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Sexual Precocity in a 16-Month-Old
$ ^5 c1 W# _* @Boy Induced by Indirect Topical
3 @4 Z, o0 T0 }+ g. {4 XExposure to Testosterone5 j8 K' _4 o4 Z, U8 b) H2 {8 J
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 w, u, [( M9 W6 z( Jand Kenneth R. Rettig, MD1( ?% V; c/ K$ B; X2 X
Clinical Pediatrics# U- a5 p3 T) W1 f$ [, r }
Volume 46 Number 6
9 ~0 ]: P$ p* {# iJuly 2007 540-543
. t& _, N) C) J© 2007 Sage Publications
( [- u4 `. `8 I. L) ^8 X* H# |10.1177/0009922806296651
4 i$ I: p- c+ q7 r9 n1 Qhttp://clp.sagepub.com+ @) ?5 f# t6 h$ r) l/ g# a J% B
hosted at
* P$ y* p1 l+ x: p' c' r* y7 ^0 S# O/ uhttp://online.sagepub.com. n0 Q- d7 u& u. D1 {- A
Precocious puberty in boys, central or peripheral,/ P6 x$ q" t6 v0 P/ z) w# T* P$ C
is a significant concern for physicians. Central
( z3 s9 ]1 W% @) A1 v6 @precocious puberty (CPP), which is mediated; L- ]0 T2 K: x
through the hypothalamic pituitary gonadal axis, has
9 i3 V/ Y7 W3 O$ J. H( ^a higher incidence of organic central nervous system
7 I0 f( }" Q8 Q4 @6 `/ q+ {lesions in boys.1,2 Virilization in boys, as manifested
2 _' v* S. R: a: {" Uby enlargement of the penis, development of pubic
7 Z# _* i4 E% C$ E2 Whair, and facial acne without enlargement of testi-
4 _6 U% S1 Y5 ]5 X- z& h' d# Ccles, suggests peripheral or pseudopuberty.1-3 We
& m3 \5 L( l7 z: G5 W; K: C6 `report a 16-month-old boy who presented with the
' S. r5 o8 {9 ?" i8 C/ M; w3 {enlargement of the phallus and pubic hair develop-4 p S: y2 R I1 c# A9 E
ment without testicular enlargement, which was due, D' t; Z# S" P, d+ P
to the unintentional exposure to androgen gel used by3 g& Q+ m+ M) B9 S* }8 o# S
the father. The family initially concealed this infor-
' I5 u! u6 V: v9 E) Qmation, resulting in an extensive work-up for this8 Y: ]3 B+ g0 Z+ @. J( H
child. Given the widespread and easy availability of
' O0 M! [( \" i% Q% R% `testosterone gel and cream, we believe this is proba-
- C: v9 g# u2 ^! p8 Dbly more common than the rare case report in the
& L0 r( x5 _4 b& M, |# T) J; Q8 M N. H* dliterature.4 `8 ]: O7 `) S1 e
Patient Report
; Y9 a1 `3 X% E! _* I+ R, ]' y: m2 ^A 16-month-old white child was referred to the
/ n( N$ o( P* s0 y% {1 y hendocrine clinic by his pediatrician with the concern
" y, i/ r' y% X! @: A4 n6 Q" [1 uof early sexual development. His mother noticed* V8 o9 c9 ?! Z* A
light colored pubic hair development when he was
% P4 Y9 v0 q& _: D7 x3 BFrom the 1Division of Pediatric Endocrinology, 2University of
c4 Y! b0 p: Y0 a V0 p" B1 uSouth Alabama Medical Center, Mobile, Alabama.; ^. D) C0 u V' r
Address correspondence to: Samar K. Bhowmick, MD, FACE,
+ u! r& x3 B; |5 q4 R/ xProfessor of Pediatrics, University of South Alabama, College of4 f% r& a0 f2 w4 @$ g3 g
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 u4 }1 ]$ R: Y0 u/ B0 m, z
e-mail: [email protected].# M5 @/ T, P# b s, h! u: x
about 6 to 7 months old, which progressively became$ v( \$ E/ M4 s
darker. She was also concerned about the enlarge-
1 R, I- E* Y- Y6 D1 ]ment of his penis and frequent erections. The child
, L0 x% y M; }) h$ e+ V! N5 z6 Xwas the product of a full-term normal delivery, with4 Y3 w- x! Y# e k" m+ i
a birth weight of 7 lb 14 oz, and birth length of% A- t6 o( \. j" v' l
20 inches. He was breast-fed throughout the first year0 ~0 q$ \1 Q, N% W' n. \$ y
of life and was still receiving breast milk along with
. X. c5 v4 L; p3 _7 \. e( Vsolid food. He had no hospitalizations or surgery,6 R! C; O. q! q4 `( Z/ s! l% r
and his psychosocial and psychomotor development
3 l) E* G+ K2 F, ~was age appropriate.
6 V" l+ R; t2 \/ N4 u7 q8 RThe family history was remarkable for the father,
% n& a' R6 _0 v) J: G' S' z; ^who was diagnosed with hypothyroidism at age 16,
2 P& x) J4 g$ v9 ?; L3 y1 h3 hwhich was treated with thyroxine. The father’s
. W1 a8 L5 x' X4 I- H( l4 y$ sheight was 6 feet, and he went through a somewhat
1 @9 Q: D7 c5 i/ R0 Nearly puberty and had stopped growing by age 14.
9 _+ h3 E* U. d& a: vThe father denied taking any other medication. The
8 q. v3 t1 k: G3 F& a& k4 Gchild’s mother was in good health. Her menarche5 ~: s. z9 ]. ~: K
was at 11 years of age, and her height was at 5 feet D( p5 B- Z9 ]4 R$ W
5 inches. There was no other family history of pre-1 |* n }4 d( @& T" f$ p
cocious sexual development in the first-degree rela-/ [7 g) i* ?* s: K: y
tives. There were no siblings.6 k: i7 U+ x$ ]1 q" C) p% M
Physical Examination3 _2 v- c3 u# Q% t" T
The physical examination revealed a very active,! X6 k/ _; l: u1 D! W& o/ U: `$ t
playful, and healthy boy. The vital signs documented2 i. S1 v3 x% Z
a blood pressure of 85/50 mm Hg, his length was# ]+ a* x# }) P w$ r0 J0 P
90 cm (>97th percentile), and his weight was 14.4 kg; M) ~" A7 s, Z2 @/ p0 ~, Q
(also >97th percentile). The observed yearly growth
$ D2 ?1 ^5 T6 Cvelocity was 30 cm (12 inches). The examination of7 L4 Y& i7 s& B& s
the neck revealed no thyroid enlargement.
/ E3 O! r! f* UThe genitourinary examination was remarkable for
( R2 l: f7 T" j/ ~5 Eenlargement of the penis, with a stretched length of
y0 M9 `: c8 r. {7 E- |0 d8 cm and a width of 2 cm. The glans penis was very well
8 N! ^7 O' T, E& Hdeveloped. The pubic hair was Tanner II, mostly around# w; j. `# l) d9 g8 A
540% B& o1 m1 i) w4 V3 f5 o* O- P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 i2 W- h: A3 p3 o
the base of the phallus and was dark and curled. The! E; _( p& s; I9 I4 y
testicular volume was prepubertal at 2 mL each.
* g4 A7 h8 Y6 j4 B, \* bThe skin was moist and smooth and somewhat% p3 i. X; V# o2 m2 i
oily. No axillary hair was noted. There were no
8 ~% b; z2 j, E0 C x: Jabnormal skin pigmentations or café-au-lait spots.
8 U1 g, Z- j. e% y1 lNeurologic evaluation showed deep tendon reflex 2+
. f; w' U1 T* Rbilateral and symmetrical. There was no suggestion
& g- m9 B' G1 U1 |" | Aof papilledema.. ^$ N! C% d' |" \. l
Laboratory Evaluation
$ X- i) K1 M) ^& f3 wThe bone age was consistent with 28 months by; x H/ [3 O6 [
using the standard of Greulich and Pyle at a chrono-$ Z, A3 n7 t: h p- ~
logic age of 16 months (advanced).5 Chromosomal
. s' o( q4 N- W, L% Z }karyotype was 46XY. The thyroid function test' s) s5 b1 H* g9 a, t6 w: V, h; U
showed a free T4 of 1.69 ng/dL, and thyroid stimu-/ r5 J: I* P5 r- B( m& |
lating hormone level was 1.3 µIU/mL (both normal).
# R, @' L; `/ \The concentrations of serum electrolytes, blood' Z4 m+ r' h; X3 O d
urea nitrogen, creatinine, and calcium all were
' T6 x* D* b! C! x2 `: h% mwithin normal range for his age. The concentration
, i6 ?( R8 ~0 v: M( n: vof serum 17-hydroxyprogesterone was 16 ng/dL( R; ~7 ? w7 Y7 U
(normal, 3 to 90 ng/dL), androstenedione was 206 W2 L1 t m# `+ N0 y
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
: U M1 K8 x/ v! R# mterone was 38 ng/dL (normal, 50 to 760 ng/dL),+ k( { {6 n* }7 G" F
desoxycorticosterone was 4.3 ng/dL (normal, 7 to6 |' A+ z: m; G6 I5 ], _
49ng/dL), 11-desoxycortisol (specific compound S); v) D' Q, o6 @
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ v6 f1 n" @; n8 b4 J Atisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) I8 w& Q+ P+ m% j* U$ A4 ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),& G! v1 f4 t' b* S
and β-human chorionic gonadotropin was less than8 b& i& K( O+ z% L( B# T
5 mIU/mL (normal <5 mIU/mL). Serum follicular, }5 S% M5 r* m' z- {, A: m' A# T$ |
stimulating hormone and leuteinizing hormone5 _) y6 X' o; m9 g* ?
concentrations were less than 0.05 mIU/mL
4 J: Y0 N2 e2 P* ]3 N(prepubertal).
0 q% h( u9 h2 ^* p4 jThe parents were notified about the laboratory
! \8 ?2 Z- g4 H% t8 w: I; Xresults and were informed that all of the tests were% D5 W1 u$ _6 M5 Z5 u
normal except the testosterone level was high. The
+ v$ ]& A8 M; o7 ^2 p2 {5 J1 d' A5 Cfollow-up visit was arranged within a few weeks to: D9 E7 I6 N5 U% g
obtain testicular and abdominal sonograms; how-0 f2 i& z, j7 N, e/ [1 U7 e
ever, the family did not return for 4 months.% E, R- C2 ?, I5 p9 s/ e
Physical examination at this time revealed that the3 g) b' o. x9 G! O) `
child had grown 2.5 cm in 4 months and had gained
! ~+ z! `' {4 Q- _. l/ Z4 w2 kg of weight. Physical examination remained& F6 Q+ k% @. S! Q3 g: ~" e
unchanged. Surprisingly, the pubic hair almost com-! K8 p0 f$ N* _3 d4 L8 u
pletely disappeared except for a few vellous hairs at& g% [3 C2 Y, b7 o* [- j4 q4 b
the base of the phallus. Testicular volume was still 2
3 F/ U9 p, m$ x" ~# W1 h* Z7 wmL, and the size of the penis remained unchanged.
* q# Y6 v& `4 ~5 `( i$ q+ tThe mother also said that the boy was no longer hav-" X- ~: C* ?1 O
ing frequent erections.
( k; `1 W6 v6 P9 u: d0 f0 u# uBoth parents were again questioned about use of
& V, A; f4 `5 r# m( b( R' F" dany ointment/creams that they may have applied to
+ k* P; G- F8 j7 D6 \% {& lthe child’s skin. This time the father admitted the, e! ~# b# G- v; G9 x. ~
Topical Testosterone Exposure / Bhowmick et al 541
3 Y+ @: W. t* I% _' M- {, @use of testosterone gel twice daily that he was apply-
0 o* c" Z) M# h3 a# Z7 Ying over his own shoulders, chest, and back area for- N4 W! _* R! {' p8 }+ g0 H
a year. The father also revealed he was embarrassed& L) d( d. k+ t3 @( e4 K4 O
to disclose that he was using a testosterone gel pre-% F% `4 ^1 m9 X* U" f
scribed by his family physician for decreased libido
1 ~6 p- ]) Q. @2 M3 Q4 Q9 k4 dsecondary to depression.9 M Q6 _4 j+ z: k% K1 `, q* b
The child slept in the same bed with parents.
: }6 B5 q. h6 y7 OThe father would hug the baby and hold him on his- S1 I+ N! _9 e' o
chest for a considerable period of time, causing sig-6 t" H& I3 m {) M7 c# r# O+ D
nificant bare skin contact between baby and father., a* x$ {; P' m
The father also admitted that after the phone call,. b% H" |% U9 d# B+ s3 R
when he learned the testosterone level in the baby. R& ]3 N; x# ~5 k' a' C4 E( T u" L
was high, he then read the product information& \' P: h. Z0 ]4 l
packet and concluded that it was most likely the rea-
5 K* j+ X$ ~5 A+ m/ Vson for the child’s virilization. At that time, they; P2 @# M4 Q. k
decided to put the baby in a separate bed, and the
* |. H( K# _1 e7 a6 mfather was not hugging him with bare skin and had
$ l' f1 R6 Y0 ^; E4 N' jbeen using protective clothing. A repeat testosterone
, D, s% b0 o* n+ etest was ordered, but the family did not go to the# e/ j; F# H% y7 e
laboratory to obtain the test.2 E/ G/ I; u. b% ^% G# ]
Discussion7 r3 S: t# J+ h/ }
Precocious puberty in boys is defined as secondary
9 H% o( _2 h1 Gsexual development before 9 years of age.1,4( J/ }9 X3 W0 x, ]) s" f
Precocious puberty is termed as central (true) when& U2 L! X" r! G+ A. d- e
it is caused by the premature activation of hypo-
& G. M% O8 A+ x g9 G- rthalamic pituitary gonadal axis. CPP is more com- E# ]" v/ ?+ Y4 M
mon in girls than in boys.1,3 Most boys with CPP
: W$ w; @' e# x( } C; `% Gmay have a central nervous system lesion that is
6 K* Y$ T6 p, V; Cresponsible for the early activation of the hypothal-/ U. |4 [6 ^% c% g& y J
amic pituitary gonadal axis.1-3 Thus, greater empha-* J7 A# Q0 |9 ^. H7 N6 k9 Z8 d
sis has been given to neuroradiologic imaging in! A0 R3 ]* I3 |, {( J* M3 B
boys with precocious puberty. In addition to viril-/ I f: S) j3 S# T+ u) q' Q5 y
ization, the clinical hallmark of CPP is the symmet-6 a4 Z/ ^3 I) B0 {8 Q. R
rical testicular growth secondary to stimulation by
8 x @: ~3 `6 R& L0 M* Zgonadotropins.1,3
5 H9 @6 A/ G; H' m+ WGonadotropin-independent peripheral preco-. U, s$ A1 [. M. o" |3 h
cious puberty in boys also results from inappropriate
5 i! x9 U, ^; t+ N( F5 }* iandrogenic stimulation from either endogenous or
& Z7 C2 i8 k5 l/ pexogenous sources, nonpituitary gonadotropin stim-* y9 g3 e% n, N/ S8 @
ulation, and rare activating mutations.3 Virilizing
: y& l" g6 g+ x, n/ f- }0 e/ Z6 L" Qcongenital adrenal hyperplasia producing excessive
" h; u% _. l; x% }) o$ W7 Padrenal androgens is a common cause of precocious
( c- p A! J) ]$ L# I6 V# qpuberty in boys.3,42 ] j- ] j3 L* x( u
The most common form of congenital adrenal4 {8 A, u$ s# _6 B- C
hyperplasia is the 21-hydroxylase enzyme deficiency.
/ W; m% s9 I0 P [' M1 P2 J$ QThe 11-β hydroxylase deficiency may also result in
# e" @) e L. b, t0 E5 Y1 Cexcessive adrenal androgen production, and rarely, ^4 P) K9 f0 }: u. A
an adrenal tumor may also cause adrenal androgen2 ~2 @% }8 {* a' Q3 ~
excess.1,35 l4 }& U1 ?5 M, o9 a
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 Z0 w. Q) R& C6 b D; r542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: Y. T" A9 x" HA unique entity of male-limited gonadotropin-2 N. q/ ]# x: u g% d, G, g, `
independent precocious puberty, which is also known7 \' \8 k; K) z
as testotoxicosis, may cause precocious puberty at a- \# S1 @+ K4 c$ t' ~. B
very young age. The physical findings in these boys) Y* }' A2 b2 {! v) [; d
with this disorder are full pubertal development,
! J$ E1 y* A- t6 `* n8 s7 k" nincluding bilateral testicular growth, similar to boys1 j U* c: Q8 s2 ~9 U
with CPP. The gonadotropin levels in this disorder
+ M S/ f! h! S6 u: X+ P7 P) kare suppressed to prepubertal levels and do not show3 x" }1 L5 ~- n2 |& i$ q6 x5 P
pubertal response of gonadotropin after gonadotropin-
5 u X" _0 _- @: u- V) yreleasing hormone stimulation. This is a sex-linked2 R3 D! e7 E: F" D4 T1 j8 w9 @
autosomal dominant disorder that affects only
1 k# M, T! B& L4 N) \2 \males; therefore, other male members of the family
+ S4 v6 s5 b9 A/ ~" kmay have similar precocious puberty.3
+ f! w) y! K3 [( @0 s1 U9 vIn our patient, physical examination was incon-* u, {. R; D9 a0 r
sistent with true precocious puberty since his testi-
8 W* G4 {0 v0 a0 xcles were prepubertal in size. However, testotoxicosis
: K$ G9 J0 z1 O2 x# x T$ ?3 X5 xwas in the differential diagnosis because his father
& D$ m- e) T9 d+ D9 O* Astarted puberty somewhat early, and occasionally,1 |9 C y r: \- X: b! k# Z9 S% ?
testicular enlargement is not that evident in the) Z9 u; K* q0 p# ^6 l" V. ~
beginning of this process.1 In the absence of a neg-- d; U( l5 Z1 p
ative initial history of androgen exposure, our7 [9 @3 w, R, T" k8 @5 @
biggest concern was virilizing adrenal hyperplasia,
7 ?' b5 e0 D% u! ], _+ d: `either 21-hydroxylase deficiency or 11-β hydroxylase. q# |# C* ?4 f
deficiency. Those diagnoses were excluded by find-
, C5 W4 c- ~' ~. w5 _; q" t& Uing the normal level of adrenal steroids.
4 X, m0 R7 n& |2 V8 F v7 f4 X' Y) P1 zThe diagnosis of exogenous androgens was strongly
* G; Y; Q+ L' }' E, ~suspected in a follow-up visit after 4 months because l4 `0 z6 J# k2 n; Y& u9 T
the physical examination revealed the complete disap-
|8 \- {8 G1 Q8 v! ^ Cpearance of pubic hair, normal growth velocity, and; j2 A/ e- f$ Y2 x0 z" z8 T, n3 u6 V
decreased erections. The father admitted using a testos-
; R( e' Y+ |, P/ k! s& f! \terone gel, which he concealed at first visit. He was
* M* h0 p( t1 \/ d8 }& Q8 nusing it rather frequently, twice a day. The Physicians’
6 V1 Z. ]& R. O: zDesk Reference, or package insert of this product, gel or
e, q. }! N- Ncream, cautions about dermal testosterone transfer to9 i1 E' r8 e9 r2 W/ |
unprotected females through direct skin exposure.( M1 ]' X7 Z/ T# k# j! F. M8 E
Serum testosterone level was found to be 2 times the
) v) ]( m T2 L1 f; ]( Ybaseline value in those females who were exposed to% B+ y/ M. Q1 \+ ]
even 15 minutes of direct skin contact with their male4 ~. d% d% F8 L9 ~' J
partners.6 However, when a shirt covered the applica-
: |, w( q3 |9 w! Q, M3 M/ i2 d$ btion site, this testosterone transfer was prevented.
9 q, ]; Z) x, M# s9 k* l' w6 f5 K6 @Our patient’s testosterone level was 60 ng/mL,
& \$ ?3 Q* R6 X8 Z, @) W$ b3 ]which was clearly high. Some studies suggest that6 u0 h% q* L$ e1 u! y2 o
dermal conversion of testosterone to dihydrotestos-8 Q4 I1 p4 E9 p6 X& w
terone, which is a more potent metabolite, is more
' t& S4 `3 a0 Tactive in young children exposed to testosterone$ b+ `. |6 Q4 r: u
exogenously7; however, we did not measure a dihy-
& U" s0 e4 I; i3 w4 V0 Ydrotestosterone level in our patient. In addition to I( K w f. w0 q* ]9 @
virilization, exposure to exogenous testosterone in9 N6 X. `/ o6 D, ^* Q6 v1 @
children results in an increase in growth velocity and* N/ L. }$ ^2 z
advanced bone age, as seen in our patient.# `9 I( u1 x5 g
The long-term effect of androgen exposure during
8 N. K3 Y% g% i$ L8 i0 ]% Bearly childhood on pubertal development and final
' K4 O) a" ?2 {2 Y8 Oadult height are not fully known and always remain6 ?' K9 E( ^8 F# L2 F1 o) @
a concern. Children treated with short-term testos-2 y5 N: F! G6 Z' j* Y/ l
terone injection or topical androgen may exhibit some, Y2 ~- h7 B+ O! s- y
acceleration of the skeletal maturation; however, after, ?- _# `2 P* A; }) m. C; C
cessation of treatment, the rate of bone maturation
; d' z; w% [" h3 c1 z$ g$ d& |decelerates and gradually returns to normal.8,9, U b, \6 \1 O4 M
There are conflicting reports and controversy1 Z8 [- L* K5 G' |
over the effect of early androgen exposure on adult
+ O/ S7 a( r- j6 ^penile length.10,11 Some reports suggest subnormal
1 w# ]# w/ z! J7 T8 I3 ladult penile length, apparently because of downreg-" _4 q/ `# K+ ~) W
ulation of androgen receptor number.10,12 However,
6 ^+ |7 {' j- I! a: TSutherland et al13 did not find a correlation between( B0 r+ O) _' u9 s8 p: C8 a% p
childhood testosterone exposure and reduced adult
# @* }* d- c( Y |penile length in clinical studies. |% V5 V* H' K: S0 w3 j- A" b
Nonetheless, we do not believe our patient is
& @' w' b0 _# t! K, A. u& [: Kgoing to experience any of the untoward effects from
, h$ \6 H; _$ s# Xtestosterone exposure as mentioned earlier because
/ T5 m4 Z5 g- M3 [0 Ithe exposure was not for a prolonged period of time.
, X) i# F* X! a+ F( D! AAlthough the bone age was advanced at the time of/ s' Z/ B- _( E# i
diagnosis, the child had a normal growth velocity at% j9 o3 O: W% Z1 S. n6 }+ V3 ]% i" r
the follow-up visit. It is hoped that his final adult- ?% u5 E* h: t [% r
height will not be affected.
+ g* E1 x2 }/ b) a$ P7 L! HAlthough rarely reported, the widespread avail-
5 T2 ^" o; I7 D! j% |! \ability of androgen products in our society may
9 d4 Z- ^9 o- j2 S2 _: U9 L* cindeed cause more virilization in male or female
, B5 S* _9 r2 S" J* a; ichildren than one would realize. Exposure to andro-
, N$ u ]/ G8 s; X# @7 u0 H Mgen products must be considered and specific ques-) Z; E' }5 E2 ?, I0 r8 p
tioning about the use of a testosterone product or4 W+ \; a* A, y0 p6 |
gel should be asked of the family members during
" ?; S! n% W8 i$ U5 Nthe evaluation of any children who present with vir-5 i, D6 i, R- z) x2 |6 t
ilization or peripheral precocious puberty. The diag-/ I6 s. \" K- _7 d; y# l3 V$ a
nosis can be established by just a few tests and by
. _4 T/ j( t6 happropriate history. The inability to obtain such a
# E- N; p2 `$ \6 ^, whistory, or failure to ask the specific questions, may
2 Q7 U5 ~! f7 V9 p8 ], `4 ~result in extensive, unnecessary, and expensive
2 ], i% K3 x% }8 F" ^" Rinvestigation. The primary care physician should be2 V# `) a3 X) S" [
aware of this fact, because most of these children
" {/ ^8 T, B2 vmay initially present in their practice. The Physicians’, D$ d3 S* n7 d% f1 ^* y0 X1 H, F
Desk Reference and package insert should also put a
6 E7 n0 C' O2 bwarning about the virilizing effect on a male or
8 b0 W4 G7 f: d0 d' X3 ffemale child who might come in contact with some-
- p( e8 M, B' L) y }one using any of these products." x, Q3 t, ]+ u, M
References; W& L6 V$ b0 z* j
1. Styne DM. The testes: disorder of sexual differentiation
7 u. L3 i; ?2 k7 H9 A: Q6 t' E) Hand puberty in the male. In: Sperling MA, ed. Pediatric% n% ]1 t, d7 E" G; j
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& H5 S1 _0 e# ]5 g; N M+ I
2002: 565-628.
; D+ j2 ?5 q5 X, Y I# V& q/ O2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( A% w( ^4 t/ G/ f9 D" ~2 v# l" J
puberty in children with tumours of the suprasellar pineal |
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