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Sexual Precocity in a 16-Month-Old
$ u' t+ h! c  F# p2 {( TBoy Induced by Indirect Topical
$ i' b% J4 t; [: D6 DExposure to Testosterone9 |4 o. [) m' Z9 z
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( g0 L( \3 ^6 [3 K6 R
and Kenneth R. Rettig, MD1& B* o- Q3 E9 o5 D) S/ Y; `7 C
Clinical Pediatrics5 i% h  n1 @2 W# u* Z
Volume 46 Number 6
6 h1 A% o6 z5 O2 ]( u, QJuly 2007 540-543% |2 T! U3 w6 F' @8 Y
© 2007 Sage Publications( r: o" _4 U: o
10.1177/00099228062966516 d" i5 @) a2 V  Z: m3 a+ a2 U& l
http://clp.sagepub.com
' }+ T8 e* n4 ]8 n! \5 f5 H# phosted at
& z+ w/ X. M& y. zhttp://online.sagepub.com
. J' M( ?) y& jPrecocious puberty in boys, central or peripheral,7 I2 o- J; O+ D' n3 O
is a significant concern for physicians. Central; b4 v! ~% Y9 A+ G& }1 e6 I
precocious puberty (CPP), which is mediated
- }9 H1 i% n8 F! Qthrough the hypothalamic pituitary gonadal axis, has1 }% G5 x8 d  I4 J4 N9 C
a higher incidence of organic central nervous system
# e% o  D/ K- L) Y' Y& Y- ilesions in boys.1,2 Virilization in boys, as manifested8 G8 U: b# H( n. A
by enlargement of the penis, development of pubic( x, i/ b5 Z, A" o5 H" I- T
hair, and facial acne without enlargement of testi-
$ m9 g3 R" \, ^+ Z( S3 y* Q9 E# Bcles, suggests peripheral or pseudopuberty.1-3 We. s9 a( t( ?9 Z+ e- v8 i6 O/ u
report a 16-month-old boy who presented with the% W# n, x% H% W; f% b5 i/ x$ ?- `
enlargement of the phallus and pubic hair develop-2 G" ~* Z$ i# H0 S8 @% y& G: c' j# N3 u# _
ment without testicular enlargement, which was due  I7 p2 l' x. q6 Z3 f) y1 H( r
to the unintentional exposure to androgen gel used by$ H# o0 |2 g2 w5 M: G" C! v
the father. The family initially concealed this infor-( Y& c) R' }- I+ o/ D& h# V- v* y+ |
mation, resulting in an extensive work-up for this7 Z) a9 M+ A" _$ K! @' {& P* F" a/ l
child. Given the widespread and easy availability of- N0 {$ ?* d2 G# U/ O# ]+ B; y
testosterone gel and cream, we believe this is proba-
$ V  J8 c/ B4 e. Cbly more common than the rare case report in the
2 W$ {* N' d0 f' s* D0 t1 |literature.4; ^" G/ N. ?8 q0 c3 w9 K
Patient Report  U* U% m  o* A
A 16-month-old white child was referred to the3 G) {- ?0 |/ \2 }9 `, }! T0 t! u
endocrine clinic by his pediatrician with the concern6 Y! m8 t; j4 ^/ X- Q& s) A! T
of early sexual development. His mother noticed
0 b( ?3 m# c# l6 jlight colored pubic hair development when he was% x+ M3 a- ^6 O" S
From the 1Division of Pediatric Endocrinology, 2University of" ^" d6 K0 o* m2 U, r) l. P
South Alabama Medical Center, Mobile, Alabama.; s7 @% W3 G4 u
Address correspondence to: Samar K. Bhowmick, MD, FACE,
2 O2 A6 w9 ?1 |; gProfessor of Pediatrics, University of South Alabama, College of. S* k- d8 _! Z( N
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; T, o/ `2 H3 h5 H! Me-mail: [email protected].
* x; d6 n, |" H" Z% ]/ rabout 6 to 7 months old, which progressively became( Y$ q. R- {4 n$ \6 b6 F/ _
darker. She was also concerned about the enlarge-3 V/ g, m6 ~2 R
ment of his penis and frequent erections. The child5 g, y/ f7 a; Z/ E
was the product of a full-term normal delivery, with
1 `7 s/ p5 {; k0 @- I* X7 |a birth weight of 7 lb 14 oz, and birth length of
, @% U( b% V2 S: ?20 inches. He was breast-fed throughout the first year" l  [& \! f  X0 m# I
of life and was still receiving breast milk along with
( O0 t/ q; S8 o( Vsolid food. He had no hospitalizations or surgery,4 ~6 ^; t2 H* h! g
and his psychosocial and psychomotor development
/ z, k* [- ^% ~% `- Lwas age appropriate.
1 K& K% x% ~3 m2 N, y# NThe family history was remarkable for the father,
4 `. [: l1 a6 g# c5 R, v) ]% i1 Uwho was diagnosed with hypothyroidism at age 16,
5 i+ s1 r; h* G0 Q8 A( lwhich was treated with thyroxine. The father’s; c; U7 {5 _2 G3 a+ Y; d
height was 6 feet, and he went through a somewhat0 ?3 a, ?7 l1 H7 j* t' a* \0 J
early puberty and had stopped growing by age 14.
, ^* `# K$ x# Y9 YThe father denied taking any other medication. The
; D+ I& @5 [. C4 V; f8 @! r; I- mchild’s mother was in good health. Her menarche, N. P6 a, z4 ]) ?8 t0 V
was at 11 years of age, and her height was at 5 feet4 x% }2 W+ C0 N5 ~
5 inches. There was no other family history of pre-: n6 B) T( o9 s: a
cocious sexual development in the first-degree rela-
# g" h$ S2 T1 G* ?9 qtives. There were no siblings.( ?; E7 U, p  S
Physical Examination
( e2 w2 `( y7 H; x# a" G+ iThe physical examination revealed a very active,
7 Z! h9 u, I3 d% B6 w' Cplayful, and healthy boy. The vital signs documented1 W& S3 x: ^4 _8 R$ I( \* e& @
a blood pressure of 85/50 mm Hg, his length was2 y; K2 u/ q* k4 K& f! \: V
90 cm (>97th percentile), and his weight was 14.4 kg
; w8 X# r; A5 [(also >97th percentile). The observed yearly growth4 p. W) D4 G8 L/ Z9 g
velocity was 30 cm (12 inches). The examination of6 U% j4 k2 V& B8 {+ O
the neck revealed no thyroid enlargement.
$ O1 g0 ^. I+ b8 a; P3 p/ y3 UThe genitourinary examination was remarkable for
& P3 s. N  S; P5 W% T" E4 {  qenlargement of the penis, with a stretched length of: R+ N: w) q1 |; ~5 Q) ~
8 cm and a width of 2 cm. The glans penis was very well
- D6 b# H  S" g$ F/ m3 zdeveloped. The pubic hair was Tanner II, mostly around* I3 s4 Z; ]- w7 t( c6 @
540
" ]2 m( e7 B$ C; E1 x+ l) Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 j5 Q) y0 D  j% ]  Pthe base of the phallus and was dark and curled. The
5 H% c1 t/ t" t# M% h' Ctesticular volume was prepubertal at 2 mL each.0 c4 k$ _( f7 J6 O
The skin was moist and smooth and somewhat
1 B8 u! [2 f# d) K. ~! N& Zoily. No axillary hair was noted. There were no
9 T. }, E' O  v5 A$ o! ]+ habnormal skin pigmentations or café-au-lait spots.  O% }, F* Z0 o# a  m. T
Neurologic evaluation showed deep tendon reflex 2+
5 u. C: e8 O7 Q( L! r% u; Xbilateral and symmetrical. There was no suggestion" J. o0 E& `) j
of papilledema.. m% Z/ k6 T. J- B! y0 c
Laboratory Evaluation
) a( b+ y; c; uThe bone age was consistent with 28 months by9 B! {" L) k% Z; a4 `0 Z! F1 W: d
using the standard of Greulich and Pyle at a chrono-
/ e( F- ~4 `. o) |# c5 Clogic age of 16 months (advanced).5 Chromosomal4 k. S" {  X1 ]4 V! w
karyotype was 46XY. The thyroid function test
, h0 h9 C& C2 y- ]. i" q: d. r1 E3 Ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-( L+ ^3 Z# [+ U8 `- s/ ^
lating hormone level was 1.3 µIU/mL (both normal).8 y) [& i6 o4 b+ @, Y; M
The concentrations of serum electrolytes, blood
5 j4 m# W" G# b5 T( _urea nitrogen, creatinine, and calcium all were, M; v, C# [; r' n
within normal range for his age. The concentration
- g6 ]+ V1 C% Q5 G3 Hof serum 17-hydroxyprogesterone was 16 ng/dL
+ u4 v2 U0 K0 V1 X: H(normal, 3 to 90 ng/dL), androstenedione was 20: B! |' ?$ B! R, Q  R" }. T
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! |/ C- k+ i5 \! @9 [$ M3 v. {+ |terone was 38 ng/dL (normal, 50 to 760 ng/dL),
; W5 W; K+ j* l: wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 s7 N& x  v8 [) y  k5 b49ng/dL), 11-desoxycortisol (specific compound S)
$ y' w' ^5 C/ \& @: z, Rwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" b7 l9 j, P) G0 n; b) D
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# a! \. ~0 |: M6 }% q# |# `" s
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 ~+ c! z; `, G9 R2 Eand β-human chorionic gonadotropin was less than
. k. I* P: F! m5 mIU/mL (normal <5 mIU/mL). Serum follicular
) t+ n# G6 ?: A+ Z; A2 c# E' L0 p' {5 Astimulating hormone and leuteinizing hormone0 B& q$ h7 L6 {
concentrations were less than 0.05 mIU/mL
' G1 I/ T$ l* D' d8 W0 Y7 X(prepubertal).
' M) t% W' J  z/ X- DThe parents were notified about the laboratory
, I' X1 J9 ?7 _' R8 O7 P* X5 i: Cresults and were informed that all of the tests were9 I, W) d4 m' L1 [3 ^6 B5 _$ ]
normal except the testosterone level was high. The
. ?* d9 u0 ]$ f6 P: I- K) A2 Xfollow-up visit was arranged within a few weeks to! V. i8 G9 E, l# g! l' x' ]
obtain testicular and abdominal sonograms; how-
" G) H- R- }0 T4 u' `0 W! lever, the family did not return for 4 months.
0 B! u1 f/ Q( ^3 K* {" L- c# BPhysical examination at this time revealed that the3 I: \% H7 o1 E; o4 Z- p
child had grown 2.5 cm in 4 months and had gained
, z  h/ J4 R- k5 Z2 kg of weight. Physical examination remained$ s; z3 o' x0 W' O8 M# h
unchanged. Surprisingly, the pubic hair almost com-2 u5 ]( J, j4 z+ q, a! a
pletely disappeared except for a few vellous hairs at
/ }3 E0 B6 D1 W/ R( U8 V0 g; Sthe base of the phallus. Testicular volume was still 2$ h: J6 `) o! F3 f& D
mL, and the size of the penis remained unchanged.0 c/ Q1 e. F& M% m. S+ N& _
The mother also said that the boy was no longer hav-
% `8 T4 L. H. ~/ m0 cing frequent erections." A! A5 w# q, n2 M! C! e% F
Both parents were again questioned about use of
& z7 Z1 F* b, m+ s6 b. B2 a( Z: Wany ointment/creams that they may have applied to8 B2 @! \# M  R! m; S& N
the child’s skin. This time the father admitted the: f) q* n/ ^4 ~+ j# ]
Topical Testosterone Exposure / Bhowmick et al 5415 Q( Y7 f7 w/ t) p8 T
use of testosterone gel twice daily that he was apply-
! t" ~4 X% ~- G9 g$ N& P) jing over his own shoulders, chest, and back area for+ T8 }4 k! ?+ y9 A3 n5 C
a year. The father also revealed he was embarrassed+ k) @/ E2 _* Q# d7 f$ M
to disclose that he was using a testosterone gel pre-
( v8 Y/ P6 @9 {6 r4 M9 D! Ascribed by his family physician for decreased libido$ J( B/ `  d/ @2 {8 \" v$ `* s
secondary to depression.
! B0 U# B4 D% ]: H5 f$ E- ZThe child slept in the same bed with parents.
" [6 T7 W8 F1 \The father would hug the baby and hold him on his
* Y$ V4 O$ {  ^$ y' k1 p* G( Schest for a considerable period of time, causing sig-8 B% b1 S5 p, u4 u
nificant bare skin contact between baby and father.
/ J* O3 I9 M) x( j$ n0 QThe father also admitted that after the phone call,
! o9 E$ V/ M4 E0 [when he learned the testosterone level in the baby& v; Y% U5 p5 N( b$ E' D
was high, he then read the product information1 R7 ?2 H. u0 N5 L  H0 Z; [! T
packet and concluded that it was most likely the rea-5 C+ K5 h& g1 R! k
son for the child’s virilization. At that time, they
1 w8 g$ X: K% G8 edecided to put the baby in a separate bed, and the$ B0 Z( a  Q5 v* q6 ?
father was not hugging him with bare skin and had
! S% @, b; b0 A7 p$ Dbeen using protective clothing. A repeat testosterone
0 P4 F8 Q; f5 ?, x5 k3 Htest was ordered, but the family did not go to the6 ]/ g: X0 }$ a8 ~! v% \7 Q0 w: T
laboratory to obtain the test.
$ m- b5 Q3 K4 Z3 _8 e' iDiscussion
; z# ^2 w& q0 P8 ?6 B4 ]Precocious puberty in boys is defined as secondary% O4 r& g* g$ H4 T  \
sexual development before 9 years of age.1,42 n3 ]; P0 E! o, d: |  s' @  G
Precocious puberty is termed as central (true) when
+ C1 l# p, M4 ^3 S1 O8 o* Rit is caused by the premature activation of hypo-
$ I  q/ I) R- |! a! g; gthalamic pituitary gonadal axis. CPP is more com-5 B( |5 @6 P" D0 n, }2 p6 C
mon in girls than in boys.1,3 Most boys with CPP  p- ^- @# K6 N
may have a central nervous system lesion that is$ R# k. S" R" t' V- d  C& J9 |
responsible for the early activation of the hypothal-  V' @% V6 b+ o" `/ N; p
amic pituitary gonadal axis.1-3 Thus, greater empha-" S8 Q: q. S+ _  d  e: p2 x( F
sis has been given to neuroradiologic imaging in! `( ~- ]5 R# d- H) D% t1 q
boys with precocious puberty. In addition to viril-  t8 x# N% r/ X" u1 C9 d
ization, the clinical hallmark of CPP is the symmet-
- H5 b6 ~/ x5 Z6 z4 h' Orical testicular growth secondary to stimulation by
. w0 b" v' T6 M3 G8 N! `. ]+ Mgonadotropins.1,3
7 t# o) z' A2 z: ]9 ~8 X( QGonadotropin-independent peripheral preco-
6 D. {5 i4 \! Ycious puberty in boys also results from inappropriate" G9 q- T- {5 E  b. ^/ k4 V" u/ `
androgenic stimulation from either endogenous or/ r+ }* C/ n5 B7 J
exogenous sources, nonpituitary gonadotropin stim-1 m; L4 l* ~( R
ulation, and rare activating mutations.3 Virilizing
( I2 ~6 `9 E1 h# T% `congenital adrenal hyperplasia producing excessive
: s% a9 Y' i  U5 x) }. P6 ~adrenal androgens is a common cause of precocious5 \3 B* }* ^# _
puberty in boys.3,4. h/ ]( h; b9 L
The most common form of congenital adrenal
" Y$ k/ @# L: L# U2 ]hyperplasia is the 21-hydroxylase enzyme deficiency.
0 a* R$ |! Y2 s% H4 ^9 TThe 11-β hydroxylase deficiency may also result in
0 C9 z0 g, A$ F$ {  L6 Pexcessive adrenal androgen production, and rarely,
3 |# t! ~2 m( j2 L! Q9 Dan adrenal tumor may also cause adrenal androgen
0 v  O6 `  S  v$ k+ aexcess.1,38 A9 h& m9 ]6 h* p; M2 i+ m+ e
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  Z! G  z! k8 y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 ~$ I$ @: o, O( w9 i/ S0 dA unique entity of male-limited gonadotropin-; P8 ^- M! R* D' y% `# N, C
independent precocious puberty, which is also known9 f! N1 y+ J, t# X  l
as testotoxicosis, may cause precocious puberty at a4 ]  e% ~$ E; P( ^
very young age. The physical findings in these boys  M# U  |: T: y7 S+ _' f
with this disorder are full pubertal development,
" a* y7 Z% a9 z% @  J" ^' z. Xincluding bilateral testicular growth, similar to boys4 E8 \4 c3 N: G2 c
with CPP. The gonadotropin levels in this disorder, B) m3 @# k1 K* O
are suppressed to prepubertal levels and do not show
; ~# p2 _% z! ?pubertal response of gonadotropin after gonadotropin-# O+ b8 n" ?& \
releasing hormone stimulation. This is a sex-linked7 c8 d; K0 n; Z3 [" ~
autosomal dominant disorder that affects only
7 ?% h. Y" ]/ G9 v& K7 b/ S) ]males; therefore, other male members of the family
* D2 o! {( V6 D. Y! c1 cmay have similar precocious puberty.37 s1 ^9 o6 K  U" A' y: f4 |/ N
In our patient, physical examination was incon-( c- Z5 E; W6 `7 T8 r3 B( r7 o
sistent with true precocious puberty since his testi-
* V# Q0 q% x9 E$ kcles were prepubertal in size. However, testotoxicosis+ A( \% l7 q  o3 M7 g
was in the differential diagnosis because his father
, d+ H$ A  b6 t* l! H# hstarted puberty somewhat early, and occasionally,
* u8 D0 `( {1 R" c( [8 vtesticular enlargement is not that evident in the# b+ b! o% t4 I3 {- b, }+ x) h8 L4 X
beginning of this process.1 In the absence of a neg-; s6 {7 h+ f; {: k- `
ative initial history of androgen exposure, our
% P! T5 n4 ~. t2 k6 ?, F! ?biggest concern was virilizing adrenal hyperplasia,
* Z" I' S1 C; w9 T# `9 Seither 21-hydroxylase deficiency or 11-β hydroxylase
/ A5 T- s2 x5 G3 A$ \4 O: K/ Mdeficiency. Those diagnoses were excluded by find-
" x+ i; z$ v. L4 ring the normal level of adrenal steroids.3 m8 H6 V. q/ t1 Q5 `/ i) p
The diagnosis of exogenous androgens was strongly
6 _. y! F8 i* z: l. D/ g! Xsuspected in a follow-up visit after 4 months because
0 c$ \  v" l. N6 }9 W5 q/ L+ S6 R' Ythe physical examination revealed the complete disap-* }6 Z; v# i7 C9 Z  o0 ^
pearance of pubic hair, normal growth velocity, and. z9 F4 g$ S; b- a1 R
decreased erections. The father admitted using a testos-
5 c( \! P! y* Y  {" B9 V0 _/ Dterone gel, which he concealed at first visit. He was
4 g( N" t( b; Gusing it rather frequently, twice a day. The Physicians’
3 h+ e0 c! P0 mDesk Reference, or package insert of this product, gel or- _- _8 ]- \0 J7 Y$ l' s
cream, cautions about dermal testosterone transfer to2 I! Z2 z4 I0 b( R
unprotected females through direct skin exposure.8 e4 s( O# b6 k2 h3 m: W
Serum testosterone level was found to be 2 times the( O9 `, \% |0 Q" C4 D2 b
baseline value in those females who were exposed to5 }, P/ p0 b' t2 m2 M; d. }4 V
even 15 minutes of direct skin contact with their male
) J4 D1 T$ t$ Y$ o# |; n* spartners.6 However, when a shirt covered the applica-
2 `6 L0 |/ E& M5 c' Ttion site, this testosterone transfer was prevented.4 l) K5 j! Q% K5 [2 N0 D' n4 j
Our patient’s testosterone level was 60 ng/mL,6 v' I  E9 M9 n6 J/ Z
which was clearly high. Some studies suggest that( P' I" ?3 _4 _3 a: U- t  Y
dermal conversion of testosterone to dihydrotestos-4 C9 i) B; A) Q- v+ J4 z
terone, which is a more potent metabolite, is more: g1 J' ]' l8 V  [: b# |; a$ m/ Z) T
active in young children exposed to testosterone! o& \' X+ |# t2 z/ K) f
exogenously7; however, we did not measure a dihy-: W4 Y5 |9 ?; [0 q0 `) @
drotestosterone level in our patient. In addition to
6 x' ^3 E2 v0 W: ]0 tvirilization, exposure to exogenous testosterone in
: v0 `: ?$ P3 Pchildren results in an increase in growth velocity and
8 t8 @% l; I; g) J3 }, E- E; a) Zadvanced bone age, as seen in our patient.* o  X$ e/ t! Y5 a. {) ~4 Y8 }0 K
The long-term effect of androgen exposure during
5 z: ^# m' L- X; o* x; ^early childhood on pubertal development and final
' ]" S  `! p/ Yadult height are not fully known and always remain0 `- x! w$ V/ w% Y# ^. ]! v! c
a concern. Children treated with short-term testos-
$ G: y$ l4 j; ~, B) rterone injection or topical androgen may exhibit some
! g; L6 k* L) ?# xacceleration of the skeletal maturation; however, after& g7 s* j7 z7 q6 F) L7 A) P1 ?
cessation of treatment, the rate of bone maturation
8 W! R7 q) K- }, @decelerates and gradually returns to normal.8,96 t% H0 a$ b! s) D0 d3 `+ m
There are conflicting reports and controversy
7 C  R/ w- }. R8 c3 U9 ~& w) aover the effect of early androgen exposure on adult
- {- n& W, J% Tpenile length.10,11 Some reports suggest subnormal
7 H7 r: k0 K! [" b6 j6 ^adult penile length, apparently because of downreg-
0 d+ k5 g# k" kulation of androgen receptor number.10,12 However,
0 I) n1 n' U$ C1 ~  t+ CSutherland et al13 did not find a correlation between
4 Z- D6 l# @+ P' ]( hchildhood testosterone exposure and reduced adult
* I8 {; o5 J$ xpenile length in clinical studies.
4 [" l9 ?6 K/ ]4 L; D- {" FNonetheless, we do not believe our patient is
* c' F. W9 K5 Qgoing to experience any of the untoward effects from
8 S! ~& b, H% B$ Btestosterone exposure as mentioned earlier because
# o8 h  ]% ]9 t" H! t# o- pthe exposure was not for a prolonged period of time.
6 P5 u# q9 K5 Q3 q& CAlthough the bone age was advanced at the time of: Z' B6 v9 C' [
diagnosis, the child had a normal growth velocity at
' f' i5 a8 F1 N& d" T7 }% Lthe follow-up visit. It is hoped that his final adult; |  m: N- _1 N- {1 S, y8 g
height will not be affected.9 E. W9 k, V9 p7 U& L- G
Although rarely reported, the widespread avail-
4 @: N8 K% B: M  _ability of androgen products in our society may
4 Y+ U0 z. Y6 M2 f7 r1 Eindeed cause more virilization in male or female# Y" ~1 g& Y7 y
children than one would realize. Exposure to andro-
' s# E6 j* |+ N5 @gen products must be considered and specific ques-$ c- J; r" G  w/ T+ R3 k
tioning about the use of a testosterone product or/ s! G0 \) t4 P7 ]8 R4 S) C2 K
gel should be asked of the family members during7 B3 ?5 U$ f) |5 C- D4 D' Q# C( s* F
the evaluation of any children who present with vir-8 F; \4 N# `5 ]& @! O# z
ilization or peripheral precocious puberty. The diag-
" k% e+ \% L% w! l4 i$ znosis can be established by just a few tests and by# T+ Y; ]8 E# O% Q& f+ _( T
appropriate history. The inability to obtain such a
6 \7 t  M& e' V% C4 _2 khistory, or failure to ask the specific questions, may/ k2 G6 x; F+ o' f5 h' s7 n5 t
result in extensive, unnecessary, and expensive/ i9 d: y5 T1 K, ]+ k
investigation. The primary care physician should be3 j0 K4 V1 {) t: G1 k9 {5 e/ l
aware of this fact, because most of these children5 k- G! X1 s, Y) _
may initially present in their practice. The Physicians’
4 t5 b! {5 X. q8 J% @  q, }; xDesk Reference and package insert should also put a' @) b; O/ r  Y6 G  ?
warning about the virilizing effect on a male or* K- y; M% Q- p  G
female child who might come in contact with some-
+ ?4 m4 m. F+ Rone using any of these products.! k$ Y& y: ?4 n) h1 |7 t
References/ Y( u0 H: v. {2 t" ^; m
1. Styne DM. The testes: disorder of sexual differentiation
; V) x2 [8 Q2 l% i8 C1 f# eand puberty in the male. In: Sperling MA, ed. Pediatric2 B4 w4 }* F8 @, _3 x8 o
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;/ H4 {$ a/ B* E( C. |3 F
2002: 565-628.3 I( B! c9 l; x2 @( P0 L
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 {1 S6 R3 W( w/ ~, }, B, D; _( a- ~puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old1 Z/ ?2 o' m  h& A7 N+ J9 [5 m
Boy Induced by Indirect Topical% L* D- v6 ]. A2 I9 L4 n! z  r/ C
Exposure to Testosterone: B- A- q& p* \6 \% R2 F0 t
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 W# _5 G# Z* n# Y9 e0 u$ I. [
and Kenneth R. Rettig, MD1
! s- J- w9 u$ \: eClinical Pediatrics
8 Z8 |: s3 T2 _5 \Volume 46 Number 6% F% x$ O  I+ b7 K' W, f$ u
July 2007 540-5435 g1 n4 I7 c+ n5 A
© 2007 Sage Publications0 k4 H8 r+ {; q- D/ t! I  e
10.1177/0009922806296651
! i) M! I# \! ~http://clp.sagepub.com
: H: m  h$ q# ?hosted at
* J2 @4 |/ t% G6 N2 H; l. S: nhttp://online.sagepub.com' E. Y: g% T: H" p
Precocious puberty in boys, central or peripheral,: }% h6 a5 H# {$ B; [
is a significant concern for physicians. Central% [: y3 ?9 u) d6 t
precocious puberty (CPP), which is mediated
* `' p4 O7 j, V# R% s. }* U8 |through the hypothalamic pituitary gonadal axis, has
$ w1 i( v( t% p4 B6 U7 Ca higher incidence of organic central nervous system- W# K- ~% C9 v2 k
lesions in boys.1,2 Virilization in boys, as manifested
- Y' p( o. S& ]by enlargement of the penis, development of pubic
$ x  }- P4 h, Z' I# l; S( Ohair, and facial acne without enlargement of testi-. H/ c3 y6 L7 r  c* R1 z# w
cles, suggests peripheral or pseudopuberty.1-3 We% n% N  C& k5 R5 q' e
report a 16-month-old boy who presented with the
: i1 O: b3 @$ aenlargement of the phallus and pubic hair develop-
+ }( O( \2 s% V8 G4 ?6 h5 O$ s# Oment without testicular enlargement, which was due1 O. G( n2 H: o5 l
to the unintentional exposure to androgen gel used by
2 _4 ]& X# ?6 S7 {( jthe father. The family initially concealed this infor-! j0 L, o: K2 W! i
mation, resulting in an extensive work-up for this
4 y6 I" g7 r% a1 `6 W; Vchild. Given the widespread and easy availability of
: H  A: L" s$ B+ U6 Xtestosterone gel and cream, we believe this is proba-% [  q: U  ]0 z' e
bly more common than the rare case report in the
4 `2 l7 N- C! K) Z/ Y$ k- w0 mliterature.4
. Y9 n/ L; H4 g% {Patient Report
( r- O, B" C' Q7 Q+ e$ JA 16-month-old white child was referred to the. K3 }- t( {) T7 V: ]1 `0 T
endocrine clinic by his pediatrician with the concern
" u3 P7 \; k7 f& |  V8 Q6 L+ Eof early sexual development. His mother noticed- I7 u7 m3 E. }6 k8 P
light colored pubic hair development when he was/ x$ L( H# i) h5 L& V: a. k& \
From the 1Division of Pediatric Endocrinology, 2University of
% I) v, e' e1 {( Z: u2 vSouth Alabama Medical Center, Mobile, Alabama.0 y' a$ Z+ b8 X+ ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,
( p$ ]/ k2 k+ b- `6 T7 E" ?Professor of Pediatrics, University of South Alabama, College of/ j- G7 Y/ w, }& {9 y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! ?* P6 t( ]" x5 o3 n2 de-mail: [email protected].9 m' \6 \" L+ A
about 6 to 7 months old, which progressively became
% m! o8 J1 H/ @% A- Zdarker. She was also concerned about the enlarge-  k  A# t' D) H' Y& n$ ^) Y2 Y7 G
ment of his penis and frequent erections. The child% e% U0 Q4 U* A0 ~! i- y3 a; q; z& i
was the product of a full-term normal delivery, with
; z% S6 x) T2 ~9 Q6 Q/ ba birth weight of 7 lb 14 oz, and birth length of
- m& U9 r: T% f20 inches. He was breast-fed throughout the first year
& b8 a* b$ F- A8 m8 uof life and was still receiving breast milk along with! `1 V: U( S1 u8 q
solid food. He had no hospitalizations or surgery,+ f$ [0 N: `5 y) h$ L, Z' b! ?5 ~
and his psychosocial and psychomotor development
( k0 Y0 e( w& f% E- Z) lwas age appropriate.6 ]/ H' N; _+ y1 ~
The family history was remarkable for the father,
8 i  w. y* `6 U/ s9 @who was diagnosed with hypothyroidism at age 16,% Y4 U1 H) Y+ F: s7 K/ u
which was treated with thyroxine. The father’s: F. w: w  Z: r4 e) q
height was 6 feet, and he went through a somewhat) b/ ?- g, d3 ^2 n5 f& N
early puberty and had stopped growing by age 14.1 S5 J" l7 Y6 n/ j7 q% {; y0 y) r
The father denied taking any other medication. The
2 Q3 O. [+ J+ l, o. {+ U) Mchild’s mother was in good health. Her menarche
, l9 f( N# Z0 M1 H2 q. awas at 11 years of age, and her height was at 5 feet
' ?( i* e9 w% }5 inches. There was no other family history of pre-
7 r! L9 U; }4 x- ^cocious sexual development in the first-degree rela-
. L7 m' J1 q, A% Wtives. There were no siblings.
1 t' F% j8 B  _8 t: I; s9 k4 zPhysical Examination
+ {& |8 V0 V0 S! [0 P' W) @+ RThe physical examination revealed a very active,
4 i* K# X7 i  Qplayful, and healthy boy. The vital signs documented
1 m4 [  T' m" ^( w; ia blood pressure of 85/50 mm Hg, his length was, E  U5 e6 y, e( l; F
90 cm (>97th percentile), and his weight was 14.4 kg0 R; V& O  x3 f! u2 S6 w
(also >97th percentile). The observed yearly growth" }, A0 j4 U6 ]7 F$ i
velocity was 30 cm (12 inches). The examination of
: b7 `9 n( T) S' jthe neck revealed no thyroid enlargement.! {4 S! b4 X4 p& G5 v9 Y4 h! w
The genitourinary examination was remarkable for3 v* n6 l% }/ n7 E6 m7 L' X
enlargement of the penis, with a stretched length of
2 l0 w" R2 V6 Z7 p+ t" i9 H0 i( Q8 cm and a width of 2 cm. The glans penis was very well  j) Y) T9 L9 K1 }4 M+ U
developed. The pubic hair was Tanner II, mostly around9 d; \" R5 k/ e& ^
540
4 K- J9 J: N+ a7 |; Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 D3 U; Y4 w% I* mthe base of the phallus and was dark and curled. The
$ C( o' M" ]. H! @& S% R: }testicular volume was prepubertal at 2 mL each.! [2 s+ I8 ~0 {  F& S' o) f4 M
The skin was moist and smooth and somewhat
; S( z2 ]# R' ?$ v: q* e! foily. No axillary hair was noted. There were no* S1 _! c8 I  t1 B0 j
abnormal skin pigmentations or café-au-lait spots.
9 E2 V! \/ Q) f2 I* I# C1 NNeurologic evaluation showed deep tendon reflex 2+1 ?6 _8 I% n+ W7 }4 B% b
bilateral and symmetrical. There was no suggestion7 H# [9 M- e: k/ W
of papilledema.( @2 ]2 l9 R; X
Laboratory Evaluation+ h7 D: R2 E$ v# j: v  F! }
The bone age was consistent with 28 months by  ]2 c0 M$ [8 l  v2 k  v3 `8 {
using the standard of Greulich and Pyle at a chrono-
3 B( u  p( r* Qlogic age of 16 months (advanced).5 Chromosomal
' R* r* b! n% B2 b; W. H2 ~karyotype was 46XY. The thyroid function test1 }  j" M$ h5 x5 A/ U
showed a free T4 of 1.69 ng/dL, and thyroid stimu-" \0 X; J5 ~! W1 G
lating hormone level was 1.3 µIU/mL (both normal).
4 W" K$ ]0 r+ C3 j) PThe concentrations of serum electrolytes, blood
7 |' E6 R# D( @5 Hurea nitrogen, creatinine, and calcium all were
! T% E9 W6 K! E$ ?9 s4 S. h" B6 uwithin normal range for his age. The concentration7 ?" q# ^3 {4 Q7 I- l
of serum 17-hydroxyprogesterone was 16 ng/dL# ?3 y  P( L; K1 X* L. t, Z( z8 a
(normal, 3 to 90 ng/dL), androstenedione was 20
6 {  W* d7 I  b: Ong/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ |8 {& C: l8 [9 ^! V
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 i/ J" E- d" C+ xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
% P% a# v8 }# V: i3 R49ng/dL), 11-desoxycortisol (specific compound S)
/ Z' O( I( F9 W1 [! wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) d* |2 k% t( a) X( K( Ttisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total6 d) P0 E+ {( w! H) R
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* G; c3 Z& }' O3 Mand β-human chorionic gonadotropin was less than0 x: ^' `: p; I1 |; E  O2 f
5 mIU/mL (normal <5 mIU/mL). Serum follicular/ w  s1 ^1 E, D# C$ L
stimulating hormone and leuteinizing hormone
$ [( a5 }& l. J3 w4 nconcentrations were less than 0.05 mIU/mL1 r" e# k% k# R) ]: ~
(prepubertal)." x0 g# q8 F$ a: }" c0 E
The parents were notified about the laboratory
& Y6 X) F' ^2 U# }8 a* v% fresults and were informed that all of the tests were( |0 j$ @) |) o/ m0 g" i2 K$ {& l
normal except the testosterone level was high. The
4 E6 U# i* \# y  Z$ n1 `follow-up visit was arranged within a few weeks to- S( E9 D% f& r* R9 j
obtain testicular and abdominal sonograms; how-6 W  q. x: l9 p; q* Y8 V# o8 `
ever, the family did not return for 4 months.1 x# C/ t" d# i7 f* F5 _
Physical examination at this time revealed that the2 ?7 w9 g( r, Y6 u% V/ G. F$ g5 g$ m
child had grown 2.5 cm in 4 months and had gained
+ b- @) w; \$ b; }2 kg of weight. Physical examination remained
! H! p% R0 Z/ ^9 i; J+ Tunchanged. Surprisingly, the pubic hair almost com-
- j' z, I  G0 n6 b, J+ spletely disappeared except for a few vellous hairs at- m4 C4 I, @. B/ z7 X9 ?6 U
the base of the phallus. Testicular volume was still 2
4 K, s' u* n- K/ `. \mL, and the size of the penis remained unchanged.
- [( H+ F' M5 X0 p% f4 tThe mother also said that the boy was no longer hav-
- g) A' ^- w% v* Z' n' Xing frequent erections.
* K6 |. _+ W% C# UBoth parents were again questioned about use of3 z- x! s. H' ~( m
any ointment/creams that they may have applied to
, W+ X1 M' v; B1 W1 m* H2 \the child’s skin. This time the father admitted the
% T* b/ x. p( G! {$ rTopical Testosterone Exposure / Bhowmick et al 541( R3 p5 h0 s5 ?/ |! m/ N
use of testosterone gel twice daily that he was apply-5 B4 r4 [3 x! e1 K2 i2 j
ing over his own shoulders, chest, and back area for
: t: J, p3 H9 B0 La year. The father also revealed he was embarrassed
: i& o' a# c" q+ F. Y+ T* h$ ~to disclose that he was using a testosterone gel pre-
6 ^5 L& i* B  k) Yscribed by his family physician for decreased libido
: k) [! d1 D9 s$ k2 ssecondary to depression.! u' K, S7 X2 ]+ i8 `/ t
The child slept in the same bed with parents.
- t2 t8 n+ N3 o6 K, o5 J$ sThe father would hug the baby and hold him on his9 s+ K3 a$ \  B% ~+ K
chest for a considerable period of time, causing sig-
, v, q$ g- G7 R& o- `nificant bare skin contact between baby and father.; i7 G1 I1 {4 |) E
The father also admitted that after the phone call,
7 u. g" V2 C: X4 `% ywhen he learned the testosterone level in the baby
3 Q; |; R- s8 a- s& fwas high, he then read the product information5 d9 b7 z8 F5 c# ]- s: Z1 v
packet and concluded that it was most likely the rea-
8 p% v  d" s/ u( H7 `son for the child’s virilization. At that time, they' P- X/ @* K" [6 ?2 r
decided to put the baby in a separate bed, and the/ k0 g, q) K; U. I
father was not hugging him with bare skin and had, c+ w# [1 y+ |
been using protective clothing. A repeat testosterone
; B6 Q/ t: v9 itest was ordered, but the family did not go to the
- l: K6 R7 t* v% glaboratory to obtain the test.5 j9 u" K  a0 |, ~) I
Discussion+ @# q3 b9 `$ d1 W
Precocious puberty in boys is defined as secondary
8 r8 ?# f1 X" a1 ksexual development before 9 years of age.1,4
6 n9 o. z! n6 XPrecocious puberty is termed as central (true) when: x/ U: q. S$ M( S+ V
it is caused by the premature activation of hypo-
% O: v0 W7 ]# e# g  J; _- Wthalamic pituitary gonadal axis. CPP is more com-
8 Q' X( j; t5 P' kmon in girls than in boys.1,3 Most boys with CPP1 o' o6 S  l$ B) ~
may have a central nervous system lesion that is5 x) l9 n' z7 J' O
responsible for the early activation of the hypothal-
$ J" I1 q' ^0 e# J( tamic pituitary gonadal axis.1-3 Thus, greater empha-  Y+ R  M; T+ C$ g1 v
sis has been given to neuroradiologic imaging in
8 d# j6 [0 d+ M/ s2 Lboys with precocious puberty. In addition to viril-  Z. X7 N0 O+ {0 A" ?1 p, z+ }1 {/ a
ization, the clinical hallmark of CPP is the symmet-5 ^! V, f& q/ [
rical testicular growth secondary to stimulation by- B5 W% L8 z1 L- \! v0 z# ?& [
gonadotropins.1,3; U# {/ u: Q4 f. V
Gonadotropin-independent peripheral preco-
* L: {6 W- o7 Z" X: Q- Q% ycious puberty in boys also results from inappropriate. Y+ L  [( w! [5 z. W
androgenic stimulation from either endogenous or9 X2 A$ y9 j  p- u4 c
exogenous sources, nonpituitary gonadotropin stim-
6 ~, b" A# i2 N9 D- k# [  julation, and rare activating mutations.3 Virilizing+ h, W. }6 f% @1 N
congenital adrenal hyperplasia producing excessive
4 {: g! x: f1 n, iadrenal androgens is a common cause of precocious$ M! s3 a, j3 O9 A2 d; q! H2 ~, i2 ~
puberty in boys.3,4
3 H8 R9 j( |; o' }* B5 lThe most common form of congenital adrenal
# @+ A4 I* z" lhyperplasia is the 21-hydroxylase enzyme deficiency.* ~; J. i7 [$ n5 t5 I
The 11-β hydroxylase deficiency may also result in
+ v. P6 o9 H4 a, c) k6 O) Sexcessive adrenal androgen production, and rarely,
% P; r7 h' p' }' i, Gan adrenal tumor may also cause adrenal androgen! m' T7 U0 s2 H+ p4 Z
excess.1,32 z, g2 k) l  ~* \2 k) M- j  A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" L- \, O5 u5 M
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007" z& Y' M7 i' R; s1 z6 w
A unique entity of male-limited gonadotropin-0 f. F+ L. \8 w; ^( J  X/ _
independent precocious puberty, which is also known
0 E, v4 E$ u% t' H% }: M4 Fas testotoxicosis, may cause precocious puberty at a
6 v5 C' r% h* C. Y! @/ A# R7 Svery young age. The physical findings in these boys! I' ?, `$ ]& q' ]. R
with this disorder are full pubertal development,! ~) Z+ a- a* O' Y! k* n' f
including bilateral testicular growth, similar to boys
  |  B- k  x( B" i3 nwith CPP. The gonadotropin levels in this disorder
  S2 P2 o9 h/ E' @3 m+ zare suppressed to prepubertal levels and do not show
% y$ p; B1 T( D9 Ypubertal response of gonadotropin after gonadotropin-
- E3 w% W( C4 i. {" p/ V& dreleasing hormone stimulation. This is a sex-linked( D+ p/ p2 X  P6 \( x- _
autosomal dominant disorder that affects only6 u+ D& ^$ w8 o6 L2 O" }% X
males; therefore, other male members of the family
4 C7 D  \. U  X* g1 f$ {may have similar precocious puberty.3
* h* c& T7 V  ?! [1 f  }9 n& uIn our patient, physical examination was incon-, u- _7 \; R. [9 C4 X8 ^" e- F
sistent with true precocious puberty since his testi-
: i0 c) o9 J3 l  p. }7 Rcles were prepubertal in size. However, testotoxicosis
( Z, o! R- {/ e' k6 @was in the differential diagnosis because his father; j, W: N7 W; {: D$ t4 Y
started puberty somewhat early, and occasionally,$ k, M7 z& j: ^* t9 @
testicular enlargement is not that evident in the
1 v" _* i; H! g7 g* X$ ibeginning of this process.1 In the absence of a neg-- N; I: Z# z+ a4 M3 y5 V
ative initial history of androgen exposure, our3 n' j+ |! x6 [0 B6 _
biggest concern was virilizing adrenal hyperplasia,# Z2 j+ \# U1 J, r
either 21-hydroxylase deficiency or 11-β hydroxylase
0 K* c: B( P. E, _deficiency. Those diagnoses were excluded by find-3 m+ c  a: Q- I. L/ }6 I- V# d% c
ing the normal level of adrenal steroids.3 n3 t9 l/ S4 c# O- f
The diagnosis of exogenous androgens was strongly  D: }0 ?- u* s$ u1 o. n6 o7 x
suspected in a follow-up visit after 4 months because5 E5 `2 t, U( d
the physical examination revealed the complete disap-
. Q' F- q; ~7 {2 e& N- Dpearance of pubic hair, normal growth velocity, and
6 v( c$ _# i; T: W) Ddecreased erections. The father admitted using a testos-1 M8 r4 ~9 P  J& N4 E
terone gel, which he concealed at first visit. He was3 f" k+ F2 ?% U  ^! D7 z8 x/ N, |
using it rather frequently, twice a day. The Physicians’1 I. b6 R- p8 D' {
Desk Reference, or package insert of this product, gel or6 o& b4 @8 I/ j, s
cream, cautions about dermal testosterone transfer to5 K% j8 m9 |# x
unprotected females through direct skin exposure.
, F8 s% z. O$ R9 s8 X/ ?! J! sSerum testosterone level was found to be 2 times the
' ~4 q, {, ]: V1 L" @+ U6 l* ^baseline value in those females who were exposed to, K& r8 s- V% q  n, Z7 Z+ X  u" a
even 15 minutes of direct skin contact with their male
$ {9 X5 k3 Z+ a6 z. g7 vpartners.6 However, when a shirt covered the applica-+ A( t" K+ A& l* b
tion site, this testosterone transfer was prevented.4 `. ~! E  q' {( L
Our patient’s testosterone level was 60 ng/mL,9 [' y5 z& w" Z* X/ |
which was clearly high. Some studies suggest that
4 L9 K7 ?) \% }2 K4 qdermal conversion of testosterone to dihydrotestos-$ N- N0 @% n6 m7 f4 K# M
terone, which is a more potent metabolite, is more* J! F# A5 Q# I; ^1 L
active in young children exposed to testosterone% L; O* f$ I2 E; d6 [) S
exogenously7; however, we did not measure a dihy-
& n  ^1 a% c0 W# Q( O) Edrotestosterone level in our patient. In addition to
' m! ]5 y- @9 u+ d4 s0 o& Tvirilization, exposure to exogenous testosterone in/ a# K) n$ Z* K& \" T8 I
children results in an increase in growth velocity and
0 I! N9 N9 y  u  f: I5 I2 U" Ladvanced bone age, as seen in our patient.
0 l! \3 V+ @& J: oThe long-term effect of androgen exposure during
+ g9 X" \" o: i' }3 t! Xearly childhood on pubertal development and final
; r7 ~% B; i) ?# B4 t8 gadult height are not fully known and always remain: @# y3 Z7 X: k9 s
a concern. Children treated with short-term testos-
( T5 c; Q: ~4 f0 J7 a# ?- @( }terone injection or topical androgen may exhibit some
; D3 |) o( x' N1 Y6 x) W6 }% Uacceleration of the skeletal maturation; however, after
; h, N2 K4 {8 K7 n/ A9 d/ A/ vcessation of treatment, the rate of bone maturation0 Q% V- U& M4 |  k; W
decelerates and gradually returns to normal.8,9
; ^& M- z4 |" \" H) r  MThere are conflicting reports and controversy* r( m4 d/ B1 n+ F$ L4 R
over the effect of early androgen exposure on adult8 t$ m( `+ s! k/ G2 i0 C% x
penile length.10,11 Some reports suggest subnormal
0 H( Y. D( l) jadult penile length, apparently because of downreg-
0 P. I' ~& V8 P; _2 S0 Nulation of androgen receptor number.10,12 However,# t- Y, {/ H4 p  S
Sutherland et al13 did not find a correlation between# u, `+ G6 T, ^3 x8 o
childhood testosterone exposure and reduced adult1 D/ R& ]% z2 m' d8 F1 G7 s& T; K
penile length in clinical studies.
) |7 |7 h) W  x- dNonetheless, we do not believe our patient is4 _( h& O! G% f9 {
going to experience any of the untoward effects from
- N- w1 `& @% X  _testosterone exposure as mentioned earlier because7 n; e$ H- g$ D& m/ n7 @. ?
the exposure was not for a prolonged period of time.$ W, H% o: `& @2 Z/ N0 N9 ^+ ], J/ S
Although the bone age was advanced at the time of7 ^( {" e. t4 J: A) x3 ?
diagnosis, the child had a normal growth velocity at
8 }9 ^+ z2 ~3 D9 i0 \the follow-up visit. It is hoped that his final adult+ R. m6 Y& l3 ?" e0 f( [2 J
height will not be affected.
  k+ [" D- N. f$ ]/ d2 uAlthough rarely reported, the widespread avail-
( V) A& k4 L) G. w& W8 fability of androgen products in our society may
/ ~+ J# H. m2 d# m+ N8 h8 m) Oindeed cause more virilization in male or female
, \5 m  h- g' Y5 T& h3 e3 x: qchildren than one would realize. Exposure to andro-/ ?& R: I* e  T+ z- z5 k, `6 H4 K
gen products must be considered and specific ques-7 R! s9 n6 M( c/ Z
tioning about the use of a testosterone product or! W& M/ Z8 j# j0 V
gel should be asked of the family members during. ~+ ^" E# t7 h9 A# l6 I
the evaluation of any children who present with vir-) v7 w8 V" H7 B7 k, P- Z
ilization or peripheral precocious puberty. The diag-
  T! N+ Z' R" S/ S& q; F. ?nosis can be established by just a few tests and by
. A4 z/ i+ z2 q9 h" n+ Jappropriate history. The inability to obtain such a; b, w5 V3 g) z9 l; E
history, or failure to ask the specific questions, may
1 g* g4 @8 r4 Q6 q- A# V4 w2 Vresult in extensive, unnecessary, and expensive
/ A9 b3 Y3 e, |investigation. The primary care physician should be/ [2 _! c9 O' ~
aware of this fact, because most of these children9 [* h! {( g: {
may initially present in their practice. The Physicians’
( e% }0 R- g. m; ^Desk Reference and package insert should also put a
, c# C8 P7 G6 ^4 h# X7 ]/ C  ewarning about the virilizing effect on a male or
% E' G, A4 E% `0 b1 U8 e/ efemale child who might come in contact with some-; w  i/ C1 j2 h: w
one using any of these products.
! Z+ F0 t1 l# {2 T( }References, _+ `9 D& y2 E8 A
1. Styne DM. The testes: disorder of sexual differentiation
: g9 R+ n( \. a2 c# \and puberty in the male. In: Sperling MA, ed. Pediatric
' W4 _! b. _" p4 f/ R# REndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
# |% U9 c: d% M. P2002: 565-628.
6 c2 w% a% F/ B4 ~$ L2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- D4 Z8 t* C) Q6 r" r( lpuberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
" A& f0 @* b8 z' x, X& d; `
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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