# t4 m3 \0 c4 T! athe neck revealed no thyroid enlargement.; w( `2 ?/ g0 `0 W
The genitourinary examination was remarkable for
5 e4 b) X" a0 M- Tenlargement of the penis, with a stretched length of: Y1 F' b" A) }* U$ A3 E
8 cm and a width of 2 cm. The glans penis was very well8 P9 f: e& Y8 V G3 f
developed. The pubic hair was Tanner II, mostly around
! Y" c& N z0 Z O( d+ V& X540
O( J- l+ {5 Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" G* D0 c' e& v* p9 Pthe base of the phallus and was dark and curled. The
2 V& M! e, x. Q& @" t8 }testicular volume was prepubertal at 2 mL each.5 V/ v8 B9 i4 ]4 T0 D
The skin was moist and smooth and somewhat$ o! k p! P' r2 y9 _
oily. No axillary hair was noted. There were no0 A1 m, p/ A" {4 F" P; x0 Q
abnormal skin pigmentations or café-au-lait spots.0 K S2 x1 o4 x! ^* ^! a3 g
Neurologic evaluation showed deep tendon reflex 2+) ^4 s$ a! c9 u& o
bilateral and symmetrical. There was no suggestion
# G& I1 L+ W. g4 `% {+ Yof papilledema.
" D6 ~( [* ^! s% o4 g6 ?- b% d7 rLaboratory Evaluation8 J5 N0 O# K& Y, `
The bone age was consistent with 28 months by4 e* d8 m0 W/ y% A( L8 u) r) a$ B
using the standard of Greulich and Pyle at a chrono-) d7 Z4 N/ Z6 E% D
logic age of 16 months (advanced).5 Chromosomal
8 {' p# M# N- b1 {karyotype was 46XY. The thyroid function test1 t6 E- ^0 L& w0 e5 M& e
showed a free T4 of 1.69 ng/dL, and thyroid stimu- W5 I& y8 t' z7 E3 a* J% u# n" I$ P
lating hormone level was 1.3 µIU/mL (both normal).
# o" c$ w: _, gThe concentrations of serum electrolytes, blood
# W) L3 \0 v4 N7 Gurea nitrogen, creatinine, and calcium all were5 g4 B# `. @8 q2 G
within normal range for his age. The concentration
, U: ]7 u3 t0 h8 V0 @) T! Y$ o; ~of serum 17-hydroxyprogesterone was 16 ng/dL
& f- A+ v4 U# _* k! h4 [% W1 ]) z(normal, 3 to 90 ng/dL), androstenedione was 20& r5 d1 h% {0 `5 i
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 J4 f4 p9 ]# V0 d% U; r* m
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
% E3 j$ N" b, ]; X+ b1 B9 Ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ y# E. t, v; L& q49ng/dL), 11-desoxycortisol (specific compound S)
) S( ]/ |5 Y+ Wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor- f+ }; h- v2 t, a/ w u1 L
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: }7 C$ F1 D9 b- n7 j$ d& R% k# ^testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& b$ d3 M V7 ]& X* c0 band β-human chorionic gonadotropin was less than- v( \" c& Q, N, |
5 mIU/mL (normal <5 mIU/mL). Serum follicular4 s' E) `; m5 c& p9 k
stimulating hormone and leuteinizing hormone+ |9 o9 l8 C, W# o- B9 {, d
concentrations were less than 0.05 mIU/mL; `) H/ {' D) w' X# @+ j5 T
(prepubertal)./ o Y. v% V6 |3 S
The parents were notified about the laboratory
2 a7 L! g6 i: M7 h) Kresults and were informed that all of the tests were; J( F$ N2 c2 L1 g
normal except the testosterone level was high. The
6 d3 u: ]( {6 [ q! Ofollow-up visit was arranged within a few weeks to" G) e+ ]1 t3 G
obtain testicular and abdominal sonograms; how-. y( j& t( t* G0 g& @2 j6 k
ever, the family did not return for 4 months.. ]+ x" A$ O5 ^4 N, p; {8 G
Physical examination at this time revealed that the' w4 q0 K/ `6 `1 ~5 k) M0 e" B
child had grown 2.5 cm in 4 months and had gained
2 V% I% N, A) y! M7 g% Z2 kg of weight. Physical examination remained
4 [6 ~1 v8 x" Ounchanged. Surprisingly, the pubic hair almost com-( B4 |" a( n! `3 p5 b3 _
pletely disappeared except for a few vellous hairs at
3 f, O+ n. ~ N1 L# e ^the base of the phallus. Testicular volume was still 2& G+ k( S/ D2 Q4 p( R
mL, and the size of the penis remained unchanged.
& D( G# s3 e% a* c/ RThe mother also said that the boy was no longer hav-# f. A$ ]# D3 b+ K9 E! ]6 X. y
ing frequent erections.- ^: k7 a* n( h P$ Y) T& h
Both parents were again questioned about use of
0 V6 ]1 R: w/ e5 ^any ointment/creams that they may have applied to
9 x6 U6 X9 q0 E' kthe child’s skin. This time the father admitted the. J. r/ c$ V, f5 _6 t
Topical Testosterone Exposure / Bhowmick et al 5415 n$ L# o4 g% ?6 P
use of testosterone gel twice daily that he was apply-
* @) x) \1 t! x- o3 ~! }1 X, ding over his own shoulders, chest, and back area for
3 X! T4 j5 P C7 f" J9 ?9 A$ _# _a year. The father also revealed he was embarrassed& ?5 }4 j- c |& B- N, h$ ^
to disclose that he was using a testosterone gel pre-9 r! q8 u, {; R) S& a
scribed by his family physician for decreased libido0 S* G) V! W# `" V% g3 l- W
secondary to depression.5 d* Y8 t5 {: T4 ^( E
The child slept in the same bed with parents.
, G2 @0 [) N+ o0 t4 bThe father would hug the baby and hold him on his# g5 i J8 ^# X% h/ C E, n* l
chest for a considerable period of time, causing sig-) @9 x* o, R* C$ K
nificant bare skin contact between baby and father.
; F1 ?" T9 p: l, }$ V8 IThe father also admitted that after the phone call,
3 ?; _. p3 z2 X0 Y* nwhen he learned the testosterone level in the baby8 j3 B- q" f0 L
was high, he then read the product information$ m1 K; r7 {4 p* ~
packet and concluded that it was most likely the rea-$ m- Y* i5 _. m3 f. c/ _/ v- O
son for the child’s virilization. At that time, they
' _: t8 c) R" e1 Y. ?7 W* ^+ K6 |decided to put the baby in a separate bed, and the5 x, B' p1 b2 J) G3 e; ^" l
father was not hugging him with bare skin and had& C6 Y2 A J; s1 `. I- o2 z
been using protective clothing. A repeat testosterone
5 B5 A- Y/ H) X2 ctest was ordered, but the family did not go to the- j4 d& l# F/ _( e" M9 [- P: n
laboratory to obtain the test./ z% G3 n) w5 a% k( A @
Discussion5 W* d4 l" T- g! O, l
Precocious puberty in boys is defined as secondary
" i8 L- ]. D/ k$ w2 r2 m& zsexual development before 9 years of age.1,45 Q- o* `0 W9 h; W/ \
Precocious puberty is termed as central (true) when
, N1 H4 Q+ x5 I. Y) \, @it is caused by the premature activation of hypo-: t4 L+ W4 O+ G5 B0 F: G8 }7 \0 i) ?
thalamic pituitary gonadal axis. CPP is more com-
: j1 H) e9 j' l* ymon in girls than in boys.1,3 Most boys with CPP
" i5 n, A- K, }- Cmay have a central nervous system lesion that is
# R+ [/ \# Z4 M+ jresponsible for the early activation of the hypothal-
- t. i* o# X2 d5 W( xamic pituitary gonadal axis.1-3 Thus, greater empha-
" y- L* Q, T" d2 Tsis has been given to neuroradiologic imaging in
6 f7 r& {& p3 i4 C7 u7 m+ B" Jboys with precocious puberty. In addition to viril-' F; ?* m: N8 M# k1 L
ization, the clinical hallmark of CPP is the symmet-5 y* r5 s9 @2 w; C: N Y' l2 Q1 r
rical testicular growth secondary to stimulation by
4 V* w) U4 Z2 a9 Xgonadotropins.1,3
& L6 `, F1 {) x! Z! E @& y6 ~! BGonadotropin-independent peripheral preco-" [: p* I; D# Y5 S- _( A
cious puberty in boys also results from inappropriate2 p2 w+ u2 Q- X0 m
androgenic stimulation from either endogenous or8 @/ O& ^7 |$ r V! U" @; Z
exogenous sources, nonpituitary gonadotropin stim-7 j y6 \/ `$ c$ U/ S) _
ulation, and rare activating mutations.3 Virilizing
, o/ _0 k9 u; Qcongenital adrenal hyperplasia producing excessive
/ N4 I k/ h- [( e, Tadrenal androgens is a common cause of precocious, q* [ j, [ }" ?4 T1 p6 z
puberty in boys.3,4' S8 @! f3 ?7 _% {
The most common form of congenital adrenal
- T8 h) C5 n# h D9 W& u* {hyperplasia is the 21-hydroxylase enzyme deficiency.
" T1 C, E: c; v! R/ F) zThe 11-β hydroxylase deficiency may also result in
L5 _ C2 G5 p$ w! J. b5 o$ h0 C/ K: \" Yexcessive adrenal androgen production, and rarely,# u5 T7 d" S: k s
an adrenal tumor may also cause adrenal androgen
' l2 P/ r: D- D# R v9 Y1 m$ w& Jexcess.1,3
8 E, U" u/ K8 E; v- ?% G% eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ p- |/ V$ B. D542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
" `( y2 N0 c% `+ S6 T4 E8 DA unique entity of male-limited gonadotropin-2 z \9 Y0 u% m- M
independent precocious puberty, which is also known
$ K6 ^& L& N$ t9 t! q. e/ V' @8 [as testotoxicosis, may cause precocious puberty at a( n* K h+ G; e- p' I
very young age. The physical findings in these boys
% @$ k' a+ n3 Zwith this disorder are full pubertal development,
; G- ]- F# g |including bilateral testicular growth, similar to boys
+ Q1 M/ l2 Z* d5 D3 f$ o$ ^with CPP. The gonadotropin levels in this disorder
: { P5 b, a9 ^) G3 Oare suppressed to prepubertal levels and do not show3 ^: o/ v/ \& q3 L& O. F# T) Y
pubertal response of gonadotropin after gonadotropin-
, p/ a, G6 H" f2 ^releasing hormone stimulation. This is a sex-linked
7 ~9 f* o- F) I: e; o+ b. fautosomal dominant disorder that affects only
+ B( m$ F4 M! }2 E# u. Bmales; therefore, other male members of the family% I; j- A4 _( J" U/ v8 w5 t
may have similar precocious puberty.3
" k; ~4 y4 M) B: ?! E1 {) B9 XIn our patient, physical examination was incon-$ f. c1 t1 ]0 A4 J* H2 n9 J
sistent with true precocious puberty since his testi-8 t5 b9 w W2 n' m% G O
cles were prepubertal in size. However, testotoxicosis
" D; @; _7 v! dwas in the differential diagnosis because his father1 ^: }8 V% Y, k
started puberty somewhat early, and occasionally,6 w2 E& l; H9 h9 Q* W5 a
testicular enlargement is not that evident in the
; [- w; q* a5 }beginning of this process.1 In the absence of a neg-- N( K" f! c, _& {
ative initial history of androgen exposure, our
4 |1 g* Y7 [9 T; a4 h1 Xbiggest concern was virilizing adrenal hyperplasia,5 Y2 e m) x# U
either 21-hydroxylase deficiency or 11-β hydroxylase
/ X( B1 Q1 m$ d6 @0 P3 `2 hdeficiency. Those diagnoses were excluded by find-$ @# L; c; T a7 g$ n
ing the normal level of adrenal steroids.! j2 p X8 Z# H4 q. o; R
The diagnosis of exogenous androgens was strongly) I6 c4 Z' {7 i; p$ q0 W
suspected in a follow-up visit after 4 months because
S1 H3 J" E5 d# h4 cthe physical examination revealed the complete disap-3 y& p4 I6 k4 S8 D$ _# K; N
pearance of pubic hair, normal growth velocity, and
# l1 ?+ `2 Z7 X3 k) jdecreased erections. The father admitted using a testos-
7 N" q2 \# ^0 q, f( ~terone gel, which he concealed at first visit. He was
; [/ ^. ]/ j! D. d4 w, f+ {0 `using it rather frequently, twice a day. The Physicians’
O9 R; {5 g6 t4 {5 |Desk Reference, or package insert of this product, gel or+ e! X% i' d* Y' W
cream, cautions about dermal testosterone transfer to# p0 h1 L" c6 D5 B7 K8 J% `$ o9 z
unprotected females through direct skin exposure.2 L$ Z) ]6 V. P" o# u0 t
Serum testosterone level was found to be 2 times the
% F+ L& X' L+ p5 D% N6 pbaseline value in those females who were exposed to/ w S+ s/ |) R/ e0 y+ F. c
even 15 minutes of direct skin contact with their male+ w" c" `& J6 q, l1 ], q
partners.6 However, when a shirt covered the applica-
n) ?; D% H, R; Ytion site, this testosterone transfer was prevented.
9 k5 x% ]# T' v& r( i5 f+ d( B$ zOur patient’s testosterone level was 60 ng/mL,
' k* c, B: r' S$ c# ?which was clearly high. Some studies suggest that. x; c% Y# d. L2 V' V
dermal conversion of testosterone to dihydrotestos-2 E6 }9 u( F- y$ f# T( f7 b% s0 f8 D
terone, which is a more potent metabolite, is more
' B$ E R9 |9 o' \active in young children exposed to testosterone
4 g+ z8 a. i+ ^" ]# D7 b5 y$ Q4 sexogenously7; however, we did not measure a dihy-9 m; B% z- [: d, n- u
drotestosterone level in our patient. In addition to
' e$ x! U$ u# \, |5 [- Rvirilization, exposure to exogenous testosterone in" \" `9 {9 g: l2 q$ }5 D6 c8 A
children results in an increase in growth velocity and4 q% ^. _2 U( ^
advanced bone age, as seen in our patient.
2 ?+ p8 A6 n1 Q' ]6 yThe long-term effect of androgen exposure during
' l u7 X0 J6 k! ~; ?5 pearly childhood on pubertal development and final
- ?8 w J. h0 _: J- P t$ Padult height are not fully known and always remain7 I: I3 V) S/ q4 W1 a3 P6 E" E7 U7 S
a concern. Children treated with short-term testos-$ o. B( @/ ?/ y) L6 q- P6 r3 z
terone injection or topical androgen may exhibit some( _4 f2 ?% H0 G) c5 i8 u, n- U
acceleration of the skeletal maturation; however, after
2 N$ {* D9 _: {. tcessation of treatment, the rate of bone maturation
- M2 ~4 o9 P* o# A1 i% Tdecelerates and gradually returns to normal.8,9
1 P \7 H( w* F7 @$ R9 l3 \- E/ dThere are conflicting reports and controversy- R) E% T* H4 n7 x$ E
over the effect of early androgen exposure on adult
: g( D' o9 [5 v0 F% hpenile length.10,11 Some reports suggest subnormal
+ e! n! C0 q* n6 } l' Cadult penile length, apparently because of downreg-
: V/ W$ @. E# iulation of androgen receptor number.10,12 However,* O+ i$ w% O; ^
Sutherland et al13 did not find a correlation between( H8 \8 s5 x: a
childhood testosterone exposure and reduced adult
* J. M5 V, i) h4 s4 G9 p) t# gpenile length in clinical studies.5 L' E& W% R4 @* W' Y
Nonetheless, we do not believe our patient is2 ]6 D4 s7 K$ E) @8 s' `
going to experience any of the untoward effects from
4 I) n+ A3 q d h/ t. atestosterone exposure as mentioned earlier because" K- v7 e/ g& o8 P
the exposure was not for a prolonged period of time.
( L& R4 g" A7 v2 VAlthough the bone age was advanced at the time of2 e# q3 G3 b8 ?5 N8 Y, U
diagnosis, the child had a normal growth velocity at5 a. A7 A \0 b! K7 y+ |/ K
the follow-up visit. It is hoped that his final adult5 h6 U& l# n1 `4 E5 d! B( o
height will not be affected.
, t9 d* Z2 g# T+ Y% S1 bAlthough rarely reported, the widespread avail-& c2 F5 ~0 k& \# W' X+ d- |% k
ability of androgen products in our society may9 I: n/ v# c* \3 @1 B6 `- ?" v
indeed cause more virilization in male or female9 C" c: E& M% n# M" s
children than one would realize. Exposure to andro-
, ?- ^; I& g9 ^. d$ A' x' cgen products must be considered and specific ques-
% R& _/ `/ A8 h( ntioning about the use of a testosterone product or
1 Z/ l/ U' m, igel should be asked of the family members during( x) B# d8 _! G6 N
the evaluation of any children who present with vir-+ D7 W/ F; Y3 F& y8 @* k4 q
ilization or peripheral precocious puberty. The diag-* S- S4 k0 [% n' S
nosis can be established by just a few tests and by7 e* @" i" c9 C
appropriate history. The inability to obtain such a4 J4 S6 e4 J! x; r) t6 l. t
history, or failure to ask the specific questions, may- u: E/ g6 D% t0 x6 Q
result in extensive, unnecessary, and expensive
' F/ s- ]1 A |5 y6 d9 Minvestigation. The primary care physician should be
- `( P. f3 R; z% `* l5 u% K8 t Taware of this fact, because most of these children7 t# H. c/ q. F( I) @4 N
may initially present in their practice. The Physicians’9 {4 ^$ Y2 h! ]0 k+ a) `! s: Y
Desk Reference and package insert should also put a
2 e; O7 D2 D. ~' z3 s; Ywarning about the virilizing effect on a male or6 f5 T5 q9 ?& z1 y6 Y1 |
female child who might come in contact with some-
/ n6 O0 K9 I) C) C0 x1 F9 fone using any of these products.
* j9 \2 \4 A# r1 H8 r, wReferences
* C6 c# ?6 H% M* \2 m W1. Styne DM. The testes: disorder of sexual differentiation- F- `, ]1 x( q
and puberty in the male. In: Sperling MA, ed. Pediatric
. W$ e5 |5 X; t" m/ C( [+ L: }Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 ^. R) v& O* ?) K2002: 565-628.
7 ~, t" `$ r/ k4 \1 p2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; q1 @, E9 a& E' r1 f8 G* C
puberty in children with tumours of the suprasellar pineal |
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